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Dysregulation of EMT Drives the Progression to Clinically Aggressive Sarcomatoid Bladder Cancer.
Guo, Charles C; Majewski, Tadeusz; Zhang, Li; Yao, Hui; Bondaruk, Jolanta; Wang, Yan; Zhang, Shizhen; Wang, Ziqiao; Lee, June Goo; Lee, Sangkyou; Cogdell, David; Zhang, Miao; Wei, Peng; Grossman, H Barton; Kamat, Ashish; Duplisea, Jonathan James; Ferguson, James Edward; Huang, He; Dadhania, Vipulkumar; Gao, Jianjun; Dinney, Colin; Weinstein, John N; Baggerly, Keith; McConkey, David; Czerniak, Bogdan.
Afiliação
  • Guo CC; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Majewski T; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Zhang L; Department of Environmental Health, University of Cincinnati, Cincinnati, OH, USA.
  • Yao H; Department of Bioinformatics & Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Bondaruk J; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Wang Y; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Zhang S; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Wang Z; Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Lee JG; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Lee S; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Cogdell D; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Zhang M; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Wei P; Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Grossman HB; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Kamat A; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Duplisea JJ; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Ferguson JE; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Huang H; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Dadhania V; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Gao J; Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Dinney C; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Weinstein JN; Department of Bioinformatics & Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • Baggerly K; Department of Bioinformatics & Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
  • McConkey D; Johns Hopkins Greenberg Bladder Cancer Institute, Johns Hopkins University, Baltimore, MD, USA.
  • Czerniak B; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: bczernia@mdanderson.org.
Cell Rep ; 27(6): 1781-1793.e4, 2019 05 07.
Article em En | MEDLINE | ID: mdl-31067463
ABSTRACT
Sarcomatoid urothelial bladder cancer (SARC) displays a high propensity for distant metastasis and is associated with short survival. We report a comprehensive genomic analysis of 28 cases of SARC and 84 cases of conventional urothelial carcinoma (UC), with the TCGA cohort of 408 muscle-invasive bladder cancers serving as the reference. SARCs show a distinct mutational landscape, with enrichment of TP53, RB1, and PIK3CA mutations. They are related to the basal molecular subtype of conventional UCs and could be divided into epithelial-basal and more clinically aggressive mesenchymal subsets on the basis of TP63 and its target gene expression levels. Other analyses reveal that SARCs are driven by downregulation of homotypic adherence genes and dysregulation of the EMT network, and nearly half exhibit a heavily infiltrated immune phenotype. Our observations have important implications for prognostication and the development of more effective therapies for this highly lethal variant of bladder cancer.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sarcoma / Neoplasias da Bexiga Urinária / Progressão da Doença / Transição Epitelial-Mesenquimal Limite: Adult / Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Ano de publicação: 2019 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sarcoma / Neoplasias da Bexiga Urinária / Progressão da Doença / Transição Epitelial-Mesenquimal Limite: Adult / Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Ano de publicação: 2019 Tipo de documento: Article