Nature Communications (Apr 2022)

MTAP deficiency creates an exploitable target for antifolate therapy in 9p21-loss cancers

  • 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

DOI
https://doi.org/10.1038/s41467-022-29397-z
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 12

Abstract

Read online

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.