Article
SETD2 loss-of-function promotes renal cancer branched evolution through replication stress and impaired DNA repair.
Oncogene - 12 Nov 2015
Kanu N, Grönroos E, Martinez P, Burrell R A, Yi Goh X, Bartkova J, Maya-Mendoza A, Mistrík M, Rowan A J, Patel H, Rabinowitz A, East P, Wilson G, Santos C R, McGranahan N, Gulati S, Gerlinger M, Birkbak N J, Joshi T, Alexandrov L B, Stratton M R, Powles T, Matthews N, Bates P A, Stewart A, Szallasi Z, Larkin J, Bartek J, Swanton C
Abstract excerpt
Defining mechanisms that generate intratumour heterogeneity and branched evolution may inspire novel therapeutic approaches to limit tumour diversity and adaptation. SETD2 (Su(var), Enhancer of zeste, Trithorax-domain containing 2) trimethylates histone-3 lysine-36 (H3K36me3) at sites of active transcription and is mutated in diverse tumour types, including clear cell renal carcinomas (ccRCCs). Distinct SETD2...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.