What is the significance of K-ras (KRAS) mutations in human cancers?

K-ras (KRAS) mutations are significant in human cancers primarily because they cause the RAS protein to remain in an active state. Under normal conditions, the RAS protein is involved in signaling pathways that control cell growth and differentiation. When a mutation occurs in the KRAS gene, it frequently leads to a protein that cannot hydrolyze GTP (the active form) to GDP (the inactive form). As a result, the mutated RAS protein continues to relay growth signals even in the absence of external growth factors. This unregulated signaling can drive uncontrolled cell proliferation and contribute to the development and progression of various cancers, making KRAS mutations a critical target in cancer research and treatment.

The other mentioned options do not adequately reflect the effects of KRAS mutations. For instance, tumor suppression is typically associated with loss of function mutations in tumor suppressor genes, rather than in oncogenes like KRAS. Kinase inhibition is not a direct consequence of KRAS mutations; rather, mutated KRAS can lead to sustained activation of downstream signaling pathways, including those involving kinases. Additionally, KRAS mutations generally do not initiate apoptosis; instead, they promote cell survival and proliferation, contributing to tumorigenesis.