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Author

Joshua Armenia

Other affiliations: National Institutes of Health
Bio: Joshua Armenia is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Prostate cancer & Medicine. The author has an hindex of 30, co-authored 53 publications receiving 10006 citations. Previous affiliations of Joshua Armenia include National Institutes of Health.

Papers published on a yearly basis

Papers
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Journal ArticleDOI
Adam Abeshouse1, Jaeil Ahn1, Rehan Akbani1, Adrian Ally1  +308 moreInstitutions (1)
05 Nov 2015-Cell
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

Journal ArticleDOI
05 Apr 2018-Cell
TL;DR: This work charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity.

1,841 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

Journal ArticleDOI
Peter J. Campbell1, Gad Getz2, Jan O. Korbel3, Joshua M. Stuart4  +1329 moreInstitutions (238)
06 Feb 2020-Nature
TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
Abstract: Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1,2,3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10,11,12,13,14,15,16,17,18.

1,600 citations

Journal ArticleDOI
Katherine A Hoadley1, Christina Yau2, Christina Yau3, Toshinori Hinoue4  +735 moreInstitutions (16)
05 Apr 2018-Cell
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


Cited by
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01 Feb 2015
TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.

4,409 citations

Journal ArticleDOI
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

Journal ArticleDOI
17 Apr 2018-Immunity
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

Journal ArticleDOI
Dan R. Robinson1, Eliezer M. Van Allen2, Eliezer M. Van Allen3, Yi-Mi Wu1, Nikolaus Schultz4, Robert J. Lonigro1, Juan Miguel Mosquera, Bruce Montgomery5, Mary-Ellen Taplin3, Colin C. Pritchard5, Gerhardt Attard6, Gerhardt Attard7, Himisha Beltran, Wassim Abida4, Robert K. Bradley5, Jake Vinson4, Xuhong Cao1, Pankaj Vats1, Lakshmi P. Kunju1, Maha Hussain1, Felix Y. Feng1, Scott A. Tomlins, Kathleen A. Cooney1, David Smith1, Christine Brennan1, Javed Siddiqui1, Rohit Mehra1, Yu Chen4, Yu Chen8, Dana E. Rathkopf4, Dana E. Rathkopf8, Michael J. Morris4, Michael J. Morris8, Stephen B. Solomon4, Jeremy C. Durack4, Victor E. Reuter4, Anuradha Gopalan4, Jianjiong Gao4, Massimo Loda, Rosina T. Lis3, Michaela Bowden3, Michaela Bowden9, Stephen P. Balk10, Glenn C. Gaviola9, Carrie Sougnez2, Manaswi Gupta2, Evan Y. Yu5, Elahe A. Mostaghel5, Heather H. Cheng5, Hyojeong Mulcahy5, Lawrence D. True11, Stephen R. Plymate5, Heidi Dvinge5, Roberta Ferraldeschi6, Roberta Ferraldeschi7, Penny Flohr6, Penny Flohr7, Susana Miranda6, Susana Miranda7, Zafeiris Zafeiriou6, Zafeiris Zafeiriou7, Nina Tunariu7, Nina Tunariu6, Joaquin Mateo6, Joaquin Mateo7, Raquel Perez-Lopez6, Raquel Perez-Lopez7, Francesca Demichelis8, Francesca Demichelis12, Brian D. Robinson, Marc H. Schiffman8, David M. Nanus, Scott T. Tagawa, Alexandros Sigaras8, Kenneth Eng8, Olivier Elemento8, Andrea Sboner8, Elisabeth I. Heath13, Howard I. Scher4, Howard I. Scher8, Kenneth J. Pienta14, Philip W. Kantoff3, Johann S. de Bono7, Johann S. de Bono6, Mark A. Rubin, Peter S. Nelson, Levi A. Garraway3, Levi A. Garraway2, Charles L. Sawyers4, Arul M. Chinnaiyan 
21 May 2015-Cell
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