https://www.selleckchem.com/products/ca-170.html
Inhibition of SRC signaling by dasatinib augmented DNA damage in -null prostate cancer cells. Moreover, knockdown increased PARPi sensitivity in -null prostate cancer cells. 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 PARPis and SRC inhibitors may be a promising therapeutic strategy for patients with -null mCRPC. This work suggests that SRC activation may be a potential mechani
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