DNA repair

DNA repair comprises cellular processes that detect and correct damage or errors in DNA. These processes preserve genome integrity and limit mutations.

Base excision repair: A pathway that removes damaged or inappropriate bases and replaces them using the intact DNA strand as a template. It corrects small base lesions that do not substantially distort the DNA helix.
DNA: A molecule that stores hereditary information in a sequence of nucleotides, usually arranged as two complementary strands. Its paired strands provide the information and templates that many repair pathways preserve.
Tomas Lindahl: A Swedish biochemist whose work established the enzymatic basis of DNA repair and characterized base excision repair. His studies showed that DNA is chemically unstable and requires continual repair.
Xeroderma pigmentosum: A group of inherited disorders marked by extreme sensitivity to ultraviolet light and greatly increased skin-cancer risk. Defects in nucleotide excision repair leave ultraviolet lesions unrepaired.
Mutation: A heritable change in the nucleotide sequence of genetic material. Damage that escapes repair can become a permanent mutation after DNA replication.
Nucleotide excision repair: A pathway that removes a short stretch of DNA containing a bulky, helix-distorting lesion and resynthesizes it. It excises lesions such as ultraviolet-induced photoproducts that disrupt the DNA helix.
DNA damage: Chemical or physical alterations to DNA that disrupt its structure, base sequence, or ability to be copied. Repair begins when cellular systems recognize these diverse forms of damage.
Paul Modrich: An American biochemist who elucidated the mechanism of DNA mismatch repair. His work explained how cells identify and correct replication mismatches.
Lynch syndrome: An inherited cancer predisposition syndrome commonly caused by pathogenic variants in DNA mismatch repair genes. Its tumors often show mismatch-repair deficiency and elevated microsatellite instability.
Carcinogenesis: The multistep process by which normal cells acquire changes that enable cancer development. Accumulated mutations from failed repair can contribute to the emergence of cancer.

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