The Role of Genetics in Cancer: Oncogenes and Tumor Suppressor Genes

Cancer is fundamentally a genetic disease driven by alterations in the cellular genome that disrupt normal mechanisms of proliferation, differentiation, and cell death. Among the most critical genetic factors involved in carcinogenesis are oncogenes and tumor suppressor genes. Oncogenes arise from the activation of proto-oncogenes through mutations, gene amplification, or chromosomal rearrangements, leading to the production of overactive proteins that promote uncontrolled cell growth and survival. In contrast, tumor suppressor genes normally function to inhibit cell division, repair DNA damage, or induce apoptosis; their inactivation by loss-of-function mutations, deletions, or epigenetic silencing removes essential brakes on cell proliferation. The balance between oncogene activation and tumor suppressor gene inactivation is a key determinant of malignant transformation and tumor progression. Classic examples include activation of RAS and MYC oncogenes, and loss of function of TP۵۳, RB۱, and BRCA۱/۲ tumor suppressor genes. In addition, germline mutations in specific cancer-associated genes contribute to hereditary cancer syndromes, while somatic mutations accumulate during a person's lifetime under the influence of environmental and lifestyle factors. Understanding the molecular mechanisms by which oncogenes and tumor suppressor genes regulate cell cycle control, genomic stability, and signaling pathways has led to the development of targeted therapies, personalized medicine approaches, and improved diagnostic and prognostic tools. This paper reviews the fundamental roles of oncogenes and tumor suppressor genes in cancer biology and highlights their clinical implications for prevention, diagnosis, and treatment.

کلیدواژه ها:

Oncogenes ، Tumor suppressor genes ، Carcinogenesis ، Genetic mutations ، Targeted cancer therapy