Somatic mutations are DNA alterations that occur after birth and are not inherited from a parent. These mutations can accumulate over time due to factors like environmental exposure or cellular replication errors. As they build up, they can disrupt normal cellular processes and are frequently linked to the development of cancer.
One key mechanism involves tumor suppressor genes genes that regulate cell division and repair damaged DNA. When somatic mutations inactivate these genes, it can lead to uncontrolled cell growth. A well-known example is the TP53 gene, often called the “guardian of the genome”, which helps prevent abnormal cell proliferation. Mutations in TP53 are among the most common alterations found across various cancer types.
Conversely, somatic mutations can also activate oncogenes genes that stimulate cell growth and division. Normally, these genes are tightly regulated, but when mutations cause them to remain permanently active, they can drive the formation and progression of tumors.
Environmental Factors: Exposure to carcinogens such as tobacco smoke, ultraviolet (UV) radiation, or certain chemicals can significantly increase the risk of acquiring somatic mutations. Over time, these mutations may accumulate in specific cells, potentially disrupting normal cellular function and contributing to cancer development.