Question

K-Ras is a proto-oncogene that is activated in 95% of all pancreatic cancers. Which of the following mutations is likely to increase cell division rate and potentially lead to cancer? (Select ALL that apply.)

A. A nonsense mutation close to the start codon of the K-Ras gene

B. A translocation that puts the K-Ras gene near an active repressor region of DNA

C. Methylation of multiple C residues in the K-Ras promoter region

D. Duplication of the K-Ras gene

E. Insertion of a viral promoter sequence next to K-Ras, which activates transcription of K-Ras

F. Deletion of the K-Ras gene

Answer 1

Mutations likely to lead to cancer by increasing cell division rates in the K-Ras gene include duplication of the gene, insertion of a viral promoter sequence, and gain of function mutations that continuously activate cell proliferation pathways.

Step-by-step explanation:

K-Ras is a proto-oncogene involved in cell division regulation, and specific mutations can lead to its transformation into an oncogene, leading to the potential development of cancer by increasing the cell division rate. When investigating the types of mutations that could increase cell division rate and potentially lead to cancer, the following apply:

• Duplication of the K-Ras gene could result in an overexpression of the K-Ras protein, which can enhance the cell division signaling pathways, thereby increasing the rate of cell division.
• Insertion of a viral promoter sequence next to K-Ras, which activates transcription of K-Ras, can also lead to overexpression of the K-Ras protein, thus promoting increased cell division rates.
• A gain of function mutation in RAS protein can result in the continued activation of pathways that encourage cell proliferation, contributing to cancer development.

Other mutations listed, such as nonsense mutations, repressor region translocations, promoter region methylation, and gene deletions, are more likely to decrease K-Ras activity and are not associated with increased cell division rates that lead to cancer.