Chapter 19: Problem 5
What is the role of the retinoblastoma protein in cell-cycle regulation? Is the retinoblastoma gene a tumor-suppressor gene or an oncogene?
Chapter 19: Problem 5
What is the role of the retinoblastoma protein in cell-cycle regulation? Is the retinoblastoma gene a tumor-suppressor gene or an oncogene?
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Get started for freeCompare 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.
How does the environment contribute to cancer?
In this chapter, we focused on cancer as a genetic disease, with an emphasis on the relationship between cancer, the cell cycle, and DNA damage, as well as on the multiple steps that lead to cancer. (a) How do we know that malignant tumors arise from a single cell that contains mutations? (b) How do we know that cancer development requires more than one mutation? (c) How do we know that cancer cells contain defects in DNA repair?
Those who inherit a mutant allele of the \(R B 1\) gene are at risk for developing a bone cancer called osteosarcoma. You suspect that in these cases, osteosarcoma requires a mutation in the second \(R B 1\) allele, and you have cultured some osteosarcoma cells and obtained a cDNA clone of a normal human \(R B I\) gene. A colleague sends you a research paper revealing that a strain of cancer-prone mice develop malignant tumors when injected with osteosarcoma cells, and you obtain these mice. Using these three resources, what experiments would you perform to determine (a) whether osteosarcoma cells carry two \(R B 1\) mutations, (b) whether osteosarcoma cells produce any \(\mathrm{pRB}\) protein, and (c) if the addition of a normal \(R B 1\) gene will change the cancer-causing notential of astensarcama cells?
A 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.
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