Question 1

Which of the following genes is NOT classified as a tumor suppressor?

Accepted Answer

A) MGMT 
B) p16INK4A 
C) PTEN 
D) VHL 
E) None of the above 
A) MGMT 
B) p16INK4A 
C) PTEN 
D) VHL 
E) None of the above A

Question 2

Which of the following statements about NF1 is FALSE?

Accepted Answer

A) It regulates Ras signaling through positive feedback control mechanisms. 
B) Cells lacking NF1 have higher levels of GTP-bound Ras. 
C) NF1 is known as a Ras-GAP. 
D) B and C. 
E) None of the above. 
A) It regulates Ras signaling through positive feedback control mechanisms. 
B) Cells lacking NF1 have higher levels of GTP-bound Ras. 
C) NF1 is known as a Ras-GAP. 
D) B and C. 
E) None of the above. A

Question 3

You are studying cancer cells,and hypothesize that you have found a previously unidentified tumor suppressor gene.Which of the following results would support your hypothesis?

Accepted Answer

A) You have found loss of heterozygosity in the locus containing your gene in a number of human lung cancer samples. 
B) You have identified a gain-of-function mutation in this gene that results in the transformation of normal cells. 
C) Functional analysis has revealed that the wild-type form of the gene that you have identified serves to drive proliferation. 
D) B and C. 
E) None of the above. 
A) You have found loss of heterozygosity in the locus containing your gene in a number of human lung cancer samples. 
B) You have identified a gain-of-function mutation in this gene that results in the transformation of normal cells. 
C) Functional analysis has revealed that the wild-type form of the gene that you have identified serves to drive proliferation. 
D) B and C. 
E) None of the above. A

Question 4

Which of the following is TRUE of methylation in cancer cells?

Accepted Answer

A) Overall levels of methylation throughout the cancer cell genome often increase. 
B) There is an increase in DNA methyltransferase enzyme activity. 
C) Areas of CpG islands are hypomethylated. 
D) Areas of CpG islands become methylated inappropriately. 
E) None of the above. 
A) Overall levels of methylation throughout the cancer cell genome often increase. 
B) There is an increase in DNA methyltransferase enzyme activity. 
C) Areas of CpG islands are hypomethylated. 
D) Areas of CpG islands become methylated inappropriately. 
E) None of the above.

Question 5

The APC protein

Accepted Answer

A) Is essential for degrading β-catenin. 
B) Causes increased activation of β-catenin. 
C) Helps to regulate cell motility. 
D) A and C. 
E) None of the above. 
A) Is essential for degrading β-catenin. 
B) Causes increased activation of β-catenin. 
C) Helps to regulate cell motility. 
D) A and C. 
E) None of the above.

Question 6

You are studying a cell line in which the loss of just one copy of a tumor suppressor gene provides a growth advantage for the cells.This would be an example of genetic

Accepted Answer

A) Haplosufficiency. 
B) Heteroinsufficiency. 
C) Haploinsufficiency. 
D) Unilateral mutation. 
E) None of the above. 
A) Haplosufficiency. 
B) Heteroinsufficiency. 
C) Haploinsufficiency. 
D) Unilateral mutation. 
E) None of the above.

Question 7

Inactivation of tumor suppressor genes can occur as the result of

Accepted Answer

A) Somatic mutation. 
B) Promoter demethylation. 
C) Loss of heterozygosity. 
D) A and C. 
E) None of the above. 
A) Somatic mutation. 
B) Promoter demethylation. 
C) Loss of heterozygosity. 
D) A and C. 
E) None of the above.

Question 8

Sporadic cases of retinoblastoma require

Accepted Answer

A) One inactivating somatic mutation in one copy of Rb. 
B) Two somatic inactivating mutations,one in each of the two copies of Rb. 
C) One somatic mutation in Rb,leading to its activation. 
D) Two somatic mutations in a copy of Rb,leading to its activation. 
E) None of the above. 
A) One inactivating somatic mutation in one copy of Rb. 
B) Two somatic inactivating mutations,one in each of the two copies of Rb. 
C) One somatic mutation in Rb,leading to its activation. 
D) Two somatic mutations in a copy of Rb,leading to its activation. 
E) None of the above.

Question 9

Single nucleotide polymorphism markers SNPs)are found approximately how far apart across the genome?

Accepted Answer

A) Every 1 megabase 
B) Every 10 megabases 
C) Every 1 kilobase 
D) Every 10 kilobases 
E) None of the above 
A) Every 1 megabase 
B) Every 10 megabases 
C) Every 1 kilobase 
D) Every 10 kilobases 
E) None of the above

Question 10

When a normal cell and a cancer cell were fused,the resulting hybrids lost the ability to form tumors in mice.This suggests that

Accepted Answer

A) The cancer cell alleles are dominant over the normal cell alleles. 
B) The cancer cell alleles are recessive to the normal cell alleles. 
C) The normal and cancer cell alleles are co-dominant. 
D) The original tumor formed as a result of infection by a tumor virus. 
E) None of the above. 
A) The cancer cell alleles are dominant over the normal cell alleles. 
B) The cancer cell alleles are recessive to the normal cell alleles. 
C) The normal and cancer cell alleles are co-dominant. 
D) The original tumor formed as a result of infection by a tumor virus. 
E) None of the above.

Question 11

HIF-1α levels may go up when

Accepted Answer

A) Oxygen conditions are at normal physiologic levels. 
B) Cells are experiencing hypoxic conditions. 
C) Oxygen levels are high. 
D) HIF-1α is bound to pVHL. 
E) C and D. 
A) Oxygen conditions are at normal physiologic levels. 
B) Cells are experiencing hypoxic conditions. 
C) Oxygen levels are high. 
D) HIF-1α is bound to pVHL. 
E) C and D.

Which of the following genes is NOT classified as a tumor suppressor?

Which of the following statements about NF1 is FALSE?

You are studying cancer cells,and hypothesize that you have found a previously unidentified tumor suppressor gene.Which of the following results would support your hypothesis?

Which of the following is TRUE of methylation in cancer cells?

The APC protein

You are studying a cell line in which the loss of just one copy of a tumor suppressor gene provides a growth advantage for the cells.This would be an example of genetic

Inactivation of tumor suppressor genes can occur as the result of

Sporadic cases of retinoblastoma require

Single nucleotide polymorphism markers SNPs)are found approximately how far apart across the genome?

When a normal cell and a cancer cell were fused,the resulting hybrids lost the ability to form tumors in mice.This suggests that

HIF-1α levels may go up when

The Biology and Genetics of Cells and Organisms

The Nature of Cancer

Tumor Viruses

Cellular Oncogenes

Growth Factors,receptors,and Cancer

Cytoplasmic Signaling Circuitry Programs Many of the Traits of Cancer

Prb and Control of the Cell Cycle Clock

P53 and Apoptosis: Master Guardian and Executioner

Eternal Life: Cell Immortalization and Tumorigenesis

Multi-Step Tumorigenesis

Maintenance of Genomic Integrity and the Development of Cancer

Dialogue Replaces Monologue: Heterotypic Interactions and the Biology of Angiogenesis

Moving Out: Invasion and Metastasis

Crowd Control: Tumor Immunology and Immunotherapy

The Rational Treatment of Cancer

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Exam 7: Tumor Suppressor Genes

Which of the following genes is NOT classified as a tumor suppressor?

Which of the following statements about NF1 is FALSE?

You are studying cancer cells,and hypothesize that you have found a previously unidentified tumor suppressor gene.Which of the following results would support your hypothesis?

Which of the following is TRUE of methylation in cancer cells?

The APC protein

You are studying a cell line in which the loss of just one copy of a tumor suppressor gene provides a growth advantage for the cells.This would be an example of genetic

Inactivation of tumor suppressor genes can occur as the result of

Sporadic cases of retinoblastoma require

Single nucleotide polymorphism markers SNPs)are found approximately how far apart across the genome?

When a normal cell and a cancer cell were fused,the resulting hybrids lost the ability to form tumors in mice.This suggests that

HIF-1α levels may go up when

The Biology and Genetics of Cells and Organisms

The Nature of Cancer

Tumor Viruses

Cellular Oncogenes

Growth Factors,receptors,and Cancer

Cytoplasmic Signaling Circuitry Programs Many of the Traits of Cancer

Prb and Control of the Cell Cycle Clock

P53 and Apoptosis: Master Guardian and Executioner

Eternal Life: Cell Immortalization and Tumorigenesis

Multi-Step Tumorigenesis

Maintenance of Genomic Integrity and the Development of Cancer

Dialogue Replaces Monologue: Heterotypic Interactions and the Biology of Angiogenesis

Moving Out: Invasion and Metastasis

Crowd Control: Tumor Immunology and Immunotherapy

The Rational Treatment of Cancer

Filters