DNA Repair Pathways in Carcinogenesis: Mechanisms, Modulation, and Future Directions for Cancer Prevention

Abstract

DNA repair mechanisms are prime custodians of genomic integrity and their deregulation is essentially a central feature during oncogenesis. This study surveys the molecular pathways of micro base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), and dual strand repair (DSBR) through homologous recombination (HR) and by no means homologous end joining (NHEJ), and this is by particular attention to the way that they take part in carcinogenic adjustment. Clinical data show that germline BRCA1/2, MLH1, and MSH2 mutations systems cause susceptibility to hereditary cancer, and somatic variants of the repair genes promote tumorigenesis. Further, the epigenetic silencing of the repair capacity as well as oxidative stress and oncogenic signal transduction pathways also play a role in the chemoresistance and the development of the disease. Existing treatment approaches, such as PARP inhibitors and immune checkpoint manipulation are specific modalities, in addition to synthetic lethality approaches, assessed within this study as interventional and preventative measures. Education on repair pathway control can guide the precise oncology, early indication makers, translation of the oncology prevention method, which in turn can control morbidity and enhance the prognosis of the patient