Deck 23: DNA Replication

Question 1

Human cells contain genes that induce tumor growth when mutated. In their normal state, these genes are called

A) oncogenes.
B) cellular oncogenes.
C) viral oncogenes.
D) proto-oncogenes.
E) sub-oncogenes.

Answer 1

D

Question 2

Retroviruses are responsible for which of the following conditions?

A) AIDS
B) Rous sarcoma
C) Mouse mammary tumor
D) Feline leukemia
E) All of the above

Answer 2

E

Question 3

Metastatic cancer is

A) terminally differentiated.
B) malignant.
C) invasive.
D) A, B, C
E) B and C only

Answer 3

E

Question 4

Cancer may arise as a result of

A) spontaneous mutations.
B) mutations associated with viral infection.
C) mutations associated with chemical mutagens.
D) mutations associated with radiation.
E) all of the above.

Question 5

What is the cellular target of HIV?

A) Granulocytes
B) Red blood cells
C) Neurons
D) Helper T cells
E) Hepatocytes

Question 6

A v-onc gene may be found in

A) human cells.
B) retroviruses.
C) bacteria.
D) fowl.
E) bacteriophages.

Question 7

Which of the following statements is not true?

A) Certain types of virus can cause cancer.
B) Some cancers stem from hyperactivated telomerase enzymes.
C) Neoplasia is another term for cancerous cells.
D) Melanomas are commonly caused by ionizing radiation.
E) About half the people with cancer have a mutation in a p53 gene.

Question 8

Cell proliferation is culture is normally limited by

A) cytophagy.
B) nutrient limitation.
C) contact inhibition.
D) quorum sensing.
E) competition.

Question 9

In sporadic (nonhereditary) cancers, mutations occur in ________ cells.

A) mammary
B) somatic
C) germ
D) undifferentiated
E) T

Question 10

In normal cells, p53 protein acts as a

A) GTPase inhibitor.
B) tumor suppressor.
C) proto-oncogene activator.
D) signal transducer.
E) None of the above

Question 11

Agents that can induce cancer through mutagenesis are called

A) mutagens.
B) carcinogens.
C) cancerogens.
D) destabilizers.
E) none of the above.

Question 12

The "two-hit" model for cancer development suggests that

A) a person without family history will never develop cancer.
B) cancers are often caused by two mutational events in a cell's life.
C) all types of cancer are hereditary.
D) All of the above
E) None of the above

Question 13

Unilateral retinoblastoma suggests that the cancer

A) developed spontaneously.
B) was radiation-induced.
C) will become metastatic.
D) was inherited.
E) is viral in nature.

Question 14

________ play a pivotal role in programmed cell death.

A) Proto-oncogenes
B) Oncogenes
C) Telomeres
D) Telomerases
E) Cyclins

Question 15

Which type of gene is often mutated in cancer?

A) Tumor suppressor gene
B) Mutator gene
C) Proto-oncogene
D) A, B, C
E) None of the above

Question 16

________ are implicated in breast, colon, and lung cancer.

A) Viral oncogenes
B) Mutator genes
C) Proto-oncogenes
D) Tumor suppressor genes
E) None of the above

Question 17

Cancer is best defined as

A) immune dysfunction.
B) viral malignancy.
C) regulated differentiation of tissue.
D) uncontrolled and abnormal cell division.
E) cellular deregulation.

Question 18

A mutant proto-oncogene is a(n)

A) growth factor.
B) virus.
C) suppressor.
D) oncogene.
E) mutator.

Question 19

Protein kinases are enzymes that normally catalyze the

A) phosphorylation of ADP.
B) formation of peptide bonds in proteins.
C) phosphorylation of cellular proteins.
D) synthesis of kinins.
E) degradation of cellular proteins.

Question 20

In retroviruses, the pol gene product is a(n)

A) reverse transcriptase.
B) DNA polymerase.
C) integrase.
D) recombinase.
E) RNA polymerase.

Question 21

It is a widespread, popular belief that radiation in small doses is healthful. What should be your response to this claim in light of what you learned in this chapter?

Question 22

The only genes necessary for the retroviral lifecycle are gag and pol.

Question 23

Explain how retinoblastoma appears dominant in pedigrees, when in fact the mutations underlying this cancer are recessive.

Question 24

The nucleic acid of retroviral provirus is composed of RNA.

Question 25

Telomerase is not a cause of cancer, yet can play a role in helping cancerous cells. How?

Question 26

Tumor suppressor gene mutations express in dominant fashion.

Question 27

The products of tumor suppressor genes stimulate cell proliferation, while the products of proto-oncogenes inhibit cell proliferation.

Question 28

The terms proto-oncogene and oncogene may give the misleading impression that these are genes "for" cancer waiting to be turned on. What are these genes, in terms of normal function, and what name might have been given to them to reflect this function rather than their role in cancer?

Question 29

Ionizing radiation is emitted at low levels by many natural objects in the environment, including some rocks and gases.

Question 30

Describe Knudson's 1971 two-mutation model: When and where are the mutations posited to occur?

Question 31

The process of relaying a growth-stimulatory or growth-inhibitory signal in response to an extracellular factor binding at the cell surface is called intercell signaling.

Question 32

Why, in the two-hit mutation model of cancer, is a germ cell/somatic cell mutational combination more likely than two somatic cell mutations?

Question 33

Terminally differentiated cells are noncancerous, normal cells.

Question 34

Some carcinogens act on the genome directly, while others act indirectly through chemical conversion.

Question 35

Li-Fraumeni syndrome is a rare inherited disease that greatly increases a person's risk of developing several types of cancer. This disease stems from a mutation in the TP53 tumor suppressor gene (Nichols et al. 2001. Cancer Epidemiol Biomarkers Prev 10:83-87). In most cases, approximately 95 percent of the mutations can be detected by sequence analysis of exons 4 through 9. If you isolated and analyzed DNA from a Li-Fraumeni patient, what genotype should you find in DNA isolated from (a) normal tissue, and (b) malignant tissue?

Question 36

Reverse transcriptase, the enzyme responsible for copying viral RNA into cDNA prior to integration into the host genome, lacks 3'-to-5' exonuclease "proofreading" ability. This may seem like a disadvantage to organisms that depend on such enzymes, but in fact they turn it to their advantage. How is this so?

Question 37

Programmed cell death, or apoptosis, is a necessary and useful property of cells. Why is this so?

Question 38

Wild-type mutator genes produce substances that induce point mutations and chromosomal rearrangements.

Question 39

People suffering from the genetic disease xeroderma pigmentosum have compromised DNA repair mechanisms, making them extremely sensitive to genetic damage from sunlight. Without taking measures to minimize exposure, these individuals typically succumb to skin cancer in childhood or early adulthood-a visceral demonstration of the mutagenicity of ultraviolet radiation. Yet, deliberate exposure in the form of sunbathing is very popular with some segments of the population. Why do you think this is so, and how might public health professionals raise awareness of the danger in which these people place themselves?

Question 40

List the ways in which proto-oncogenes may be converted to oncogenes.

Question 41

Each year, large parts of Australia fall within the sizable hole in the Earth's ozone layer that forms over the Antarctic, a situation that is likely linked to the high skin cancer rate found in that country. The protective motto in many parts of Australia is "slip, slap, slop"-slip on a shirt, slap on a hat, and slop on sunscreen. At the molecular level, what exactly are the mutagenic effects of UVA and UVB radiation?

Question 42

Suppose you are studying a rare spontaneous cancer in cats, which you suspect is retrovirus-induced. What kinds of retroviral insertion could lead to cancer, and what kind of genetic signature would you look for to distinguish between them?

Question 43

What is metastasis, and why is metastatic cancer the most difficult cancer to treat?

Question 44

What kinds of cancers might someday be treated with iRNAs, which you learned about in Chapters 20 and 21?