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Cancer develops when cells accumulate mutations that disrupt the normal controls on growth and division. Under normal circumstances, proto-oncogenes promote cell division in response to growth signals, while tumour suppressor genes (such as TP53 and RB1) act as brakes. DNA repair mechanisms correct errors that arise during replication. Cancer typically requires the disabling of multiple safeguards — often 4–7 key mutations — which is why it usually develops over years or decades. When an oncogene is mutated into a permanently "on" state, or when tumour suppressors are inactivated, cells can divide uncontrollably. The resulting tumour is not genetically uniform; it continues to evolve under Darwinian selection, with sub-clones that happen to grow faster, evade the immune system, or resist drugs becoming dominant. This intra-tumour heterogeneity is a primary reason cancer is so difficult to cure: a drug that kills 99% of cells may spare a resistant sub-clone that repopulates the tumour. Additional hallmarks of cancer include the ability to stimulate angiogenesis (blood vessel growth to supply the tumour), invade surrounding tissues, and metastasise to distant organs.
answered by Omniscientia Team · 183 words · 18 Mar 2026