Dr. Camidge on MET as a Target in Lung Cancer
D. Ross Camidge, MD, director, Thoracic Oncology Clinical Program, program director, Thoracic Oncology Clinical and Translational Research Fellowship, University of Colorado Denver, discusses MET and if it is still a relevant target in lung cancer.
D. Ross Camidge, MD, director, Thoracic Oncology Clinical Program, program director, Thoracic Oncology Clinical and Translational Research Fellowship, University of Colorado Denver, discusses MET and if it is still a relevant target in lung cancer.
MET can still be a target in lung cancer; however, it depends on what biomarker is being examined, what agent is being used, and what patients are selected, Camidge explains. Data suggest that MET is a primary driver in some subsets of lung cancer through high-level MET amplification.
However, this matters where oncologists add a cut-point. The cut-point also determines how well a patient is dependent on the MET pathway.
MET exon-14 skipping, a driver twice as common as high-level MET amplification, is occurring in approximately 4% of patients with lung adenocarcinoma, Camidge says. This trims the ubiquitin ligase domain on MET and creates a more stable protein. MET exon-14 skipping is also sensitive to MET inhibitors, such as crizotinib.
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