Attenuation of SRC kinase activity augments PARP inhibitor-mediated synthetic lethality in BRCA2-altered prostate tumors.
CONCLUSIONS: This work suggests that SRC activation may be a potential mechanism of PARPi resistance and that treatment with SRC inhibitors may overcome this resistance. Our preclinical study demonstrates that combining PARPi and SRC inhibitors may be a promising therapeutic strategy for patients with BRCA2-null mCRPC.
PMID: 33334906 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - Category: Cancer & Oncology Authors: Chakraborty G, Khan Patail N, Hirani R, Nandakumar S, Mazzu YZ, Yoshikawa Y, Atiq MO, Jehane L, Stopsack KH, Lee GM, Abida W, Morris MJ, Mucci LA, Danila DC, Kantoff PW Tags: Clin Cancer Res Source Type: research