Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001002182 | EGA |
REPOSITORIES: EGA
McKinney Matthew M Moffitt Andrea B AB Gaulard Philippe P Travert Marion M De Leval Laurence L Nicolae Alina A Raffeld Mark M Jaffe Elaine S ES Pittaluga Stefania S Xi Liqiang L Heavican Tayla T Iqbal Javeed J Belhadj Karim K Delfau-Larue Marie Helene MH Fataccioli Virginie V Czader Magdalena B MB Lossos Izidore S IS Chapman-Fredricks Jennifer R JR Richards Kristy L KL Fedoriw Yuri Y Ondrejka Sarah L SL Hsi Eric D ED Low Lawrence L Weisenburger Dennis D Chan Wing C WC Mehta-Shah Neha N Horwitz Steven S Bernal-Mizrachi Leon L Flowers Christopher R CR Beaven Anne W AW Parihar Mayur M Baseggio Lucile L Parrens Marie M Moreau Anne A Sujobert Pierre P Pilichowska Monika M Evens Andrew M AM Chadburn Amy A Au-Yeung Rex K H RK Srivastava Gopesh G Choi William W L WW Goodlad John R JR Aurer Igor I Basic-Kinda Sandra S Gascoyne Randy D RD Davis Nicholas S NS Li Guojie G Zhang Jenny J Rajagopalan Deepthi D Reddy Anupama A Love Cassandra C Levy Shawn S Zhuang Yuan Y Datta Jyotishka J Dunson David B DB Davé Sandeep S SS
Cancer discovery 20170125 4
Hepatosplenic T-cell lymphoma (HSTL) is a rare and lethal lymphoma; the genetic drivers of this disease are unknown. Through whole-exome sequencing of 68 HSTLs, we define recurrently mutated driver genes and copy-number alterations in the disease. Chromatin-modifying genes, including <i>SETD2, INO80</i>, and <i>ARID1B</i>, were commonly mutated in HSTL, affecting 62% of cases. HSTLs manifest frequent mutations in <i>STAT5B</i> (31%), <i>STAT3</i> (9%), and <i>PIK3CD</i> (9%), for which there cur ...[more]