Question 1

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

Accepted Answer

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

Question 2

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

Accepted Answer

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. 
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. A

Question 3

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

Accepted Answer

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. 
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. C

Question 4

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

Accepted Answer

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

Question 5

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

Question 6

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

Accepted Answer

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. 
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 7

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

Accepted Answer

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

Question 8

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

Accepted Answer

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

Question 9

Genetic testing for cancer can

Accepted Answer

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. 
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 10

The enzyme telomerase is essential for unlimited cell division since

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..

Question 11

What is the relationship between chromosomal stability and proliferation?

Accepted Answer

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. 
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 12

The current model of cancer development is that

Accepted Answer

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. 
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 13

Why are some individuals are predisposed to getting cancer?

Accepted Answer

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. 
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 14

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

Accepted Answer

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. 
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 15

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

Accepted Answer

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. 
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.

Question 16

The activity of Rb is regulated by

Accepted Answer

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

Question 17

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

Accepted Answer

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

Question 18

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

Accepted Answer

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 
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 19

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

Accepted Answer

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

Question 20

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?

Accepted Answer

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. 
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.

Exam 19: The Genetics of Cancer

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

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

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

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

Which statement best describes the action of polypeptide growth factors?

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

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

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

Genetic testing for cancer can

The enzyme telomerase is essential for unlimited cell division since

What is the relationship between chromosomal stability and proliferation?

The current model of cancer development is that

Why are some individuals are predisposed to getting cancer?

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

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

The activity of Rb is regulated by

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

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

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

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?

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 Genomes

Analyzing Genomic Information

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

Genetics of Complex Traits

Filters