Can we treat cancer by restoring tumor suppressor function such as mutated p53 or pRb?  If so, how can this be?

In some cancer cells, a specific gene has been duplicated many times. Is this gene likely to be an oncogene or a tumor-suppressor gene? Explain your reasoning

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!

Cancer can arise spontaneously, but it can also be induced as a result of environmental factors such as sun exposure, infections, and tobacco smoking. If you were asked to help allocate resources to cancer research, what emphasis would you place on research to find cancer cures, compared to that placed on education about cancer prevention?

How Mutations Cause Cancer Phenotypes?

Many of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride.  Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?

Acquired mutation in the p53 gene is the most common genetic alteration found in human cancer (> 50% of all cancers). A germline mutation in p53 is the causative lesion of Li- Fraumeni familial cancer syndrome. In many tumors, one p53 allele on chromosome 17p is deleted and the other is mutated. What type of protein is encoded by the p53 gene? (A) Caspase (B) DNA repair enzyme (C) Membrane cell adhesion molecule (D) Serine phosphatase (E) Telomerase (F) Transcription factor (G) Tyrosine kinase

Do more mutations necessarily mean that more cancer-causing genes are faulty? Why or why not?

Hi, can you elaborate about these two concepts: 1) Can telomere inhibition be good cancer treatment?  2) Can cancer steam cells hypothesis be a good / bad approach?

Let’s suppose you were interested in developing drugs to preventepigenetic changes that may contribute to cancer. What cellularproteins would be the target of your drugs? What possible sideeffects might your drugs cause?