A second hit might arise because of viral infection. Tumor-initiating viruses often target RB1 for inactivation. What advantage would a virus gain by inactivating RB function in the host cell? Human papillomavirus (HPV) is an example of a virus that inactivates RB and causes tumors. Which cancer is HPV infection most closely associated with? How is HPV able to inactivate RB? (3-4 sentences only)

The Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction.   Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV?  If it does, what is the relationship between P53 and P63? Thank you!

The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?

One of the ways that we know what the RB protein does in cells is that its inactivation is a common priority of tumor-initiating viruses. What advantage would a virus gain by inactivating RB function in its host cell?