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When a cell carries extra copies of a gene, sometimes 50 or more instead of the normal two, so it makes far too much of that protein. HER2 amplification in breast cancer is the classic example and is what trastuzumab exploits; MET amplification is a common escape route from EGFR inhibitors in lung cancer.
Amplification is a copy-number change: a segment of DNA containing the gene is duplicated, sometimes to 50 or more copies, either within the chromosome or on separate circles of DNA (ecDNA). More copies mean more RNA and more protein, so an amplified oncogene behaves as if permanently over-activated. It is detected by in situ hybridisation (FISH/ISH) or sequencing and is a drug target in its own right: HER2 amplification is what trastuzumab and T-DXd exploit, and MET amplification is a common way lung cancers escape EGFR inhibitors.
In plain words · A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers.
Showing the target this term concerns: HER2.
Shares MET, Trastuzumab deruxtecan, HER2, Non-small-cell lung cancer.
Shares Trastuzumab deruxtecan, HER2, Non-small-cell lung cancer.
Shares HER2-low and HER2-ultralow, Trastuzumab deruxtecan, HER2.
Shares Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer, Non-small-cell lung cancer.
Shares HER2-low and HER2-ultralow, Trastuzumab deruxtecan, HER2.
Shares HER2-low and HER2-ultralow, Trastuzumab deruxtecan, Trastuzumab, HER2.
Shares Trastuzumab deruxtecan, Trastuzumab, HER2.
Shares HER2-low and HER2-ultralow, Trastuzumab deruxtecan, HER2.