Nature Communications (Aug 2021)
Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
- Ninghui Mao,
- Zeda Zhang,
- Young Sun Lee,
- Danielle Choi,
- Aura Agudelo Rivera,
- Dan Li,
- Cindy Lee,
- Samuel Haywood,
- Xiaoping Chen,
- Qing Chang,
- Guotai Xu,
- Hsuan-An Chen,
- Elisa de Stanchina,
- Charles Sawyers,
- Neal Rosen,
- Andrew C. Hsieh,
- Yu Chen,
- Brett S. Carver
Affiliations
- Ninghui Mao
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Zeda Zhang
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Young Sun Lee
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Danielle Choi
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Aura Agudelo Rivera
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Dan Li
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Cindy Lee
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Samuel Haywood
- Department of Surgery, Memorial Sloan Kettering Cancer Center
- Xiaoping Chen
- Antitumor Assessment Core Facility, Memorial Sloan Kettering Cancer Center
- Qing Chang
- Antitumor Assessment Core Facility, Memorial Sloan Kettering Cancer Center
- Guotai Xu
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Hsuan-An Chen
- Louis V. Gerstner Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center
- Elisa de Stanchina
- Antitumor Assessment Core Facility, Memorial Sloan Kettering Cancer Center
- Charles Sawyers
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Neal Rosen
- Molecular Pharmacology Program, Memorial Sloan Kettering Cancer Center
- Andrew C. Hsieh
- Divisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center
- Yu Chen
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- Brett S. Carver
- Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
- DOI
- https://doi.org/10.1038/s41467-021-25341-9
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 13
Abstract
Understanding the mechanisms driving PI3K isoform dependency in prostate cancer can help the design of future clinical trials. Here, the authors show that gain-of-function mutations in PIK3CA or PIK3CB can confer PI3K p110 isoform dependency and that the direct inhibition of AKT may be superior to PI3K inhibition in PTEN-deficient prostate cancers.
