Question 1

In its active form, the Ras protein is associated with

Accepted Answer

A) DNA. 
B) ATP. 
C) GTP. 
D) RNA. 
E) GDP. 
A) DNA. 
B) ATP. 
C) GTP. 
D) RNA. 
E) GDP. C

Question 2

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

Accepted Answer

A) cyclin. 
B) proto-oncogene. 
C) reverse transcriptase. 
D) tumor-suppressor gene. 
A) cyclin. 
B) proto-oncogene. 
C) reverse transcriptase. 
D) tumor-suppressor gene. B

Question 3

The enzyme telomerase is essential for unlimited cell division because

Accepted Answer

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. 
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. B

Question 4

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

Accepted Answer

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. 
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.

Question 5

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

Accepted Answer

A) True 
 B)False

Question 6

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

Accepted Answer

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. 
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.

Question 7

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

Accepted Answer

A) True 
 B)False

Question 8

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

Accepted Answer

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. 
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.

Question 9

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

Accepted Answer

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. 
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.

Question 10

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

Accepted Answer

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. 
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.

Question 11

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.

Accepted Answer

A) True 
 B)False

Question 12

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

Accepted Answer

A) True 
 B)False

Question 13

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?

Accepted Answer

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. 
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.

Question 14

A cellular process that results in cell death is

Accepted Answer

A) apoptosis. 
B) contact inhibition. 
C) posttranslational control. 
D) metastasis. 
A) apoptosis. 
B) contact inhibition. 
C) posttranslational control. 
D) metastasis.

Question 15

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

Accepted Answer

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 
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

Question 16

Which statement best describes the action of polypeptide growth factors?

Accepted Answer

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. 
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.

Question 17

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

Accepted Answer

A) polyploidy. 
B) a single missing chromosome. 
C) a single extra chromosome. 
D) a normal set of chromosomes because only point mutations have occurred. 
A) polyploidy. 
B) a single missing chromosome. 
C) a single extra chromosome. 
D) a normal set of chromosomes because only point mutations have occurred.

Question 18

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

Accepted Answer

A) Polymerases 
B) Oncogenes 
C) Activators 
D) Tumor-suppressor genes 
A) Polymerases 
B) Oncogenes 
C) Activators 
D) Tumor-suppressor genes

Question 19

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

Accepted Answer

A) p53 
B) p21 
C) Growth factors 
D) Cyclins 
A) p53 
B) p21 
C) Growth factors 
D) Cyclins

Question 20

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

Accepted Answer

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. 
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.

Exam 20: The Genetics of Cancer

In its active form, the Ras protein is associated with

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

The enzyme telomerase is essential for unlimited cell division because

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

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

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

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

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

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

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

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.

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

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 cellular process that results in cell death is

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

Which statement best describes the action of polypeptide growth factors?

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

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

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

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

Genetics: the Study of Biological Information

Mendels Principles of Heredity

Extensions to Mendels Laws

The Chromosome Theory of Inheritance

Linkage, Recombination, and the Mapping of Genes on Chromosomes

DNA Structure, Replication, and Recombination

Anatomy and Function of a Gene: Dissection Through Mutation

Gene Expression: the Flow of Information From Dna to Rna to Protein

Digital Analysis of Dna

Genome Annotation

Analyzing Genomic Variation

The Eukaryotic Chromosome

Chromosomal Rearrangements and Changes in Chromosome Number

Bacterial Genetics

Organellar Inheritance

Gene Regulation in Prokaryotes

Gene Regulation in Eukaryotes

Manipulating the Genomes of Eukaryotes

The Genetic Analysis of Development

Variation and Selection in Populations

The Genetics of Complex Traits

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