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In a subset of patients with non–small-cell lung cancer (NSCLC), increases in MET copy number have been hypothesized to lead to excessive amounts of MET protein, autoaggregation, ligand-independent MET signaling, and oncogenic addiction to the MET pathway. The same process has also been described as one mechanism of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR-mutant NSCLC. Changes in MET copy number represent a continuous variable that can be assessed in different ways: either the ratio of MET relative to another region of chromosome 7, such as CEP7 (to show true amplification), or the absolute number of MET copies, which can also be increased by polysomy. Consequently, the persistent problem with MET copy number studies has been to define a threshold for any given methodology above which aMET-directed therapy will likely be active. Less stringent criteria may include more patients but could dilute the clinical benefit in the treated population. More stringent criteria will identify fewer patients: those who may derive the greatest clinical benefit, but potentially excluding others who will still derive some benefit.

journal of clinical oncology

<i>MET</i> Copy Number as a Secondary Driver of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance in <i>EGFR</i>-Mutant Non–Small-Cell Lung Cancer

MET Copy Number as a Secondary Driver of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance in EGFR-Mutant Non–Small-Cell Lung Cancer