Deck 20: Genetics of Cancer

Question 1

Hereditary retinoblastoma is an autosomal dominant hereditary cancer.Cells from retinal tumors in a child who has this disease possess

A)evidence of non-disjunction in all autosomes.
B)one non-functional copy of the retinoblastoma gene.
C)two non-functional copies of the retinoblastoma gene.
D)trisomy for the retinblastoma gene.
E)a dominant mutation in the retinoblastoma gene.

Answer 1

C

Question 2

Which of the following is not likely to be a tumor suppressor?

A)A growth factor receptor
B)A checkpoint protein
C)A DNA repair enzyme
D)An apoptosis-promoting factor
E)The negative regulator of a CDK

Answer 2

A

Question 3

Cancer is best defined as

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

Answer 3

B

Question 4

Protein kinases are enzymes that normally catalyze the

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

Question 5

Malignant breast,colon,and lung cancers typically have

A)mutated tumor suppressor genes.
B)active oncogenes.
C)chromosomal abnormalities.
D)activated telomerase.
E)All of these

Question 6

Metastatic cancer is

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

Question 7

Retroviruses are responsible for which of the following conditions?

A)Rous sarcoma
B)AIDS
C)Feline leukemia
D)Mouse mammary tumors
E)All of these

Question 8

A proto-oncogene that gains function due to amplification,translocation to a more transcriptionally active area of the genome,or a mutation that causes either an increase in function or the suppression of down-regulation,is

A)a pseudo-oncogene.
B)recessive.
C)dominant.
D)an oncogene.
E)C and D only

Question 9

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

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

Question 10

________ play a pivotal role in programmed cell death.

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

Question 11

Apoptosis is

A)rapid cell division.
B)caused by proto-oncogenes.
C)the change in shape of a cell when it becomes cancerous.
D)programmed cell death.
E)None of these

Question 12

Which of the following statements is not true?

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

Question 13

v-onc genes are found in

A)vital cells.
B)viral cells.
C)cancer-causing retroviruses.
D)very rapidly growing cells.
E)bacteriophages.

Question 14

Cell proliferation in culture is normally limited by

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

Question 15

Mutations in a normal growth-stimulating gene are most likely to have no effect or to cause

A)the loss of responsiveness to growth stimulation in the cell with the mutant gene.
B)the cell with the mutant gene to become cancerous.
C)excessive growth in the cells surrounding the one with the mutant gene.
D)a mutator effect in the cell with the mutant gene.
E)apoptosis of the cell with the mutant gene.

Question 16

Cancer may arise as a result of

A)mutations associated with viral infection.
B)mutations associated with chemical mutagens.
C)mutations associated with radiation.
D)spontaneous mutations.
E)All of these

Question 17

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

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

Question 18

Small DNA tumor viruses such as SV40 and HPV have viral oncogenes that are not homologs of host cell genes.Some of these novel viral oncogenes make proteins that exert their tumorigenic effect by

A)binding to and inactivating pRB.
B)making Gag,Pol and Env proteins more active.
C)causing cellular proto-oncogenes to mutate into oncogenes.
D)causing apoptosis in target tissues.
E)inactivating the immune system.

Question 19

Agents that can induce cancer through mutagenesis are called

A)destabilizers.
B)cancerogens.
C)mutagens.
D)carcinogens.
E)None of these

Question 20

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.How is this advantageous to organisms that depend on such enzymes?

Question 21

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

Question 22

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

Question 23

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

Question 24

Most cancer deaths in the United States are caused by radiation-induced cancer.

Question 25

How does telomerase,which is not a cause of cancer,nonetheless play a role in its development?

Question 26

Inherited mutant tumor suppressors produce a dominant susceptibility to cancer,but the mutant alleles are actually recessive in the cancer.

Question 27

Terminally differentiated cells are noncancerous,normal cells.

Question 28

The nucleic acid of retroviral provirus is composed of RNA.

Question 29

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

Question 30

People with 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 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 31

Some carcinogens act on the genome directly,while others are converted to mutagenic substances by the cells's enzymes.

Question 32

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

Question 33

The Bcl-2 gene product in its normal form can be activated to prevent cells from undergoing apoptosis (programmed cell death)in specific circumstances.It is a carefully regulated gene,being "turned on" only under specific circumstances.A null mutation in Bcl-2 leads to excessive cell loss.Some Bcl-2 mutation can cause a "gain of function" in which the protein is active all the time.
a.In the terms used in this chapter,what would the normal version be called?
b.What would the gain-of-function mutation be called?
c.How would you expect the gain-of-function mutation to be involved in cancer?

Question 34

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

Question 35

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

Question 36

In normal cells,p53 protein acts as

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

Question 37

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

Question 38

When oncologists (scientists who study cancer)refer to "transformation," they mean something different from what the word "transformation" signifies when used by biotechnologists.Explain the difference between the two uses of the term in genetics.

Question 39

The terms proto-oncogene and oncogene may give the misleading impression that these are "genes for cancer" that are 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 40

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

Question 41

At the molecular level,what exactly are the mutagenic effects of UVA and UVB radiation?

Question 42

What kinds of cancers might eventually be treated with RNAi,which you learned about in

Question 43

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% 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?
b.malignant tissue?

Question 44

BRCA1 is a gene involved in repair of double-stranded DNA breaks.Mutant forms of this gene are linked to a substantial proportion of familial breast cancers.A woman who inherits a certain allele of the gene has about a 60-80% chance of getting breast cancer,as well as an elevated chance of getting ovarian cancer,in her lifetime.
a.Why don't a higher percentage of women with the mutation get breast cancer?
b.How would the breast cancer inheritance caused by BRCA1 be described in Mendelian terms?

Question 45

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?