If MET amplification is documented in NSCLC, why is crizotinib considered to have

If MET amplification is documented in NSCLC, why is crizotinib considered to have "targeted activity" against this tumor profile? What support suggests high activity in patients with tumors manifesting this genetic alteration?

If MET amplification is documented in NSCLC, why is crizotinib considered by the NCCN to have “targeted activity” against this tumor profile? What clinical study-based support—improvements in PFS and/or OS—suggests high activity of this agent in patients with tumors manifesting this genetic alteration?


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Presenter

Alexander Drilon, MD

Alexander Drilon, MD

Medical Oncologist
Memorial Sloan Kettering Cancer Center
New York, NY, USA