In the development of colorectal neoplasia, what oncogene is typically activated after mutations in the APC gene?

In the development of colorectal neoplasia, the activation of the K-ras oncogene is a critical step that typically follows mutations in the APC gene. The adenomatous polyposis coli (APC) gene is a tumor suppressor gene, and mutations in this gene are often the first hit in the multistep process leading to colorectal cancer. The loss of function of APC leads to the accumulation of beta-catenin, which can activate transcription of oncogenes, including K-ras.

Once the APC gene is mutated and function is lost, subsequent mutations often occur, including activation of the K-ras oncogene. This activation promotes cellular proliferation and contributes to the progression of adenomas to more advanced neoplastic lesions. K-ras mutations are particularly characteristic of the colorectal cancer pathway, leading to the development of malignant tumors.

The other options presented, such as p53 and Rb, are indeed involved in tumorigenesis but typically represent later events in the progression of colorectal cancer or do not directly follow APC mutations in the context of this specific pathway. For instance, mutations in the p53 tumor suppressor gene usually occur after the initial activation of K-ras and play a role in the transition to carcinoma.