THE ROLE OF DNA REPAIR MECHANISMS IN CANCER DEVELOPMENT
Abstract
The stability of the human genome depends on the efficiency of DNA repair systems that safeguard cells against mutagenic damage. DNA molecules are continuously exposed to harmful agents such as ultraviolet radiation, ionizing radiation, reactive oxygen species, and chemical mutagens. To maintain genetic integrity, cells have developed precise repair mechanisms that detect and correct DNA lesions. Failure in these processes leads to mutation accumulation, chromosomal instability, and, ultimately, cancer. The principal DNA repair pathways include base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. Each system operates through specific enzymes and signaling cascades to maintain genomic fidelity. Mutations in repair genes such as BRCA1, BRCA2, MLH1, and TP53 are strongly linked to hereditary and sporadic cancers. This article discusses the biological principles of DNA repair, the consequences of their dysfunction, and the therapeutic implications for oncology.
Keywords
DNA repair, cancer, genomic instability, mutations, base excision repair, homologous recombination, mismatch repair, BRCA genes.
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