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Cancer & Aging > Exam I > Flashcards

Exam I Flashcards

1
Q

1) The Nature of Cancer

1. Loss of function occurs in _________ & _________ genes.

A

1) The Nature of Cancer

1. Loss of function occurs in tumor suppressor & caretaker genes.

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2
Q

1) The Nature of Cancer

2. Gain of function occurs in _____-genes.

A

1) The Nature of Cancer

2. Gain of function occurs in oncogenes.

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3
Q

1) The Nature of Cancer

3. Which cell cycle checkpoint is the “point of no return?”

A

1) The Nature of Cancer

3. The restriction point (R point)/ G1/S checkpoint in the G1 phase

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4
Q

1) The Nature of Cancer

4. What does the migration pattern of a G6PD protein on a starch gel suggest?

A

1) The Nature of Cancer
4. That tumor cells within a tumor mass constitute MONOCLONAL GROWTH (enzymes likely were descendants of a common ancestor that already had a pattern of X-activation)

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5
Q

1) The Nature of Cancer

5. Explain the Warburg effect and possible effects on tumor growth and development.

A

1) The Nature of Cancer
5. The Warburg effect is when cancer cells switch their normal metabolism mechanism (oxidative phosphorylation) to aerobic glycolysis

Effects: Creates an immunosuppressive environment to inhibit immune response

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6
Q

1) The Nature of Cancer

6. What does the Ames Test suggest?

A

1) The Nature of Cancer

6. The Ames test suggests that a mutagenic chemical might also be carcinogenic

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7
Q

2) The Genetic Basis of Cancer

1. Describe a...
      A. Silent mutation
      B. Missence mutation
      C. Nonsense mutation
      D. Frameshift mutation
A

2) The Genetic Basis of Cancer

  A. Silent mutation: when the change of a base does not affect the amnio acid (wobble hypothesis)

  B.  Missence mutation: the change of a base changes the amnio acid

  C. Nonsense mutation: when the change of a base makes a stop codon

  D. When the addition of a base moves all other bases over one spot
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8
Q

2) The Genetic Basis of Cancer
2. Mutations outside the coding region can still impact gene expression, which of the following are regions known to affect gene expression when mutated?

  A. Silent mutation
  B. Nonsense caution
  C. Missense mutation
  D. Frameshift mutation
A

2) The Genetic Basis of Cancer

  B. Nonsense mutation

Because nonsense mutations cause termination signals that stop any more translation

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9
Q

2) The Genetic Basis of Cancer

3. What is a proto-oncogene? A tumor suppressor gene?

A

2) The Genetic Basis of Cancer

Proto-oncogene:

 - A gain of function gene
 - Normally grows, but can become permanently turned on
 - This can cause cells to grow out of control (cancer)

Tumor Suppressor Gene:

 - Loss of function gene
 - Normally grows, but can become permanently turned off
 - This can cause the unregulated growth of cells (cancer)
 - Example: p53
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10
Q

2) The Genetic Basis of Cancer

  1. What is a dominant negative mutation?
    Haploinsufficiency?
A

2) The Genetic Basis of Cancer

Dominant Negative Mutation: A mutation whose gene product adversely affects the normal, wild-type gene product within the same cell

Haploinsufficiency: When one copy of a gene is inactivated or deleted and the remaining functional copy of the gene is not adequate to produce the needed gene product to preserve normal function (seen in Marfan syndrome)

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11
Q

2) The Genetic Basis of Cancer

5. What is an amorphic phenotype? What is a hypomorphic phenotype?

A

2) The Genetic Basis of Cancer

Amorphic: no function

Hypomorphic: decreased function

  • Loss of function *
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12
Q

2) The Genetic Basis of Cancer

6. What is a hypermorphic phenotype? What is a neomorphic phenotype?

A

2) The Genetic Basis of Cancer

Hypermorphic: increased function

Neomorphic: new function

  • Gain of function *
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13
Q

2) The Genetic Basis of Cancer

7. What does “clonally derived heterogenous population” mean in relation to a tumor mass?

A

2) The Genetic Basis of Cancer

Means that the majority of cells in a tumor are NOT genetically identical

This is because there are so many different mutations throughout the subclones of a tumor

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14
Q

2) The Genetic Basis of Cancer

8. What are driver mutations? What are passenger mutations?

A

2) The Genetic Basis of Cancer

Driver mutations: mutations with STRONG links to cancer

Passenger mutations: mutations with NO links to cancer

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15
Q

3) The Origin of Tumors/ Oncogenes

1. The failure of temperature sensitive mutants of RSV to transform cells at high temperatures is because _____.

A

3) The Origin of Tumors/ Oncogenes

A viral gene is present and V-SRC is inactive at high temperatures.

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16
Q

3) The Origin of Tumors/ Oncogenes
2. A comparison of the genome sizes of transformation competent RSV, replication competent RSV, and transformation-defective mutants show that loss of oncogenicity is correlated with loss of about 20% of the genome. What gene does the lost genome sequence code for?

A

3) The Origin of Tumors/ Oncogenes

The lost sequences represent the src gene which is not essential for virus replication.

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17
Q

3) The Origin of Tumors/ Oncogenes

3. Is C-SRC a proto-oncogene or an oncogene? Is V-SRC a proto-oncogene or an oncogene?

A

3) The Origin of Tumors/ Oncogenes

C-SRC: Proto-oncogene

V-SRC: Oncogene (bc it lacks the c-terminal domain (Y-527))

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18
Q

3) The Origin of Tumors/ Oncogenes

4. Ectodomain deletion in the cell-surface receptor gene EGFR forms a ligand-independent oncoprotein called ____.

A

3) The Origin of Tumors/ Oncogenes

ErbB

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19
Q

3) The Origin of Tumors/ Oncogenes

5. Valine –> Gln mutation in the cell-surface receptor gene Her2 form a ligand-independent oncoprotein called ____.

A

3) The Origin of Tumors/ Oncogenes

Neu

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20
Q

3) The Origin of Tumors/ Oncogenes

6. Gleevec is a small molecule kinase inhibitor against _____ kinase.

A

3) The Origin of Tumors/ Oncogenes

BCR-ABL

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21
Q

3) The Origin of Tumors/ Oncogenes

  1. Her-2 is a gene that encodes a glycoprotein that is a member of the family of Epidermal growth factor (EGF) receptor tyrosine kinases. Her-2 gene amplification is observed in 30% of breast cancers.
    In a breast cancer patient that over-expresses Her-2 gene, would you characterize the gene encoding Her-2 protein as an oncogene, tumor suppressor gene or a proto-oncogene? Why?
A

3) The Origin of Tumors/ Oncogenes

Oncogene

  • Not tumor suppressor gene because: Her-2 can over express, it is a gain of function gene (rules out tumor suppressor gene, which is a loss of function gene)
  • Not a proto-oncogene because: proto-oncogenes are not yet over expressed. Since the patient has already experienced over-expression (amplification), this is an oncogene
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22
Q

3) The Origin of Tumors/ Oncogenes
8. For each mutation, determine whether c-myc is expressed and how cell proliferation changes.

 A. Ras protein that continues to stay in its GDP bound form.
 B. RAF protein that lacks its kinase domain.
 C. EGF receptor that lacks its extracellular domain. 
 D. MAPK that is constitutively phosphorylated at its active site. 
 E.c-myc gene that has a constitutively active promoter.
A

3) The Origin of Tumors/ Oncogenes

 A. c-myc expressed?: no how cell proliferation changes?: decreased 
 B. c-myc expressed?: no  how cell proliferation changes?: decreased
 C. c-myc expressed?: no how cell proliferation changes?: decreased
 D. c-myc expressed?: yes how cell proliferation changes?: increased 
 E. c-myc expressed?: yes  how cell proliferation changes?: increased
  • Not sure about these *
23
Q

3) The Origin of Tumors/ Oncogenes

9. How is c-SRC kept inactive?

A

3) The Origin of Tumors/ Oncogenes

The c-terminal domain (Y-527)

24
Q

3) The Origin of Tumors/ Oncogenes

10. What is the structural distinction between c-SRC and v-SRC? How does this difference confer the v-SRC oncogenic?

A

3) The Origin of Tumors/ Oncogenes

C-SRC: Has a c-terminal domain (Y-527) that makes it active OR inactive (proto-oncogenic)

V-SRC: Lacks a c-terminal domain (Y-527) that makes it constantly active (oncogenic)

25
Q

3) The Origin of Tumors/ Oncogenes

11. What human tumors can be clearly tied to viral infections (2)?

A

3) The Origin of Tumors/ Oncogenes
- Cervical carcinomas (HPV)
- Hepatomas (HBV, HCV, HAV) (liver carcinomas)

26
Q

4) Tumor Supressor Genes

  1. In the tumor phenotypic progeny cells, the mutated cancer allele is:
    Dominant gain of function or recessive loss of function?
A

4) Tumor Supressor Genes

Dominant gain of function

27
Q

4) Tumor Supressor Genes
2. The classical two hits theory suggests that both alleles of the tumor suppressor gene need to be mutated for tumor development. However, for some TSGs, tumor development was significantly accelerated with mutation in only one allele, which is called _______.

A

4) Tumor Supressor Genes

haploinsufficiency

28
Q

4) Tumor Supressor Genes
3. The “two hit” hypothesis: loss of heterozygosity

 A. What would you call a mutation that happens suddenly with no family history (the child was not born with the mutation)?

 B. What would you call a mutation that a child is born with?
A

4) Tumor Supressor Genes

 A. Somatic mutation

 B. Germ-line mutation
29
Q

4) Tumor Supressor Genes
4. p53 is solely a transcriptional _____.

 A. Activator
 B. Suppressor
 C. Neither
A

4) Tumor Supressor Genes

 A. Activator
30
Q

4) Tumor Supressor Genes
5. Tumor protein p53 (aka TP53) functions as a _____.

 A. Monomer
 B. Dimer
 C. Trimer
 D. Tetramer
A

4) Tumor Supressor Genes

 D. Tetramer
31
Q

4) Tumor Supressor Genes
6. Accelerated tumor development was seen in both dominant-negative transgenic mice and heterogenous p53 knockout mice.

Please identify the corresponding mechanisms for each mouse
model: (less functional multimers, haploinsufficiency, promoter methylation, proteasomal degradation)

Dominant-negative transgenic mice:
Heterogenous p53 knockout mice:

A

4) Tumor Supressor Genes

Dominant-negative transgenic mice: promoter methylation

Heterogenous p53 knockout mice: proteasomal degradation

32
Q

4) Tumor Supressor Genes
7. The p53 gene has the important role of cellular homeostasis because it has the power to:

     A. Halt mitosis
     B. Lead to repair of damaged DNA
     C. Trigger cell death/ apoptosis
     D. A & B
     E. All of the above are correct
A

4) Tumor Supressor Genes

 E. All of the above are correct
33
Q

4) Tumor Supressor Genes
8. What is the main function of Rb?

 A. Transcription factor for p21, a protein that stops cell proliferation

 B. Binds and inhibits the activity of a transcription factor (E2F)  that, when not bound, stimulates cell division

 C. Cell surface protein that binds growth factors and promotes the cell cycle

 D. Pigment molecule that prevents eye cancers

 E. Protein channel in the cell membrane that allows ATP to travel from one side to the other
A

4) Tumor Supressor Genes

 B. Binds and inhibits the activity of a transcription factor (E2F)  that, when not bound, stimulates cell division
34
Q

4) Tumor Supressor Genes
9. Which of the following are NOT found in genetically normal cells?

 A. Tumor suppressors
 B. Proto-oncogenes
 C. Oncogenes
 D. Proteins that stimulate cell division
 E. Proteins that inhibit cell division
A

4) Tumor Supressor Genes

 C. Oncogenes
35
Q

4) Tumor Supressor Genes
10. Which of the following statements BEST explains loss of heterozygosity?

 A. When a mutation occurs in the only functional copy of a gene and renders it dysfunctional.

 B. When a person inherits one dysfunctional copy of a tumor suppressor gene.

 C. When a person inherits two dysfunctional copies of a tumor suppressor gene.

 D. When a cell loses the ability to regulate its growth and begins to grow and divide  uncontrollably, resulting in a tumor.
A

4) Tumor Supressor Genes

 A. When a mutation occurs in the only functional copy of a gene and renders it dysfunctional.
36
Q

4) Tumor Supressor Genes
11. Which of the following types of protein could be coded by a tumor suppressor gene?

 A. A protein which forms part of a growth factor signaling pathway.

 B. A protein which codes for a DNA repair enzyme.

 C. A protein which helps prevent apoptosis.

 D. A protein which controls progression through the cell cycle.
A

4) Tumor Supressor Genes

 D. A protein which controls progression through the cell cycle.
37
Q

4) Tumor Supressor Genes
12. Which one of the following statements about p53 is false?

 A. It was the first oncogene to be identified.

 B. It is a transcription factor that contains a DNA binding domain and a transactivation domain 

 C. The mechanism by which p53 becomes activated is dependent on the nature of the stress signal.
A

4) Tumor Supressor Genes

 A. It was the first oncogene to be identified.
38
Q

4) Tumor Supressor Genes
13. Which of the following statements about Retinoblastoma is false?

 A. Familial retinoblastoma involves inheriting one germline mutation in the Rb gene and acquiring a second mutation later in life.

 B. In the familial form of the disease, one mutated gene increases the probability that a second mutation will occur.

 C. In sporadic retinoblastoma, mutations occur in both alleles of the Rb gene in the same retinoblast after birth.

 D. The mechanism of action of the Rb gene in cancer does not follow the concept of a tumor suppressor gene two-hit hypothesis.
A

4) Tumor Supressor Genes

 D. The mechanism of action of the Rb gene in cancer does not follow the concept of a tumor suppressor gene two-hit hypothesis.
39
Q

4) Tumor Supressor Genes
14. What is the role of PTEN (phosphate and tensin homolog) on chromosome 10?

 A. Dephosphorylation of PIP2 to form PIP3.

 B. Dephosphorylation of the membrane lipid PIP3 to form PIP2.

 C. To remove inhibitory signals and hence induce kinase activity.
A

4) Tumor Supressor Genes

 B. Dephosphorylation of the membrane lipid PIP3 to form PIP2.
40
Q

4) Tumor Supressor Genes
15. Viral protein products interact with pRB. Identify which one of the following is a correct statement.

 A. HPV E6
 B. HPV E7
 C. HIV TaT
A

4) Tumor Supressor Genes

 B. HPV E7
41
Q

5) Genome Instability & Cancer

1. Chromosomal instability (CIN) includes ____ and ____ CINs.

A

5) Genome Instability & Cancer

Stable and unstable

42
Q

5) Genome Instability & Cancer

2. Dysfunction in DNA replication causes ____ CIN and dysfunction in segregation causes ____ CIN.

A

5) Genome Instability & Cancer

Stable
Unstable

43
Q

5) Genome Instability & Cancer
3. What theory is proposed to explain the discrepancy in the mutation rate between the normal spontaneous mutation rate of human somatic cells and the mutation rate observed in human cancers?

A

5) Genome Instability & Cancer

Mutator phenotype

44
Q

5) Genome Instability & Cancer
4. Which of the following structures are part of the telomere for protecting natural t-chromosomal DNA ends?

 A. T-loop
 B. Shelterin
 C. Actin
 D. Tubulin
A

5) Genome Instability & Cancer

 B. Shelterin
45
Q

5) Genome Instability & Cancer

5. In cancer cells, telomeres are maintained either by _____ or by a mechanism known as ______.

A

5) Genome Instability & Cancer

Telomerase expression

Alternative lengthening of telomeres

46
Q

6) Oncogenetic Pathways
1. Which of the following statements is not a phenotypic trait of cancer cells?

 A. Independence from external growth signals

  B. Insensitivity to antiproliferative signals

  C. Sensitivity to death signals

  D. Tissue invasion and metastasis
A

6) Oncogenetic Pathways

C. Sensitivity to death signals

47
Q

6) Oncogenetic Pathways
2. Which of the following domains are known to interact with phosphorylated intracellular domain of receptor tyrosine kinases?

A. Abl
B. SH2
C. Ph domain
D. Phox domain

A

6) Oncogenetic Pathways

B. SH2

48
Q

6) Oncogenetic Pathways
3. Which of the following mechanisms are known to mediate Mutation Induced Ligand Independent Receptor Dimerization?

A. S-S bond formation
B. Leucine zipper
C. Coiled-coil
D. Zinc finger

A

6) Oncogenetic Pathways

C. Coiled-coil

49
Q

6) Oncogenetic Pathways
4. Cytoplasmic tyrosine kinase can be maintained in inactive form by:

A. Trans-inhibitors
B. Acetylation
C. Methylation
D. Intramolecular constraints

A

6) Oncogenetic Pathways

D. Intramolecular constraints

50
Q

6) Oncogenetic Pathways

The positions of the three most frequent codon mutations in Ras are:

A) G12, G13, and Q61
B) S17, A18, and Q22
C) D30, E31, and Y32
D) Others

A

6) Oncogenetic Pathways

A) G12, G13, and Q61

51
Q

6) Oncogenetic Pathways
6. In the APC/Wnt pathway, identify the potential “gain of function” and “loss of function” mutations that could lead to constant activation of the pathway.

A

6) Oncogenetic Pathways

Gain of function: beta-cat

Loss of function: AXIN and APC

52
Q

6) Oncogenetic Pathways

7. C-myc binds to ____ to form a heterodimer which binds to ____ consensus DNA to activate transcription.

A

6) Oncogenetic Pathways

MAX

E box

53
Q

6) Oncogenetic Pathways

8. Phosphorylation at S62 by RAS/RAF ____ and ____ c-myc.

A

6) Oncogenetic Pathways

Activates

Stabilizes

54
Q

6) Oncogenetic Pathways

9. Phosphorylation at T58 by PI3K/AKT ____ c-myc and is associated with ____.

A

6) Oncogenetic Pathways

Inhibits

Degradation

Cancer & Aging (3 decks)

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