Revision Cancer cells escape limits on proliferation

1. RevisionCancer cells escape limits on proliferation

5. Sample Questions 1. You are treating a cancer patient by injecting an expression vector containing the (retinoblastoma) Rb gene directly into the tumor. Explain the following observations from what you know about the role of Rb in cell cycle regulation: A. The tumor growth decreased to half the original size in the first two weeks of therapy. B. You inadvertently transfected the tumor with a constitutively phosphorylated version of Rb and now the tumor has grown back to the original size. C. After the initial decrease in size, the tumor no longer responded to the Rb gene therapy and upon further analysis you discover that the cancer cells contained a deletion in the gene coding for p53. D. After the initial decrease in size, the tumor no longer responded to the Rb gene therapy and upon further analysis you discover that the cancer cells contained an oncogenic E2F transcription factor. E. After the initial decrease in size the tumor no longer responded to the Rb gene therapy and upon further analysis you discover that the cancer cells were overexpressing cyclin dependent kinase.

6. 2. Activation of a proto-oncogene to an oncogene can occur by all of the following mechanisms except: A. gene amplification B. translocation C. point mutation D. mutation of both alleles to the recessive genotype

7. 3. Which of the following genes encodes a tyrosine kinase which was the first viral oncogene identified? A. src B. abl C. raf D. Ras E. Akt

8. 4. Neoplastic cells in nearly all patients with chronic myelogenous leukemia contain a characteristic chromosomal translocation (the Philadelphia chromosome) that generates which of the following molecular events? A. Amplification of the myc gene B. Mutation in the Rb gene C. Fusion of the bcr and abl genes D. Deletion of p53 E. Point mutation in Ras

9. 5. Several oncogenes have been shown to be altered versions of genes encoding growth factor membrane receptors. By which mechanism do these altered receptors contribute to neoplastic cell transformation? A. They act as a permanently switched on growth signal in the absence of growth factor. B. They bind the growth factor irreversibly. C. They bind directly to the nuclear membrane. D. They decrease the production of growth factors. E. They enhance the GTPase activity of small G-proteins.

10. 6. A DNA virus can induce tumor formation by: A. Dephosphorylating Rb B. Inducing apoptosis in the host cells C. Activating p53 D. Inserting src into the host DNA E. Inducing G0 in the host cells

11. 7. The ras gene encodes a 21kD G-protein that is important in normal cell growth control. Approximately 30% of human cancers carry a mutated ras gene. The most common carcinogenic mutation is the substitution of glycine at position 12 with valine. Because of this mutation the ras protein is unable to: A. Bind the guanine-nucleotide exchange factor known as SOS. B. Bind GTP. C. Hydrolyze GTP. D. Binds its GTPase-activating protein known as ras-GAP. E. Dissociates from its beta-subunit and gamma-subunit partners.

12. 8. You have a cancer cell line that overexpresses EGFR (epidermal growth factor receptor. For which of the conditions will the cells not proliferate? Use of SCH6636, a farnesyl transferase inhibitor. Cetuximab, a monoclonal antibody to EGFR. PD184352, a MEK (MAP kinase kinase) inhibitor STI-571, which inhibits Abl kinase activity

13. 9. Which of the following cells have the potential to develop a tumor? Cell expressing a deletion in mdm2 the protein that phoshporylates and inactivates p53 Cell expressing a dominant negative Ras with a T17N mutation Cell expressing Ras T17N but constitutively active Raf kinase Cell overexpressing cip1/p21 Cell overexpressing wee kinase (chk1)

14. 10. When compound X is applied alone several times to the skin it induces cancer. Compound Y applied by itself does not induce cancer. However, only one dose of compound X followed by several doses of compound Y induces cancer. Which of the following statements best describes compounds X and Y? A. Both X and Y are tumor initiators. B. Both X and Y are tumor promoters. C. X is a tumor promoter and Y is a tumor initiator. D. X is a tumor initiator and y is a tumor promoter. E. Y probably induces mutations but X does not.