학술논문
MTAP deficiency creates an exploitable target for antifolate therapy in 9p21-loss cancers
Document Type
article
Author
Omar Alhalabi; Jianfeng Chen; Yuxue Zhang; Yang Lu; Qi Wang; Sumankalai Ramachandran; Rebecca Slack Tidwell; Guangchun Han; Xinmiao Yan; Jieru Meng; Ruiping Wang; Anh G. Hoang; Wei-Lien Wang; Jian Song; Lidia Lopez; Alex Andreev-Drakhlin; Arlene Siefker-Radtke; Xinqiao Zhang; William F. Benedict; Amishi Y. Shah; Jennifer Wang; Pavlos Msaouel; Miao Zhang; Charles C. Guo; Bogdan Czerniak; Carmen Behrens; Luisa Soto; Vassiliki Papadimitrakopoulou; Jeff Lewis; Waree Rinsurongkawong; Vadeerat Rinsurongkawong; Jack Lee; Jack Roth; Stephen Swisher; Ignacio Wistuba; John Heymach; Jing Wang; Matthew T. Campbell; Eleni Efstathiou; Mark Titus; Christopher J. Logothetis; Thai H. Ho; Jianjun Zhang; Linghua Wang; Jianjun Gao
Source
Nature Communications, Vol 13, Iss 1, Pp 1-12 (2022)
Subject
Language
English
ISSN
2041-1723
Abstract
The deficiency of MTAP, an enzyme of the adenine salvage pathway, occurs in some cancers. Here the authors perform a small cohort phase II clinical trial with metastatic MTAP-deficient urothelial cancer (UC) and show an increased overall response when comparing to MTAP-proficient UC patients.