Ch25 Genetics Basis of Cancer | Test Bank – 7th Edition

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1) Select the events that can convert a proto-oncogene into an oncogene. (Check all that apply.)

A) Viral integration near the proto-oncogene
B) Missense mutations
C) Translocation
D) Aneuploidy
E) Gene amplification

2) After genetic testing, a person is identified with an inherited mutation associated with a specific class of cancer. Select the statements that are true about this person. (Check all that apply.)

A) The person will definitely develop cancer in his or her lifetime.
B) The person is predisposed to the development of cancer.
C) The mutation is probably in a tumor suppressor gene.
D) The person may pass the trait on to his or her offspring.

3) How can a tumor suppressor gene lose its function? (Check all that apply.)

A) Gene mutation
B) Duplication
C) Aberrant DNA methylation
D) Aneuploidy leading to loss of the tumor suppressor gene

4) Select the events that must occur for inherited retinoblastoma to develop. (Check all that apply.)

A) An individual must have two mutated copies of the Rb gene.
B) The p53 gene must be mutated.
C) E2F is no longer regulated by Rb.
D) The cell proceeds uncontrolled through cell division.

5) Indicate the roles of growth factors in the cell cycle. (Check all that apply.)

A) They act as repair proteins that fix DNA damage in the cell.
B) Growth factors bind to a receptor and initiate a signal cascade in the cell.
C) Their binding changes gene transcription.
D) They allow the cell to progress through the cell cycle.

6) You are studying the role of a novel histone demethylase in cancer. This histone demethylase normally functions to "close" the chromatin. A loss-of-function mutation in the gene for this histone demethylase has been linked to a number of tumor types. You decide to look at the expression of a number of known tumor-suppressor genes and oncogenes in cells that carry this mutation. Select the genes whose expression is likely to be affected by this mutation in a way that could lead to cancer. (Check all that apply.)

A) BRCA-2
B) APC
C) fos
D) src
E) myc

7) Select the genetic changes that are associated with the development of colorectal cancer. (Check all that apply.)

A) Loss of APC
B) Activation of ras
C) Loss of DCC
D) Loss of p53
E) Loss of myc
F) Activation of NF1

8) The term that indicates that cancer has begun to migrate to other parts of the body is __________.

A) malignant
B) benign
C) metastatic
D) invasive
E) clonal

9) The majority of human cancers are caused by __________.

A) viral infections
B) inherited mutations
C) spontaneous mutations
D) carcinogens

10) A gene that promotes the development of cancer is called a/an __________.

A) clone
B) tumor suppressor gene
C) mutagen
D) carcinogen
E) oncogene

11) The first cancer-causing virus to be isolated was __________.

A) RSV in chickens
B) Hepatitis B in humans
C) SSV in monkeys
D) ALV in mice
E) SV40 in humans

12) An oncogene form of Ras would have ___________.

A) decreased GTPase activity
B) an inability to bind GTP
C) increased susceptibility to growth factors
D) inability to bind Raf-1

13) When GTP is bound to Ras, it is in the __________ form.

A) active
B) inactive

14) Chronic myelogenous leukemia is an example of a proto-oncogene activation by __________.

A) the action of a virus
B) a missense mutation
C) a translocation
D) gene amplification
E) None of these choices are correct.

15) What is p53?

A) A caspase
B) A proto-oncogene
C) A transcription factor
D) A tumor-suppressor gene
E) None of these choices are correct.

16) When are caspases active?

A) During the normal cell cycle
B) In apotosis
C) Following viral integration
D) During DNA replication

17) Checkpoint proteins are encoded by ________.

A) oncogenes
B) growth factors
C) proto-oncogenes
D) tumor-suppressor genes

18) A _______ is a cellular gene that has the potential to become an oncogene.

A) carcinogen
B) proto-oncogene
C) tumor-suppressorgenes
D) caspase gene

19) An environmental agent that causes cancer is called a __________.

A) carcinogen
B) malignant agent
C) invasive agent
D) metastatic agent

20) A common way of studying methylation in cells is to sequence DNA samples before and after modification with sodium bisulfite. The sodium bisulfite deaminates cytosine residues, generating uracil residues, therefore resulting in a change in the sequence as compared to the non-modified DNA. Sodium bisulfite does not react with 5-methylcytosine so there will be no change in the sequence of those modified bases. When tumors are sequenced to study methylation patterns and epigenetic control, what would be the best control for sequencing using this technique?

A) Non-cancerous tissue DNA from a different individual but from the same organ
B) Liver DNA from the same individual that the cancer sample is from
C) DNA from non-cancerous tissue from the same individual's organ as the cancer
D) A combination of DNA from liver, brain, and muscle from the same individual that has the cancer

21) In cancer cells one allele of the tumor suppressor gene p53 is frequently mutated so that the protein is inactive, not produced, or deleted. The other allele will usually have a normal sequence and the promoter remains intact but the gene is not expressed. Sequencing with sodium bisulfite modification of DNA can be used to detect which cytosines are methylated. If the cancer cell DNA is sequenced what would be the anticipated results?

A) Cytosines in or near the promoter region will be methylated.
B) Cytosines in or near the promoter will not be methylated.
C) Cytosines in the coding region will have an increased methylation.
D) There will be no differences in the methylation pattern of the promoter of p53 from a cancer cell and a normal cell.

22) You have sequenced the genome of tumor cells from a cancer patient and compared it to the genome of normal cells from the same patient. You find that in the tumor cells, a gene contains a nonsense mutation. The function of the protein encoded by this gene is not known. What can you predict about this gene?

A) This gene is likely to encode a tumor-suppressor.
B) The gene is likely to encode a proto-oncogene.
C) The gene could encode either a tumor-suppressor gene or a proto-oncogene.

23) You have sequenced the genome of tumor cells from a cancer patient and compared it to the genome of normal cells from the same patient. You find that in the tumor cells, a gene contains a number of changes in its promoter region. The function of the protein encoded by this gene is not known. What can you predict about this gene?

A) This gene is likely to encode a tumor-suppressor.
B) The gene is likely to encode a proto-oncogene.
C) The gene could encode either a tumor-suppressor gene or a proto-oncogene.

24) You have sequenced the genome of tumor cells from a cancer patient and compared it to the genome of normal cells from the same patient. You find that in the tumor cells, a histone acetyltransferase is deactivated. What can you accurately predict from this finding?

A) As a result of the mutant histone acetyltransferase, an oncogene was activated.
B) As a result of the mutant histone acetyltransferase, a tumor suppressor was deactivated.
C) As a result of the mutant histone acetyltransferase, a tumor suppressor may have been deactivated or an oncogene activated.

25) An oncogene may promote cancer by keeping the cell growth pathway in the off position.

⊚ true
⊚ false

26) Programmed cell death is called genome maintenance.

⊚ true
⊚ false

27) Cancer is considered clonal because daughter cells from a cancer cell have the same genetic makeup as the parent cell.

⊚ true
⊚ false

28) DNA damage is sensed by E2F at the G 1 and G 2 checkpoints.

⊚ true
⊚ false

29) Expression of a tumor suppressor gene can be impaired if its promoter is hypermethylated.

⊚ true
⊚ false

30) A promoter mutation can turn a proto-oncogene into an oncogene.

⊚ true
⊚ false