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@comment{{Command line: bib2bib ../bibli.bib -c 'subject:"csbcbook" or keywords:"csbcbook"' -ob tmp.bib}}
@article{Veer2008Enabling,
author = {{van't Veer}, L. J. and Bernards, R.},
title = {Enabling personalized cancer medicine through analysis of gene-expression
patterns.},
journal = {Nature},
year = {2008},
volume = {452},
pages = {564--570},
number = {7187},
month = {Apr},
abstract = {Therapies for patients with cancer have changed gradually over the
past decade, moving away from the administration of broadly acting
cytotoxic drugs towards the use of more-specific therapies that are
targeted to each tumour. To facilitate this shift, tests need to
be developed to identify those individuals who require therapy and
those who are most likely to benefit from certain therapies. In particular,
tests that predict the clinical outcome for patients on the basis
of the genes expressed by their tumours are likely to increasingly
affect patient management, heralding a new era of personalized medicine.},
doi = {10.1038/nature06915},
pdf = {../local/Veer2008Enabling.pdf},
file = {Veer2008Enabling.pdf:Veer2008Enabling.pdf:PDF},
institution = {Agendia BV, Louwesweg 6, 1066 EC Amsterdam, The Netherlands.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nature06915},
pmid = {18385730},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1038/nature06915}
}
@article{Aguda1999Oncogene,
author = {Aguda, B. D.},
title = {Instabilities in phosphorylation-dephosphorylation cascades and cell
cycle checkpoints},
journal = {Oncogene},
year = {1999},
volume = {18},
pages = {2846-51},
number = {18},
abstract = {The G2-M checkpoint in the cell cycle is identified with a set of
phosphorylation-dephosphorylation (PD) cycles involving Cdc25 and
the maturation-promoting factor (MPF); these PD cycles are coupled
in a way that generates an instability. This instability arises out
of a transcritical bifurcation which could be exploited by the G2
DNA damage checkpoint pathway in order to arrest or delay entry into
mitosis. The coupling between PD cycles involving Wee1 and MPF does
not lead to an instability and therefore Wee1 may not be a crucial
target of the checkpoint pathway. A set of PD cycles exhibiting transcritical
bifurcation also possesses the integrative ability of a checkpoint
for 'checking' that prerequisites are satisfied prior to the next
cell cycle event. Such a set of coupled PD cycles is suggested to
be a core mechanism of cell cycle checkpoints.},
keywords = {csbcbook}
}
@article{Aguda1999PNAS,
author = {Aguda, B. D.},
title = {A quantitative analysis of the kinetics of the G(2) DNA damage checkpoint
system},
journal = {Proc Natl Acad Sci U S A},
year = {1999},
volume = {96},
pages = {11352-7},
number = {20},
abstract = {A detailed model of the G(2) DNA damage checkpoint (G2DDC) system
is presented that includes complex regulatory networks of the mitotic
kinase Cdc2, phosphatase Cdc25, Wee1 kinase, and damage signal transduction
pathways involving Chk1 and p53. Assumptions on the kinetic equations
of the G2DDC are made, and computer simulations are carried out to
demonstrate how the various subsystems operate to delay or arrest
cell cycle progression. The detailed model could be used to explain
various experiments relevant to G2DDC reported recently, including
the nuclear export of 14-3-3-bound Cdc25, the down-regulation of
cyclin B1 expression by p53, the effect of Chk1 and p53 on Cdc25
levels, and Wee1 degradation. It also is shown that, under certain
conditions, p53 is necessary to sustain a G(2) arrest.},
keywords = {csbcbook}
}
@article{Aguda2003CellCycle,
author = {Aguda, B. D. and Algar, C. K.},
title = {A structural analysis of the qualitative networks regulating the
cell cycle and apoptosis},
journal = {Cell Cycle},
year = {2003},
volume = {2},
pages = {538-44},
number = {6},
abstract = {This paper proposes an integration and modular organization of the
complex regulatory networks involved in the mammalian cell cycle,
apoptosis, and related intracellular signaling cascades. A common
node linking the cell cycle and apoptosis permits the possibility
of coordinate control between the initiation of these two cellular
processes. From this node, pathways emanate that lead to the activation
of cyclin-dependent kinases (in the cell cycle) and caspases (in
apoptosis). Computer simulations are carried out to demonstrate that
the proposed network architecture and certain module-module interactions
can account for the experimentally observed sequence of cellular
events (quiescence, cell cycle, and apoptosis) as the transcriptional
activities of E2F-1 and c-Myc are increased. Despite the lack of
quantitative kinetic data on most of the pathways, it is demonstrated
that there can be meaningful conclusions regarding system stability
that arise from the topology of the network. It is shown that only
cycles in the network graph determine stability. Thus, several positive
and negative feedback loops are identified from a literature review
of the major pathways involved in the initiation of the cell cycle
and of apoptosis.},
keywords = {csbcbook}
}
@article{Aguda2007PLOSCompBiol,
author = {Aguda, B. D. and Goryachev, A. B.},
title = {From pathways databases to network models of switching behavior},
journal = {PLoS Comput Biol},
year = {2007},
volume = {3},
pages = {1674-8},
number = {9},
keywords = {csbcbook}
}
@article{Aguda1999CellProl,
author = {Aguda, B. D. and Tang, Y.},
title = {The kinetic origins of the restriction point in the mammalian cell
cycle},
journal = {Cell Prolif},
year = {1999},
volume = {32},
pages = {321-35},
number = {5},
abstract = {A detailed model mechanism for the G1/S transition in the mammalian
cell cycle is presented and analysed by computer simulation to investigate
whether the kinetic origins of the restriction point (R-point) can
be identified. The R-point occurs in mid-to-late G1 phase and marks
the transition between mitogen-dependent to mitogen-independent progression
of the cell cycle. For purposes of computer simulations, the R-point
is defined as the first point in time after mitosis where cutting
off mitogen stimulation does not prevent the cell reaching the threshold
activity of cyclin-E/cdk2 required for entry into S phase. The key
components of the network that generate a dynamic switching behaviour
associated with the R-point include a positive feedback loop between
cyclin-E/cdk2 and Cdc25A, along with the mutually negative interaction
between the cdk inhibitor p27Kip1 and cyclin-E/cdk2. Simulations
of the passage through the R-point were carried out and the factors
affecting the position of the R-point in G1 are determined. The detailed
model also shows various points in the network where the activation
of cyclin-E/cdk2 can be initiated with or without the involvement
of the retinoblastoma protein.},
keywords = {csbcbook}
}
@article{Aguilera2008Genome,
author = {Aguilera, A. and G{\'o}mez-Gonz{\'a}lez, B.},
title = {Genome instability: a mechanistic view of its causes and consequences.},
journal = {Nat. Rev. Genet.},
year = {2008},
volume = {9},
pages = {204--217},
number = {3},
month = {Mar},
abstract = {Genomic instability in the form of mutations and chromosome rearrangements
is usually associated with pathological disorders, and yet it is
also crucial for evolution. Two types of elements have a key role
in instability leading to rearrangements: those that act in trans
to prevent instability--among them are replication, repair and S-phase
checkpoint factors--and those that act in cis--chromosomal hotspots
of instability such as fragile sites and highly transcribed DNA sequences.
Taking these elements as a guide, we review the causes and consequences
of instability with the aim of providing a mechanistic perspective
on the origin of genomic instability.},
doi = {10.1038/nrg2268},
pdf = {../local/Aguilera2008Genome.pdf},
file = {Aguilera2008Genome.pdf:Aguilera2008Genome.pdf:PDF},
institution = {Centro Andaluz de Biologia Molecular y Medicina Regenerativa CABIMER,
Universidad de Sevilla-CSIC, Avd. Américo Vespucio s/n, 41092 Sevilla,
Spain. aguilo@us.es},
keywords = {csbcbook},
owner = {jp},
pii = {nrg2268},
pmid = {18227811},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1038/nrg2268}
}
@book{Alberts2002Molecular,
title = {Molecular Biology of the Cell},
publisher = {Garland Science, Taylor \& Francis Group, LLC},
year = {2002},
author = {Alberts, B. and Johnson, A. and Lewis, J. and Raff, M. and Roberts,
K. and Walter, P.},
note = {Fourth Edition},
annote = {Fourth Edition},
keywords = {csbcbook}
}
@article{Albertson2003Chromosome,
author = {Albertson, D. G. and Collins, C. and McCormick, F. and Gray, J. W.},
title = {Chromosome aberrations in solid tumors},
journal = {Nat. Genet.},
year = {2003},
volume = {34},
pages = {369--376},
number = {4},
month = {Aug},
abstract = {Chromosome aberrations in human solid tumors are hallmarks of gene
deregulation and genome instability. This review summarizes current
knowledge regarding aberrations, discusses their functional importance,
suggests mechanisms by which aberrations may form during cancer progression
and provides examples of clinical advances that have come from studies
of chromosome aberrations.},
doi = {10.1038/ng1215},
pdf = {../local/Albertson2003Chromosome.pdf},
file = {Albertson2003Chromosome.pdf:Albertson2003Chromosome.pdf:PDF},
institution = {Cancer Research Institute, University of California San Francisco,
San Francisco, California 94143-0808, USA. albertson@cc.ucsf.edu},
keywords = {csbcbook},
owner = {jp},
pii = {ng1215},
pmid = {12923544},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1038/ng1215}
}
@article{Albertson2003Genomic,
author = {Albertson, D. G. and Pinkel, D.},
title = {Genomic microarrays in human genetic disease and cancer},
journal = {Hum. Mol. Genet.},
year = {2003},
volume = {12 Spec No 2},
pages = {R145--R152},
month = {Oct},
abstract = {Alterations in the genome that lead to changes in DNA sequence copy
number are a characteristic of solid tumors and are found in association
with developmental abnormalities and/or mental retardation. Comparative
genomic hybridization (CGH) can be used to detect and map these changes.
Recent improvements in the resolution and sensitivity of CGH have
been possible through implementation of microarray-based CGH (array
CGH). Here we discuss the performance characteristics of different
array platforms and review some of the recent applications of array
CGH in cancer and medical genetics.},
doi = {10.1093/hmg/ddg261},
pdf = {../local/Albertson2003Genomic.pdf},
file = {Albertson2003Genomic.pdf:Albertson2003Genomic.pdf:PDF},
institution = {Department of Laboratory Medicine, University of California San Francisco,
San Francisco, CA 94143-0808,USA. albertson@cc.ucsf.edu},
keywords = {csbcbook},
owner = {jp},
pii = {ddg261},
pmid = {12915456},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1093/hmg/ddg261}
}
@article{Alizadeh2000Distinct,
author = {Alizadeh, A. A. and Eisen, M. B. and Davis, R. E. and Ma, C. and
Lossos, I. S. and Rosenwald, A. and Boldrick, J. C. and Sabet, H.
and Tran, T. and Yu, X. and Powell, J. I. and Yang, L. and Marti,
G. E. and Moore, T. and Hudson, J. and Lu, L. and Lewis, D. B. and
Tibshirani, R. and Sherlock, G. and Chan, W. C. and Greiner, T. C.
and Weisenburger, D. D. and Armitage, J. O. and Warnke, R. and Levy,
R. and Wilson, W. and Grever, M. R. and Byrd, J. C. and Botstein,
D. and Brown, P. O. and Staudt, L. M.},
title = {Distinct types of diffuse large {B}-cell lymphoma identified by gene
expression profiling},
journal = {Nature},
year = {2000},
volume = {403},
pages = {503--511},
number = {6769},
month = {Feb},
abstract = {Diffuse large B-cell lymphoma (DLBCL), the most common subtype of
non-Hodgkin's lymphoma, is clinically heterogeneous: 40\% of patients
respond well to current therapy and have prolonged survival, whereas
the remainder succumb to the disease. We proposed that this variability
in natural history reflects unrecognized molecular heterogeneity
in the tumours. Using DNA microarrays, we have conducted a systematic
characterization of gene expression in B-cell malignancies. Here
we show that there is diversity in gene expression among the tumours
of DLBCL patients, apparently reflecting the variation in tumour
proliferation rate, host response and differentiation state of the
tumour. We identified two molecularly distinct forms of DLBCL which
had gene expression patterns indicative of different stages of B-cell
differentiation. One type expressed genes characteristic of germinal
centre B cells ('germinal centre B-like DLBCL'); the second type
expressed genes normally induced during in vitro activation of peripheral
blood B cells ('activated B-like DLBCL'). Patients with germinal
centre B-like DLBCL had a significantly better overall survival than
those with activated B-like DLBCL. The molecular classification of
tumours on the basis of gene expression can thus identify previously
undetected and clinically significant subtypes of cancer.},
doi = {10.1038/35000501},
pdf = {../local/Alizadeh2000Distinct.pdf},
file = {Alizadeh2000Distinct.pdf:local/Alizadeh2000Distinct.pdf:PDF},
institution = {Department of Biochemistry, Stanford University School of Medicine,
California 94305, USA.},
keywords = {csbcbook},
owner = {jp},
pmid = {10676951},
timestamp = {2008.11.15},
url = {http://dx.doi.org/10.1038/35000501}
}
@article{Aouba2007Les,
author = {Aouba, A. and P{\'e}quignot, F. and Le Toullec, A. and Jougla, E.},
title = {Les causes médicales de d{\'e}c{\`e}s en {France} en 2004 et leur
évolution 1980-2004},
journal = {Bulletin {\'e}pid{\'e}miologique hebdomadaire},
year = {2007},
volume = {35-36},
pages = {308--314},
pdf = {../local/Aouba2007Les.pdf},
file = {Aouba2007Les.pdf:Aouba2007Les.pdf:PDF},
keywords = {csbcbook},
url = {http://www.invs.sante.fr/beh/2007/35_36/beh_35_36_2007.pdf}
}
@article{Bagci2008PLOS1,
author = {Bagci, E. Z. and Vodovotz, Y. and Billiar, T. R. and Ermentrout,
B. and Bahar, I.},
title = {Computational insights on the competing effects of nitric oxide in
regulating apoptosis},
journal = {PLoS One},
year = {2008},
volume = {3},
pages = {e2249},
number = {5},
abstract = {Despite the establishment of the important role of nitric oxide (NO)
on apoptosis, a molecular-level understanding of the origin of its
dichotomous pro- and anti-apoptotic effects has been elusive. We
propose a new mathematical model for simulating the effects of nitric
oxide (NO) on apoptosis. The new model integrates mitochondria-dependent
apoptotic pathways with NO-related reactions, to gain insights into
the regulatory effect of the reactive NO species N(2)O(3), non-heme
iron nitrosyl species (FeL(n)NO), and peroxynitrite (ONOO(-)). The
biochemical pathways of apoptosis coupled with NO-related reactions
are described by ordinary differential equations using mass-action
kinetics. In the absence of NO, the model predicts either cell survival
or apoptosis (a bistable behavior) with shifts in the onset time
of apoptotic response depending on the strength of extracellular
stimuli. Computations demonstrate that the relative concentrations
of anti- and pro-apoptotic reactive NO species, and their interplay
with glutathione, determine the net anti- or pro-apoptotic effects
at long time points. Interestingly, transient effects on apoptosis
are also observed in these simulations, the duration of which may
reach up to hours, despite the eventual convergence to an anti-apoptotic
state. Our computations point to the importance of precise timing
of NO production and external stimulation in determining the eventual
pro- or anti-apoptotic role of NO.},
keywords = {csbcbook}
}
@article{Bagci2006BiophysJ,
author = {Bagci, E. Z. and Vodovotz, Y. and Billiar, T. R. and Ermentrout,
G. B. and Bahar, I.},
title = {Bistability in apoptosis: roles of bax, bcl-2, and mitochondrial
permeability transition pores},
journal = {Biophys J},
year = {2006},
volume = {90},
pages = {1546-59},
number = {5},
abstract = {We propose a mathematical model for mitochondria-dependent apoptosis,
in which kinetic cooperativity in formation of the apoptosome is
a key element ensuring bistability. We examine the role of Bax and
Bcl-2 synthesis and degradation rates, as well as the number of mitochondrial
permeability transition pores (MPTPs), on the cell response to apoptotic
stimuli. Our analysis suggests that cooperative apoptosome formation
is a mechanism for inducing bistability, much more robust than that
induced by other mechanisms, such as inhibition of caspase-3 by the
inhibitor of apoptosis (IAP). Simulations predict a pathological
state in which cells will exhibit a monostable cell survival if Bax
degradation rate is above a threshold value, or if Bax expression
rate is below a threshold value. Otherwise, cell death or survival
occur depending on initial caspase-3 levels. We show that high expression
rates of Bcl-2 can counteract the effects of Bax. Our simulations
also demonstrate a monostable (pathological) apoptotic response if
the number of MPTPs exceeds a threshold value. This study supports
our contention, based on mathematical modeling, that cooperativity
in apoptosome formation is critically important for determining the
healthy responses to apoptotic stimuli, and helps define the roles
of Bax, Bcl-2, and MPTP vis-a-vis apoptosome formation.},
keywords = {csbcbook}
}
@article{Bentele2004JCB,
author = {Bentele, M. and Lavrik, I. and Ulrich, M. and Stosser, S. and Heermann,
D. W. and Kalthoff, H. and Krammer, P. H. and Eils, R.},
title = {Mathematical modeling reveals threshold mechanism in CD95-induced
apoptosis},
journal = {J Cell Biol},
year = {2004},
volume = {166},
pages = {839-51},
number = {6},
abstract = {Mathematical modeling is required for understanding the complex behavior
of large signal transduction networks. Previous attempts to model
signal transduction pathways were often limited to small systems
or based on qualitative data only. Here, we developed a mathematical
modeling framework for understanding the complex signaling behavior
of CD95(APO-1/Fas)-mediated apoptosis. Defects in the regulation
of apoptosis result in serious diseases such as cancer, autoimmunity,
and neurodegeneration. During the last decade many of the molecular
mechanisms of apoptosis signaling have been examined and elucidated.
A systemic understanding of apoptosis is, however, still missing.
To address the complexity of apoptotic signaling we subdivided this
system into subsystems of different information qualities. A new
approach for sensitivity analysis within the mathematical model was
key for the identification of critical system parameters and two
essential system properties: modularity and robustness. Our model
describes the regulation of apoptosis on a systems level and resolves
the important question of a threshold mechanism for the regulation
of apoptosis.},
keywords = {csbcbook}
}
@article{Bhalla1999Emergent,
author = {Bhalla, U. S. and Iyengar, R.},
title = {Emergent Properties of Networks of Biological Signaling Pathways},
journal = {Science},
year = {1999},
volume = {283},
pages = {381-387},
number = {5400},
doi = {10.1126/science.283.5400.381},
eprint = {http://www.sciencemag.org/cgi/reprint/283/5400/381.pdf},
pdf = {../local/Bhalla1999Emergent.pdf},
file = {Bhalla1999Emergent.pdf:Bhalla1999Emergent.pdf:PDF},
keywords = {csbcbook},
url = {http://www.sciencemag.org/cgi/content/abstract/283/5400/381}
}
@article{Billerey1996Etude,
author = {Billerey, C. and Boccon-Gibod, L.},
title = {Etude des variations inter-pathologistes dans l'{\'e}valuation du
grade et du stade des tumeurs v{\'e}sicales},
journal = {Progr{\`e}s en Urologie},
year = {1996},
volume = {6},
pages = {49--57},
pdf = {../local/Billerey1996Etude.pdf},
file = {Billerey1996Etude.pdf:Billerey1996Etude.pdf:PDF},
keywords = {csbcbook, csbcbook-ch3},
url = {http://www.urofrance.org/fileadmin/documents/data/PU/1996/PU-1996-00070049/TEXF-PU-1996-00070049.PDF}
}
@article{Blow2008DNA,
author = {Blow, N.},
title = {{DNA} sequencing: generation next-next},
journal = {Nat. Meth.},
year = {2008},
volume = {5},
pages = {267-274},
number = {3},
abstract = {Emboldened by the success of next-generation sequencing, scientists
are pursuing the holy grail of genomics—the '$1,000 genome'—with
single-molecule approaches. Nathan Blow reports.},
doi = {10.1038/nmeth0308-267},
pdf = {../local/Blow2008DNA.pdf},
file = {Blow2008DNA.pdf:Blow2008DNA.pdf:PDF},
keywords = {csbcbook-ch2, csbcbook},
owner = {jp},
url = {http://dx.doi.org/10.1038/nmeth0308-267}
}
@article{Breslin2005Signal,
author = {Breslin, T. and Krogh, M. and Peterson, C. and Troein, C.},
title = {Signal transduction pathway profiling of individual tumor samples.},
journal = {BMC Bioinformatics},
year = {2005},
volume = {6},
pages = {163},
abstract = {Signal transduction pathways convey information from the outside of
the cell to transcription factors, which in turn regulate gene expression.
Our objective is to analyze tumor gene expression data from microarrays
in the context of such pathways.We use pathways compiled from the
TRANSPATH/TRANSFAC databases and the literature, and three publicly
available cancer microarray data sets. Variation in pathway activity,
across the samples, is gauged by the degree of correlation between
downstream targets of a pathway. Two correlation scores are applied;
one considers all pairs of downstream targets, and the other considers
only pairs without common transcription factors. Several pathways
are found to be differentially active in the data sets using these
scores. Moreover, we devise a score for pathway activity in individual
samples, based on the average expression value of the downstream
targets. Statistical significance is assigned to the scores using
permutation of genes as null model. Hence, for individual samples,
the status of a pathway is given as a sign, + or -, and a p-value.
This approach defines a projection of high-dimensional gene expression
data onto low-dimensional pathway activity scores. For each dataset
and many pathways we find a much larger number of significant samples
than expected by chance. Finally, we find that several sample-wise
pathway activities are significantly associated with clinical classifications
of the samples.This study shows that it is feasible to infer signal
transduction pathway activity, in individual samples, from gene expression
data. Furthermore, these pathway activities are biologically relevant
in the three cancer data sets.},
doi = {10.1186/1471-2105-6-163},
pdf = {../local/Breslin2005Signal.pdf},
file = {Breslin2005Signal.pdf:Breslin2005Signal.pdf:PDF},
institution = {Complex Systems Division, Department of Theoretical Physics, University
of Lund, Sölvegatan 14A, SE-223 62 Lund, Sweden. thomas@thep.lu.se},
keywords = {csbcbook-ch4},
language = {eng},
medline-pst = {epublish},
owner = {jp},
pii = {1471-2105-6-163},
pmid = {15987529},
timestamp = {2011.08.06},
url = {http://dx.doi.org/10.1186/1471-2105-6-163}
}
@article{Buyse2006Validation,
author = {Buyse, M. and Loi, S. and van't Veer, S. and Viale, G. and Delorenzi,
M. and Glas, A. M. and Saghatchian d'Assignies, M. and Bergh, J.
and Lidereau, R. and Ellis, P. and Harris, A. and Bogaerts, J. and
Therasse, P. and Floore, A. and Amakrane, M. and Piette, F. and Rutgers,
E. and Sotiriou, C. and Cardoso, F. and Piccart, M. J. and T. R.
A. N. S. B. I. G. Consortium},
title = {Validation and clinical utility of a 70-gene prognostic signature
for women with node-negative breast cancer.},
journal = {J. Natl. Canc. Inst.},
year = {2006},
volume = {98},
pages = {1183--1192},
number = {17},
month = {Sep},
abstract = {BACKGROUND: A 70-gene signature was previously shown to have prognostic
value in patients with node-negative breast cancer. Our goal was
to validate the signature in an independent group of patients. METHODS:
Patients (n = 307, with 137 events after a median follow-up of 13.6
years) from five European centers were divided into high- and low-risk
groups based on the gene signature classification and on clinical
risk classifications. Patients were assigned to the gene signature
low-risk group if their 5-year distant metastasis-free survival probability
as estimated by the gene signature was greater than 90\%. Patients
were assigned to the clinicopathologic low-risk group if their 10-year
survival probability, as estimated by Adjuvant! software, was greater
than 88\% (for estrogen receptor [ER]-positive patients) or 92\%
(for ER-negative patients). Hazard ratios (HRs) were estimated to
compare time to distant metastases, disease-free survival, and overall
survival in high- versus low-risk groups. RESULTS: The 70-gene signature
outperformed the clinicopathologic risk assessment in predicting
all endpoints. For time to distant metastases, the gene signature
yielded HR = 2.32 (95\% confidence interval [CI] = 1.35 to 4.00)
without adjustment for clinical risk and hazard ratios ranging from
2.13 to 2.15 after adjustment for various estimates of clinical risk;
clinicopathologic risk using Adjuvant! software yielded an unadjusted
HR = 1.68 (95\% CI = 0.92 to 3.07). For overall survival, the gene
signature yielded an unadjusted HR = 2.79 (95\% CI = 1.60 to 4.87)
and adjusted hazard ratios ranging from 2.63 to 2.89; clinicopathologic
risk yielded an unadjusted HR = 1.67 (95\% CI = 0.93 to 2.98). For
patients in the gene signature high-risk group, 10-year overall survival
was 0.69 for patients in both the low- and high-clinical risk groups;
for patients in the gene signature low-risk group, the 10-year survival
rates were 0.88 and 0.89, respectively. CONCLUSIONS: The 70-gene
signature adds independent prognostic information to clinicopathologic
risk assessment for patients with early breast cancer.},
doi = {10.1093/jnci/djj329},
pdf = {../local/Buyse2006Validation.pdf},
file = {Buyse2006Validation.pdf:Buyse2006Validation.pdf:PDF},
institution = {International Drug Development Institute, Brussels, Belgium.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {16954471},
timestamp = {2009.10.17},
url = {http://dx.doi.org/10.1093/jnci/djj329}
}
@article{Calin2006MicroRNA,
author = {Calin, G. A. and Croce, C. M.},
title = {Micro{RNA} signatures in human cancers},
journal = {Nat. Rev. Cancer},
year = {2006},
volume = {6},
pages = {857--866},
number = {11},
month = {Nov},
abstract = {MicroRNA (miRNA) alterations are involved in the initiation and progression
of human cancer. The causes of the widespread differential expression
of miRNA genes in malignant compared with normal cells can be explained
by the location of these genes in cancer-associated genomic regions,
by epigenetic mechanisms and by alterations in the miRNA processing
machinery. MiRNA-expression profiling of human tumours has identified
signatures associated with diagnosis, staging, progression, prognosis
and response to treatment. In addition, profiling has been exploited
to identify miRNA genes that might represent downstream targets of
activated oncogenic pathways, or that target protein-coding genes
involved in cancer.},
doi = {10.1038/nrc1997},
pdf = {../local/Calin2006MicroRNA.pdf},
file = {Calin2006MicroRNA.pdf:Calin2006MicroRNA.pdf:PDF},
institution = {Department of Molecular Virology, Immunology and Medical Genetics
and Comprehensive Cancer Center, Ohio State University, Columbus,
Ohio 43210, USA.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nrc1997},
pmid = {17060945},
timestamp = {2009.10.17},
url = {http://dx.doi.org/10.1038/nrc1997}
}
@article{Calin2006MicroRNA-cancer,
author = {Calin, G.A. and Croce, C. M.},
title = {{MicroRNA}-cancer connection: the beginning of a new tale},
journal = {Cancer Res.},
year = {2006},
volume = {66},
pages = {7390--7394},
number = {15},
month = {Aug},
abstract = {Cancer initiation and progression can involve microRNAs (miRNA), which
are small noncoding RNAs that can regulate gene expression. Their
expression profiles can be used for the classification, diagnosis,
and prognosis of human malignancies. Loss or amplification of miRNA
genes has been reported in a variety of cancers, and altered patterns
of miRNA expression may affect cell cycle and survival programs.
Germ-line and somatic mutations in miRNAs or polymorphisms in the
mRNAs targeted by miRNAs may also contribute to cancer predisposition
and progression. We propose that alterations in miRNA genes play
a critical role in the pathophysiology of many, perhaps all, human
cancers.},
doi = {10.1158/0008-5472.CAN-06-0800},
pdf = {../local/Calin2006MicroRNA-cancer.pdf},
file = {Calin2006MicroRNA-cancer.pdf:Calin2006MicroRNA-cancer.pdf:PDF},
institution = {Department of Molecular Virology, Immunology, and Medical Genetics,
Ohio State University, 400 12th Avenue, Columbus, OH 43210, USA.},
keywords = {csbcbook},
owner = {jp},
pii = {66/15/7390},
pmid = {16885332},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1158/0008-5472.CAN-06-0800}
}
@article{Calzone2006BIOCHAM,
author = {Calzone, L. and Fages, F. and Soliman, S.},
title = {{BIOCHAM: an environment for modeling biological systems and formalizing
experimental knowledge}},
journal = {Bioinformatics},
year = {2006},
volume = {22},
pages = {1805-1807},
number = {14},
abstract = {Summary: BIOCHAM (the BIOCHemical Abstract Machine) is a software
environment for modeling biochemical systems. It is based on two
aspects: (1) the analysis and simulation of boolean, kinetic and
stochastic models and (2) the formalization of biological properties
in temporal logic. BIOCHAM provides tools and languages for describing
protein networks with a simple and straightforward syntax, and for
integrating biological properties into the model. It then becomes
possible to analyze, query, verify and maintain the model with respect
to those properties. For kinetic models, BIOCHAM can search for appropriate
parameter values in order to reproduce a specific behavior observed
in experiments and formalized in temporal logic. Coupled with other
methods such as bifurcation diagrams, this search assists the modeler/biologist
in the modeling process. Availability: BIOCHAM (v. 2.5) is a free
software available for download, with example models, at http://contraintes.inria.fr/BIOCHAM/
Contact: Sylvain.Soliman@inria.fr},
doi = {10.1093/bioinformatics/btl172},
eprint = {http://bioinformatics.oxfordjournals.org/cgi/reprint/22/14/1805.pdf},
pdf = {../local/Calzone2006BIOCHAM.pdf},
file = {Calzone2006BIOCHAM.pdf:Calzone2006BIOCHAM.pdf:PDF},
keywords = {csbcbook},
url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/22/14/1805}
}
@article{Calzone2008comprehensive,
author = {Calzone, L. and Gelay, A. and Zinovyev, A. and Radvanyi, F. and Barillot,
E.},
title = {A comprehensive modular map of molecular interactions in {RB/E2F}
pathway.},
journal = {Mol. Syst. Biol.},
year = {2008},
volume = {4},
pages = {173},
abstract = {We present, here, a detailed and curated map of molecular interactions
taking place in the regulation of the cell cycle by the retinoblastoma
protein (RB/RB1). Deregulations and/or mutations in this pathway
are observed in most human cancers. The map was created using Systems
Biology Graphical Notation language with the help of CellDesigner
3.5 software and converted into BioPAX 2.0 pathway description format.
In the current state the map contains 78 proteins, 176 genes, 99
protein complexes, 208 distinct chemical species and 165 chemical
reactions. Overall, the map recapitulates biological facts from approximately
350 publications annotated in the diagram. The network contains more
details about RB/E2F interaction network than existing large-scale
pathway databases. Structural analysis of the interaction network
revealed a modular organization of the network, which was used to
elaborate a more summarized, higher-level representation of RB/E2F
network. The simplification of complex networks opens the road for
creating realistic computational models of this regulatory pathway.},
doi = {10.1038/msb.2008.7},
pdf = {../local/Calzone2008comprehensive.pdf},
file = {Calzone2008comprehensive.pdf:Calzone2008comprehensive.pdf:PDF},
institution = {Institut Curie, Service Blolnforrnatique, Paris, France.},
keywords = {csbcbook},
owner = {jp},
pii = {msb20087},
pmid = {18319725},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1038/msb.2008.7}
}
@article{Chen2007BiophysJ,
author = {Chen, C. and Cui, J. and Lu, H. and Wang, R. and Zhang, S. and Shen,
P.},
title = {Modeling of the role of a Bax-activation switch in the mitochondrial
apoptosis decision},
journal = {Biophys J},
year = {2007},
volume = {92},
pages = {4304-15},
number = {12},
abstract = {We performed in silico modeling of the regulatory network of mitochondrial
apoptosis through which we examined the role of a Bax-activation
switch in governing the mitochondrial apoptosis decision. Two distinct
modeling methods were used in this article. One is continuous and
deterministic, comprised of a set of ordinary differential equations.
The other, carried out in a discrete manner, is based on a cellular
automaton, which takes stochastic fluctuations into consideration.
We focused on dynamic properties of the mitochondrial apoptosis regulatory
network. The roles of Bcl-2 family proteins in cellular responses
to apoptotic stimuli were examined. In our simulations, a self-amplification
process of Bax-activation is indicated. Further analysis suggests
that the core module of Bax-activation is bistable in both deterministic
and stochastic models, and this feature is robust to noise and wide
ranges of parameter variation. When coupling with Bax-polymerization,
it forms a one-way-switch, which governs irreversible behaviors of
Bax-activation even with attenuation of apoptotic stimulus. Together
with the growing biochemical evidence, we propose a novel molecular
switch mechanism embedded in the mitochondrial apoptosis regulatory
network and give a plausible explanation for the all-or-none, irreversible
character of mitochondrial apoptosis.},
keywords = {csbcbook}
}
@article{Chen2007FEBS,
author = {Chen, C. and Cui, J. and Zhang, W. and Shen, P.},
title = {Robustness analysis identifies the plausible model of the Bcl-2 apoptotic
switch},
journal = {FEBS Lett},
year = {2007},
volume = {581},
pages = {5143-50},
number = {26},
abstract = {In this paper two competing models of the B-cell lymphoma 2 (Bcl-2)
apoptotic switch were contrasted by mathematical modeling and robustness
analysis. Since switch-like behaviors are required for models that
attempt to explain the all-or-none decisions of apoptosis, ultrasensitivity
was employed as a criterion for comparison. Our results successfully
exhibit that the direct activation model operates more reliably to
achieve a robust switch in cellular conditions. Moreover, by investigating
the robustness of other important features of the Bcl-2 apoptotic
switch (including low Bax basal activation, inhibitory role of anti-apoptotic
proteins and insensitivity to small perturbations) the direct activation
model was further supported. In all, we identified the direct activation
model as a more plausible explanation for the Bcl-2 apoptotic switch.},
keywords = {csbcbook}
}
@article{Chen2008Mapping,
author = {Wei Chen and Vera Kalscheuer and Andreas Tzschach and Corinna Menzel
and Reinhard Ullmann and Marcel Holger Schulz and Fikret Erdogan
and Na Li and Zofia Kijas and Ger Arkesteijn and Isidora Lopez Pajares
and Margret Goetz-Sothmann and Uwe Heinrich and Imma Rost and Andreas
Dufke and Ute Grasshoff and Birgitta Glaeser and Martin Vingron and
H. Hilger Ropers},
title = {Mapping translocation breakpoints by next-generation sequencing.},
journal = {Genome Res.},
year = {2008},
volume = {18},
pages = {1143--1149},
number = {7},
month = {Jul},
abstract = {Balanced chromosome rearrangements (BCRs) can cause genetic diseases
by disrupting or inactivating specific genes, and the characterization
of breakpoints in disease-associated BCRs has been instrumental in
the molecular elucidation of a wide variety of genetic disorders.
However, mapping chromosome breakpoints using traditional methods,
such as in situ hybridization with fluorescent dye-labeled bacterial
artificial chromosome clones (BAC-FISH), is rather laborious and
time-consuming. In addition, the resolution of BAC-FISH is often
insufficient to unequivocally identify the disrupted gene. To overcome
these limitations, we have performed shotgun sequencing of flow-sorted
derivative chromosomes using "next-generation" (Illumina/Solexa)
multiplex sequencing-by-synthesis technology. As shown here for three
different disease-associated BCRs, the coverage attained by this
platform is sufficient to bridge the breakpoints by PCR amplification,
and this procedure allows the determination of their exact nucleotide
positions within a few weeks. Its implementation will greatly facilitate
large-scale breakpoint mapping and gene finding in patients with
disease-associated balanced translocations.},
doi = {10.1101/gr.076166.108},
pdf = {../local/Chen2008Mapping.pdf},
file = {Chen2008Mapping.pdf:Chen2008Mapping.pdf:PDF},
institution = {Max Planck Institute for Molecular Genetics, 14195 Berlin, Germany.
wei@molgen.mpg.de},
keywords = {ngs, csbcbook, csbcbook-ch2},
owner = {jp},
pii = {gr.076166.108},
pmid = {18326688},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1101/gr.076166.108}
}
@article{Chen2002Gene,
author = {Chen, X. and Cheung, S. T. and So, S. and Fan, S. T. and Barry, C.
and Higgins, J. and Lai, K.-M. and Ji, J. and Dudoit, S. and Ng,
I. O L. and {Van De Rijn}, M. and Botstein, D. and Brown, P. O.},
title = {Gene expression patterns in human liver cancers.},
journal = {Mol. Biol. Cell},
year = {2002},
volume = {13},
pages = {1929--1939},
number = {6},
month = {Jun},
abstract = {Hepatocellular carcinoma (HCC) is a leading cause of death worldwide.
Using cDNA microarrays to characterize patterns of gene expression
in HCC, we found consistent differences between the expression patterns
in HCC compared with those seen in nontumor liver tissues. The expression
patterns in HCC were also readily distinguished from those associated
with tumors metastatic to liver. The global gene expression patterns
intrinsic to each tumor were sufficiently distinctive that multiple
tumor nodules from the same patient could usually be recognized and
distinguished from all the others in the large sample set on the
basis of their gene expression patterns alone. The distinctive gene
expression patterns are characteristic of the tumors and not the
patient; the expression programs seen in clonally independent tumor
nodules in the same patient were no more similar than those in tumors
from different patients. Moreover, clonally related tumor masses
that showed distinct expression profiles were also distinguished
by genotypic differences. Some features of the gene expression patterns
were associated with specific phenotypic and genotypic characteristics
of the tumors, including growth rate, vascular invasion, and p53
overexpression.},
doi = {10.1091/mbc.02-02-0023},
pdf = {../local/Chen2002Gene.pdf},
file = {Chen2002Gene.pdf:Chen2002Gene.pdf:PDF},
institution = {Department of Biochemistry, Stanford University School of Medicine,
Stanford, California 94305, USA.},
keywords = {csbcbook-ch3, csbcbook},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {12058060},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1091/mbc.02-02-0023}
}
@article{Chi2008year,
author = {Chi, K. R.},
title = {The year of sequencing},
journal = {Nat. Methods},
year = {2008},
volume = {5},
pages = {11--14},
number = {1},
month = {Jan},
abstract = {In 2007, the next-generation sequencing technologies have come into
their own with an impressive array of successful applications. Kelly
Rae Chi reports.},
doi = {10.1038/nmeth1154},
pdf = {../local/Chi2008year.pdf},
file = {Chi2008year.pdf:Chi2008year.pdf:PDF},
keywords = {csbcbook, csbcbook-ch2},
owner = {jp},
pmid = {18175410},
timestamp = {2009.10.13},
url = {http://dx.doi.org/10.1038/nmeth1154}
}
@article{Chin2008Translating,
author = {Chin, L. and Gray, J. W.},
title = {Translating insights from the cancer genome into clinical practice.},
journal = {Nature},
year = {2008},
volume = {452},
pages = {553--563},
number = {7187},
month = {Apr},
abstract = {Cancer cells have diverse biological capabilities that are conferred
by numerous genetic aberrations and epigenetic modifications. Today's
powerful technologies are enabling these changes to the genome to
be catalogued in detail. Tomorrow is likely to bring a complete atlas
of the reversible and irreversible alterations that occur in individual
cancers. The challenge now is to work out which molecular abnormalities
contribute to cancer and which are simply 'noise' at the genomic
and epigenomic levels. Distinguishing between these will aid in understanding
how the aberrations in a cancer cell collaborate to drive pathophysiology.
Past successes in converting information from genomic discoveries
into clinical tools provide valuable lessons to guide the translation
of emerging insights from the genome into clinical end points that
can affect the practice of cancer medicine.},
doi = {10.1038/nature06914},
pdf = {../local/Chin2008Translating.pdf},
file = {Chin2008Translating.pdf:Chin2008Translating.pdf:PDF},
institution = {Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney
Street, Boston, Massachusetts 02115, USA. lynda_chin@dfci.harvard.edu},
keywords = {csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nature06914},
pmid = {18385729},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1038/nature06914}
}
@article{Choi2007Coupled,
author = {Choi, H.-S. and Han, S. and Yokota, H. and Cho, K.-H.},
title = {Coupled positive feedbacks provoke slow induction plus fast switching
in apoptosis},
journal = {FEBS Letters},
year = {2007},
volume = {581},
pages = {2684 - 2690},
number = {14},
abstract = {Apoptosis is a form of a programmed cell death for multicellular organisms
to remove unwanted or damaged cells. This critical choice of cellular
fate is an all-or-none process, but its dynamics remains unraveled.
The switch-like apoptotic decision has to be reliable, and once a
pro-apoptotic fate is determined it requires fast and irreversible
execution. One of the key regulators in apoptosis is caspase-3. Interestingly,
activated caspase-3 quickly executes apoptosis, but it takes considerable
time to activate it. Here, we have analyzed this slow induction plus
fast switching mechanism of caspase-3 through mathematical modeling
and computational simulation. First, we have shown that two positive
feedbacks, composed of caspase-8 and XIAP, are essential for the
slow induction plus fast switching behavior of caspase-3. Second,
we have found that XIAP in the feedback loops primarily regulates
induction time of caspase-3. In many cancer cells activation of caspase-3
is suppressed. Our results suggest that reinforcement of the positive
feedback by XIAP, which relieves XIAP-mediated caspase-3 inhibition,
might favor a pro-apoptotic cellular fate.},
doi = {DOI: 10.1016/j.febslet.2007.05.016},
pdf = {../local/Choi2007Coupled.pdf},
file = {Choi2007Coupled.pdf:Choi2007Coupled.pdf:PDF},
issn = {0014-5793},
keywords = {csbcbook},
url = {http://www.sciencedirect.com/science/article/B6T36-4NSR1M2-F/2/1d13173e1580459d4c4430a96116dc3d}
}
@article{Cianfrocca2004Prognostic,
author = {Cianfrocca, M. and Goldstein, L. J.},
title = {Prognostic and predictive factors in early-stage breast cancer},
journal = {Oncologist},
year = {2004},
volume = {9},
pages = {606--616},
number = {6},
abstract = {Breast cancer is the most common malignancy among American women.
Due to increased screening, the majority of patients present with
early-stage breast cancer. The Oxford Overview Analysis demonstrates
that adjuvant hormonal therapy and polychemotherapy reduce the risk
of recurrence and death from breast cancer. Adjuvant systemic therapy,
however, has associated risks and it would be useful to be able to
optimally select patients most likely to benefit. The purpose of
adjuvant systemic therapy is to eradicate distant micrometastatic
deposits. It is essential therefore to be able to estimate an individual
patient's risk of harboring clinically silent micrometastatic disease
using established prognostic factors. It is also beneficial to be
able to select the optimal adjuvant therapy for an individual patient
based on established predictive factors. It is standard practice
to administer systemic therapy to all patients with lymph node-positive
disease. However, there are clearly differences among node-positive
women that may warrant a more aggressive therapeutic approach. Furthermore,
there are many node-negative women who would also benefit from adjuvant
systemic therapy. Prognostic factors therefore must be differentiated
from predictive factors. A prognostic factor is any measurement available
at the time of surgery that correlates with disease-free or overall
survival in the absence of systemic adjuvant therapy and, as a result,
is able to correlate with the natural history of the disease. In
contrast, a predictive factor is any measurement associated with
response to a given therapy. Some factors, such as hormone receptors
and HER2/neu overexpression, are both prognostic and predictive.},
doi = {10.1634/theoncologist.9-6-606},
pdf = {../local/Cianfrocca2004Prognostic.pdf},
file = {Cianfrocca2004Prognostic.pdf:Cianfrocca2004Prognostic.pdf:PDF},
institution = {D.O., Fox Chase Cancer Center, 333 Cottman Ave, Philadelphia, Pennsylvania
19111, USA. M_Cianfrocca@fccc.edu},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {9/6/606},
pmid = {15561805},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1634/theoncologist.9-6-606}
}
@article{Cianfrocca2009New,
author = {Cianfrocca, M. and Gradishar, W.},
title = {New molecular classifications of breast cancer},
journal = {CA Cancer J. Clin.},
year = {2009},
volume = {59},
pages = {303--313},
number = {5},
abstract = {Traditionally, pathologic determinations of tumor size, lymph node
status, endocrine receptor status, and human epidermal growth factor
receptor 2 (HER2) status have driven prognostic predictions and adjuvant
therapy recommendations for patients with early stage breast cancer.
However, these prognostic and predictive factors are relatively crude
measures, resulting in many patients being overtreated or undertreated.
As a result of gene expression assays, there is growing recognition
that breast cancer is a molecularly heterogeneous disease. Evidence
from gene expression microarrays suggests the presence of multiple
molecular subtypes of breast cancer. The recent commercial availability
of gene expression profiling techniques that predict risk of disease
recurrence as well as potential chemotherapy benefit have shown promise
in refining clinical decision making. These techniques will be reviewed
in this article.},
doi = {10.3322/caac.20029},
pdf = {../local/Cianfrocca2009New.pdf},
file = {Cianfrocca2009New.pdf:Cianfrocca2009New.pdf:PDF},
institution = {Division of Hematology/Oncology, Northwestern University, Feinberg
School of Medicine, Robert H. Lurie Comprehensive Cancer Center,
Chicago, IL 60611, USA. m-cianfrocca@northwestern.edu},
keywords = {csbcbook, breastcancer},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {59/5/303},
pmid = {19729680},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.3322/caac.20029}
}
@article{Ciliberto2005CellCycle,
author = {Ciliberto, A. and Novak, B. and Tyson, J. J.},
title = {Steady states and oscillations in the p53/Mdm2 network},
journal = {Cell Cycle},
year = {2005},
volume = {4},
pages = {488-93},
number = {3},
abstract = {p53 is activated in response to events compromising the genetic integrity
of a cell. Recent data show that p53 activity does not increase steadily
with genetic damage but rather fluctuates in an oscillatory fashion.
Theoretical studies suggest that oscillations can arise from a combination
of positive and negative feedbacks or from a long negative feedback
loop alone. Both negative and positive feedbacks are present in the
p53/Mdm2 network, but it is not known what roles they play in the
oscillatory response to DNA damage. We developed a mathematical model
of p53 oscillations based on positive and negative feedbacks in the
p53/Mdm2 network. According to the model, the system reacts to DNA
damage by moving from a stable steady state into a region of stable
limit cycles. Oscillations in the model are born with large amplitude,
which guarantees an all-or-none response to damage. As p53 oscillates,
damage is repaired and the system moves back to a stable steady state
with low p53 activity. The model reproduces experimental data in
quantitative detail. We suggest new experiments for dissecting the
contributions of negative and positive feedbacks to the generation
of oscillations.},
keywords = {csbcbook}
}
@article{Coe2007Resolving,
author = {Coe, B. P. and Ylstra, B. and Carvalho, B. and Meijer, G. A. and
Macaulay, C. and Lam, W. L.},
title = {Resolving the resolution of array {CGH}},
journal = {Genomics},
year = {2007},
volume = {89},
pages = {647--653},
number = {5},
month = {May},
abstract = {Many recent technologies have been designed to supplant conventional
metaphase CGH technology with the goal of refining the description
of segmental copy number status throughout the genome. However, the
emergence of new technologies has led to confusion as to how to describe
adequately the capabilities of each array platform. The design of
a CGH array can incorporate a uniform or a highly variable element
distribution. This can lead to bias in the reporting of average or
median resolutions, making it difficult to provide a fair comparison
of platforms. In this report, we propose a new definition of resolution
for array CGH technology, termed "functional resolution," that incorporates
the uniformity of element spacing on the array, as well as the sensitivity
of each platform to single-copy alterations. Calculation of these
metrics is automated through the development of a Java-based application,
"ResCalc," which is applicable to any array CGH platform.},
doi = {10.1016/j.ygeno.2006.12.012},
pdf = {../local/Coe2007Resolving.pdf},
file = {Coe2007Resolving.pdf:Coe2007Resolving.pdf:PDF},
institution = {British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver,
BC, Canada V5Z 1L3. bcoe@bccrc.ca},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {S0888-7543(07)00004-3},
pmid = {17276656},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1016/j.ygeno.2006.12.012}
}
@article{Cowell2007application,
author = {Cowell, J.K. and Hawthorn, L.},
title = {The application of microarray technology to the analysis of the cancer
genome},
journal = {Curr. Mol. Med.},
year = {2007},
volume = {7},
pages = {103--120},
number = {1},
month = {Feb},
abstract = {The identification of genetic events that are involved in the development
of human cancer has been facilitated through the development and
application of a diverse series of high resolution, high throughput
microarray platforms. Essentially there are two types of array; those
that carry PCR products from cloned nucleic acids (e.g. cDNA, BACs,
cosmids) and those that use oligonucleotides. Each has advantages
and disadvantages but it is now possible to survey genome wide DNA
copy number abnormalities and expression levels to allow correlations
between losses, gains and amplifications in tumor cells with genes
that are over- and under-expressed in the same samples. The gene
expression arrays that provide estimates of mRNA levels in tumors
have given rise to exon-specific arrays that can identify both gene
expression levels, alternative splicing events and mRNA processing
alterations. Oligonucleotide arrays are also being used to interrogate
single nucleotide polymorphisms (SNPs) throughout the genome for
linkage and association studies and these have been adapted to quantify
copy number abnormalities and loss of heterozygosity events. To identify
as yet unknown transcripts tiling arrays across the genome have been
developed which can also identify DNA methylation changes and be
used to identify DNA-protein interactions using ChIP on Chip protocols.
Ultimately DNA sequencing arrays will allow resequencing of chromosome
regions and whole genomes. With all of these capabilities becoming
routine in genomics laboratories, the idea of a systematic characterization
of the sum genetic events that give rise to a cancer cell is rapidly
becoming a reality.},
institution = {Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo,
New York 14263, USA. john.cowell@roswellpark.org},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {17311536},
timestamp = {2009.10.18}
}
@article{Crick1970Central,
author = {Crick, F.},
title = {Central Dogma of Molecular Biology},
journal = {Nature},
year = {1970},
volume = {227},
pages = {561--563},
abstract = {The central dogma of molecular biology deals with the detailed
residue-by-residue transfer of sequential information. It states
that such informatfon cannot be transferred from protein to either
proteln or nucleic acid.},
pdf = {../local/Crick1970Central.pdf},
file = {Crick1970Central.pdf:Crick1970Central.pdf:PDF},
keywords = {csbcbook},
owner = {jp},
url = {http://profiles.nlm.nih.gov/SC/B/C/C/H/_/scbcch.pdf}
}
@article{Croce2009Causes,
author = {Carlo M. Croce},
title = {Causes and consequences of {microRNA} dysregulation in cancer},
journal = {Nat Rev Genet},
year = {2009},
volume = {10},
pages = {704--714},
number = {10},
month = oct,
doi = {10.1038/nrg2634},
pdf = {../local/Croce2009Causes.pdf},
file = {Croce2009Causes.pdf:Croce2009Causes.pdf:PDF},
issn = {1471-0056},
keywords = {csbcbook},
owner = {phupe},
timestamp = {2009.10.15},
url = {http://dx.doi.org/10.1038/nrg2634}
}
@article{Croce2008Oncogenes,
author = {Croce, C. M.},
title = {Oncogenes and cancer.},
journal = {N. Engl. J. Med.},
year = {2008},
volume = {358},
pages = {502--511},
number = {5},
month = {Jan},
doi = {10.1056/NEJMra072367},
pdf = {../local/Croce2008Oncogenes.pdf},
file = {Croce2008Oncogenes.pdf:Croce2008Oncogenes.pdf:PDF},
institution = {Department of Molecular Virology, Immunology, and Medical Genetics
and the Human Cancer Genetics Program, Ohio State University Medical
Center, Columbus, OH 43210, USA. carlo.croce@osumc.edu},
keywords = {csbcbook},
owner = {jp},
pii = {358/5/502},
pmid = {18234754},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1056/NEJMra072367}
}
@article{Cui2008Two,
author = {Cui, J. and Chen, C. and Lu, H. and Sun, T. and Shen, P.},
title = {Two Independent Positive Feedbacks and Bistability in the Bcl-2 Apoptotic
Switch},
journal = {PLoS ONE},
year = {2008},
volume = {3},
pages = {e1469},
number = {1},
month = {01},
abstract = {Background - The complex interplay between B-cell lymphoma 2 (Bcl-2)
family proteins constitutes a crucial checkpoint in apoptosis. Its
detailed molecular mechanism remains controversial. Our former modeling
studies have selected the ‘Direct Activation Model’ as a better explanation
for experimental observations. In this paper, we continue to extend
this model by adding interactions according to updating experimental
findings. Methodology/Principal Findings - Through mathematical simulation
we found bistability, a kind of switch, can arise from a positive
(double negative) feedback in the Bcl-2 interaction network established
by anti-apoptotic group of Bcl-2 family proteins. Moreover, Bax/Bak
auto-activation as an independent positive feedback can enforce the
bistability, and make it more robust to parameter variations. By
ensemble stochastic modeling, we also elucidated how intrinsic noise
can change ultrasensitive switches into gradual responses. Our modeling
result agrees well with recent experimental data where bimodal Bax
activation distributions in cell population were found. Conclusions/Significance
- Along with the growing experimental evidences, our studies successfully
elucidate the switch mechanism embedded in the Bcl-2 interaction
network and provide insights into pharmacological manipulation of
Bcl-2 apoptotic switch as further cancer therapies.},
doi = {10.1371/journal.pone.0001469},
pdf = {../local/Cui2008Two.pdf},
file = {Cui2008Two.pdf:Cui2008Two.pdf:PDF},
keywords = {csbcbook},
publisher = {Public Library of Science},
url = {http://dx.plos.org/10.1371/journal.pone.0001469}
}
@article{Davies2005Array,
author = {Davies, J. J. and Wilson, I. M. and Lam, W. L.},
title = {Array {CGH} technologies and their applications to cancer genomes},
journal = {Chromosome Res.},
year = {2005},
volume = {13},
pages = {237--248},
number = {3},
abstract = {Cancer is a disease characterized by genomic instability. Comparative
genomic hybridization (CGH) is a technique designed for detecting
segmental genomic alterations. Recent advances in array-based CGH
technology have enabled examination of chromosomal regions in unprecedented
detail, revolutionizing our understanding of tumour genomes. A number
of array-based technologies have been developed, aiming to improve
the resolution of CGH, enabling researchers to refine and define
regions in the genome that may be causal to cancer, and facilitating
gene discovery at a rapid rate. This article reviews the various
array CGH platforms and their use in the study of cancer genomes.
In addition, the need for high-resolution analysis is discussed as
well as the importance of studying early-stage disease to discover
genetic alterations that may be causal to cancer progression and
aetiology.},
doi = {10.1007/s10577-005-2168-x},
pdf = {../local/Davies2005Array.pdf},
file = {Davies2005Array.pdf:Davies2005Array.pdf:PDF},
institution = {British Columbia Cancer Research Centre, 675 W 10th Ave., Vancouver
BC, V5Z 1L3, Canada. jdavies@bccrc.ca},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {15868418},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1007/s10577-005-2168-x}
}
@article{Declercq2009RIP,
author = {Declercq, W. and Vanden Berghe, T. and Vandenabeele, P.},
title = {{RIP} Kinases at the Crossroads of Cell Death and Survival},
journal = {Cell},
year = {2009},
volume = {138},
pages = {229-232},
number = {2},
doi = {10.1016/j.cell.2009.07.006},
pdf = {../local/Declercq2009RIP.pdf},
file = {Declercq2009RIP.pdf:Declercq2009RIP.pdf:PDF},
keywords = {csbcbook},
url = {http://dx.doi.org/10.1016/j.cell.2009.07.006}
}
@article{Eissing2004Bistability,
author = {Eissing, T. and Conzelmann, H. and Gilles, E. D. and Allgower, F.
and Bullinger, E. and Scheurich, P.},
title = {Bistability Analyses of a Caspase Activation Model for Receptor-induced
Apoptosis},
journal = {J. Biol. Chem.},
year = {2004},
volume = {279},
pages = {36892-36897},
number = {35},
abstract = {Apoptosis is an important physiological process crucially involved
in development and homeostasis of multicellular organisms. Although
the major signaling pathways have been unraveled, a detailed mechanistic
understanding of the complex underlying network remains elusive.
We have translated here the current knowledge of the molecular mechanisms
of the death-receptor-activated caspase cascade into a mathematical
model. A reduction down to the apoptotic core machinery enables the
application of analytical mathematical methods to evaluate the system
behavior within a wide range of parameters. Using parameter values
from the literature, the model reveals an unstable status of survival
indicating the need for further control. Based on recent publications
we tested one additional regulatory mechanism at the level of initiator
caspase activation and demonstrated that the resulting system displays
desired characteristics such as bistability. In addition, the results
from our model studies allowed us to reconcile the fast kinetics
of caspase 3 activation observed at the single cell level with the
much slower kinetics found at the level of a cell population.},
doi = {10.1074/jbc.M404893200},
eprint = {http://www.jbc.org/content/279/35/36892.full.pdf+html},
pdf = {../local/Eissing2004Bistability.pdf},
file = {Eissing2004Bistability.pdf:Eissing2004Bistability.pdf:PDF},
keywords = {csbcbook},
url = {http://www.jbc.org/content/279/35/36892.abstract}
}
@article{Eissing2007Response,
author = {Eissing, T. and Waldherr, S. and Allgower, F. and Scheurich, P. and
Bullinger, E.},
title = {Response to Bistability in Apoptosis: Roles of Bax, Bcl-2, and Mitochondrial
Permeability Transition Pores},
journal = {Biophysical Journal},
year = {2007},
volume = {92},
pages = {3332 - 3334},
number = {9},
doi = {10.1529/biophysj.106.100362},
pdf = {../local/Eissing2007Response.pdf},
file = {Eissing2007Response.pdf:Eissing2007Response.pdf:PDF},
issn = {0006-3495},
keywords = {csbcbook},
url = {http://www.sciencedirect.com/science/article/B94RW-4TR4KB1-1B/2/8c4f12571fa01055b7dea12984318e9f}
}
@article{Eissing2007Responsea,
author = {Eissing, T. and Waldherr, S. and Allgower, F. and Scheurich, P. and
Bullinger, E.},
title = {Response to Bistability in Apoptosis: Roles of Bax, Bcl-2, and Mitochondrial
Permeability Transition Pores},
journal = {Biophys. J.},
year = {2007},
volume = {92},
pages = {3332--3334},
number = {9},
doi = {10.1529/biophysj.106.100362},
issn = {0006-3495},
keywords = {csbcbook},
owner = {jp},
timestamp = {2012.05.11},
url = {http://www.sciencedirect.com/science/article/B94RW-4TR4KB1-1B/2/8c4f12571fa01055b7dea12984318e9f}
}
@article{Ellis1992Pathological,
author = {Ellis, I. O. and Galea, M. and Broughton, N. and Locker, A. and Blamey,
R. W. and Elston, C. W.},
title = {Pathological prognostic factors in breast cancer. II. Histological
type. Relationship with survival in a large study with long-term
follow-up.},
journal = {Histopathology},
year = {1992},
volume = {20},
pages = {479--489},
number = {6},
month = {Jun},
abstract = {The histological tumour type determined by current criteria has been
investigated in a consecutive series of 1621 women with primary operable
breast carcinoma, presenting between 1973 and 1987. All women underwent
definitive surgery with node biopsy and none received adjuvant systemic
therapy. Special types, tubular, invasive cribriform and mucinous,
with a very favourable prognosis can be identified. A common type
of tumour recognized by our group and designated tubular mixed carcinoma
is shown to be prognostically distinct from carcinomas of no special
type; it has a characteristic histological appearance and is the
third most common type in this series. Analysis of subtypes of lobular
carcinoma confirms differing prognoses. The classical, tubulo-lobular
and lobular mixed types are associated with a better prognosis than
carcinomas of no special type; this is not so for the solid variant.
Tubulo-lobular carcinoma in particular has an extremely good prognosis
similar to tumours included in the 'special type' category above.
Neither medullary carcinoma nor atypical medullary carcinoma are
found to carry a survival advantage over carcinomas of no special
type. The results confirm that histological typing of human breast
carcinoma can provide useful prognostic information.},
doi = {10.1111/j.1365-2559.1992.tb01032.x},
pdf = {../local/Ellis1992Pathological.pdf},
file = {Ellis1992Pathological.pdf:Ellis1992Pathological.pdf:PDF},
institution = {Department of Histopathology, City Hospital, Nottingham, UK.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {1607149},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1111/j.1365-2559.1992.tb01032}
}
@article{Elston1991Pathological,
author = {Elston, C. W. and Ellis, I. O.},
title = {Pathological prognostic factors in breast cancer. I. The value of
histological grade in breast cancer: experience from a large study
with long-term follow-up.},
journal = {Histopathology},
year = {1991},
volume = {19},
pages = {403--410},
number = {5},
month = {Nov},
abstract = {Morphological assessment of the degree of differentiation has been
shown in numerous studies to provide useful prognostic information
in breast cancer, but until recently histological grading has not
been accepted as a routine procedure, mainly because of perceived
problems with reproducibility and consistency. In the Nottingham/Tenovus
Primary Breast Cancer Study the most commonly used method, described
by Bloom & Richardson, has been modified in order to make the criteria
more objective. The revised technique involves semiquantitative evaluation
of three morphological features--the percentage of tubule formation,
the degree of nuclear pleomorphism and an accurate mitotic count
using a defined field area. A numerical scoring system is used and
the overall grade is derived from a summation of individual scores
for the three variables: three grades of differentiation are used.
Since 1973, over 2200 patients with primary operable breast cancer
have been entered into a study of multiple prognostic factors. Histological
grade, assessed in 1831 patients, shows a very strong correlation
with prognosis; patients with grade I tumours have a significantly
better survival than those with grade II and III tumours (P less
than 0.0001). These results demonstrate that this method for histological
grading provides important prognostic information and, if the grading
protocol is followed consistently, reproducible results can be obtained.
Histological grade forms part of the multifactorial Nottingham prognostic
index, together with tumour size and lymph node stage, which is used
to stratify individual patients for appropriate therapy.},
doi = {10.1111/j.1365-2559.1991.tb00229.x},
pdf = {../local/Elston1991Pathological.pdf},
file = {Elston1991Pathological.pdf:Elston1991Pathological.pdf:PDF},
institution = {Department of Histopathology, City Hospital, Nottingham, UK.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {1757079},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1111/j.1365-2559.1991.tb00229.x}
}
@article{Esquela-Kerscher2006Oncomirs,
author = {Esquela-Kerscher, A. and Slack, F. J.},
title = {Oncomirs - micro{RNA}s with a role in cancer.},
journal = {Nat. Rev. Cancer},
year = {2006},
volume = {6},
pages = {259--269},
number = {4},
month = {Apr},
abstract = {MicroRNAs (miRNAs) are an abundant class of small non-protein-coding
RNAs that function as negative gene regulators. They regulate diverse
biological processes, and bioinformatic data indicates that each
miRNA can control hundreds of gene targets, underscoring the potential
influence of miRNAs on almost every genetic pathway. Recent evidence
has shown that miRNA mutations or mis-expression correlate with various
human cancers and indicates that miRNAs can function as tumour suppressors
and oncogenes. miRNAs have been shown to repress the expression of
important cancer-related genes and might prove useful in the diagnosis
and treatment of cancer.},
doi = {10.1038/nrc1840},
pdf = {../local/Esquela-Kerscher2006Oncomirs.pdf},
file = {Esquela-Kerscher2006Oncomirs.pdf:Esquela-Kerscher2006Oncomirs.pdf:PDF},
institution = { Developmental Biology, 266 Whitney Avenue, New Haven, Connecticut
06520, USA.},
keywords = {csbcbook},
owner = {jp},
pii = {nrc1840},
pmid = {16557279},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1038/nrc1840}
}
@article{Esteller2008Epigenetics,
author = {Esteller, M.},
title = {Epigenetics in cancer},
journal = {N. Engl. J. Med.},
year = {2008},
volume = {358},
pages = {1148--1159},
number = {11},
month = {Mar},
doi = {10.1056/NEJMra072067},
pdf = {../local/Esteller2008Epigenetics.pdf},
file = {Esteller2008Epigenetics.pdf:Esteller2008Epigenetics.pdf:PDF},
institution = {Cancer Epigenetics Laboratory, Spanish National Cancer Research Center,
Madrid, Spain. mesteller@cnio.es},
keywords = {csbcbook},
owner = {jp},
pii = {358/11/1148},
pmid = {18337604},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1056/NEJMra072067}
}
@article{Esteller2007Cancer,
author = {Esteller, M.},
title = {Cancer epigenomics: {DNA} methylomes and histone-modification maps},
journal = {Nat. Rev. Genet.},
year = {2007},
volume = {8},
pages = {286--298},
number = {4},
month = {Apr},
abstract = {An altered pattern of epigenetic modifications is central to many
common human diseases, including cancer. Many studies have explored
the mosaic patterns of DNA methylation and histone modification in
cancer cells on a gene-by-gene basis; among their results has been
the seminal finding of transcriptional silencing of tumour-suppressor
genes by CpG-island-promoter hypermethylation. However, recent technological
advances are now allowing cancer epigenetics to be studied genome-wide
- an approach that has already begun to provide both biological insight
and new avenues for translational research. It is time to 'upgrade'
cancer epigenetics research and put together an ambitious plan to
tackle the many unanswered questions in this field using epigenomics
approaches.},
doi = {10.1038/nrg2005},
pdf = {../local/Esteller2007Cancer.pdf},
file = {Esteller2007Cancer.pdf:Esteller2007Cancer.pdf:PDF},
institution = {Cancer Epigenetics Laboratory, Spanish National Cancer Centre (CNIO),
Melchor Fernandez Almagro 3, 28029 Madrid, Spain. mesteller@cnio.es},
keywords = {csbcbook},
owner = {jp},
pii = {nrg2005},
pmid = {17339880},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1038/nrg2005}
}
@article{Fabbri2008MicroRNAs,
author = {Fabbri, M. and Croce, C. M. and Calin, G. A.},
title = {{MicroRNAs}},
journal = {Cancer J.},
year = {2008},
volume = {14},
pages = {1--6},
number = {1},
abstract = {MicroRNAs (miRNAs) are small, noncoding RNAs with regulatory functions,
which play an important role in many human diseases, including cancer.
An emerging number of studies show that miRNAs can act either as
oncogenes or as tumor suppressor genes or sometimes as both. Germline,
somatic mutations and polymorphisms can contribute to cancer predisposition.
miRNA expression levels have diagnostic and prognostic implications,
and their roles as anticancer therapeutic agents is promising and
currently under investigation.},
doi = {10.1097/PPO.0b013e318164145e},
institution = {Human Cancer Genetics, Molecular Virology, Immunology and Medical
Genetics, Ohio State University, Columbus, OH, USA.},
keywords = {csbcbook},
owner = {jp},
pii = {00130404-200801000-00001},
pmid = {18303474},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1097/PPO.0b013e318164145e}
}
@article{Filipowicz2008Mechanisms,
author = {Filipowicz, W. and Bhattacharyya, S. N. and Sonenberg, N.},
title = {Mechanisms of post-transcriptional regulation by micro{RNA}s: are
the answers in sight?},
journal = {Nat. Rev. Genet.},
year = {2008},
volume = {9},
pages = {102--114},
number = {2},
month = {Feb},
abstract = {MicroRNAs constitute a large family of small, approximately 21-nucleotide-long,
non-coding RNAs that have emerged as key post-transcriptional regulators
of gene expression in metazoans and plants. In mammals, microRNAs
are predicted to control the activity of approximately 30\% of all
protein-coding genes, and have been shown to participate in the regulation
of almost every cellular process investigated so far. By base pairing
to mRNAs, microRNAs mediate translational repression or mRNA degradation.
This Review summarizes the current understanding of the mechanistic
aspects of microRNA-induced repression of translation and discusses
some of the controversies regarding different modes of microRNA function.},
doi = {10.1038/nrg2290},
pdf = {../local/Filipowicz2008Mechanisms.pdf},
file = {Filipowicz2008Mechanisms.pdf:Filipowicz2008Mechanisms.pdf:PDF},
institution = {Friedrich Miescher Institute for Biomedical Research, 4002 Basel,
Switzerland. witold.filipowicz@fmi.ch},
keywords = {csbcbook},
owner = {jp},
pii = {nrg2290},
pmid = {18197166},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1038/nrg2290}
}
@article{Finetti2008Sixteen-kinase,
author = {Finetti, P. and Cervera, N. and Charafe-Jauffret, E. and Chabannon,
C. and Charpin, C. and Chaffanet, M. and Jacquemier, J. and Viens,
P. and Birnbaum, D. and Bertucci, F.},
title = {Sixteen-kinase gene expression identifies luminal breast cancers
with poor prognosis},
journal = {Cancer Res.},
year = {2008},
volume = {68},
pages = {767--776},
number = {3},
month = {Feb},
abstract = {Breast cancer is a heterogeneous disease made of various molecular
subtypes with different prognosis. However, evolution remains difficult
to predict within some subtypes, such as luminal A, and treatment
is not as adapted as it should be. Refinement of prognostic classification
and identification of new therapeutic targets are needed. Using oligonucleotide
microarrays, we profiled 227 breast cancers. We focused our analysis
on two major breast cancer subtypes with opposite prognosis, luminal
A (n = 80) and basal (n = 58), and on genes encoding protein kinases.
Whole-kinome expression separated luminal A and basal tumors. The
expression (measured by a kinase score) of 16 genes encoding serine/threonine
kinases involved in mitosis distinguished two subgroups of luminal
A tumors: Aa, of good prognosis and Ab, of poor prognosis. This classification
and its prognostic effect were validated in 276 luminal A cases from
three independent series profiled across different microarray platforms.
The classification outperformed the current prognostic factors in
univariate and multivariate analyses in both training and validation
sets. The luminal Ab subgroup, characterized by high mitotic activity
compared with luminal Aa tumors, displayed clinical characteristics
and a kinase score intermediate between the luminal Aa subgroup and
the luminal B subtype, suggesting a continuum in luminal tumors.
Some of the mitotic kinases of the signature represent therapeutic
targets under investigation. The identification of luminal A cases
of poor prognosis should help select appropriate treatment, whereas
the identification of a relevant kinase set provides potential targets.},
doi = {10.1158/0008-5472.CAN-07-5516},
pdf = {../local/Finetti2008Sixteen-kinase.pdf},
file = {Finetti2008Sixteen-kinase.pdf:Finetti2008Sixteen-kinase.pdf:PDF},
institution = {UMR599 Inserm, Institut Paoli-Calmettes, Laboratoire d'Oncologie
Moléculaire, Centre de Recherche en Cancérologie de Marseille, Marseille,
France.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {68/3/767},
pmid = {18245477},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1158/0008-5472.CAN-07-5516}
}
@article{Freeman2006Copy,
author = {Freeman, J. L. and Perry, G. H. and Feuk, L. and Redon, R. and McCarroll,
S. A. and Altshuler, D. M. and Aburatani, H. and Jones, K. W. and
Tyler-Smith, C. and Hurles, M. E. and Carter, N. P. and Scherer,
S. W. and Lee, C.},
title = {Copy number variation: new insights in genome diversity},
journal = {Genome Res},
year = {2006},
volume = {16},
pages = {949--961},
number = {8},
month = {Aug},
abstract = {DNA copy number variation has long been associated with specific chromosomal
rearrangements and genomic disorders, but its ubiquity in mammalian
genomes was not fully realized until recently. Although our understanding
of the extent of this variation is still developing, it seems likely
that, at least in humans, copy number variants (CNVs) account for
a substantial amount of genetic variation. Since many CNVs include
genes that result in differential levels of gene expression, CNVs
may account for a significant proportion of normal phenotypic variation.
Current efforts are directed toward a more comprehensive cataloging
and characterization of CNVs that will provide the basis for determining
how genomic diversity impacts biological function, evolution, and
common human diseases.},
doi = {10.1101/gr.3677206},
pdf = {../local/Freeman2006Copy.pdf},
file = {Freeman2006Copy.pdf:Freeman2006Copy.pdf:PDF},
institution = {Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts
02115, USA.},
keywords = {cgh, csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {gr.3677206},
pmid = {16809666},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1101/gr.3677206}
}
@article{Frigola2006Epigenetic,
author = {Frigola, J. and Song, J. and Stirzaker, C. and Hinshelwood, R. A.
and Peinado, M. A. and Clark, S. J.},
title = {Epigenetic remodeling in colorectal cancer results in coordinate
gene suppression across an entire chromosome band},
journal = {Nat. Genet.},
year = {2006},
volume = {38},
pages = {540--549},
number = {5},
month = {May},
abstract = {We report a new mechanism in carcinogenesis involving coordinate long-range
epigenetic gene silencing. Epigenetic silencing in cancer has always
been envisaged as a local event silencing discrete genes. However,
in this study of silencing in colorectal cancer, we found common
repression of the entire 4-Mb band of chromosome 2q.14.2, associated
with global methylation of histone H3 Lys9. DNA hypermethylation
within the repressed genomic neighborhood was localized to three
separate enriched CpG island 'suburbs', with the largest hypermethylated
suburb spanning 1 Mb. These data change our understanding of epigenetic
gene silencing in cancer cells: namely, epigenetic silencing can
span large regions of the chromosome, and both DNA-methylated and
neighboring unmethylated genes can be coordinately suppressed by
global changes in histone modification. We propose that loss of gene
expression can occur through long-range epigenetic silencing, with
similar implications as loss of heterozygosity in cancer.},
doi = {10.1038/ng1781},
pdf = {../local/Frigola2006Epigenetic.pdf},
file = {Frigola2006Epigenetic.pdf:Frigola2006Epigenetic.pdf:PDF},
institution = {Cancer Program, Garvan Institute of Medical Research, 384 Victoria
Street, Darlinghurst, Sydney 2010, New South Wales, Australia.},
keywords = {csbcbook},
owner = {jp},
pii = {ng1781},
pmid = {16642018},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1038/ng1781}
}
@article{Fussenegger2000NatBio,
author = {Fussenegger, M. and Bailey, J. and Varner, J.},
title = {A mathematical model of caspase function in apoptosis},
journal = {Nat. Biotechnol.},
year = {2000},
volume = {18},
pages = {768-774},
abstract = {Caspases (cysteine-containing aspartate-specific proteases) are at
the core of the cell's suicide machinery. These enzymes, once activated,
dismantle the cell by selectively cleaving key proteins after aspartate
residues. The events culminating in caspase activation are the subject
of intense study because of their role in cancer, and neurodegenerative
and autoimmune disorders. Here we present a mechanistic mathematical
model, formulated on the basis of newly emerging information, describing
key elements of receptor-mediated and stress-induced caspase activation.
We have used mass-conservation principles in conjunction with kinetic
rate laws to formulate ordinary differential equations that describe
the temporal evolution of caspase activation. Qualitative strategies
for the prevention of caspase activation are simulated and compared
with experimental data. We show that model predictions are consistent
with available information. Thus, the model could aid in better understanding
caspase activation and identifying therapeutic approaches promoting
or retarding apoptotic cell death.},
doi = {doi:10.1038/77589},
pdf = {../local/Fuster2005sweet.pdf},
file = {Fuster2005sweet.pdf:Fuster2005sweet.pdf:PDF},
keywords = {csbcbook}
}
@article{Galluzzi2008Cell,
author = {Galluzzi, L. and Kroemer, G.},
title = {Necroptosis: A Specialized Pathway of Programmed Necrosis},
journal = {Cell},
year = {2008},
volume = {135},
pages = {1161-1163},
number = {7},
note = {doi: DOI: 10.1016/j.cell.2008.12.004},
keywords = {csbcbook}
}
@article{Gaudet2005MCPorteomics,
author = {Gaudet, S. and Janes, K. A. and Albeck, J. G. and Pace, E. A. and
Lauffenburger, D. A. and Sorger, P. K.},
title = {A Compendium of Signals and Responses Triggered by Prodeath and Prosurvival
Cytokines},
journal = {Mol Cell Proteomics},
year = {2005},
volume = {4},
pages = {1569-1590},
number = {10},
abstract = {Cell-signaling networks consist of proteins with a variety of functions
(receptors, adaptor proteins, GTPases, kinases, proteases, and transcription
factors) working together to control cell fate. Although much is
known about the identities and biochemical activities of these signaling
proteins, the ways in which they are combined into networks to process
and transduce signals are poorly understood. Network-level understanding
of signaling requires data on a wide variety of biochemical processes
such as posttranslational modification, assembly of macromolecular
complexes, enzymatic activity, and localization. No single method
can gather such heterogeneous data in high throughput, and most studies
of signal transduction therefore rely on series of small, discrete
experiments. Inspired by the power of systematic datasets in genomics,
we set out to build a systematic signaling dataset that would enable
the construction of predictive models of cell-signaling networks.
Here we describe the compilation and fusion of [~]10,000 signal and
response measurements acquired from HT-29 cells treated with tumor
necrosis factor-{alpha}, a proapoptotic cytokine, in combination
with epidermal growth factor or insulin, two prosurvival growth factors.
Nineteen protein signals were measured over a 24-h period using kinase
activity assays, quantitative immunoblotting, and antibody microarrays.
Four different measurements of apoptotic response were also collected
by flow cytometry for each time course. Partial least squares regression
models that relate signaling data to apoptotic response data reveal
which aspects of compendium construction and analysis were important
for the reproducibility, internal consistency, and accuracy of the
fused set of signaling measurements. We conclude that it is possible
to build self-consistent compendia of cell-signaling data that can
be mined computationally to yield important insights into the control
of mammalian cell responses.},
keywords = {csbcbook}
}
@article{GevaZatorsky2006MSB,
author = {Geva-Zatorsky, N. and Rosenfeld, N. and Itzkovitz, S. and Milo, R.
and Sigal, A. and Dekel, E. and Yarnitzky, T. and Liron, Y. and Polak,
P. and Lahav, G. and Alon, U.},
title = {Oscillations and variability in the p53 system},
journal = {Mol Syst Biol},
year = {2006},
volume = {2},
pages = {2006 0033},
abstract = {Understanding the dynamics and variability of protein circuitry requires
accurate measurements in living cells as well as theoretical models.
To address this, we employed one of the best-studied protein circuits
in human cells, the negative feedback loop between the tumor suppressor
p53 and the oncogene Mdm2. We measured the dynamics of fluorescently
tagged p53 and Mdm2 over several days in individual living cells.
We found that isogenic cells in the same environment behaved in highly
variable ways following DNA-damaging gamma irradiation: some cells
showed undamped oscillations for at least 3 days (more than 10 peaks).
The amplitude of the oscillations was much more variable than the
period. Sister cells continued to oscillate in a correlated way after
cell division, but lost correlation after about 11 h on average.
Other cells showed low-frequency fluctuations that did not resemble
oscillations. We also analyzed different families of mathematical
models of the system, including a novel checkpoint mechanism. The
models point to the possible source of the variability in the oscillations:
low-frequency noise in protein production rates, rather than noise
in other parameters such as degradation rates. This study provides
a view of the extensive variability of the behavior of a protein
circuit in living human cells, both from cell to cell and in the
same cell over time.},
keywords = {csbcbook}
}
@article{Golub1999Molecular,
author = {Golub, T. R. and Slonim, D. K. and Tamayo, P. and Huard, C. and Gaasenbeek,
M. and Mesirov, J. P. and Coller, H. and Loh, M. L. and Downing,
J. R. and Caligiuri, M. A. and Bloomfield, C. D. and Lander, E. S.},
title = {Molecular classification of cancer: class discovery and class prediction
by gene expression monitoring},
journal = {Science},
year = {1999},
volume = {286},
pages = {531--537},
abstract = {Although cancer classification has improved over the past 30 years,
there has been no general approach for identifying new cancer classes
(class discovery) or for assigning tumors to known classes (class
prediction). Here, a generic approach to cancer classification based
on gene expression monitoring by DNA microarrays is described and
applied to human acute leukemias as a test case. A class discovery
procedure automatically discovered the distinction between acute
myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) without
previous knowledge of these classes. An automatically derived class
predictor was able to determine the class of new leukemia cases.
The results demonstrate the feasibility of cancer classification
based solely on gene expression moni- toring and suggest a general
strategy for discovering and predicting cancer classes for other
types of cancer, independent of previous biological knowledge.},
doi = {10.1126/science.286.5439.531},
pdf = {../local/Golub1999Molecular.pdf},
file = {Golub1999Molecular.pdf:Golub1999Molecular.pdf:PDF},
keywords = {csbcbook, csbcbook-ch3, csbcbook-ch4},
subject = {microarray},
url = {http://dx.doi.org/10.1126/science.286.5439.531}
}
@article{Han2008Apoptosis,
author = {Han, L. and Zhao, Y. and Jia, X.},
title = {Mathematical modeling identified c-FLIP as an apoptotic switch in
death receptor induced apoptosis},
journal = {Apoptosis},
year = {2008},
volume = {13},
pages = {1198-204},
number = {10},
abstract = {Apoptosis is an essential process to get rid of injured or unwanted
cells. In this study, we proposed a mathematical modeling for death
receptor mediated apoptosis to investigate the role of c-FLIP in
controlling the balance between apoptosis and survival. In order
to get insight into how NF-kappa B mediated pro-survival pathway
affects the outcome of our modeling, we implemented reduced models
without taking such regulation into consideration. Our simulation
revealed that c-FLIP could act as a pivotal death or life switch
and this switch-like behavior is bistable, irreversible, and robust.
We introduce a new term, probability apoptosis, to delineate the
likelihood in occurrence of apoptosis events. This simulation system
is plausible and may offer several valuable clinical indications
for the abnormal apoptosis related disease, such as cancer.},
keywords = {csbcbook}
}
@article{Hanahan2000hallmarks,
author = {Hanahan, D. and Weinberg, R. A.},
title = {The hallmarks of cancer},
journal = {Cell},
year = {2000},
volume = {100},
pages = {57--70},
doi = {10.1016/S0092-8674(00)81683-9},
pdf = {../local/Hanahan2000hallmarks.pdf},
file = {Hanahan2000hallmarks.pdf:local/Hanahan2000hallmarks.pdf:PDF},
keywords = {csbcbook, csbcbook-mustread},
owner = {jp},
url = {http://dx.doi.org/10.1016/S0092-8674(00)81683-9}
}
@article{Heiner2004Biosystems,
author = {Heiner, M. and Koch, I. and Will, J.},
title = {Model validation of biological pathways using Petri nets--demonstrated
for apoptosis},
journal = {Biosystems},
year = {2004},
volume = {75},
pages = {15--28},
number = {1-3},
abstract = {This paper demonstrates the first steps of a new integrating methodology
to develop and analyse models of biological pathways in a systematic
manner using well established Petri net technologies. The whole approach
comprises step-wise modelling, animation, model validation as well
as qualitative and quantitative analysis for behaviour prediction.
In this paper, the first phase is addressed how to develop and validate
a qualitative model, which might be extended afterwards to a quantitative
model. The example used in this paper is devoted to apoptosis, the
genetically programmed cell death. Apoptosis is an essential part
of normal physiology for most metazoan species. Disturbances in the
apoptotic process could lead to several diseases. The signal transduction
pathway of apoptosis includes highly complex mechanisms to control
and execute programmed cell death. This paper explains how to model
and validate this pathway using qualitative Petri nets. The results
provide a mathematically unique and valid model enabling the confirmation
of known properties as well as new insights in this pathway.},
keywords = {csbcbook}
}
@article{Hoheisel2006Microarray,
author = {Hoheisel, J. D.},
title = {Microarray technology: beyond transcript profiling and genotype analysis},
journal = {Nat Rev Genet},
year = {2006},
volume = {7},
pages = {200--210},
number = {3},
month = {Mar},
abstract = {Understanding complex functional mechanisms requires the global and
parallel analysis of different cellular processes. DNA microarrays
have become synonymous with this kind of study and, in many cases,
are the obvious platform to achieve this aim. They have already made
important contributions, most notably to gene-expression studies,
although the true potential of this technology is far greater. Whereas
some assays, such as transcript profiling and genotyping, are becoming
routine, others are still in the early phases of development, and
new areas of application, such as genome-wide epigenetic analysis
and on-chip synthesis, continue to emerge.},
doi = {10.1038/nrg1809},
pdf = {../local/Hoheisel2006Microarray.pdf},
file = {Hoheisel2006Microarray.pdf:Hoheisel2006Microarray.pdf:PDF},
institution = {Division of Functional Genome Analysis, Deutsches Krebsforschungszentrum,
Im Neuenheimer Feld 580, 69120 Heidelberg, Germany. J.Hoheisel@dkfz.de},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nrg1809},
pmid = {16485019},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1038/nrg1809}
}
@article{Hornberg2006Cancer,
author = {Hornberg, J. J. and Bruggeman, F. J. and Westerhoff, H. V. and Lankelma,
J.},
title = {Cancer: a Systems Biology disease.},
journal = {Biosystems},
year = {2006},
volume = {83},
pages = {81--90},
number = {2-3},
abstract = {Cancer research has focused on the identification of molecular differences
between cancerous and healthy cells. The emerging picture is overwhelmingly
complex. Molecules out of many parallel signal transduction pathways
are involved. Their activities appear to be controlled by multiple
factors. The action of regulatory circuits, cross-talk between pathways
and the non-linear reaction kinetics of biochemical processes complicate
the understanding and prediction of the outcome of intracellular
signaling. In addition, interactions between tumor and other cell
types give rise to a complex supra-cellular communication network.
If cancer is such a complex system, how can one ever predict the
effect of a mutation in a particular gene on a functionality of the
entire system? And, how should one go about identifying drug targets?
Here, we argue that one aspect is to recognize, where the essence
resides, i.e. recognize cancer as a Systems Biology disease. Then,
more cancer biologists could become systems biologists aiming to
provide answers to some of the above systemic questions. To this
aim, they should integrate the available knowledge stemming from
quantitative experimental results through mathematical models. Models
that have contributed to the understanding of complex biological
systems are discussed. We show that the architecture of a signaling
network is important for determining the site at which an oncologist
should intervene. Finally, we discuss the possibility of applying
network-based drug design to cancer treatment and how rationalized
therapies, such as the application of kinase inhibitors, may benefit
from Systems Biology.},
doi = {10.1016/j.biosystems.2005.05.014},
pdf = {../local/Hornberg2006Cancer.pdf},
file = {Hornberg2006Cancer.pdf:Hornberg2006Cancer.pdf:PDF},
institution = {Cell Biology, BioCentrum Amsterdam, Faculty of Earth and Life Sciences,
Vrije Universiteit, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands.
jorrit.hornberg@falw.vu.nl},
keywords = {csbcbook, csbcbook-mustread},
owner = {jp},
pii = {S0303-2647(05)00117-6},
pmid = {16426740},
timestamp = {2009.10.11},
url = {http://dx.doi.org/10.1016/j.biosystems.2005.05.014}
}
@article{Hua2005JImmunol,
author = {Hua, F. and Cornejo, M. G. and Cardone, M. H. and Stokes, C. L. and
Lauffenburger, D. A.},
title = {Effects of Bcl-2 levels on Fas signaling-induced caspase-3 activation:
molecular genetic tests of computational model predictions},
journal = {J Immunol},
year = {2005},
volume = {175},
pages = {985--95},
number = {2},
abstract = {Fas-induced apoptosis is a critical process for normal immune system
development and function. Although many molecular components in the
Fas signaling pathway have been identified, a systematic understanding
of how they work together to determine network dynamics and apoptosis
itself has remained elusive. To address this, we generated a computational
model for interpreting and predicting effects of pathway component
properties. The model integrates current information concerning the
signaling network downstream of Fas activation, through both type
I and type II pathways, until activation of caspase-3. Unknown parameter
values in the model were estimated using experimental data obtained
from human Jurkat T cells. To elucidate critical signaling network
properties, we examined the effects of altering the level of Bcl-2
on the kinetics of caspase-3 activation, using both overexpression
and knockdown in the model and experimentally. Overexpression was
used to distinguish among alternative hypotheses for inhibitory binding
interactions of Bcl-2 with various components in the mitochondrial
pathway. In comparing model simulations with experimental results,
we find the best agreement when Bcl-2 blocks the release of cytochrome
c by binding to both Bax and truncated Bid instead of Bax, truncated
Bid, or Bid alone. Moreover, although Bcl-2 overexpression strongly
reduces caspase-3 activation, Bcl-2 knockdown has a negligible effect,
demonstrating a general model finding that varying the expression
levels of signal molecules frequently has asymmetric effects on the
outcome. Finally, we demonstrate that the relative dominance of type
I vs type II pathways can be switched by varying particular signaling
component levels without changing network structure.},
keywords = {csbcbook}
}
@article{Hudis2007Trastuzumab,
author = {Hudis, C.A.},
title = {Trastuzumab--mechanism of action and use in clinical practice.},
journal = {N. Engl. J. Med.},
year = {2007},
volume = {357},
pages = {39--51},
number = {1},
month = {Jul},
doi = {10.1056/NEJMra043186},
pdf = {../local/Hudis2007Trastuzumab.pdf},
file = {Hudis2007Trastuzumab.pdf:Hudis2007Trastuzumab.pdf:PDF},
institution = {Breast Cancer Medicine Service, Solid Tumor Division, Department
of Medicine, Memorial Sloan-Kettering Cancer Center, New York, USA.
hudisc@mskcc.org},
keywords = {csbcbook},
owner = {jp},
pii = {357/1/39},
pmid = {17611206},
timestamp = {2009.10.09},
url = {http://dx.doi.org/10.1056/NEJMra043186}
}
@article{Iafrate2004Detection,
author = {A. John Iafrate and Lars Feuk and Miguel N Rivera and Marc L Listewnik
and Patricia K Donahoe and Ying Qi and Stephen W Scherer and Charles
Lee},
title = {Detection of large-scale variation in the human genome},
journal = {Nat. Genet.},
year = {2004},
volume = {36},
pages = {949--951},
number = {9},
month = {Sep},
abstract = {We identified 255 loci across the human genome that contain genomic
imbalances among unrelated individuals. Twenty-four variants are
present in > 10\% of the individuals that we examined. Half of these
regions overlap with genes, and many coincide with segmental duplications
or gaps in the human genome assembly. This previously unappreciated
heterogeneity may underlie certain human phenotypic variation and
susceptibility to disease and argues for a more dynamic human genome
structure.},
doi = {10.1038/ng1416},
pdf = {../local/Iafrate2004Detection.pdf},
file = {Iafrate2004Detection.pdf:Iafrate2004Detection.pdf:PDF},
institution = {Department of Pathology, Brigham and Women's Hospital, 20 Shattuck
St., Thorn 6-28, Boston, Massachusetts 02115, USA.},
keywords = {cgh, csbcbook, csbcbook-ch2},
owner = {jp},
pii = {ng1416},
pmid = {9},
timestamp = {2009.02.08},
url = {http://dx.doi.org/10.1038/ng1416}
}
@article{Irizarry2003Exploration,
author = {Irizarry, R. A. and Hobbs, B. and Collin, F. and Beazer-Barclay,
Y. D. and Antonellis, K. J. and Scherf, U. and Speed, T. P.},
title = {Exploration, normalization, and summaries of high density oligonucleotide
array probe level datas},
journal = {Biostatistics},
year = {2003},
volume = {4},
pages = {249--264},
number = {2},
month = {Apr},
abstract = {In this paper we report exploratory analyses of high-density oligonucleotide
array data from the Affymetrix GeneChip system with the objective
of improving upon currently used measures of gene expression. Our
analyses make use of three data sets: a small experimental study
consisting of five MGU74A mouse GeneChip arrays, part of the data
from an extensive spike-in study conducted by Gene Logic and Wyeth's
Genetics Institute involving 95 HG-U95A human GeneChip arrays; and
part of a dilution study conducted by Gene Logic involving 75 HG-U95A
GeneChip arrays. We display some familiar features of the perfect
match and mismatch probe (PM and MM) values of these data, and examine
the variance-mean relationship with probe-level data from probes
believed to be defective, and so delivering noise only. We explain
why we need to normalize the arrays to one another using probe level
intensities. We then examine the behavior of the PM and MM using
spike-in data and assess three commonly used summary measures: Affymetrix's
(i) average difference (AvDiff) and (ii) MAS 5.0 signal, and (iii)
the Li and Wong multiplicative model-based expression index (MBEI).
The exploratory data analyses of the probe level data motivate a
new summary measure that is a robust multi-array average (RMA) of
background-adjusted, normalized, and log-transformed PM values. We
evaluate the four expression summary measures using the dilution
study data, assessing their behavior in terms of bias, variance and
(for MBEI and RMA) model fit. Finally, we evaluate the algorithms
in terms of their ability to detect known levels of differential
expression using the spike-in data. We conclude that there is no
obvious downside to using RMA and attaching a standard error (SE)
to this quantity using a linear model which removes probe-specific
affinities.},
doi = {10.1093/biostatistics/4.2.249},
pdf = {../local/Irizarry2003Exploration.pdf},
file = {Irizarry2003Exploration.pdf:Irizarry2003Exploration.pdf:PDF},
institution = {Department of Biostatistics, Johns Hopkins University, Baltimore,
MD 21205, USA. rafa@jhu.edu},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {4/2/249},
pmid = {12925520},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1093/biostatistics/4.2.249}
}
@article{Ishkanian2004tiling,
author = {Ishkanian, A. S. and Malloff, C. A. and Watson, S. K. and DeLeeuw,
R. J. and Chi, B. and Coe, B. P. and Snijders, A. and Albertson,
D. G. and Pinkel, D. and Marra, M. A. and Ling, V. and MacAulay,
C. and Lam, W. L.},
title = {A tiling resolution {DNA} microarray with complete coverage of the
human genome},
journal = {Nat. Genet.},
year = {2004},
volume = {36},
pages = {299--303},
number = {3},
month = {Mar},
abstract = {We constructed a tiling resolution array consisting of 32,433 overlapping
BAC clones covering the entire human genome. This increases our ability
to identify genetic alterations and their boundaries throughout the
genome in a single comparative genomic hybridization (CGH) experiment.
At this tiling resolution, we identified minute DNA alterations not
previously reported. These alterations include microamplifications
and deletions containing oncogenes, tumor-suppressor genes and new
genes that may be associated with multiple tumor types. Our findings
show the need to move beyond conventional marker-based genome comparison
approaches, that rely on inference of continuity between interval
markers. Our submegabase resolution tiling set for array CGH (SMRT
array) allows comprehensive assessment of genomic integrity and thereby
the identification of new genes associated with disease.},
doi = {10.1038/ng1307},
pdf = {../local/Ishkanian2004tiling.pdf},
file = {Ishkanian2004tiling.pdf:Ishkanian2004tiling.pdf:PDF},
institution = {British Columbia Cancer Research Centre, 601 West 10th Avenue, Vancouver,
British Columbia V5Z 1L3, Canada.},
keywords = {csbcbook, microarray},
owner = {jp},
pii = {ng1307},
pmid = {14981516},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1038/ng1307}
}
@article{Jablonka2002changing,
author = {Jablonka, A. and Lamb, M. J.},
title = {The changing concept of epigenetics},
journal = {Ann N Y Acad Sci},
year = {2002},
volume = {981},
pages = {82--96},
month = {Dec},
abstract = {We discuss the changing use of epigenetics, a term coined by Conrad
Waddington in the 1940s, and how the epigenetic approach to development
differs from the genetic approach. Originally, epigenetics referred
to the study of the way genes and their products bring the phenotype
into being. Today, it is primarily concerned with the mechanisms
through which cells become committed to a particular form or function
and through which that functional or structural state is then transmitted
in cell lineages. We argue that modern epigenetics is important not
only because it has practical significance for medicine, agriculture,
and species conservation, but also because it has implications for
the way in which we should view heredity and evolution. In particular,
recognizing that there are epigenetic inheritance systems through
which non-DNA variations can be transmitted in cell and organismal
lineages broadens the concept of heredity and challenges the widely
accepted gene-centered neo-Darwinian version of Darwinism.},
institution = {Cohn Institute for the History and Philosophy of Science and Ideas,
Tel Aviv University, Tel Aviv 69978, Israel. jablonka@post.tau.ac.il},
keywords = {csbcbook},
owner = {jp},
pmid = {12547675},
timestamp = {2009.10.11}
}
@article{Janoueix-Lerosey2005Preferential,
author = {Isabelle Janoueix-Lerosey and Philippe Hupé and Zofia Maciorowski
and Philippe La Rosa and Gudrun Schleiermacher and Gaëlle Pierron
and Stéphane Liva and Emmanuel Barillot and Olivier Delattre},
title = {Preferential occurrence of chromosome breakpoints within early replicating
regions in neuroblastoma.},
journal = {Cell Cycle},
year = {2005},
volume = {4},
pages = {1842--1846},
number = {12},
month = {Dec},
abstract = {Neuroblastoma (NB) is a frequent paediatric extra cranial solid tumor
characterized by the occurrence of unbalanced chromosome translocations,
frequently, but not exclusively, involving chromosomes 1 and 17.
We have used a 1 Mb resolution BAC array to further refine the mapping
of breakpoints in NB cell lines. Replication timing profiles were
evaluated in 7 NB cell lines, using DNAs from G1 and S phases flow
sorted nuclei hybridised on the same array. Strikingly, these replication
timing profiles were highly similar between the different NB cell
lines. Furthermore, a significant level of similarity was also observed
between NB cell lines and lymphoblastoid cells. A segmentation analysis
using the Adaptative Weights Smoothing procedure was performed to
determine regions of coordinate replication. More than 50\% of the
breakpoints mapped to early replicating regions, which account for
23.7\% of the total genome. The breakpoints frequency per 10(8) bases
was therefore 10.84 for early replicating regions, whereas it was
only 2.94 for late replicating regions, these difference being highly
significant (p < 10(-4)). This strong association was also observed
when chromosomes 1 and 17, the two most frequent translocation partners
in NB were excluded from the statistical analysis. These results
unambiguously establish a link between unbalanced translocations,
whose most likely mechanism of occurrence relies on break-induced
replication, and early replication of the genome.},
pdf = {../local/Janoueix-Lerosey2005Preferential.pdf},
file = {Janoueix-Lerosey2005Preferential.pdf:Janoueix-Lerosey2005Preferential.pdf:PDF},
institution = {Laboratoire de Pathologie Moléculaire des Cancers, Institut Curie,
Paris, France.},
keywords = {csbcbook, csbcbook-ch2},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {2257},
pmid = {16294040},
timestamp = {2009.10.18},
url = {http://www.landesbioscience.com/journals/cc/article/2257/}
}
@article{Johnson2005Kinomics,
author = {Johnson, S. A. and Hunter, T.},
title = {Kinomics: methods for deciphering the kinome.},
journal = {Nat. Methods},
year = {2005},
volume = {2},
pages = {17--25},
number = {1},
month = {Jan},
abstract = {Phosphorylation by protein kinases is the most widespread and well-studied
signaling mechanism in eukaryotic cells. Phosphorylation can regulate
almost every property of a protein and is involved in all fundamental
cellular processes. Cataloging and understanding protein phosphorylation
is no easy task: many kinases may be expressed in a cell, and one-third
of all intracellular proteins may be phosphorylated, representing
as many as 20,000 distinct phosphoprotein states. Defining the kinase
complement of the human genome, the kinome, has provided an excellent
starting point for understanding the scale of the problem. The kinome
consists of 518 kinases, and every active protein kinase phosphorylates
a distinct set of substrates in a regulated manner. Deciphering the
complex network of phosphorylation-based signaling is necessary for
a thorough and therapeutically applicable understanding of the functioning
of a cell in physiological and pathological states. We review contemporary
techniques for identifying physiological substrates of the protein
kinases and studying phosphorylation in living cells.},
doi = {10.1038/nmeth731},
pdf = {../local/Johnson2005Kinomics.pdf},
file = {Johnson2005Kinomics.pdf:Johnson2005Kinomics.pdf:PDF},
institution = {Molecular and Cell Biology Laboratory, Salk Institute, 10010 North
Torrey Pines Road, La Jolla, California 92037, USA.},
keywords = {csbcbook, csbcbook-ch2},
owner = {jp},
pii = {nmeth731},
pmid = {15789031},
timestamp = {2009.10.13},
url = {http://dx.doi.org/10.1038/nmeth731}
}
@article{Kallioniemi2008CGH,
author = {Kallioniemi, A.},
title = {{CGH} microarrays and cancer.},
journal = {Curr Opin Biotechnol},
year = {2008},
volume = {19},
pages = {36--40},
number = {1},
month = {Feb},
abstract = {Genetic alterations are a key feature of cancer cells and typically
target biological processes and pathways that contribute to cancer
pathogenesis. Array-based comparative genomic hybridization (aCGH)
has provided a wealth of new information on copy number changes in
cancer on a genome-wide level and aCGH data have also been utilized
in cancer classification. More importantly, aCGH analyses have allowed
highly accurate localization of specific genetic alterations that,
for example, are associated with tumor progression, therapy response,
or patient outcome. The genes involved in these aberrations are likely
to contribute to cancer pathogenesis, and the high-resolution mapping
by aCGH greatly facilitates the subsequent identification of these
cancer-associated genes.},
doi = {10.1016/j.copbio.2007.11.004},
pdf = {../local/Kallioniemi2008CGH.pdf},
file = {Kallioniemi2008CGH.pdf:Kallioniemi2008CGH.pdf:PDF},
institution = {Laboratory of Cancer Genetics, Tampere University Hospital and Institute
of Medical Technology, University of Tampere, Biokatu 6, Tampere
FI-33014, Finland. anne.kallioniemi@uta.fi},
keywords = {csbcbook, csbcbook-ch2, cgh},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {S0958-1669(07)00148-6},
pmid = {18162393},
timestamp = {2009.10.18},
url = {http://dx.doi.org/10.1016/j.copbio.2007.11.004}
}
@article{Kallioniemi1992Comparative,
author = {A. Kallioniemi and O. P. Kallioniemi and D. Sudar and D. Rutovitz
and J. W. Gray and F. Waldman and D. Pinkel},
title = {Comparative genomic hybridization for molecular cytogenetic analysis
of solid tumors.},
journal = {Science},
year = {1992},
volume = {258},
pages = {818--821},
number = {5083},
month = {Oct},
abstract = {Comparative genomic hybridization produces a map of DNA sequence copy
number as a function of chromosomal location throughout the entire
genome. Differentially labeled test DNA and normal reference DNA
are hybridized simultaneously to normal chromosome spreads. The hybridization
is detected with two different fluorochromes. Regions of gain or
loss of DNA sequences, such as deletions, duplications, or amplifications,
are seen as changes in the ratio of the intensities of the two fluorochromes
along the target chromosomes. Analysis of tumor cell lines and primary
bladder tumors identified 16 different regions of amplification,
many in loci not previously known to be amplified.},
pdf = {../local/Kallioniemi1992Comparative.pdf},
file = {Kallioniemi1992Comparative.pdf:Kallioniemi1992Comparative.pdf:PDF},
institution = {Department of Laboratory Medicine, University of California, San
Francisco 94143.},
keywords = {csbcbook, csbcbook-ch2, cgh},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {1359641},
timestamp = {2009.10.18},
url = {http://www.sciencemag.org/cgi/reprint/258/5083/818}
}
@article{Kim2008Insights,
author = {Eddo Kim and Amir Goren and Gil Ast},
title = {Insights into the connection between cancer and alternative splicing},
journal = {Trends Genet.},
year = {2008},
volume = {24},
pages = {7-10},
keywords = {csbcbook}
}
@article{Kitano2005NatBiotechnol,
author = {Kitano, H. and Funahashi, A. and Matsuoka, Y. and Oda, K.},
title = {Using process diagrams for the graphical representation of biological
networks},
journal = {Nat. {B}iotechnol.},
year = {2005},
volume = {8},
pages = {961-966},
abstract = {With the increased interest in understanding biological networks,
such as protein-protein interaction networks and gene regulatory
networks, methods for representing and communicating such networks
in both human- and machine-readable form have become increasingly
important. Although there has been significant progress in machine-readable
representation of networks, as exemplified by the Systems Biology
Mark-up Language (SBML) (http://www.sbml.org) issues in human-readable
representation have been largely ignored. This article discusses
human-readable diagrammatic representations and proposes a set of
notations that enhances the formality and richness of the information
represented. The process diagram is a fully state transition-based
diagram that can be translated into machine-readable forms such as
SBML in a straightforward way. It is supported by CellDesigner, a
diagrammatic network editing software (http://www.celldesigner.org/),
and has been used to represent a variety of networks of various sizes
(from only a few components to several hundred components).},
doi = {10.1038/nbt1111},
keywords = {csbcbook}
}
@article{Knudson1971Mutation,
author = {Alfred G. Knudson},
title = {Mutation and Cancer: Statistical Study of Retinoblastoma},
journal = {Proceedings of the National Academy of Sciences},
year = {1971},
volume = {68},
pages = {820-823},
keywords = {csbcbook}
}
@article{Lahav2004NatGenet,
author = {Lahav, G. and Rosenfeld, N. and Sigal, A. and Geva-Zatorsky, N. and
Levine, A. J. and Elowitz, M. B. and Alon, U.},
title = {Dynamics of the p53-Mdm2 feedback loop in individual cells},
journal = {Nat Genet},
year = {2004},
volume = {36},
pages = {147--50},
number = {2},
abstract = {The tumor suppressor p53, one of the most intensely investigated proteins,
is usually studied by experiments that are averaged over cell populations,
potentially masking the dynamic behavior in individual cells. We
present a system for following, in individual living cells, the dynamics
of p53 and its negative regulator Mdm2 (refs. 1,4-7): this system
uses functional p53-CFP and Mdm2-YFP fusion proteins and time-lapse
fluorescence microscopy. We found that p53 was expressed in a series
of discrete pulses after DNA damage. Genetically identical cells
had different numbers of pulses: zero, one, two or more. The mean
height and duration of each pulse were fixed and did not depend on
the amount of DNA damage. The mean number of pulses, however, increased
with DNA damage. This approach can be used to study other signaling
systems and suggests that the p53-Mdm2 feedback loop generates a
'digital' clock that releases well-timed quanta of p53 until damage
is repaired or the cell dies.},
keywords = {csbcbook}
}
@article{Lavrik2007JBC,
author = {Lavrik, I. N. and Golks, A. and Riess, D. and Bentele, M. and Eils,
R. and Krammer, P. H.},
title = {Analysis of CD95 threshold signaling: triggering of CD95 (FAS/APO-1)
at low concentrations primarily results in survival signaling},
journal = {J Biol Chem},
year = {2007},
volume = {282},
pages = {13664-71},
number = {18},
abstract = {Recently we generated a mathematical model (Bentele, M., Lavrik, I.,
Ulrich, M., Stosser, S., Heermann, D. W., Kalthoff, H., Krammer,
P. H., and Eils, R. (2004) J. Cell Biol. 166, 839-851) of signaling
in CD95(Fas/APO-1)-mediated apoptosis. Mathematical modeling in combination
with experimental data provided new insights into CD95-mediated apoptosis
and allowed us to establish a threshold mechanism of life and death.
Here, we further assessed the predictability of the model experimentally
by a detailed analysis of the threshold behavior of CD95 signaling.
Using the model predictions for the mechanism of the threshold behavior
we found that the CD95 DISC (death-inducing signaling complex) is
formed at the cell membrane upon stimulation with low concentrations
of agonistic anti-APO-1 monoclonal antibodies; however, activation
of procaspase-8 at the DISC is blocked due to high cellular FLICE-inhibitory
protein recruitment into the DISC. Given that death signaling does
not occur upon CD95 stimulation at low (threshold) anti-APO-1 concentrations,
we also analyzed survival signaling, focusing on mitogen-activated
protein kinase activation. Interestingly, we found that mitogen-activated
protein kinase activation takes place under threshold conditions.
These findings show that triggering of CD95 can signal both life
or death, depending on the strength of the stimulus.},
keywords = {csbcbook}
}
@article{Legewie2006PLOSCompBiol,
author = {Legewie, S. and Blathgen, N. and Herzel, H.},
title = {Mathematical Modeling Identifies Inhibitors of Apoptosis as Mediators
of Positive Feedback and Bistability},
journal = {PLoS Comput Biol},
year = {2006},
volume = {2},
pages = {e120},
number = {9},
month = {09},
abstract = {The intrinsic, or mitochondrial, pathway of caspase activation is
essential for apoptosis induction by various stimuli including cytotoxic
stress. It depends on the cellular context, whether cytochrome c
released from mitochondria induces caspase activation gradually or
in an all-or-none fashion, and whether caspase activation irreversibly
commits cells to apoptosis. By analyzing a quantitative kinetic model,
we show that inhibition of caspase-3 (Casp3) and Casp9 by inhibitors
of apoptosis (IAPs) results in an implicit positive feedback, since
cleaved Casp3 augments its own activation by sequestering IAPs away
from Casp9. We demonstrate that this positive feedback brings about
bistability (i.e., all-or-none behaviour), and that it cooperates
with Casp3-mediated feedback cleavage of Casp9 to generate irreversibility
in caspase activation. Our calculations also unravel how cell-specific
protein expression brings about the observed qualitative differences
in caspase activation (gradual versus all-or-none and reversible
versus irreversible). Finally, known regulators of the pathway are
shown to efficiently shift the apoptotic threshold stimulus, suggesting
that the bistable caspase cascade computes multiple inputs into an
all-or-none caspase output. As cellular inhibitory proteins (e.g.,
IAPs) frequently inhibit consecutive intermediates in cellular signaling
cascades (e.g., Casp3 and Casp9), the feedback mechanism described
in this paper is likely to be a widespread principle on how cells
achieve ultrasensitivity, bistability, and irreversibility.},
doi = {10.1371/journal.pcbi.0020120},
keywords = {csbcbook},
publisher = {Public Library of Science},
url = {http://dx.plos.org/10.1371/journal.pcbi.0020120}
}
@article{LevBarOr2000PNAS,
author = {Lev Bar-Or, R. and Maya, R. and Segel, L. A. and Alon, U. and Levine,
A. J. and Oren, M.},
title = {Generation of oscillations by the p53-Mdm2 feedback loop: a theoretical
and experimental study},
journal = {Proc Natl Acad Sci U S A},
year = {2000},
volume = {97},
pages = {11250--5},
number = {21},
abstract = {The intracellular activity of the p53 tumor suppressor protein is
regulated through a feedback loop involving its transcriptional target,
mdm2. We present a simple mathematical model suggesting that, under
certain circumstances, oscillations in p53 and Mdm2 protein levels
can emerge in response to a stress signal. A delay in p53-dependent
induction of Mdm2 is predicted to be required, albeit not sufficient,
for this oscillatory behavior. In line with the predictions of the
model, oscillations of both p53 and Mdm2 indeed occur on exposure
of various cell types to ionizing radiation. Such oscillations may
allow cells to repair their DNA without risking the irreversible
consequences of continuous excessive p53 activation.},
keywords = {csbcbook}
}
@article{Li2009BriefBioinform,
author = {Li, C. and Courtot, M. and Le Novere, N. and Laibe, C.},
title = {BioModels.net Web Services, a free and integrated toolkit for computational
modelling software},
journal = {Brief Bioinform},
year = {2009},
abstract = {Exchanging and sharing scientific results are essential for researchers
in the field of computational modelling. BioModels.net defines agreed-upon
standards for model curation. A fundamental one, MIRIAM (Minimum
Information Requested in the Annotation of Models), standardises
the annotation and curation process of quantitative models in biology.
To support this standard, MIRIAM Resources maintains a set of standard
data types for annotating models, and provides services for manipulating
these annotations. Furthermore, BioModels.net creates controlled
vocabularies, such as SBO (Systems Biology Ontology) which strictly
indexes, defines and links terms used in Systems Biology. Finally,
BioModels Database provides a free, centralised, publicly accessible
database for storing, searching and retrieving curated and annotated
computational models. Each resource provides a web interface to submit,
search, retrieve and display its data. In addition, the BioModels.net
team provides a set of Web Services which allows the community to
programmatically access the resources. A user is then able to perform
remote queries, such as retrieving a model and resolving all its
MIRIAM Annotations, as well as getting the details about the associated
SBO terms. These web services use established standards. Communications
rely on SOAP (Simple Object Access Protocol) messages and the available
queries are described in a WSDL (Web Services Description Language)
file. Several libraries are provided in order to simplify the development
of client software. BioModels.net Web Services make one step further
for the researchers to simulate and understand the entirety of a
biological system, by allowing them to retrieve biological models
in their own tool, combine queries in workflows and efficiently analyse
models.},
keywords = {csbcbook}
}
@article{Li2007JBiosci,
author = {Li, C. and Ge, Q. W. and Nakata, M. and Matsuno, H. and Miyano, S.},
title = {Modelling and simulation of signal transductions in an apoptosis
pathway by using timed Petri nets},
journal = {J Biosci},
year = {2007},
volume = {32},
pages = {113--27},
number = {1},
abstract = {This paper first presents basic Petri net components representing
molecular interactions and mechanisms of signalling pathways, and
introduces a method to construct a Petri net model of a signalling
pathway with these components. Then a simulation method of determining
the delay time of transitions, by using timed Petri nets - i.e. the
time taken in fi ring of each transition - is proposed based on some
simple principles that the number of tokens flowed into a place is
equivalent to the number of tokens fl owed out. Finally, the availability
of proposed method is confirmed by observing signalling transductions
in biological pathways through simulation experiments of the apoptosis
signalling pathways as an example.},
keywords = {csbcbook}
}
@article{Lowery2008MicroRNAs,
author = {Lowery, A. J. and Miller, N. and McNeill, R. E. and Kerin, M. J.},
title = {{MicroRNAs} as prognostic indicators and therapeutic targets: potential
effect on breast cancer management.},
journal = {Clin. Cancer Res.},
year = {2008},
volume = {14},
pages = {360--365},
number = {2},
month = {Jan},
abstract = {The discovery of microRNAs (miRNA) as novel modulators of gene expression
has resulted in a rapidly expanding repertoire of molecules in this
family, as reflected in the concomitant expansion of scientific literature.
MiRNAs are a category of naturally occurring RNA molecules that play
important regulatory roles in plants and animals by targeting mRNAs
for cleavage or translational repression. Characteristically, miRNAs
are noncoding, single-stranded short (18-22 nucleotides) RNAs, features
which possibly explain why they had not been intensively investigated
until recently. Accumulating experimental evidence indicates that
miRNAs play a pivotal role in many cellular functions via the regulation
of gene expression. Furthermore, their dysregulation and/or mutation
has been shown in carcinogenesis. We provide a brief review of miRNA
biogenesis and discuss the technical challenges of modifying experimental
techniques to facilitate the identification and characterization
of these small RNAs. MiRNA function and their involvement in malignancy,
particularly their putative role as oncogenes or tumor suppressors
is also discussed, with a specific emphasis on breast cancer. Finally,
we comment on the potential role of miRNAs in breast cancer management,
particularly in improving current prognostic tools and achieving
the goal of individualized cancer treatment.},
doi = {10.1158/1078-0432.CCR-07-0992},
pdf = {../local/Lowery2008MicroRNAs.pdf},
file = {Lowery2008MicroRNAs.pdf:Lowery2008MicroRNAs.pdf:PDF},
institution = {Department of Surgery, National University of Ireland, Galway, Ireland.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {14/2/360},
pmid = {18223209},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1158/1078-0432.CCR-07-0992}
}
@article{Lu2005MicroRNA,
author = {Lu, J. and Getz, G. and Miska, E. A. and Alvarez-Saavedra, E. and
Lamb, J. and Peck, D. and Sweet-Cordero, A. and Ebert, D. L. and
Mak, R. H. and Ferrando, A. A. and Downing, J. R. and Jacks, T. and
Horvitz, H. R. and Golub, T. R.},
title = {MicroRNA expression profiles classify human cancers.},
journal = {Nature},
year = {2005},
volume = {435},
pages = {834--838},
number = {7043},
month = {Jun},
abstract = {Recent work has revealed the existence of a class of small non-coding
RNA species, known as microRNAs (miRNAs), which have critical functions
across various biological processes. Here we use a new, bead-based
flow cytometric miRNA expression profiling method to present a systematic
expression analysis of 217 mammalian miRNAs from 334 samples, including
multiple human cancers. The miRNA profiles are surprisingly informative,
reflecting the developmental lineage and differentiation state of
the tumours. We observe a general downregulation of miRNAs in tumours
compared with normal tissues. Furthermore, we were able to successfully
classify poorly differentiated tumours using miRNA expression profiles,
whereas messenger RNA profiles were highly inaccurate when applied
to the same samples. These findings highlight the potential of miRNA
profiling in cancer diagnosis.},
doi = {10.1038/nature03702},
pdf = {../local/Lu2005MicroRNA.pdf},
file = {Lu2005MicroRNA.pdf:Lu2005MicroRNA.pdf:PDF},
institution = {Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141,
USA.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nature03702},
pmid = {15944708},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1038/nature03702}
}
@article{Loenning2007Breast,
author = {L{\o}nning, P. E.},
title = {Breast cancer prognostication and prediction: are we making progress?},
journal = {Ann. Oncol.},
year = {2007},
volume = {18 Suppl 8},
pages = {viii3--viii7},
month = {Sep},
abstract = {Currently, much effort is being invested in the identification of
new, accurate prognostic and predictive factors in breast cancer.
Prognostic factors assess the patient's risk of relapse based on
indicators such as intrinsic tumor biology and disease stage at diagnosis,
and are traditionally used to identify patients who can be spared
unnecessary adjuvant therapy based only on the risk of relapse. Lymph
node status and tumor size are accepted as well-defined prognostic
factors in breast cancer. Predictive factors, in contrast, determine
the responsiveness of a particular tumor to a specific treatment.
Despite recent advances in the understanding of breast cancer biology
and changing practices in disease management, with the exception
of hormone receptor status, which predicts responsiveness to endocrine
treatment, no predictive factor for response to systemic therapy
in breast cancer is widely accepted. While gene expression studies
have provided important new information with regard to tumor biology
and prognostication, attempts to identify predictive factors have
not been successful so far. This article will focus on recent advances
in prognostication and prediction, with emphasis on findings from
gene expression profiling studies.},
doi = {10.1093/annonc/mdm260},
pdf = {../local/Loenning2007Breast.pdf},
file = {Loenning2007Breast.pdf:Loenning2007Breast.pdf:PDF},
institution = {Institute of Medicine, University of Bergen, Department of Oncology,
Haukeland University Hospital, Bergen, Norway. per.lonning@helse-bergen.no},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {18/suppl_8/viii3},
pmid = {17890212},
timestamp = {2011.04.07},
url = {http://dx.doi.org/10.1093/annonc/mdm260}
}
@article{Ma2005PNAS,
author = {Ma, L. and Wagner, J. and Rice, J. J. and Hu, W. and Levine, A. J.
and Stolovitzky, G. A.},
title = {A plausible model for the digital response of p53 to DNA damage},
journal = {Proc Natl Acad Sci U S A},
year = {2005},
volume = {102},
pages = {14266--71},
number = {40},
abstract = {Recent observations show that the single-cell response of p53 to ionizing
radiation (IR) is "digital" in that it is the number of oscillations
rather than the amplitude of p53 that shows dependence on the radiation
dose. We present a model of this phenomenon. In our model, double-strand
break (DSB) sites induced by IR interact with a limiting pool of
DNA repair proteins, forming DSB-protein complexes at DNA damage
foci. The persisting complexes are sensed by ataxia telangiectasia
mutated (ATM), a protein kinase that activates p53 once it is phosphorylated
by DNA damage. The ATM-sensing module switches on or off the downstream
p53 oscillator, consisting of a feedback loop formed by p53 and its
negative regulator, Mdm2. In agreement with experiments, our simulations
show that by assuming stochasticity in the initial number of DSBs
and the DNA repair process, p53 and Mdm2 exhibit a coordinated oscillatory
dynamics upon IR stimulation in single cells, with a stochastic number
of oscillations whose mean increases with IR dose. The damped oscillations
previously observed in cell populations can be explained as the aggregate
behavior of single cells.},
keywords = {csbcbook}
}
@article{Mattick2003Challenging,
author = {John S. Mattick},
title = {Challenging the dogma: the hidden layer of non-protein-coding {RNAs}
in complex organisms},
journal = {BioEssays},
year = {2003},
volume = {25},
pages = {930-939},
keywords = {csbcbook}
}
@article{Mattick2006Non,
author = {John S. Mattick and Igor V. Makunin},
title = {Non-coding {RNA}},
journal = {Hum. Mol. Genet.},
year = {2006},
volume = {15},
pages = {R17-R29},
keywords = {csbcbook}
}
@article{Mello2004Revealing,
author = {Craig C. Mello and Darryl {Conte Jr}},
title = {Revealing the world of {RNA} interference},
journal = {Nature},
year = {2004},
volume = {43},
pages = {338-342},
keywords = {csbcbook}
}
@article{Miller2007Expression,
author = {Miller, L.D. and Liu, E.T.},
title = {Expression genomics in breast cancer research: microarrays at the
crossroads of biology and medicine},
journal = {Breast Cancer Res.},
year = {2007},
volume = {9},
pages = {206},
abstract = {Genome-wide expression microarray studies have revealed that the biological
and clinical heterogeneity of breast cancer can be partly explained
by information embedded within a complex but ordered transcriptional
architecture. Comprising this architecture are gene expression networks,
or signatures, reflecting biochemical and behavioral properties of
tumors that might be harnessed to improve disease subtyping, patient
prognosis and prediction of therapeutic response. Emerging 'hypothesis-driven'
strategies that incorporate knowledge of pathways and other biological
phenomena in the signature discovery process are linking prognosis
and therapy prediction with transcriptional readouts of tumorigenic
mechanisms that better inform therapeutic options.},
doi = {10.1186/bcr1662},
pdf = {../local/Miller2007Expression.pdf},
file = {Miller2007Expression.pdf:Miller2007Expression.pdf:PDF},
keywords = {csbcbook, csbcbook-ch3},
url = {http://dx.doi.org/10.1186/bcr1662}
}
@article{Mitelman2007Impact,
author = {Mitelman, F. and Johansson, B. and Mertens, F.},
title = {{{T}he impact of translocations and gene fusions on cancer causation}},
journal = {Nat. Rev. Cancer},
year = {2007},
volume = {7},
pages = {233--245},
keywords = {csbcbook}
}
@article{Nakabayashi2006JTB,
author = {Nakabayashi, J. and Sasaki, A.},
title = {A mathematical model for apoptosome assembly: The optimal cytochrome
c/Apaf-1 ratio},
journal = {Journal of Theoretical Biology},
year = {2006},
volume = {242},
pages = {280 - 287},
number = {2},
abstract = {Apoptosis, a highly conserved form of cell suicide, is regulated by
apoptotic signals and their transduction with caspases, a family
of cystein proteases. Caspases are constantly expressed in the normal
cells as inactive pro-enzymes. The activity of caspase is regulated
by the proteolysis. Sequential proteolytic reactions of caspases
are needed to execute apoptosis. Mitochondrial pathway is one of
these apoptotic signal pathways, in which caspases are oligomerized
into characteristic heptamer structure, called apoptosome, with caspase-9
that activate the effector caspases for apoptosis. To investigate
the dynamics of signal transduction pathway regulated by oligomerization,
we construct a mathematical model for Apaf-1 heptamer assembly process.
The model first reveals that intermediate products can remain unconverted
even after all assemble reactions are completed. The second result
of the model is that the conversion efficiency of Apaf-1 heptamer
assembly is maximized when the initial concentration of cytochrome
c is equal to that of Apaf-1. When the concentration of cytochrome
c is sufficiently larger or smaller than that of Apaf-1, the final
Apaf-1 heptamer production is decreased, because intermediate Apaf-1
oligomers (tetramers and bigger oligomers), which themselves are
unable to form active heptamer, accumulate too fast in the cells,
choking a smooth production of Apaf-1 heptamer. Slow activation of
Apaf-1 monomers and small oligomers increase the conversion efficiency.
We also study the optimal number of subunits comprising an active
oligomer that maximize the conversion efficiency in assembly process,
and found that the tetramer is the optimum.},
doi = {DOI: 10.1016/j.jtbi.2006.02.022},
issn = {0022-5193},
keywords = {csbcbook},
url = {http://www.sciencedirect.com/science/article/B6WMD-4JVT1Y9-1/2/88df2dfdc8df3b8d6a17c602e71aeb74}
}
@article{Nakabayashi2006Mathematical,
author = {Nakabayashi, J. and Sasaki, A.},
title = {A mathematical model for apoptosome assembly: The optimal cytochrome
c/Apaf-1 ratio},
journal = {J. Theor. Biol.},
year = {2006},
volume = {242},
pages = {280--287},
number = {2},
abstract = {Apoptosis, a highly conserved form of cell suicide, is regulated by
apoptotic signals and their transduction with caspases, a family
of cystein proteases. Caspases are constantly expressed in the normal
cells as inactive pro-enzymes. The activity of caspase is regulated
by the proteolysis. Sequential proteolytic reactions of caspases
are needed to execute apoptosis. Mitochondrial pathway is one of
these apoptotic signal pathways, in which caspases are oligomerized
into characteristic heptamer structure, called apoptosome, with caspase-9
that activate the effector caspases for apoptosis. To investigate
the dynamics of signal transduction pathway regulated by oligomerization,
we construct a mathematical model for Apaf-1 heptamer assembly process.
The model first reveals that intermediate products can remain unconverted
even after all assemble reactions are completed. The second result
of the model is that the conversion efficiency of Apaf-1 heptamer
assembly is maximized when the initial concentration of cytochrome
c is equal to that of Apaf-1. When the concentration of cytochrome
c is sufficiently larger or smaller than that of Apaf-1, the final
Apaf-1 heptamer production is decreased, because intermediate Apaf-1
oligomers (tetramers and bigger oligomers), which themselves are
unable to form active heptamer, accumulate too fast in the cells,
choking a smooth production of Apaf-1 heptamer. Slow activation of
Apaf-1 monomers and small oligomers increase the conversion efficiency.
We also study the optimal number of subunits comprising an active
oligomer that maximize the conversion efficiency in assembly process,
and found that the tetramer is the optimum.},
doi = {DOI: 10.1016/j.jtbi.2006.02.022},
issn = {0022-5193},
keywords = {csbcbook},
owner = {jp},
timestamp = {2012.05.11},
url = {http://www.sciencedirect.com/science/article/B6WMD-4JVT1Y9-1/2/88df2dfdc8df3b8d6a17c602e71aeb74}
}
@article{Nakamura1998ATM,
author = {Yusuke Nakamura},
title = {{ATM}: the p53 booster},
journal = {Nature Medicine},
year = {1998},
volume = {4},
pages = {1231-1232},
keywords = {csbcbook}
}
@article{Npg2007DNA,
author = {{Nature Publishing Group}},
title = {{DNA} {T}echnologies - {M}ilestones timeline},
journal = {Nature Milestones},
year = {2007},
note = {{http://www.nature.com/milestones/miledna/timeline.html}},
keywords = {csbcbook, csbcbook-ch2}
}
@article{OConnor2006BiotechnolLett,
author = {O'Connor, K. C. and Muhitch, J. W. and Lacks, D. J. and Al-Rubeai,
M.},
title = {Modeling suppression of cell death by Bcl-2 over-expression in myeloma
NS0 6A1 cells},
journal = {Biotechnol Lett},
year = {2006},
volume = {28},
pages = {1919--24},
number = {23},
abstract = {A novel population-balance model was employed to evaluate the suppression
of cell death in myeloma NS0 6A1 cells metabolically engineered to
over-express the apoptotic suppressor Bcl-2. The model is robust
in its ability to simulate cell population dynamics in batch suspension
culture and in response to thymidine-induced growth inhibition: 89
percent of simulated cell concentrations are within two standard
deviations of experimental data. Kinetic rate constants in model
equations suggest that Bcl-2 over-expression extends culture longevity
from 6 days to at least 15 days by suppressing the specific rate
of early apoptotic cell formation by more than 6-fold and necrotic
cell formation by at least 3-fold, despite nearly a 3-fold decrease
in initial cell growth rate and no significant change in the specific
rate of late apoptotic cell formation. This computational analysis
supports a mechanism in which Bcl-2 is a common mediator of early
apoptotic and necrotic events occurring at rates that are dependent
on cellular factors accumulating over time. The model has current
application to the rational design of cell cultures through metabolic
engineering for the industrial production of biopharmaceuticals.},
keywords = {csbcbook}
}
@article{Perkins2005Expanding,
author = {D O Perkins and C Jeffries and P Sullivan},
title = {Expanding the 'central dogma': the regulatory role of nonprotein
coding genes and implications for the genetic liability to schizophrenia},
journal = {Molecular Psychiatry},
year = {2005},
volume = {10},
pages = {69-78},
keywords = {csbcbook}
}
@article{Perou1999Distinctive,
author = {Perou, C. M. and Jeffrey, S. S. and {van de Rijn}, M. and Rees, C.
A. and Eisen, M. B. and Ross, D. T. and Pergamenschikov, A. and Williams,
C. F. and Zhu, S. X. and Lee, J. C. and Lashkari, D. and Shalon,
D. and Brown, P. O. and Botstein, D.},
title = {Distinctive gene expression patterns in human mammary epithelial
cells and breast cancers.},
journal = {Proc. Natl. Acad. Sci. U S A},
year = {1999},
volume = {96},
pages = {9212--9217},
number = {16},
month = {Aug},
abstract = {cDNA microarrays and a clustering algorithm were used to identify
patterns of gene expression in human mammary epithelial cells growing
in culture and in primary human breast tumors. Clusters of coexpressed
genes identified through manipulations of mammary epithelial cells
in vitro also showed consistent patterns of variation in expression
among breast tumor samples. By using immunohistochemistry with antibodies
against proteins encoded by a particular gene in a cluster, the identity
of the cell type within the tumor specimen that contributed the observed
gene expression pattern could be determined. Clusters of genes with
coherent expression patterns in cultured cells and in the breast
tumors samples could be related to specific features of biological
variation among the samples. Two such clusters were found to have
patterns that correlated with variation in cell proliferation rates
and with activation of the IFN-regulated signal transduction pathway,
respectively. Clusters of genes expressed by stromal cells and lymphocytes
in the breast tumors also were identified in this analysis. These
results support the feasibility and usefulness of this systematic
approach to studying variation in gene expression patterns in human
cancers as a means to dissect and classify solid tumors.},
doi = {10.1073/pnas.96.16.9212},
pdf = {../local/Perou1999Distinctive.pdf},
file = {Perou1999Distinctive.pdf:Perou1999Distinctive.pdf:PDF},
institution = {Department of Genetics, Stanford University School of Medicine, Stanford,
CA 94305, USA.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pmid = {10430922},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1073/pnas.96.16.9212}
}
@article{Perou2000Molecular,
author = {Perou, C M. and S{\o}rlie, T. and Eisen, M. B. and van de Rijn, M.
and Jeffrey, S. S. and Rees, C. A. and Pollack, J. R. and Ross, D.
T. and Johnsen, H. and Akslen, L. A. and Fluge, O. and Pergamenschikov,
A. and Williams, C. and Zhu, S. X. and L{\o}nning, P. E. and B{\o}rresen-Dale,
A. L. and Brown, P. O. and Botstein, D.},
title = {Molecular portraits of human breast tumours},
journal = {Nature},
year = {2000},
volume = {406},
pages = {747--752},
number = {6797},
month = {Aug},
abstract = {Human breast tumours are diverse in their natural history and in their
responsiveness to treatments. Variation in transcriptional programs
accounts for much of the biological diversity of human cells and
tumours. In each cell, signal transduction and regulatory systems
transduce information from the cell's identity to its environmental
status, thereby controlling the level of expression of every gene
in the genome. Here we have characterized variation in gene expression
patterns in a set of 65 surgical specimens of human breast tumours
from 42 different individuals, using complementary DNA microarrays
representing 8,102 human genes. These patterns provided a distinctive
molecular portrait of each tumour. Twenty of the tumours were sampled
twice, before and after a 16-week course of doxorubicin chemotherapy,
and two tumours were paired with a lymph node metastasis from the
same patient. Gene expression patterns in two tumour samples from
the same individual were almost always more similar to each other
than either was to any other sample. Sets of co-expressed genes were
identified for which variation in messenger RNA levels could be related
to specific features of physiological variation. The tumours could
be classified into subtypes distinguished by pervasive differences
in their gene expression patterns.},
doi = {10.1038/35021093},
pdf = {../local/Perou2000Molecular.pdf},
file = {Perou2000Molecular.pdf:Perou2000Molecular.pdf:PDF},
institution = {Department of Genetics, Stanford University School of Medicine, California
94305, USA.},
keywords = {breastcancer, csbcbook, csbcbook-ch3},
owner = {jp},
pmid = {10963602},
timestamp = {2009.02.04},
url = {http://dx.doi.org/10.1038/35021093}
}
@article{Philippi2009BMCSysBio,
author = {Philippi, N. and Walter, D. and Schlatter, R. and Ferreira, K. and
Ederer, M. and Sawodny, O. and Timmer, J. and Borner, C. and Dandekar,
T.},
title = {Modeling system states in liver cells: survival, apoptosis and their
modifications in response to viral infection},
journal = {BMC Syst Biol},
year = {2009},
volume = {3},
pages = {97},
abstract = {BACKGROUND: The decision pro- or contra apoptosis is complex, involves
a number of different inputs, and is central for the homeostasis
of an individual cell as well as for the maintenance and regeneration
of the complete organism. RESULTS: This study centers on Fas ligand
(FasL)-mediated apoptosis, and a complex and internally strongly
linked network is assembled around the central FasL-mediated apoptosis
cascade. Different bioinformatical techniques are employed and different
crosstalk possibilities including the integrin pathway are considered.
This network is translated into a Boolean network (74 nodes, 108
edges). System stability is dynamically sampled and investigated
using the software SQUAD. Testing a number of alternative crosstalk
possibilities and networks we find that there are four stable system
states, two states comprising cell survival and two states describing
apoptosis by the intrinsic and the extrinsic pathways, respectively.
The model is validated by comparing it to experimental data from
kinetics of cytochrome c release and caspase activation in wildtype
and Bid knockout cells grown on different substrates. Pathophysiological
modifications such as input from cytomegalovirus proteins M36 and
M45 again produces output behavior that well agrees with experimental
data. CONCLUSION: A network model for apoptosis and crosstalk in
hepatocytes shows four different system states and reproduces a number
of different conditions around apoptosis including effects of different
growth substrates and viral infections. It produces semi-quantitative
predictions on the activity of individual nodes, agreeing with experimental
data. The model (SBML format) and all data are available for further
predictions and development.},
keywords = {csbcbook}
}
@article{Pinkel2005Array,
author = {Pinkel, D. and Albertson, D. G.},
title = {Array comparative genomic hybridization and its applications in cancer},
journal = {Nat. Genet.},
year = {2005},
volume = {37 Suppl},
pages = {S11--S17},
month = {Jun},
abstract = {Alteration in DNA copy number is one of the many ways in which gene
expression and function may be modified. Some variations are found
among normal individuals, others occur in the course of normal processes
in some species and still others participate in causing various disease
states. For example, many defects in human development are due to
gains and losses of chromosomes and chromosomal segments that occur
before or shortly after fertilization, and DNA dosage-alteration
changes occurring in somatic cells are frequent contributors to cancer.
Detecting these aberrations and interpreting them in the context
of broader knowledge facilitates the identification of crucial genes
and pathways involved in biological processes and disease. Over the
past several years, array comparative genomic hybridization has proven
its value for analyzing DNA copy-number variations. Here, we discuss
the state of the art of array comparative genomic hybridization and
its applications in cancer, emphasizing general concepts rather than
specific results.},
doi = {10.1038/ng1569},
pdf = {../local/Pinkel2005Array.pdf},
file = {Pinkel2005Array.pdf:Pinkel2005Array.pdf:PDF},
institution = {Department of Laboratory Medicine and Comprehensive Cancer Center,
University of California San Francisco, Box 0808, San Francisco,
California 94143, USA. pinkel@cc.ucsf.edu},
keywords = {csbcbook, cgh, csbcbook-ch2},
owner = {jp},
pii = {ng1569},
pmid = {15920524},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1038/ng1569}
}
@article{Pinkel1998High,
author = {Pinkel, D. and Segraves, R. and Sudar, D. and Clark, S. and Poole,
I. and Kowbel, D. and Collins, C. and Kuo, W. L. and Chen, C. and
Zhai, Y. and Dairkee, S. H. and Ljung, B. M. and Gray, J. W. and
Albertson, D. G.},
title = {High resolution analysis of {DNA} copy number variation using comparative
genomic hybridization to microarrays},
journal = {Nat. Genet.},
year = {1998},
volume = {20},
pages = {207--211},
number = {2},
month = {Oct},
abstract = {Gene dosage variations occur in many diseases. In cancer, deletions
and copy number increases contribute to alterations in the expression
of tumour-suppressor genes and oncogenes, respectively. Developmental
abnormalities, such as Down, Prader Willi, Angelman and Cri du Chat
syndromes, result from gain or loss of one copy of a chromosome or
chromosomal region. Thus, detection and mapping of copy number abnormalities
provide an approach for associating aberrations with disease phenotype
and for localizing critical genes. Comparative genomic hybridization
(CGH) was developed for genome-wide analysis of DNA sequence copy
number in a single experiment. In CGH, differentially labelled total
genomic DNA from a 'test' and a 'reference' cell population are cohybridized
to normal metaphase chromosomes, using blocking DNA to suppress signals
from repetitive sequences. The resulting ratio of the fluorescence
intensities at a location on the 'cytogenetic map', provided by the
chromosomes, is approximately proportional to the ratio of the copy
numbers of the corresponding DNA sequences in the test and reference
genomes. CGH has been broadly applied to human and mouse malignancies.
The use of metaphase chromosomes, however, limits detection of events
involving small regions (of less than 20 Mb) of the genome, resolution
of closely spaced aberrations and linking ratio changes to genomic/genetic
markers. Therefore, more laborious locus-by-locus techniques have
been required for higher resolution studies. Hybridization to an
array of mapped sequences instead of metaphase chromosomes could
overcome the limitations of conventional CGH (ref. 6) if adequate
performance could be achieved. Copy number would be related to the
test/reference fluorescence ratio on the array targets, and genomic
resolution could be determined by the map distance between the targets,
or by the length of the cloned DNA segments. We describe here our
implementation of array CGH. We demonstrate its ability to measure
copy number with high precision in the human genome, and to analyse
clinical specimens by obtaining new information on chromosome 20
aberrations in breast cancer.},
doi = {10.1038/2524},
pdf = {../local/Pinkel1998High.pdf},
file = {Pinkel1998High.pdf:Pinkel1998High.pdf:PDF},
keywords = {cgh, csbcbook},
owner = {franck},
pmid = {9771718},
timestamp = {2007.09.14},
url = {http://dx.doi.org/10.1038/2524}
}
@article{Pollack1999Genome,
author = {Jonathan R. Pollack and Charles M. Perou and Ash A. Alizadeh and
Michael B. Eisen and Alexander Pergamenschikov and Cheryl F. Williams
and Stefanie S. Jeffrey and David Botstein and Patrick O. Brown},
title = {Genome-wide analysis of {DNA} copy-number changes using {cDNA} microarrays},
journal = {Nat. Genet.},
year = {1999},
volume = {23},
pages = {41-46},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Rehm2009CellDeathDiff,
author = {Rehm, M. and Huber, H. J. and Hellwig, C. T. and Anguissola, S. and
Dussmann, H. and Prehn, J. H. M.},
title = {Dynamics of outer mitochondrial membrane permeabilization during
apoptosis},
journal = {Cell Death and Differentiation},
year = {2009},
volume = {16},
pages = {613 - 623},
issn = {1350-9047},
keywords = {csbcbook},
url = {http://www.nature.com/cdd/journal/v16/n4/suppinfo/cdd2008187s1.html}
}
@article{Rehm2009Dynamics,
author = {Rehm, M. and Huber, H. J. and Hellwig, C. T. and Anguissola, S. and
Dussmann, H. and Prehn, J. H. M.},
title = {Dynamics of outer mitochondrial membrane permeabilization during
apoptosis},
journal = {Cell Death Differ.},
year = {2009},
volume = {16},
pages = {613--623},
issn = {1350-9047},
keywords = {csbcbook},
owner = {jp},
timestamp = {2012.05.11},
url = {http://www.nature.com/cdd/journal/v16/n4/suppinfo/cdd2008187s1.html}
}
@article{Reinders2008Genome,
author = {Jon Reinders and Celine Delucinge Vivier and Gregory Theiler and
Didier Chollet and Patrick Descombes and Jerzy Paszkowski},
title = {Genome-wide, high-resolution {DNA} methylation profiling using bisulfite-mediated
cytosine conversion},
journal = {Genome Res.},
year = {2008},
volume = {18},
pages = {469-76},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Rusk2008Primer,
author = {Nicole Rusk and Veronique Kiermer},
title = {Primer: Sequencing - the next generation},
journal = {Nat. Methods},
year = {2008},
volume = {5},
pages = {15},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Satzinger2008Theodor,
author = {Helga Satzinger},
title = {{T}heodor and {M}arcella {B}overi: chromosomes and cytoplasm in heredity
and development},
journal = {Nat. Rev. Genet.},
year = {2008},
volume = {9},
pages = {231-238},
keywords = {csbcbook}
}
@article{Sawyers2008cancer,
author = {Sawyers, C. L.},
title = {The cancer biomarker problem.},
journal = {Nature},
year = {2008},
volume = {452},
pages = {548--552},
number = {7187},
month = {Apr},
abstract = {Genomic technologies offer the promise of a comprehensive understanding
of cancer. These technologies are being used to characterize tumours
at the molecular level, and several clinical successes have shown
that such information can guide the design of drugs targeted to a
relevant molecule. One of the main barriers to further progress is
identifying the biological indicators, or biomarkers, of cancer that
predict who will benefit from a particular targeted therapy.},
doi = {10.1038/nature06913},
pdf = {../local/Sawyers2008cancer.pdf},
file = {Sawyers2008cancer.pdf:Sawyers2008cancer.pdf:PDF},
institution = {Howard Hughes Medical Institute, Human Oncology and Pathogenesis
Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue,
New York, New York 10065, USA.},
keywords = {csbcbook-ch3, csbcbook},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {nature06913},
pmid = {18385728},
timestamp = {2011.11.30},
url = {http://dx.doi.org/10.1038/nature06913}
}
@article{Schones2008Genome,
author = {Dustin E. Schones and Keji Zhao},
title = {Genome-wide approaches to studying chromatin modifications},
journal = {Nat. Rev. Genet.},
year = {2008},
volume = {9},
pages = {179-191},
keywords = {csbcbook, csbcbook-ch2}
}
@book{Schrodinger1944Vie,
title = {Qu'est-ce que la vie?},
publisher = {Christian Bourgois Editeur, 1986},
year = {1944},
author = {Erwin Schrödinger},
pages = {242 p},
keywords = {csbcbook},
opteditor = {Christian Bourgois}
}
@article{Schumacher2006Microarray,
author = {Schumacher, A. and Kapranov, P. and Kaminsky, Z. and Flanagan, J.
and Assadzadeh, A. and Yau, P. and Virtanen, C. and Winegarden, N.
and Cheng, J. and Gingeras, T. and Petronis, A.},
title = {{M}icroarray-based {D}{N}{A} methylation profiling: technology and
applications},
journal = {Nucleic Acids Res.},
year = {2006},
volume = {34},
pages = {528--542},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Shann2008Genome,
author = {Shann, Y.J. and Cheng, C. and Chiao, C.H. and Chen, D.T. and Li,
P.H. and Hsu, M.T.},
title = {Genome-Wide Mapping and Characterization of Hypomethylated Sites
in Human Tissues and Breast Cancer Cell Lines},
journal = {Genome Res.},
year = {2008},
volume = {18},
pages = {791-801},
keywords = {csbcbook}
}
@article{Sherr2004Principles,
author = {Charles J. Sherr},
title = {Principles of Tumor Suppression},
journal = {Cell},
year = {2004},
volume = {116},
pages = {235-246},
keywords = {csbcbook}
}
@article{Solinas1997Matrix,
author = {S. Solinas-Toldo and S. Lampel and S. Stilgenbauer and J. Nickolenko
and A. Benner and H. Dohner and T. Cremer and P. Lichter},
title = {Matrix-based comparative genomic hybridization: Biochips to screen
for genomic imbalances},
journal = {Genes Chromosomes Cancer},
year = {1997},
volume = {20},
pages = {399-407},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Southern1999Molecular,
author = {Edwin Southern and Kalim Mir and Mikhail Shchepinov},
title = {Molecular interactions on microarrays},
journal = {Nat. Genet.},
year = {1999},
volume = {21},
pages = {5-9},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Speybroeck2002From,
author = {L Van Speybroeck},
title = {From Epigenesis to Epigenetics: The Case of {C. H. Waddington}},
journal = {Annals of the New York Academy of Sciences},
year = {2002},
volume = {981},
pages = {61-81},
keywords = {csbcbook}
}
@article{Srebrow2006Connection,
author = {A. Srebrow and A. R. Kornblihtt},
title = {The connection between splicing and cancer},
journal = {J. Cell Sci.},
year = {2006},
volume = {119},
pages = {2635-2641},
keywords = {csbcbook}
}
@article{Stransky2006Regional,
author = {Stransky, N. and Vallot, C. and Reyal, F. and Bernard-Pierrot, I.
and Diez de Medina, S. G. and Segraves, R. and de Rycke, Y. and Elvin,
P. and Cassidy, A. and Spraggon, C. and Graham, A. and Southgate,
J. and Asselain, B. and Allory, Y. and Abbou, C. C. and Albertson,
D. G. and Thiery, J.-P. and Chopin, D. K. and Pinkel, D. and Radvanyi,
F.},
title = {Regional copy number-independent deregulation of transcription in
cancer},
journal = {Nat. Genet.},
year = {2006},
volume = {38},
pages = {1386--1396},
number = {12},
month = {Dec},
abstract = {Genetic and epigenetic alterations have been identified that lead
to transcriptional deregulation in cancers. Genetic mechanisms may
affect single genes or regions containing several neighboring genes,
as has been shown for DNA copy number changes. It was recently reported
that epigenetic suppression of gene expression can also extend to
a whole region; this is known as long-range epigenetic silencing.
Various techniques are available for identifying regional genetic
alterations, but no large-scale analysis has yet been carried out
to obtain an overview of regional epigenetic alterations. We carried
out an exhaustive search for regions susceptible to such mechanisms
using a combination of transcriptome correlation map analysis and
array CGH data for a series of bladder carcinomas. We validated one
candidate region experimentally, demonstrating histone methylation
leading to the loss of expression of neighboring genes without DNA
methylation.},
doi = {10.1038/ng1923},
pdf = {../local/Stransky2006Regional.pdf},
file = {Stransky2006Regional.pdf:Stransky2006Regional.pdf:PDF},
institution = {UMR 144 Centre National de la Recherche Scientifique (CNRS)/Institut
Curie, 75248 Paris Cedex 05, France.},
keywords = {csbcbook},
owner = {jp},
pii = {ng1923},
pmid = {17099711},
timestamp = {2009.10.08},
url = {http://dx.doi.org/10.1038/ng1923}
}
@article{Stratton2008Emerging,
author = {Stratton, M.R. and Rahman, N.},
title = {{{T}he emerging landscape of breast cancer susceptibility}},
journal = {Nat. Genet.},
year = {2008},
volume = {40},
pages = {17--22},
keywords = {csbcbook}
}
@article{Stucki2005JTB,
author = {Stucki, J. W. and Simon, H.-U.},
title = {Mathematical modeling of the regulation of caspase-3 activation and
degradation},
journal = {Journal of Theoretical Biology},
year = {2005},
volume = {234},
pages = {123--131},
number = {1},
abstract = {Caspases are thought to be important players in the execution process
of apoptosis. Inhibitors of apoptosis (IAPs) are able to block caspases
and therefore apoptosis. The fact that a subgroup of the IAP family
inhibits active caspases implies that not each caspase activation
necessarily leads to apoptosis. In such a scenario, however, processed
and enzymically active caspases should somehow be removed. Indeed,
IAP-caspase complexes covalently bind ubiquitin, resulting in degradation
by the 26S proteasome. Following release from mitochondria, IAP antagonists
(e.g. second mitochondrial activator of caspases (Smac)) inactivate
IAPs. Moreover, although pro-apoptotic factors such as irradiation
or anti-cancer drugs may release Smac from mitochondria in tumor
cells, high cytoplasmic survivin and ML-IAP levels might be able
to neutralize it and, consequently, IAPs would further be able to
bind activated caspases. Here, we propose a simple mathematical model,
describing the molecular interactions between Smac deactivators,
Smac, IAPs, and caspase-3, including the requirements for both induction
and prevention of apoptosis, respectively. In addition, we predict
a novel mechanism of caspase-3 degradation that might be particularly
relevant in long-living cells.},
doi = {DOI: 10.1016/j.jtbi.2004.11.011},
issn = {0022-5193},
keywords = {csbcbook},
url = {http://www.sciencedirect.com/science/article/B6WMD-4F9N72G-1/2/1dbb63d611f86dc936c8d6cb218685f0}
}
@article{Soerlie2006Gene,
author = {S{\o}rlie, T. and Perou, C. M. and Fan, C. and Geisler, S. and Aas,
T. and Nobel, A. and Anker, G. and Akslen, L. A. and Botstein, D.
and B{\o}rresen-Dale, A.-L. and L{\o}nning, P. E.},
title = {Gene expression profiles do not consistently predict the clinical
treatment response in locally advanced breast cancer},
journal = {Mol. Cancer Ther.},
year = {2006},
volume = {5},
pages = {2914--2918},
number = {11},
month = {Nov},
abstract = {Neoadjuvant treatment offers an opportunity to correlate molecular
variables to treatment response and to explore mechanisms of drug
resistance in vivo. Here, we present a statistical analysis of large-scale
gene expression patterns and their relationship to response following
neoadjuvant chemotherapy in locally advanced breast cancers. We analyzed
cDNA expression data from 81 tumors from two patient series, one
treated with doxorubicin alone (51) and the other treated with 5-fluorouracil
and mitomycin (30), and both were previously studied for correlations
between TP53 status and response to therapy. We observed a low frequency
of progressive disease within the luminal A subtype from both series
(2 of 36 versus 13 of 45 patients; P = 0.0089) and a high frequency
of progressive disease among patients with luminal B type tumors
treated with doxorubicin (5 of 8 patients; P = 0.0078); however,
aside from these two observations, no other consistent associations
between response to chemotherapy and tumor subtype were observed.
These specific associations could possibly be explained by covariance
with TP53 mutation status, which also correlated with tumor subtype.
Using supervised analysis, we could not uncover a gene profile that
could reliably (>70\% accuracy and specificity) predict response
to either treatment regimen.},
doi = {10.1158/1535-7163.MCT-06-0126},
pdf = {../local/Soerlie2006Gene.pdf},
file = {Soerlie2006Gene.pdf:Soerlie2006Gene.pdf:PDF},
institution = {Department of Medicine, Section of Oncology, Haukeland University
Hospital, N-5021 Bergen, Norway.},
keywords = {csbcbook, csbcbook-ch3},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {5/11/2914},
pmid = {17121939},
timestamp = {2011.04.07},
url = {http://dx.doi.org/10.1158/1535-7163.MCT-06-0126}
}
@article{Soerlie2001Gene,
author = {S{\o}rlie, T. and Perou, C. M. and Tibshirani, R. and Aas, T. and
Geisler, S. and Johnsen, H. and Hastie, T. and Eisen, M. B. and van
de Rijn, M. and Jeffrey, S. S. and Thorsen, T. and Quist, H. and
Matese, J. C. and Brown, P. O. and Botstein, D. and Eystein L{\o}nning,
P. and B{\o}rresen-Dale, A. L.},
title = {Gene expression patterns of breast carcinomas distinguish tumor subclasses
with clinical implications},
journal = {Proc. Natl. Acad. Sci. USA},
year = {2001},
volume = {98},
pages = {10869--10874},
number = {19},
month = {Sep},
abstract = {The purpose of this study was to classify breast carcinomas based
on variations in gene expression patterns derived from cDNA microarrays
and to correlate tumor characteristics to clinical outcome. A total
of 85 cDNA microarray experiments representing 78 cancers, three
fibroadenomas, and four normal breast tissues were analyzed by hierarchical
clustering. As reported previously, the cancers could be classified
into a basal epithelial-like group, an ERBB2-overexpressing group
and a normal breast-like group based on variations in gene expression.
A novel finding was that the previously characterized luminal epithelial/estrogen
receptor-positive group could be divided into at least two subgroups,
each with a distinctive expression profile. These subtypes proved
to be reasonably robust by clustering using two different gene sets:
first, a set of 456 cDNA clones previously selected to reflect intrinsic
properties of the tumors and, second, a gene set that highly correlated
with patient outcome. Survival analyses on a subcohort of patients
with locally advanced breast cancer uniformly treated in a prospective
study showed significantly different outcomes for the patients belonging
to the various groups, including a poor prognosis for the basal-like
subtype and a significant difference in outcome for the two estrogen
receptor-positive groups.},
doi = {10.1073/pnas.191367098},
pdf = {../local/Soerlie2001Gene.pdf},
file = {Soerlie2001Gene.pdf:Soerlie2001Gene.pdf:PDF},
institution = {cs, The Norwegian Radium Hospital, Montebello, N-0310 Oslo, Norway.},
keywords = {breastcancer, csbcbook, csbcbook-ch2},
owner = {jp},
pii = {98/19/10869},
pmid = {11553815},
timestamp = {2008.11.15},
url = {http://dx.doi.org/10.1073/pnas.191367098}
}
@article{Sorlie2003Repeated,
author = {S{\o}rlie, T. and Tibshirani, R. and Parker, J. and Hastie, T. and
Marron, J.S. and Nobel, A. and Deng, S. and Johnsen, H. and Pesich,
R. and Geisler, S. and Demeter, J. and Perou, C.M. and Lønning, P.E.
and Brown, P.O. and Børresen-Dale, A.L. and Botstein, D.},
title = {Repeated observation of breast tumor subtypes in independent gene
expression data sets},
journal = {Proc. Natl. Acad. Sci. USA},
year = {2003},
volume = {100},
pages = {8418--8423},
number = {14},
month = {Jul},
abstract = {Characteristic patterns of gene expression measured by DNA microarrays
have been used to classify tumors into clinically relevant subgroups.
In this study, we have refined the previously defined subtypes of
breast tumors that could be distinguished by their distinct patterns
of gene expression. A total of 115 malignant breast tumors were analyzed
by hierarchical clustering based on patterns of expression of 534
"intrinsic" genes and shown to subdivide into one basal-like, one
ERBB2-overexpressing, two luminal-like, and one normal breast tissue-like
subgroup. The genes used for classification were selected based on
their similar expression levels between pairs of consecutive samples
taken from the same tumor separated by 15 weeks of neoadjuvant treatment.
Similar cluster analyses of two published, independent data sets
representing different patient cohorts from different laboratories,
uncovered some of the same breast cancer subtypes. In the one data
set that included information on time to development of distant metastasis,
subtypes were associated with significant differences in this clinical
feature. By including a group of tumors from BRCA1 carriers in the
analysis, we found that this genotype predisposes to the basal tumor
subtype. Our results strongly support the idea that many of these
breast tumor subtypes represent biologically distinct disease entities.},
doi = {10.1073/pnas.0932692100},
pdf = {../local/Sorlie2003Repeated.pdf},
file = {Sorlie2003Repeated.pdf:Sorlie2003Repeated.pdf:PDF},
keywords = {csbcbook, csbcbook-ch3},
url = {http://dx.doi.org/10.1073/pnas.0932692100}
}
@article{Tomita1999Bioinformatics,
author = {Tomita, M. and Hashimoto, K. and Takahashi, K. and Shimizu, T. S.
and Matsuzaki, Y. and Miyoshi, F. and Saito, K. and Tanida, S. and
Yugi, K. and Venter, J. C. and Hutchison, C. A.},
title = {{E-CELL}: software environment for whole-cell simulation},
journal = {Bioinformatics},
year = {1999},
volume = {15},
pages = {72-84},
number = {1},
doi = {10.1093/bioinformatics/15.1.72},
eprint = {http://bioinformatics.oxfordjournals.org/cgi/reprint/15/1/72.pdf},
keywords = {csbcbook},
url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/15/1/72}
}
@article{Tompa2005Assessing,
author = {Martin Tompa and Nan Li and Timothy L Bailey and George M Church
and Bart De Moor and Eleazar Eskin and Alexander V Favorov and Martin
C Frith and Yutao Fu and W James Kent and Vsevolod J Makeev and Andrei
A Mironov and William Stafford Noble and Giulio Pavesi and Graziano
Pesole and Mireille Régnier and Nicolas Simonis and Saurabh Sinha
and Gert Thijs and Jacques Van Helden and Mathias Vandenbogaert and
Zhiping Weng and Christopher Workman and Chun Ye and Zhou Zhu},
title = {Assessing computational tools for the discovery of transcription
factor binding sites},
journal = {Nat. Biotechnol.},
year = {2005},
volume = {23},
pages = {137-144},
keywords = {csbcbook}
}
@article{Tournier2009JTB,
author = {Tournier, L. and Chaves, M.},
title = {Uncovering operational interactions in genetic networks using asynchronous
Boolean dynamics},
journal = {Journal of Theoretical Biology},
year = {2009},
volume = {260},
pages = {196--209},
number = {2},
abstract = {Biological networks of large dimensions, with their diagram of interactions,
are often well represented by a Boolean model with a family of logical
rules. The state space of a Boolean model is finite, and its asynchronous
dynamics are fully described by a transition graph in the state space.
In this context, a model reduction method will be developed for identifying
the active or operational interactions responsible for a given dynamic
behaviour. The first step in this procedure is the decomposition
of the asynchronous transition graph into its strongly connected
components, to obtain a reduced and hierarchically organized graph
of transitions. The second step consists of the identification of
a partial graph of interactions and a sub-family of logical rules
that remain operational in a given region of the state space. This
model reduction method and its usefulness are illustrated by an application
to a model of programmed cell death. The method identifies two mechanisms
used by the cell to respond to death-receptor stimulation and decide
between the survival and apoptotic pathways.},
doi = {10.1016/j.jtbi.2009.06.006},
issn = {0022-5193},
keywords = {csbcbook},
url = {http://www.sciencedirect.com/science/article/B6WMD-4WH8CGD-2/2/e9f844daaad4eef66eacf065c1416383}
}
@article{Turner2002Cellular,
author = {Bryan M. Turner},
title = {Cellular Memory and the Histone Code},
journal = {Cell},
year = {2002},
volume = {111},
pages = {285-291},
keywords = {csbcbook}
}
@article{Tusher2001Significance,
author = {Tusher, V. G. and Tibshirani, R. and Chu, G.},
title = {Significance analysis of microarrays applied to the ionizing radiation
response},
journal = {Proc. Natl. Acad. Sci. USA},
year = {2001},
volume = {98},
pages = {5116--5121},
number = {9},
month = {Apr},
abstract = {Microarrays can measure the expression of thousands of genes to identify
changes in expression between different biological states. Methods
are needed to determine the significance of these changes while accounting
for the enormous number of genes. We describe a method, Significance
Analysis of Microarrays (SAM), that assigns a score to each gene
on the basis of change in gene expression relative to the standard
deviation of repeated measurements. For genes with scores greater
than an adjustable threshold, SAM uses permutations of the repeated
measurements to estimate the percentage of genes identified by chance,
the false discovery rate (FDR). When the transcriptional response
of human cells to ionizing radiation was measured by microarrays,
SAM identified 34 genes that changed at least 1.5-fold with an estimated
FDR of 12\%, compared with FDRs of 60 and 84\% by using conventional
methods of analysis. Of the 34 genes, 19 were involved in cell cycle
regulation and 3 in apoptosis. Surprisingly, four nucleotide excision
repair genes were induced, suggesting that this repair pathway for
UV-damaged DNA might play a previously unrecognized role in repairing
DNA damaged by ionizing radiation.},
doi = {10.1073/pnas.091062498},
pdf = {../local/Tusher2001Significance.pdf},
file = {Tusher2001Significance.pdf:Tusher2001Significance.pdf:PDF},
institution = {Departments of Medicine and Biochemistry, Stanford University, 269
Campus Drive, Center for Clinical Sciences Research 1115, Stanford,
CA 94305-5151, USA.},
keywords = {csbcbook, csbcbook-ch4},
language = {eng},
medline-pst = {ppublish},
owner = {jp},
pii = {091062498},
pmid = {11309499},
timestamp = {2011.04.07},
url = {http://dx.doi.org/10.1073/pnas.091062498}
}
@article{Vaidya2007Breast,
author = {Jayant S Vaidya},
title = {Breast cancer: an artistic view},
journal = {The Lancet Oncology},
year = {2007},
volume = {8},
pages = {583-585},
keywords = {csbcbook}
}
@article{Veer2002Gene,
author = {van 't Veer, L. J. and Dai, H. and van de Vijver, M. J. and He, Y.
D. and Hart, A. A. M. and Mao, M. and Peterse, H. L. and van der
Kooy, K. and Marton, M. J. and Witteveen, A. T. and Schreiber, G.
J. and Kerkhoven, R. M. and Roberts, C. and Linsley, P. S. and Bernards,
R. and Friend, S. H.},
title = {Gene expression profiling predicts clinical outcome of breast cancers},
journal = {Nature},
year = {2002},
volume = {415},
pages = {530--536},
number = {6871},
month = {Jan},
abstract = {Breast cancer patients with the same stage of disease can have markedly
different treatment responses and overall outcome. The strongest
predictors for metastases (for example, lymph node status and histological
grade) fail to classify accurately breast tumours according to their
clinical behaviour. Chemotherapy or hormonal therapy reduces the
risk of distant metastases by approximately one-third; however, 70-80\%
of patients receiving this treatment would have survived without
it. None of the signatures of breast cancer gene expression reported
to date allow for patient-tailored therapy strategies. Here we used
DNA microarray analysis on primary breast tumours of 117 young patients,
and applied supervised classification to identify a gene expression
signature strongly predictive of a short interval to distant metastases
('poor prognosis' signature) in patients without tumour cells in
local lymph nodes at diagnosis (lymph node negative). In addition,
we established a signature that identifies tumours of BRCA1 carriers.
The poor prognosis signature consists of genes regulating cell cycle,
invasion, metastasis and angiogenesis. This gene expression profile
will outperform all currently used clinical parameters in predicting
disease outcome. Our findings provide a strategy to select patients
who would benefit from adjuvant therapy.},
doi = {10.1038/415530a},
pdf = {../local/Veer2002Gene.pdf},
file = {Veer2002Gene.pdf:Veer2002Gene.pdf:PDF},
institution = {Division of Diagnostic Oncology, The Netherlands Cancer Institute,
121 Plesmanlaan, 1066 CX Amsterdam, The Netherlands.},
keywords = {breastcancer, csbcbook, csbcbook-ch3},
owner = {jp},
pii = {415530a},
pmid = {11823860},
timestamp = {2008.11.16},
url = {http://dx.doi.org/10.1038/415530a}
}
@article{Venables2004Aberrant,
author = {Julian P. Venables},
title = {Aberrant and Alternative Splicing in Cancer},
journal = {Cancer Res.},
year = {2004},
volume = {64},
pages = {7647-7654},
keywords = {csbcbook}
}
@article{Vermeulen2008Cancer,
author = {Vermeulen, L. and Sprick, M.R. and Kemper, K. and Stassi, G. and
Medema, J.P.},
title = {{{C}ancer stem cells - old concepts, new insights}},
journal = {Cell Death and Differentiation},
year = {2008},
volume = {15},
pages = {947-58},
keywords = {csbcbook}
}
@article{Vijver2002gene-expression,
author = {van de Vijver, M. J. and He, Y. D. and van't Veer, L. J. and Dai,
H. and Hart, A. A. M. and Voskuil, D. W. and Schreiber, G. J. and
Peterse, J. L. and Roberts, C. and Marton, M. J. and Parrish, M.
and Atsma, D. and Witteveen, A. and Glas, A. and Delahaye, L. and
van der Velde, T. and Bartelink, H. and Rodenhuis, S. and Rutgers,
E. T. and Friend, S. H. and Bernards, R.},
title = {A gene-expression signature as a predictor of survival in breast
cancer},
journal = {N. Engl. J. Med.},
year = {2002},
volume = {347},
pages = {1999--2009},
number = {25},
month = {Dec},
abstract = {BACKGROUND: A more accurate means of prognostication in breast cancer
will improve the selection of patients for adjuvant systemic therapy.
METHODS: Using microarray analysis to evaluate our previously established
70-gene prognosis profile, we classified a series of 295 consecutive
patients with primary breast carcinomas as having a gene-expression
signature associated with either a poor prognosis or a good prognosis.
All patients had stage I or II breast cancer and were younger than
53 years old; 151 had lymph-node-negative disease, and 144 had lymph-node-positive
disease. We evaluated the predictive power of the prognosis profile
using univariable and multivariable statistical analyses. RESULTS:
Among the 295 patients, 180 had a poor-prognosis signature and 115
had a good-prognosis signature, and the mean (+/-SE) overall 10-year
survival rates were 54.6+/-4.4 percent and 94.5+/-2.6 percent, respectively.
At 10 years, the probability of remaining free of distant metastases
was 50.6+/-4.5 percent in the group with a poor-prognosis signature
and 85.2+/-4.3 percent in the group with a good-prognosis signature.
The estimated hazard ratio for distant metastases in the group with
a poor-prognosis signature, as compared with the group with the good-prognosis
signature, was 5.1 (95 percent confidence interval, 2.9 to 9.0; P<0.001).
This ratio remained significant when the groups were analyzed according
to lymph-node status. Multivariable Cox regression analysis showed
that the prognosis profile was a strong independent factor in predicting
disease outcome. CONCLUSIONS: The gene-expression profile we studied
is a more powerful predictor of the outcome of disease in young patients
with breast cancer than standard systems based on clinical and histologic
criteria.},
doi = {10.1056/NEJMoa021967},
pdf = {../local/Vijver2002gene-expression.pdf},
file = {Vijver2002gene-expression.pdf:local/Vijver2002gene-expression.pdf:PDF},
institution = {Division of Diagnostic Oncology, Netherlands Cancer Institute, Amsterdam,
The Netherlands.},
keywords = {breastcancer, csbcbook, csbcbook-ch3},
owner = {jp},
pii = {347/25/1999},
pmid = {12490681},
timestamp = {2008.11.16},
url = {http://dx.doi.org/10.1056/NEJMoa021967}
}
@article{Watanabe2008Endogenous,
author = {Watanabe, T. and Totoki, Y. and Toyoda, A. and Kaneda, M. and Kuramochi-Miyagawa,
S. and Obata, Y. and Chiba, H. and Kohara, Y. and Kono, T. and Nakano,
T. and Surani, M.A. and Sakaki, Y. and Sasaki, H.},
title = {{E}ndogenous si{R}{N}{A}s from naturally formed ds{R}{N}{A}s regulate
transcripts in mouse oocytes},
journal = {Nature},
year = {2008},
volume = {453},
pages = {539--543},
keywords = {csbcbook}
}
@book{Weinberg2007Biology,
title = {The biology of cancer},
publisher = {Garland Science, Taylor \& Francis Group, LLC},
year = {2007},
author = {R A Weinberg},
pages = {864 pages},
keywords = {csbcbook}
}
@techreport{Wu2003Model,
author = {Z Wu and R A Irizarry and R Gentleman and F M Murillo and F Spencer},
title = {A Model Based Background Adjustment for Oligonucleotide Expression
Arrays},
institution = {John Hopkins University, Department of Biostatistics Working Papers,
Baltimore, MD},
year = {2003},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Ylstra2006BAC,
author = {Ylstra, Bauke and Van den Ijssel, Paul and Carvalho, Beatriz and
Brakenhoff, Ruud H and Meijer, Gerrit A},
title = {{BAC to the future! or oligonucleotides: a perspective for micro
array comparative genomic hybridization (array CGH)}},
journal = {Nucleic Acids Res.},
year = {2006},
volume = {34},
pages = {445--450},
keywords = {csbcbook, csbcbook-ch2}
}
@article{Zinovyev2008Bioinformatics,
author = {Zinovyev, A. and Viara, E. and Calzone, L. and Barillot, E.},
title = {{BiNoM}: a {C}ytoscape plugin for manipulating and analyzing biological
networks},
journal = {Bioinformatics},
year = {2008},
volume = {24},
pages = {876-877},
number = {6},
abstract = {BiNoM (Biological Network Manager) is a new bioinformatics software
that significantly facilitates the usage and the analysis of biological
networks in standard systems biology formats (SBML, SBGN, BioPAX).
BiNoM implements a full-featured BioPAX editor and a method of interfaces'
for accessing BioPAX content. BiNoM is able to work with huge BioPAX
files such as whole pathway databases. In addition, BiNoM allows
the analysis of networks created with CellDesigner software and their
conversion into BioPAX format. BiNoM comes as a library and as a
Cytoscape plugin which adds a rich set of operations to Cytoscape
such as path and cycle analysis, clustering sub-networks, decomposition
of network into modules, clipboard operations and others. Availability:
Last version of BiNoM distributed under the LGPL licence together
with documentation, source code and API are available at http://bioinfo.curie.fr/projects/binom
Contact: andrei.zinovyev@curie.fr},
doi = {10.1093/bioinformatics/btm553},
eprint = {http://bioinformatics.oxfordjournals.org/cgi/reprint/24/6/876.pdf},
keywords = {csbcbook},
url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/24/6/876}
}
@comment{{jabref-meta: selector_author:}}
@comment{{jabref-meta: selector_journal:Adv. Drug Deliv. Rev.;Am. J. Hu
m. Genet.;Am. J. Pathol.;Ann. Appl. Stat.;Ann. Math. Statist.;Ann. N.
Y. Acad. Sci.;Ann. Probab.;Ann. Stat.;Artif. Intell. Med.;Bernoulli;Bi
ochim. Biophys. Acta;Bioinformatics;Biometrika;BMC Bioinformatics;Br.
J. Pharmacol.;Breast Cancer Res.;Cell;Cell. Signal.;Chem. Res. Toxicol
.;Clin. Cancer Res.;Combinator. Probab. Comput.;Comm. Pure Appl. Math.
;Comput. Chem.;Comput. Comm. Rev.;Comput. Stat. Data An.;Curr. Genom.;
Curr. Opin. Chem. Biol.;Curr. Opin. Drug Discov. Devel.;Data Min. Know
l. Discov.;Electron. J. Statist.;Eur. J. Hum. Genet.;FEBS Lett.;Found.
Comput. Math.;Genome Biol.;IEEE T. Neural Networ.;IEEE T. Pattern. An
al.;IEEE T. Signal. Proces.;IEEE Trans. Inform. Theory;IEEE Trans. Kno
wl. Data Eng.;IEEE/ACM Trans. Comput. Biol. Bioinf.;Int. J. Comput. Vi
sion;Int. J. Data Min. Bioinform.;Int. J. Qantum Chem.;J Biol Syst;J.
ACM;J. Am. Soc. Inf. Sci. Technol.;J. Am. Stat. Assoc.;J. Bioinform. C
omput. Biol.;J. Biol. Chem.;J. Biomed. Inform.;J. Cell. Biochem.;J. Ch
em. Inf. Comput. Sci.;J. Chem. Inf. Model.;J. Clin. Oncol.;J. Comput.
Biol.;J. Comput. Graph. Stat.;J. Eur. Math. Soc.;J. Intell. Inform. Sy
st.;J. Mach. Learn. Res.;J. Med. Chem.;J. Mol. BIol.;J. R. Stat. Soc.
Ser. B;Journal of Statistical Planning and Inference;Mach. Learn.;Math
. Program.;Meth. Enzymol.;Mol. Biol. Cell;Mol. Biol. Evol.;Mol. Cell.
Biol.;Mol. Syst. Biol.;N. Engl. J. Med.;Nat. Biotechnol.;Nat. Genet.;N
at. Med.;Nat. Methods;Nat. Rev. Cancer;Nat. Rev. Drug Discov.;Nat. Rev
. Genet.;Nature;Neural Comput.;Neural Network.;Neurocomputing;Nucleic
Acids Res.;Pattern Anal. Appl.;Pattern Recognit.;Phys. Rev. E;Phys. Re
v. Lett.;PLoS Biology;PLoS Comput. Biol.;Probab. Theory Relat. Fields;
Proc. IEEE;Proc. Natl. Acad. Sci. USA;Protein Eng.;Protein Eng. Des. S
el.;Protein Sci.;Protein. Struct. Funct. Genet.;Random Struct. Algorit
hm.;Rev. Mod. Phys.;Science;Stat. Probab. Lett.;Statistica Sinica;Theo
r. Comput. Sci.;Trans. Am. Math. Soc.;Trends Genet.;}}
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