Final answer:
The emergence of vemurafenib-resistant melanoma can result from additional mutations in the B-RAF gene, such as a second substitution at position 61, or from amplification of other oncogenes like c-myc, which would drive growth through alternative pathways.
Step-by-step explanation:
The genetic alteration that could result in the emergence of vemurafenib-resistant melanoma is the presence of a mutated form of the protein the drug is designed to target. In the case of vemurafenib, the drug targets the B-RAF protein with a specific mutation known as V600E. However, if the B-RAF protein undergoes further genetic alterations that change its structure, the drug may no longer be able to bind to it effectively, leading to resistance.
The correct answer to the question of which genetic alterations could result in vemurafenib-resistant melanomas is option d) p61 B-RAFV600E, amplified c-myc gene. Subsequent mutations in the same gene that is targeted by the drug (B-RAF), such as a second substitution at position 61 (p61), could potentially change the protein's structure enough to cause drug resistance. Additionally, amplification of oncogenes like c-myc can lead to resistance by driving the cancer cells' growth and survival through alternative pathways.