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How do genetic and epigenetic changes contribute to cancer development?

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Precancerous growth in a human colon — cancer View through an endoscope of a polyp, a benign precancerous growth projecting from the inner lining of the colon.

Cancer is a disease characterized by the rewiring of cellular control circuits for proliferation, differentiation, and death, driven by a combination of genetic and epigenetic alterations.1

Genetic Contributions

Cancer arises from successive mutations in three primary classes of genes:2
* Oncogenes: Derived from proto-oncogenes, these genes sustain "gain-of-function" mutations that overstimulate cell growth.32
* Tumor Suppressor Genes: These normally act as "brakes" on cell division. Mutations that inactivate both copies of these genes remove essential growth restraints.34
* Genome Surveillance Genes: These genes, such as those involved in DNA repair, identify and fix genetic damage. When these are impaired, mutations accumulate rapidly.32

Epigenetic Contributions

Epigenetic modifications—chemical changes to DNA and chromatin—regulate gene expression without altering the underlying DNA sequence. In cancer, these changes often include:15
* Hypomethylation: A general decrease in methylation, which can lead to the abnormal activation of growth-promoting genes.5
* Hypermethylation: Targeted increases in methylation that silence tumor suppressor genes, preventing them from inhibiting tumor growth.5

Together, these genetic and epigenetic insults accumulate over time, enabling cells to escape programmed controls, achieve immortality, and eventually invade distant tissues.31