Ch20 The Genetics of Cancer Full Test Bank

Genetics, 6e (Hartwell)

Chapter 20 The Genetics of Cancer

1) The enzymatic activity of CDKs is regulated by forming a complex with which proteins?

A) p53

B) p21

C) Growth factors

D) Cyclins

2) Which statement best describes the action of polypeptide growth factors?

A) They bind to intracellular receptors and trigger intracellular signal transduction pathways.

B) They bind to cell surface receptors and trigger intracellular signal transduction pathways.

C) They bind to cell surface receptors that phosphorylate cyclins.

D) They bind an intracellular receptor forming a complex that then acts as a transcription factor.

3) The retinoblastoma (Rb) protein controls progression into S phase by regulating ________ activity.

A) cyclin D

B) p53

C) CDK4

D) E2F

E) CDC28

4) The activity of Rb is controlled by

A) its phosphorylation state.

B) cyclin A.

C) E2F.

D) its poly-A tail.

E) its level of methylation.

5) Which of the following is not likely to occur if p53 is inactivated?

A) The appearance of homogenously staining regions on chromosomes

B) Increased propensity to arrest in G1

C) Inhibition of the G1 to S checkpoint

D) An increase in gene amplification in affected cells

E) Generation of chromosomes that lack telomeres and centromeres

6) A cellular process that results in cell death is

A) apoptosis.

B) contact inhibition.

C) posttranslational control.

D) metastasis.

7) Which characteristic is typical of a cancer cell but not of a normal cell?

A) Cell division is inhibited when the cell contacts neighboring cells.

B) The cell cycle lacks S phase.

C) The cell has the ability to invade surrounding tissue.

D) Cell death occurs after a limited number of divisions.

8) The enzyme telomerase is essential for unlimited cell division because

A) it is essential for DNA replication initiation at origins of replication.

B) a lack of telomerase will result in chromosome shortening and cell death.

C) it is essential for kinetochore attachment to the spindles.

D) a lack of telomerase results in decreased p53 activity.

9) A karyotype of chromosomes from a cancer cell would be most likely to exhibit

A) polyploidy.

B) a single missing chromosome.

C) a single extra chromosome.

D) a normal set of chromosomes because only point mutations have occurred.

10) The ability of a cell to move from the tissue to which it belongs to other parts of the body is known as

A) metastasis.

B) contact inhibition.

C) immune surveillance.

D) angiogenesis.

11) The current model of cancer development is that

A) cancer develops from a single cell that evolves through one to two mutations.

B) cancer develops from a single cell that evolves through multiple mutations.

C) cancer develops from multiple cells that evolve through multiple mutations.

D) cancer develops from multiple cells that evolve through one to two mutations.

12) In its active form, the Ras protein is associated with

A) DNA.

B) ATP.

C) GTP.

D) RNA.

E) GDP.

13) What is one piece of evidence that supports the hypothesis that cancers are clonal?

A) A tumor grows in a single anatomical site.

B) All cells from the same cancer have identical mutations.

C) All cells from the same tumor have identical karyotypes.

D) All cancer cells from a heterozygous woman have the same X chromosome inactivated.

E) Individuals of all ages, including children, can develop cancer.

14) What is the term for mutant alleles that can act dominantly to predispose a cell to a cancerous phenotype?

A) Polymerases

B) Oncogenes

C) Activators

D) Tumor-suppressor genes

15) How can a mutation in a tumor-suppressor gene behave as a recessive allele at the cellular level, but appear as a dominant allele in pedigree analysis?

A) Some functional protein can still be produced in a cell heterozygous for a loss-of-function allele; however, an additional mutation can inactivate the second allele, eliminating all functional protein allowing cancer to occur in many family members.

B) A single functional allele is sufficient to regulate the cell cycle, but not sufficient to promote apoptosis, allowing cancer to develop in every generation.

C) A cell with half the amount of the functional tumor-suppressor protein can form benign tumors that will occur in every generation in the pedigree.

D) Some functional protein can still be produced in a cell heterozygous for a loss-of-function allele; but loss-of-function tumor-suppressor alleles are so common in the population that many individuals are homozygous.

16) The human papillomavirus (HPV) carries a gene that functions as an oncogene by inactivating the p53 protein. The fact that the loss of p53 function is oncogenic suggests that

A) p53 normally functions to prevent uncontrolled cell division.

B) p53 is a proto-oncogene.

C) the HPV protein activates transcription of p53.

D) p53 functions at origins of replication in DNA.

17) The BRCA2 protein functions in double-strand break repair. If a woman is heterozygous for a loss-of-function allele of BRCA2, she

A) will develop cancer because two functional copies of BRCA2 are needed in every cell.

B) will not get cancer because BRCA1 can compensate for the loss of BRCA2.

C) will develop cancer after several mutations occur, even if the mutations occur in different clonal populations of cells.

D) may develop cancer because mutation of the wild-type BRCA2 allele could destroy an important DNA repair mechanism.

18) What is the relationship between genomic instability and proliferation?

A) No relationship exists between genomic instability and proliferation rate.

B) Genomic instability increases the probability of developing cells with a high rate of proliferation.

C) Genomic instability reduces the probability of developing cells with a high rate of proliferation.

D) Cells that proliferate rapidly have the most stable genomes.

19) Drugs such as Gleevec® and Herceptin® represent a modern approach to cancer treatment because they

A) target specific gene alterations that occur in some cancers.

B) target metabolic pathways that are common to all cells.

C) enhance apoptotic pathways in all cells.

D) target proteins that are present in both normal and cancer cells, but that cancer cells rely on more than normal cells do.

20) What is one reason why tumor-suppressor genes make poor druggable targets?

A) Cancer-causing mutations in tumor-suppressor genes result in loss of function.

B) Mutant alleles of tumor-suppressor genes generally result in a greater activity of the protein, which makes inhibiting the proteins more difficult.

C) Most drugs cannot distinguish the normal and mutant forms of the tumor suppressor proteins.

D) Drugs that can target-tumor suppressor proteins are difficult to deliver to cancer cells.

21) What is one current limitation of whole-genome sequencing for personalized cancer treatment?

A) The human genome is too large to be sequenced for individual patients.

B) Drugs may not exist to target the mutant genes that are identified.

C) Whole-genome sequencing reveals only mutations in coding sequences, and regulatory mutations may also be important.

D) The genomes of cells with abnormal karyotypes, such as cancer cells, cannot be sequenced reliably.

22) When autocrine stimulation is occurring, cancer cells divide in response to growth signals produced by the surrounding noncancerous cells.

23) Genomic instability in cancer cells includes both nucleotide mutations and chromosomal aberrations.

24) If cancer does not develop within one year following exposure to a mutagen, then the mutagen did not cause DNA damage.

25) If a female is heterozygous for a mutant allele of a tumor-suppressor gene, her children will be predisposed to develop cancer only if their father is also a carrier.

26) Which of the following scenarios exemplifies cancer therapy targeted toward a specific mutation?

A) A patient with leukemia receives chemotherapeutic drug that inhibits DNA synthesis.

B) A benign tumor is surgically removed from a patient's kidney.

C) A patient with melanoma receives a drug that targets a signal transduction pathway protein.

D) A patient with two mutant tumor-suppressor alleles receives radiation and a chemotherapeutic drug that blocks mitosis.

27) Rous sarcoma virus was identified when a scientist discovered that a virus passing between chickens was causing their tumors. The genome of this retrovirus includes the src gene, which encodes a tyrosine kinase that functions in signaling pathways leading to proliferation. The src gene is a

A) cyclin.

B) proto-oncogene.

C) reverse transcriptase.

D) tumor-suppressor gene.

28) A man inherited a chromosome with a deletion that removes a tumor-suppressor gene. The protein encoded by this gene normally functions in DNA damage repair. Which series of events would be most likely to lead to cancer?

A) Loss-of-heterozygosity of the tumor-suppressor gene followed by driver mutations in two different proto-oncogenes

B) A loss-of-function mutation in a proto-oncogene followed by a gain-of function mutation in a tumor-suppressor gene

C) Loss-of-heterozygosity of the tumor-suppressor gene followed by passenger mutations in several genes of unknown function

D) A gain-of-function mutation in a proto-oncogene followed by a chromosomal duplication of a region including a tumor-suppressor gene that functions the G1-to-S checkpoint