Cancer is a disease of evolution within the body. A normal cell, through a series of mutations in genes that control growth, division, and cell death, evolves into a population that no longer obeys the body's regulatory signals — outcompeting its neighbors locally, invading adjacent tissue, and eventually colonizing distant sites (metastasis). The evolutionary frame — Peter Nowell, 1976, cancer as clonal evolution — has organized oncology for nearly fifty years and explains, among other things, why most cancers eventually develop drug resistance. About 40% of people in developed countries will be diagnosed with cancer in their lifetime; about half will die of it.
Hanahan and Weinberg's hallmarks of cancer (2000, updated twice since) cast the malignant phenotype as a small set of acquired capabilities. The cell becomes self-sufficient in growth signals through activation of oncogenes (RAS, MYC, EGFR, HER2); insensitive to anti-growth signals through loss of tumor suppressors (TP53, the guardian of the genome, is mutated in roughly half of all cancers); evades apoptosis; escapes the replicative-senescence ceiling by reactivating telomerase; recruits new blood vessels; and breaks through tissue boundaries to seed distant sites — metastasis accounts for around ninety percent of cancer deaths. The 2011 update added deregulated metabolism (the Warburg effect) and immune evasion. The hallmarks fall out of evolution acting on a population of cells: most cancers require five to ten driver mutations on top of thousands of passengers.
Reading cancer as evolution-in-the-body runs through the treatment landscape. Tumor heterogeneity — a single tumor is genetically a forest of subclones, now made visible by single-cell sequencing — is the structural reason targeted therapies achieve dramatic initial responses and then fail; the drug selects for the resistant subclone already present at low frequency. The microenvironment of stroma, immune cells, and blood vessels co-evolves with the tumor. The cancer-genomics atlases (TCGA, ICGC) have catalogued driver landscapes across every major cancer type. Hereditary syndromes (BRCA1/2, Lynch, Li-Fraumeni) account for around a tenth of cases; the rest are sporadic, with carcinogens (tobacco, UV, ionizing radiation, certain viruses, chronic inflammation) acting either by raising mutation rates or altering selection.
Treatment has been transformed by targeted therapy — beginning with imatinib for BCR-ABL+ chronic myeloid leukemia and now extending across the major cancer types — and by immunotherapy, where checkpoint inhibitors (anti-PD-1, anti-CTLA-4) and CAR-T cells produce durable remissions in cases previously considered terminal. Liquid biopsies sequencing circulating tumor DNA monitor response and detect relapse; multi-cancer early-detection tests like Grail's Galleri screen many cancers simultaneously from a blood draw using methylation signatures. HPV vaccines have dramatically reduced cervical cancer; smoking cessation remains the largest prevention lever. Five-year survival has improved for most major cancers, though much of the gain has come from earlier detection rather than better treatment of advanced disease.