Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to dependence on PRMT5

J. Mavrakis, Konstantinos; Robert McDonald, E.; R. Schlabach, Michael; Billy, Éric; R. Hoffman, Gregory; de Weck, Antoine; A. Ruddy, David; Venkatesan, K.; Yu, Jianjun; McAllister, Gregg; Stump, Mark; deBeaumont, Rosalie; B. Ho, Samuel; Yue, Yingzi; Liu, Yue; Yan‐Neale, Yan; Yang, Guizhi; Lin, Fallon; Yin, Hong; Gao, Hui; Randal Kipp, D.; Zhao, Songping; T. McNamara, Joshua; R. Sprague, Elizabeth; Zheng, Bing; Lin, Ying; Shin Cho, Young; Gu, Justin; Crawford, Kenneth; Ciccone, David; C. Vitari, Alberto; Lai, Albert; Čápka, Vladimı́r; E. Hurov, Kristen; A. Porter, Jeffery; A. Tallarico, John; Mickanin, Craig; Lees, Emma; Pagliarini, Raymond; Keen, Nicholas; Schmelzle, Tobias; Hofmann, Francesco; Stegmeier, Frank; R. Sellers, William

doi:10.1126/science.aad5944

Public

Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to dependence on PRMT5

Published in Science • Feb 12, 2016

Authors:

Konstantinos J. Mavrakis

E. Robert McDonald

Michael R. Schlabach

Abstract

5-Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine salvage pathway. The MTAP gene is frequently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene CDKN2A. By interrogating data from a large-scale short hairpin RNA-mediated screen acro...

Subject

Methionine

CDKN2A

Protein arginine methyltransferase 5

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