Chiao-Ping Chen1,2, Yan-Jei Tang1,2, You-Yan Cai1, Yi-Ru Pan3, Chun-Nan Yeh3,4, Wen-Kuan Huang1,2, Chih-Hong Lo1,2, Yu-Tien Hsiao1,2, Hsuan-Jen Shih1,*, Chiao-En Wu1,2,4,5,*
Oncology Research, Vol.33, No.11, pp. 3429-3446, 2025, DOI:10.32604/or.2025.066672
- 22 October 2025
Abstract Background: KIT proto-oncogene, receptor tyrosine kinase (KIT, CD117) and platelet-derived growth factor-alpha (PDGFRA) are key drivers of gastrointestinal stromal tumors (GIST), but resistance to targeted therapy often arises from tumor protein p53 (p53) alterations and loss of cell cycle control. However, the role of p53 status in GIST therapeutic potential has rarely been studied, so this study aimed to employ both wild-type and mutant p53 GIST models to investigate how p53 dysfunction influences the efficacy of p53 pathway-targeted therapies. Methods: The efficacy of the mouse double minute 2 homolog (MDM2) inhibitor (HDM201) and the Wee1… More >