A Researchers have uncovered how lung cancer rapidly develops resistance to osimertinib, a key drug for EGFR-mutant tumors. Resistance can emerge within six to eight weeks of starting treatment, earlier than previously thought. The study identified a protein, METTL7A, as a critical driver of this process. METTL7A remodels chromatin, making it easier for cancer cells to amplify genes that promote growth and survival despite therapy.
Blocking METTL7A early in treatment prevented resistance in preclinical models, suggesting a short window after starting osimertinib when intervention could keep cancer cells sensitive to the drug. This approach targets the underlying mechanism that allows gene amplification rather than fighting it after it occurs.
Because gene amplification is a common way cancers evade targeted therapies, inhibiting METTL7A or similar pathways may offer a broad strategy to prolong the effectiveness of drugs like osimertinib and improve outcomes for patients with lung and other cancers.