Deck 19: The Genetics of Cancer

Question 1

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

A)specifically target 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 the cancer cells rely on these proteins more than normal cells.

Answer 1

specifically target gene alterations that occur in some cancers.

Question 2

What is a characteristic that is typical of a cancer cell but not of a normal cell?

A)Cell division is inhibited when they contact neighboring cells
B)Lack of an S phase in the cell cycle.
C)Ability to invade surrounding tissue.
D)Limited number of divisions before the cell dies.

Answer 2

Ability to invade surrounding tissue.

Question 3

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 which phosphorylate cyclins.
D)They make a complex with an intracellular receptor which then acts as a transcription factor.

Answer 3

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

Question 4

In its active form, the RAS protein is associated with

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

Question 5

What is the relationship between chromosomal stability and proliferation?

A)There is no relationship between chromosomal instability and proliferation rate.
B)The greater the chromosomal instability the higher the probability of getting cells that have a higher proliferation rate.
C)The greater the chromosomal instability the lower the probability of getting cells that have a higher proliferation rate.
D)A greater chromosomal instability has no impact on the proliferation rate.but a more stable genome will result in a higher proliferation rate.

Question 6

The current model of cancer development is that

A)a cancer develops from a single cell that evolves through 1-2 mutations.
B)a cancer develops from a single cell that evolves through multiple mutations.
C)a cancer develops from a multiple cells that evolve through multiple mutations.
D)a cancer develops from multiple cells that evolve through 1-2 mutations.

Question 7

The ability of a cell to move to other parts of the body is known as

A)metastasis
B)contact inhibition
C)vascularization
D)angiogenesis.

Question 8

The activity of Rb is regulated by

A)its phosphorylation state.
B)cyclin A.
C)E2F.
D)its polyA tail.
E)its level of methylation.

Question 9

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

A)Polymerases
B)Oncogenes
C)Activators
D)Tumor suppressors

Question 10

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

A)At the cellular level only one allele needs to be mutated for an en effect while in a pedigree the cancer may be vertically inherited.
B)At the cellular level both alleles need to be mutated for an en effect while in a pedigree the cancer may be vertically inherited.
C)At the cellular level one allele needs to be mutated for an en effect while in a pedigree the cancer may be horizontally inherited.
D)At the cellular level both alleles need to be mutated for an en effect while in a pedigree the cancer may be horizontally inherited.

Question 11

The retinoblastoma (Rb) protein regulates progression into S phase by regulating ___________ activity.

A)cyclin D
B)p53
C)CDK4
D)E2F
E)CDC28

Question 12

Which of the following is least likely to occur from the inactivation of p53?

A)The appearance of homogenously staining regions on chromosomes
B)Increased propensity to arrest in G₁
C)alterations in the G₁ to S checkpoint
D)An increase in gene amplification in affected cells
E)Generation of fragments of chromosomal DNA lacking telomeres and centromeres

Question 13

The human papilloma virus (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)The HPV protein is encoded by a tumor suppressor gene.
C)p53 gene expression is upregulated by the HPV protein.
D)The HPV protein functions at origins of replication on DNA.
E)p53 is a proto-oncogene.

Question 14

Why are some individuals are predisposed to getting cancer?

A)They have chromosomal deletions so that they carry fewer copies of proto-oncogenes
B)They have chromosomal duplications so that they carry more copies of proto-oncogenes
C)The individuals mutate their genes to create a cancer.
D)They inherit mutant alleles of genes that are involved in cancer development.

Question 15

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

A)Proteases
B)Nucleases
C)Growth factors
D)Cyclins

Question 16

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

A)The tumor suppressor proteins may not even be produced.
B)Tumor suppresor mutations generally result in a greater activity of the protein so that inhibiting the protein is more difficult.
C)It is difficult to distinguish with a drug the normal and mutated forms of the tumor suppressor proteins.
D)It is difficult to get the drugs that can target tumor suppressor proteins into cancer cells.

Question 17

A programmed cell change that results in cell death is referred to as

A)apoptosis.
B)contact inhibition.
C)post-translational control.
D)metastasis.

Question 18

What is a common type of genomic change that occurs in cancer cells?

A)Polyploidy
B)Decreased incidence of deletions
C)Decreased incidence of fragmentation.
D)Increased stability
E)increased chromosome loss

Question 19

The enzyme telomerase is essential for unlimited cell division since

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..

Question 20

What is one experimental result that supports the hypothesis that cancers are clonal?

A)Cancer cells all come from the same anatomical site.
B)Cells from the same cancer have identical genes mutated.
C)Cancer cells from tumors have identical karyotypes.
D)Cells from cancers of women have the same X chromosome inactivated.

Question 21

Genetic testing for cancer can

A)identify individuals that are resistant to cancer.
B)indicate increased risk of certain cancers.
C)predict the age of cancer onset in an individual.
D)eliminate the possibility that an individual will develop cancer.
E)do none of the choices.

Question 22

What kind of information will be used for personalized cancer treatment?

A)PCR and sequencing of 1-2 oncogenes
B)Whole genome sequencing.
C)PCR analysis of the RB and p53 genes.
D)PCR and sequencing of 6-10 tumor suppressor genes.