What is a consequence of DNA mutations induced by radiation exposure?

The development of secondary cancers as a consequence of DNA mutations induced by radiation exposure is a well-established phenomenon in radiation biology. When radiation interacts with cellular DNA, it can cause various types of mutations, including single-strand and double-strand breaks, which, if improperly repaired, can lead to changes in the genetic code.

These mutations can disrupt normal cellular regulation mechanisms, such as those that control cell proliferation and apoptosis. Over time, cells with mutations can accumulate additional genetic changes, leading to uncontrolled growth and the potential for malignancy. This is particularly relevant in tissues that are rapidly dividing, as these cells are more susceptible to the detrimental effects of radiation.

In contrast, other choices such as improved cellular function or expedited healing processes do not occur as a result of DNA mutations but rather indicate positive outcomes that are unrealistic in the context of radiation exposure. Decreased immune response could be a consequence of other factors but is not a direct result of DNA mutations causing cancer. Hence, the link between radiation-induced DNA mutations and the development of secondary cancers is a significant concern in understanding the long-term effects of radiation exposure.