What is a potential consequence of permanent somatic mutations in individuals with poor DNA repair?

Permanent somatic mutations can lead to an increase in the risk of cancer development, particularly in individuals with poor DNA repair mechanisms. When DNA repair processes are ineffective, mutations that occur in somatic (non-germline) cells can accumulate over time. These mutations can disrupt normal cellular functions, including critical processes that regulate the cell cycle, growth, and apoptosis (programmed cell death).

As mutations build up, there can be a transformation of normal cells into cancerous ones. This is primarily due to mutations affecting proto-oncogenes and tumor suppressor genes, which can intensify cell division and inhibit the mechanisms that typically restrain growth. Therefore, an individual's compromised ability to repair DNA not only elevates the chances of mutagenesis but also significantly heightens the potential for the development of cancerous cells.

The other choices do not reflect the consequences of somatic mutations accurately. An increased distance between cells is not directly associated with somatic mutations or poor DNA repair capabilities. Enhanced repair capabilities of DNA would suggest that the individual has a functioning DNA repair mechanism, which contradicts the premise of poor DNA repair. Lastly, suggesting a lower likelihood of developing cancer is contrary to the well-established correlation between mutations and cancer risk. Therefore, the statement