quality:corruption, stylistic:style_transfer
Pathogenesis

As with all cancers, lung cancer is triggered by mutations that allow tumor cells to endlessly multiply, stimulate blood vessel growth, avoid apoptosis (programmed cell death), generate pro-growth signalling molecules, ignore anti-growth signalling molecules, and eventually spread into surrounding tissue or metastasize throughout the body. Different tumors can acquire these abilities through different mutations, though generally cancer-contributing mutations activate oncogenes and inactivate tumor suppressors. Some mutations – called "driver mutations" – are particularly common in adenocarcinomas, and contribute disproportionately to tumor development. These typically occur in the receptor tyrosine kinases EGFR, BRAF, MET, KRAS, and PIK3CA. Similarly, some adenocarcinomas are driven by chromosomal rearrangements that result in overexpression of tyrosine kinases ALK, ROS1, NTRK, and RET. A given tumor will typically have just one driver mutation. In contrast, SCLCs rarely have these driver mutations, and instead often have mutations that have inactivated the tumor suppressors p53 and RB. A cluster of tumor suppressor genes on the short arm of chromosome 3 are often lost early in the development of all lung cancers.