Question 23.21

What characteristics of the pedigree shown in Figure 23.1 suggest that pancreatic cancer in this family is inherited as an autosomal dominant trait?

Question 23.22

If cancer is fundamentally a genetic disease, how might an environmental factor such as smoking cause cancer?

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Question 23.23

Both genes and environmental factors contribute to cancer. Table 23.2 shows that prostate cancer is 30 times as common among Caucasians from Utah as among Chinese from Shanghai. Briefly outline how you might determine if these differences in the incidence of prostate cancer are due to differences in the genetic makeup of the two populations or to differences in their environments.

Question 23.24

A couple has one child with bilateral retinoblastoma. The mother is free from cancer, but the father has unilateral retinoblastoma and he has a brother who has bilateral retinoblastoma.

• a. If the couple has another child, what is the probability that this next child will have retinoblastoma?
• b. If the next child has retinoblastoma, is it likely to be bilateral or unilateral?
• c. Explain why the father’s case of retinoblastoma is unilateral, whereas his son’s and brother’s cases are bilateral.

Question 23.25

The palladin gene, which plays a role in pancreatic cancer (see the introduction to this chapter), is said to be an oncogene. Which of its characteristics suggest that it is an oncogene rather than a tumor-suppressor gene?

Question 23.26

Mutations in the RB gene are often associated with cancer. Explain how a mutation that results in a nonfunctional RB protein contributes to cancer.

Question 23.27

Cells in a tumor contain mutated copies of a particular gene that promotes tumor growth. Gene therapy can be used to introduce a normal copy of this gene into the tumor cells. Would you expect this therapy to be effective if the mutated gene were an oncogene? A tumor-suppressor gene? Explain your reasoning.

Question 23.28

What would be the effect on the cell cycle of a drug that inhibited each of the following?

• a. MPF
• b. cyclin-E-CDK
• c. cyclin-D-CDK

Question 23.29

What would be the effect of a drug that inhibited the breakdown of cyclin B?

Question 23.30

David Seligson and his colleagues examined levels of histone protein modification in prostate tumors and their association with clinical outcomes (D. B. Seligson et al. 2005. Nature 435:1262–1266). They used antibodies to stain for acetylation at three different sites and for methylation at two different sites on histone proteins. They found that the degree of histone acetylation and methylation helped predict whether prostate cancer would return within 10 years in the patients who had a prostate tumor removed. Explain how acetylation and methylation might be associated with tumor recurrence in prostate cancer. (Hint: See Chapter 17.)

Question 23.31

Some cancers have been treated with drugs that demethylate DNA. Explain how these drugs might work. Do you think the cancer-causing genes that respond to the demethylation are likely to be oncogenes or tumor-suppressor genes? Explain your reasoning.

Question 23.32

Some cancers are consistently associated with the deletion of a particular part of a chromosome. Does the deleted region contain an oncogene or a tumor-suppressor gene? Explain.

Question 23.33

Assume that the provirus in Figure 23.14 inserts just upstream of a tumor suppressor gene. Would this be likely to cause cancer? Why or why not?