Oncogene addiction to GNAS in GNASR201 mutant tumors

• Published in: Oncogene Vol. 41; no. 35; pp. 4159 - 4168
• Main Authors: More, Aditya, Ito, Ichiaki, Haridas, Valsala, Chowdhury, Saikat, Gu, Yue, Dickson, Princess, Fowlkes, Natalie, Shen, John Paul
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 26.08.2022; Nature Publishing Group
• Subjects: 13/1; 13/100; 13/106; 13/51; 14/105; 14/5; 14/63; 38/23; 38/39; 38/77; 38/91; 42/109; 42/41; 59/5; 631/67/1504/1885; 631/67/327; 631/67/395; 64/60; Addictions; Animal models; Apoptosis; Cell Biology; Colorectal cancer; Colorectal carcinoma; Cyclic AMP; Human Genetics; Internal Medicine; Medicine; Medicine & Public Health; Mutants; Mutation; Oncogenes; Oncology; Organoids; Pancreatic cancer; Peritoneum; Phosphorylation; Protein kinase A; Therapeutic targets; Tumorigenesis; Tumors; Wnt protein; β-Catenin

The GNAS R201 gain-of-function mutation is the single most frequent cancer-causing mutation across all heterotrimeric G proteins, driving oncogenesis in various low-grade/benign gastrointestinal and pancreatic tumors. In this study, we investigated the role of GNAS and its product Gαs in tumor progr...