https://www.selleckchem.com/pr....oducts/Rapamycin.htm
Gefitinib treatment strongly blocked epithelial-like cSCC-PDX growth in the absence of and mutations, whereas tumors carrying the -activating mutation were resistant to treatment. A subset of initially responding tumors acquired resistance after long-term treatment, which was induced by the bypass from EGFR to FGFR signaling to allow tumor cell proliferation and survival upon gefitinib treatment. Pharmacologic inhibition of FGFR signaling overcame resistance to EGFR inhibitor, even in -mutated tumors. EGFR-targeted therapy may be appr
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