Cancer arises from accumulated DNA mutations that disrupt the normal functioning of cells. An explainer published in The Conversation by researchers from the Walter and Eliza Hall Institute of Medical Research outlines how genetic changes contribute to cancer development and what inherited mutations mean for individual risk.
DNA contains instructions for producing proteins, molecules that carry out virtually every function within a cell. When a mutation occurs in a gene, the resulting protein may not work correctly. Cells have dedicated repair proteins to address such errors, but if the gene encoding a repair protein is itself mutated, subsequent DNA damage may go uncorrected. Over time, accumulated mutations can cause a cell to divide uncontrollably and evade normal cell death, the hallmarks of cancer.
Mutations can occur in two ways: in reproductive cells (germline), where they can be inherited by children, or in other cell types (somatic), where they affect only the individual. Germline mutations are of particular clinical significance because every cell in the body carries the affected gene from birth, increasing the overall likelihood of cancer-driving errors accumulating over a lifetime.
Well-studied examples include the BRCA1 and BRCA2 genes, involved in DNA repair, and TP53, which normally triggers the destruction of abnormal cells. Inherited mutations in these genes are associated with meaningfully elevated cancer risk compared to the general population.
For individuals with a family history of cancer, clinical guidance recommends genetic testing and counselling, which may lead to earlier screening or other preventive measures. The authors note that while genetic risk cannot be modified, lifestyle factors, including avoiding smoking and alcohol, maintaining regular physical activity, and sun protection, may help reduce overall cancer risk.
Source: Medical Express / The Conversation
