Genetics: A Conceptual Approach

Benjamin Pierce

Chapter 23 Cancer Genetics - all with Video Answers

Educators

Chapter Questions

01:01

Problem 1

What types of evidence indicate that cancer arises from genetic changes?

Sam Limsuwannarot

Numerade Educator

00:28

Problem 2

How is cancer different from most other types of genetic diseases?

Sam Limsuwannarot

Numerade Educator

00:54

Problem 3

Outline Knudson's two-hit hypothesis of retinoblastoma and describe how it helps to explain unilateral and bilateral cases of retinoblastoma

Sam Limsuwannarot

Numerade Educator

01:02

Problem 4

Briefly explain how cancer arises through clonal evolution.

Abigail Schammel

Numerade Educator

01:10

Problem 5

What is the difference between an oncogene and a tumor-suppressor gene? Give some examples of the functions of proto-oncogenes and tumor suppressers in normal cells.

Abigail Schammel

Numerade Educator

00:37

Problem 6

What is haploinsufficiency? How might it affect cancer risk?

Sam Limsuwannarot

Numerade Educator

00:32

Problem 7

How do cyclins and CDKs differ? How do they interact in controlling the cell cycle?

Sam Limsuwannarot

Numerade Educator

00:41

Problem 8

Briefly outline the events that control the progression of cells through the $G_{1} /$ S checkpoint in the cell cycle.

Sam Limsuwannarot

Numerade Educator

04:27

Problem 9

Briefly outline the events that control the progression of cells through the $\mathrm{G}_{2} / \mathrm{M}$ checkpoint of the cell cyde.

Sana Riaz

Numerade Educator

00:42

Problem 10

What is a signal-transduction pathway? Why are mutations in components of signal-transduction pathways often associated with cancer?

Sam Limsuwannarot

Numerade Educator

00:29

Problem 11

How is the Ras protein activated and inactivated?

Sam Limsuwannarot

Numerade Educator

00:24

Problem 12

Why do mutations in genes that encode DNA-repair enzymes often produce a predisposition to cancer?

Sam Limsuwannarot

Numerade Educator

00:49

Problem 13

What role do telomeres and telomerase play in cancer progression?

Sam Limsuwannarot

Numerade Educator

00:28

Problem 14

How is an epigenetic change different from a mutation?

Sam Limsuwannarot

Numerade Educator

00:22

Problem 15

How is DNA methylation related to cancer?

Sam Limsuwannarot

Numerade Educator

00:30

Problem 16

Briefly outline some of the genetic changes commonly associated with the progression of colorectal cancer.

Sam Limsuwannarot

Numerade Educator

00:53

Problem 17

Explain how chromosome deletions, inversions, and translocation may cause cancer.

Abigail Schammel

Numerade Educator

00:26

Problem 18

Briefly outline how the Philadelphia chromosome leads to chronic myelogenous leukemia.

Sam Limsuwannarot

Numerade Educator

00:27

Problem 19

What is genomic instability? Give some ways in which genomic instability may arise.

Sam Limsuwannarot

Numerade Educator

00:57

Problem 20

How do viruses contribute to cancer?
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Abigail Schammel

Numerade Educator

01:11

Problem 21

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

Abigail Schammel

Numerade Educator

00:26

Problem 22

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

Sam Limsuwannarot

Numerade Educator

01:44

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.

Abigail Schammel

Numerade Educator

02:19

Problem 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 retin oblastoma.
a. If the couple has anot her 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.

Caroline Jones

Numerade Educator

01:10

Problem 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?

Abigail Schammel

Numerade Educator

00:29

Problem 26

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

Sam Limsuwannarot

Numerade Educator

01:22

Problem 27

Cellsin 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.

Abigail Schammel

Numerade Educator

04:32

Problem 28

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

Sana Riaz

Numerade Educator

00:24

Problem 29

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

Sam Limsuwannarot

Numerade Educator

00:59

Problem 30

David Seligson and his colleagues examined levels of histone protein modification in prostate tumors and their association withclinical 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 prost ate tumor removed. Explain how acetylation and methylation might be associated with tumor recurrence in prostate cancer. (Hint: See Chapter $17 .$ )

Sana Riaz

Numerade Educator

04:40

Problem 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.

Sana Riaz

Numerade Educator

00:36

Problem 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.

Sam Limsuwannarot

Numerade Educator

00:32

Problem 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?

Sam Limsuwannarot

Numerade Educator

01:18

Problem 34

Many cancer cells are immortal (will divide indefinitely) because they have mutat ions that allow telomerase to be expressed. How might this knowledge be used to design anticancer drugs?

Abigail Schammel

Numerade Educator

00:43

Problem 35

Bloom syndrome is an autosomal recessive disease that exhibits haploinsufficiency. A recent survey showed that people heterozygous for mutations at the $B L M$ locus are at increased risk of colon cancer. Suppose you are a genetic counselor. A young woman is referred to you whose mother has Bloom syndrome; the young woman's father has no family history of Bloom syndrome. The young woman asks whether she is likely to experience any other health problems associated with her family history of Bloom syndrome. What advice would you give her?

Sam Limsuwannarot

Numerade Educator

00:46

Problem 36

Imagine that you discover a large family in which bladder cancer is inherited as an autosomal dominant trait. Briefly outline a series of studies that you might conduct to identify the gene that causes bladder cancer in this family.

Sam Limsuwannarot

Numerade Educator

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