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The Cancer Genome Atlas Comprehensive Molecular Characterization of Renal Cell Carcinoma
Authors
Rehan Akbani
Rameen Beroukhim
+31 more
Donald P. Bottaro
Reanne Bowlby
Toni K. Choueiri
Aguirre A. De Cubas
Huihui Fan
Ewan A. Gibb
Richard A. Gibbs
Andrew K. Godwin
Scott Haake
A. Ari Hakimi
Elizabeth P. Henske
Thai H. Ho
James J. Hsieh
Rupa S. Kanchi
Bhavani Krishnan
David J. Kwaitkowski
Martin Lang
Wembin Lui
Maria J. Merino
Gordon B. Mills
Jerome Myers
Michael L. Nickerson
Victor E. Reuter
Ed Reznik
Christopher J. Ricketts
Laura S. Schmidt
C. Simon Shelley
Hui Shen
Brian Shuch
Sabina Signoretti
Christof C. Smith
Publication date
3 April 2018
Publisher
Health Sciences Research Commons
Abstract
© 2018 Renal cell carcinoma (RCC) is not a single disease, but several histologically defined cancers with different genetic drivers, clinical courses, and therapeutic responses. The current study evaluated 843 RCC from the three major histologic subtypes, including 488 clear cell RCC, 274 papillary RCC, and 81 chromophobe RCC. Comprehensive genomic and phenotypic analysis of the RCC subtypes reveals distinctive features of each subtype that provide the foundation for the development of subtype-specific therapeutic and management strategies for patients affected with these cancers. Somatic alteration of BAP1, PBRM1, and PTEN and altered metabolic pathways correlated with subtype-specific decreased survival, while CDKN2A alteration, increased DNA hypermethylation, and increases in the immune-related Th2 gene expression signature correlated with decreased survival within all major histologic subtypes. CIMP-RCC demonstrated an increased immune signature, and a uniform and distinct metabolic expression pattern identified a subset of metabolically divergent (MD) ChRCC that associated with extremely poor survival. Ricketts et al. find distinctive features of each RCC subtype, providing the foundation for development of subtype-specific therapeutic and management strategies. Somatic alteration of BAP1, PBRM1, and metabolic pathways correlates with subtype-specific decreased survival, while CDKN2A alteration, DNA hypermethylation, and Th2 immune signature correlate with decreased survival within all subtypes
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Last time updated on 03/12/2020