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

If MET amplification is documented in NSCLC, why is crizotinib considered by the NCCN to have "targeted activity" against this tumor profile? What high activity in patients with 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

Paul Mitchell, BHB, MBChB, FRACP, MD

Paul Mitchell, BHB, MBChB, FRACP, MD

Associate Professor
Senior Specialist
Austin Health Cancer Services
Director, North Eastern Metropolitan Integrated Cancer Services (NEMICS)
Melbourne, Australia