Cellular repair pathways in tumor cells

Cellular repair pathways in tumor cells refer to a collection of molecular mechanisms—including base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end-joining (NHEJ), and homologous recombination repair (HRR)—that are responsible for detecting and correcting various types of DNA damage in cancer cells. These pathways are highly active in tumor cells and contribute to both cancer cell survival and resistance to therapies like chemotherapy and radiotherapy, which rely on inducing lethal DNA damage. Specific components of these pathways, such as enzymes (PARP1), protein complexes (SWI/SNF), and regulatory genes (e.g., BRCA1/2), are considered drug targets, with several approved therapies exploiting synthetic lethality when repair pathways are defective. Research into these pathways continues to expand their role as stratification tools for therapy selection and as sources of potential biomarkers for patient outcomes.

Other names

DNA repair pathwaysDNA damage response pathwayscellular DNA repair mechanisms

Inhibition of DNA repair proteins (e.g., blocking PARP1 leads to accumulation of DNA damage and synthetic lethality in BRCA-deficient tumor cells) Synthetic lethality by targeting DNA repair pathway genes/proteins that are essential in repair-defective cancers