Author
Simone Chevalier
Other affiliations: Université de Montréal, National Institutes of Health, Montreal General Hospital ...read more
Bio: Simone Chevalier is an academic researcher from McGill University Health Centre. The author has contributed to research in topics: Prostate cancer & Prostate. The author has an hindex of 28, co-authored 70 publications receiving 6661 citations. Previous affiliations of Simone Chevalier include Université de Montréal & National Institutes of Health.
Topics: Prostate cancer, Prostate, Cancer, Biochemical recurrence, Prostatectomy
Papers published on a yearly basis
Papers
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TL;DR: The Cancer Genome Atlas (TCGA) has been used for a comprehensive molecular analysis of primary prostate carcinomas as discussed by the authors, revealing substantial heterogeneity among primary prostate cancers, evident in the spectrum of molecular abnormalities and its variable clinical course.
2,109 citations
01 Nov 2015
TL;DR: A comprehensive molecular analysis of 333 primary prostate carcinomas revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1).
Abstract: There is substantial heterogeneity among primary prostate cancers, evident in the spectrum of molecular abnormalities and its variable clinical course. As part of The Cancer Genome Atlas (TCGA), we present a comprehensive molecular analysis of 333 primary prostate carcinomas. Our results revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1). Epigenetic profiles showed substantial heterogeneity, including an IDH1 mutant subset with a methylator phenotype. Androgen receptor (AR) activity varied widely and in a subtype-specific manner, with SPOP and FOXA1 mutant tumors having the highest levels of AR-induced transcripts. 25% of the prostate cancers had a presumed actionable lesion in the PI3K or MAPK signaling pathways, and DNA repair genes were inactivated in 19%. Our analysis reveals molecular heterogeneity among primary prostate cancers, as well as potentially actionable molecular defects.
1,794 citations
TL;DR: Molecular similarities among histologically or anatomically related cancer types provide a basis for focused pan-cancer analyses, such as pan-gastrointestinal, Pan-gynecological, pan-kidney, and pan-squamous cancers, and those related by stemness features, which may inform strategies for future therapeutic development.
1,535 citations
TL;DR: The genomic and phenotypic correlates of cancer aneuploidy are defined and genome engineering is applied to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication.
660 citations
TL;DR: In this article, the authors made two errors in preparation of this manuscript and corrected them in the revised Figure S7 by re-ordering the mutations by frequency for COAD and READ independently.
303 citations
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TL;DR: UALCAN, an easy to use, interactive web-portal to perform to in-depth analyses of TCGA gene expression data, serves as a platform for in silico validation of target genes and for identifying tumor sub-group specific candidate biomarkers.
3,546 citations
Institute for Systems Biology1, BC Cancer Agency2, University of California, San Francisco3, University of North Carolina at Chapel Hill4, Columbia University5, Discovery Institute6, Massachusetts Institute of Technology7, Arizona State University8, Sage Bionetworks9, Harvard University10, Johns Hopkins University11, Stanford University12, University of Calgary13, Université libre de Bruxelles14, University of Texas MD Anderson Cancer Center15, Medical College of Wisconsin16, Qatar Airways17, Cold Spring Harbor Laboratory18, University of São Paulo19, Henry Ford Hospital20, University of Alabama at Birmingham21, Van Andel Institute22, Stony Brook University23
TL;DR: An extensive immunogenomic analysis of more than 10,000 tumors comprising 33 diverse cancer types by utilizing data compiled by TCGA identifies six immune subtypes that encompass multiple cancer types and are hypothesized to define immune response patterns impacting prognosis.
3,246 citations
University of Michigan1, Harvard University2, Massachusetts Institute of Technology3, Memorial Sloan Kettering Cancer Center4, University of Washington5, The Royal Marsden NHS Foundation Trust6, Institute of Cancer Research7, Cornell University8, Brigham and Women's Hospital9, Beth Israel Deaconess Medical Center10, University of Washington Medical Center11, University of Trento12, Wayne State University13, Johns Hopkins University14
TL;DR: This cohort study provides clinically actionable information that could impact treatment decisions for affected individuals and identified new genomic alterations in PIK3CA/B, R-spondin, BRAF/RAF1, APC, β-catenin, and ZBTB16/PLZF.
2,713 citations
01 Jan 2013
TL;DR: In this article, the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs) was described, including several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA.
Abstract: We describe the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs). We identify several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA. TERT promoter mutations are shown to correlate with elevated mRNA expression, supporting a role in telomerase reactivation. Correlative analyses confirm that the survival advantage of the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for treatment response only in classical subtype GBM. Integrative analysis of genomic and proteomic profiles challenges the notion of therapeutic inhibition of a pathway as an alternative to inhibition of the target itself. These data will facilitate the discovery of therapeutic and diagnostic target candidates, the validation of research and clinical observations and the generation of unanticipated hypotheses that can advance our molecular understanding of this lethal cancer.
2,616 citations
Nationwide Children's Hospital1, University of North Carolina at Chapel Hill2, Henry Ford Health System3, University of Texas MD Anderson Cancer Center4, Broad Institute5, Walter Reed National Military Medical Center6, Buck Institute for Research on Aging7, New York University8, University of Pittsburgh9, Sage Bionetworks10, University of California, San Francisco11, Institute for Systems Biology12
TL;DR: These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale.
1,928 citations