Chapter 19: Problem 16
Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.
Chapter 19: Problem 16
Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.
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Get started for freeA study by Bose and colleagues (1998. Blood 92: \(3362-3367\) ) and a previous study by Biernaux and others (1996. Bone Marrow Transplant 17: (Suppl.3) \(\mathrm{S} 45-\mathrm{S} 47\) ) showed that \(B C R-A B L\) fusion gene transcripts can be detected in 25 to 30 percent of healthy adults who do not develop chronic myelogenous leukemia (CML). Explain how these individuals can carry a fusion gene that is transcriptionally active and yet do not develop CML.
Compare familial and sporadic retinoblastomas in terms of genetics and age of onset. Is it possible to distinguish between these two using genetic tests? Consider the number of mutations required, loss of heterozygosity, and the two-hit hypothesis.
Review the Chapter Concepts list on page \(503 .\) These concepts relate to the multiple ways in which genetic alterations lead to the development of cancers. The sixth concept states that epigenetic effects including DNA methylation and histone modifications contribute to the genetic alterations leading to cancer. Write a short essay describing how epigenetic changes in cancer cells contribute to the development of cancers.
Can cancer be inherited or infectious?
Describe the steps by which the \(p 53\) gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that \(p 53\) is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
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