Chapter 23, Problem 18
How do normal cells protect themselves from accumulating mutations in genes that could lead to cancer? How do cancer cells differ from normal cells in these processes?
Verified Solution
This video solution was recommended by our tutors as helpful for the problem above.Video transcript
How do translocations such as the Philadelphia chromosome contribute to cancer?
Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.
DNA sequencing has provided data to indicate that cancer cells may contain tens of thousands of somatic mutations, only some of which confer a growth advantage to a cancer cell. How do scientists describe and categorize these recently discovered populations of mutations in cancer cells?
Cancer can be defined as an abnormal proliferation of cells that defy the normal regulatory controls observed by normal cells. Recently, histone deacetylation therapies have been attempted in the treatment of certain cancers [reviewed by Delcuve et al. (2009)]. Specifically, the FDA has approved histone deacetylation (HDAC) inhibitors for the treatment of cutaneous T-cell lymphoma. Explain why histone acetylation might be associated with cancer and what the rationale is for the use of HDAC inhibitors in the treatment of certain forms of cancer.
Describe the difference between an acute transforming virus and a virus that does not cause tumors.
Epigenetics is a relatively new area of genetics with a focus on phenomena that affect gene expression but do not affect DNA sequence. Epigenetic effects are quasi-stable and may be passed to progeny somatic or germ-line cells. What are known causes of epigenetic effects, and how do they relate to cancer?