Deck 16: Cancer Genetics
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Deck 16: Cancer Genetics
1
In Burkitt lymphoma, there is increased expression of the MYC gene.Which of the following BEST explains this situation?
A)A chromosome deletion has removed a tumor-suppressor gene.
B)A chromosome deletion has removed an oncogene.
C)There is a chromosome duplication that involves a segment with an oncogene.
D)A translocation has brought the MYC gene next to a different regulatory region.
E)The MYC gene has been amplified.
A)A chromosome deletion has removed a tumor-suppressor gene.
B)A chromosome deletion has removed an oncogene.
C)There is a chromosome duplication that involves a segment with an oncogene.
D)A translocation has brought the MYC gene next to a different regulatory region.
E)The MYC gene has been amplified.
D
2
Evidence that the development of cancer is a multistep process includes:
A)the observation that certain tumor-suppressor genes and oncogenes are involved in a sequential manner in the development of colon cancer.
B)the fact that proto-oncogenes are widely conserved in evolution.
C)the usual occurrence of retinoblastoma at a young age.
D)the development of a cancer as a result of activation of a single oncogene by any of a variety of mechanisms.
E)the fact that there are many genetic and epigenetic mechanisms that lead to inactivation of the same tumor-suppressor gene.
A)the observation that certain tumor-suppressor genes and oncogenes are involved in a sequential manner in the development of colon cancer.
B)the fact that proto-oncogenes are widely conserved in evolution.
C)the usual occurrence of retinoblastoma at a young age.
D)the development of a cancer as a result of activation of a single oncogene by any of a variety of mechanisms.
E)the fact that there are many genetic and epigenetic mechanisms that lead to inactivation of the same tumor-suppressor gene.
A
3
What are normal cellular genes whose products are involved in facilitating cell division to occur under appropriate conditions called?
A)Proto-oncogenes
B)Tumor-suppressor genes
C)Passenger genes
D)Inhibitor genes
E)Driver genes
A)Proto-oncogenes
B)Tumor-suppressor genes
C)Passenger genes
D)Inhibitor genes
E)Driver genes
A
4
Which of the following statements is TRUE concerning the function of proto-oncogenes?
A)They make products that act as signals to initiate cellular apoptosis.
B)Their products are components of cell growth.
C)Proto-oncogenes make products that act as cell checkpoint regulators.
D)Proto-oncogenes make products that scan the genome for DNA damage.
E)Proto-oncogenes make products that repair DNA at sites of lesions.
A)They make products that act as signals to initiate cellular apoptosis.
B)Their products are components of cell growth.
C)Proto-oncogenes make products that act as cell checkpoint regulators.
D)Proto-oncogenes make products that scan the genome for DNA damage.
E)Proto-oncogenes make products that repair DNA at sites of lesions.
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5
Which of the following types of cancer is associated with a defect in nucleotide-excision repair?
A)Retinoblastoma
B)Xeroderma pigmentosum
C)Cervical cancer
D)Chronic myelogenous leukemia
E)Bloom syndrome
A)Retinoblastoma
B)Xeroderma pigmentosum
C)Cervical cancer
D)Chronic myelogenous leukemia
E)Bloom syndrome
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6
Which of the following is a process whereby cancer cells travel to other sites in the body and establish secondary tumors?
A)Oncogenesis
B)Angiogenesis
C)Malignancy
D)Secondary tumorigenesis
E)Metastasis
A)Oncogenesis
B)Angiogenesis
C)Malignancy
D)Secondary tumorigenesis
E)Metastasis
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7
The Philadelphia chromosome is:
A)an example of an aneuploidy.
B)the result of a translocated chromosome involving parts of chromosomes 9 and 22.
C)a lengthened version of chromosome 22 that results from a recombination event with chromosome 12.
D)a shortened version of chromosome 22 that results from a deletion.
E)a lengthened version of chromosome 22 that results from a duplication.
A)an example of an aneuploidy.
B)the result of a translocated chromosome involving parts of chromosomes 9 and 22.
C)a lengthened version of chromosome 22 that results from a recombination event with chromosome 12.
D)a shortened version of chromosome 22 that results from a deletion.
E)a lengthened version of chromosome 22 that results from a duplication.
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8
Which of the following result(s)directly from metastasis?
A)Primary tumors
B)Secondary tumors
C)Tumor vascularization
D)Decreased DNA repair
E)Increased apoptosis
A)Primary tumors
B)Secondary tumors
C)Tumor vascularization
D)Decreased DNA repair
E)Increased apoptosis
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9
What kind of enzyme phosphorylates other proteins, in turn either activating or inactivating the protein?
A)Cyclin
B)Cyclin-dependent kinases
C)Telomerase
D)GTPase
E)DNA polymerase
A)Cyclin
B)Cyclin-dependent kinases
C)Telomerase
D)GTPase
E)DNA polymerase
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10
What is the rare situation called when only one of the two copies of a particular tumor-suppressor gene needs to be inactivated before there is a progression toward cancer?
A)Clonal evolution
B)Loss of heterozygosity
C)Signal transduction
D)Aneuploidy
E)Haploinsufficiency
A)Clonal evolution
B)Loss of heterozygosity
C)Signal transduction
D)Aneuploidy
E)Haploinsufficiency
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11
The increased levels of telomerase associated with many tumor cells likely promotes cancer by:
A)enhancing levels of DNA repair so that cells remain normal and have stable genomes and thus would be able to replicate their DNA and divide more often.
B)promoting the efficiency of the spindle-assembly checkpoint.
C)reducing the expression of several oncogenes.
D)allowing cells to continue to divide when, normally, chromosomes should shorten beyond a point where division would be no longer possible.
E)decreasing the number of epigenetic changes that would promote cancer.
A)enhancing levels of DNA repair so that cells remain normal and have stable genomes and thus would be able to replicate their DNA and divide more often.
B)promoting the efficiency of the spindle-assembly checkpoint.
C)reducing the expression of several oncogenes.
D)allowing cells to continue to divide when, normally, chromosomes should shorten beyond a point where division would be no longer possible.
E)decreasing the number of epigenetic changes that would promote cancer.
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12
Which of the following BEST characterizes many cancers such as colorectal cancer?
A)They result from the activation of one critical tumor-suppressor gene.
B)They result when the transition from G2 to M in the cell cycle is inhibited.
C)They result when DNA replication during the S period of the cell cycle is inhibited.
D)They result from a series of sequential mutations in a number of genes.
E)They result from decreased expression in a series of cellular oncogenes.
A)They result from the activation of one critical tumor-suppressor gene.
B)They result when the transition from G2 to M in the cell cycle is inhibited.
C)They result when DNA replication during the S period of the cell cycle is inhibited.
D)They result from a series of sequential mutations in a number of genes.
E)They result from decreased expression in a series of cellular oncogenes.
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13
Many viruses that are associated with cancers in animals are _____ that use reverse transcriptase.
A)papilloma viruses
B)Epstein-Barr virus
C)retroviruses
D)hepatitis B virus
E)None of the answers is correct.
A)papilloma viruses
B)Epstein-Barr virus
C)retroviruses
D)hepatitis B virus
E)None of the answers is correct.
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14
What is the process called by which genetic changes occur in tumors and allows them to become increasingly aggressive over time?
A)Clonal evolution
B)Metastasis
C)Loss of heterozygosity
D)Epigenetic evolution
E)Signal transduction
A)Clonal evolution
B)Metastasis
C)Loss of heterozygosity
D)Epigenetic evolution
E)Signal transduction
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15
In Burkitt lymphoma patients, despite translocation, the oncogene c-MYC remains nearly intact in its new location.Yet c-MYC is believed to be responsible for the lymphoma because the c-MYC:
A)DNA sequence undergoes hypermethylation.
B)DNA sequence is nearly intact but is inverted in the new position.
C)gene is released from inhibition by miRNAs.
D)gene is placed under the control of B-cell-specific gene regulatory sequences and is highly expressed.
E)DNA sequence undergoes several point mutations.
A)DNA sequence undergoes hypermethylation.
B)DNA sequence is nearly intact but is inverted in the new position.
C)gene is released from inhibition by miRNAs.
D)gene is placed under the control of B-cell-specific gene regulatory sequences and is highly expressed.
E)DNA sequence undergoes several point mutations.
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16
The normal activity of the retinoblastoma (Rb)protein in the cell is to:
A)inhibit p53 activity.
B)suppress transcription of tumor-suppressor genes.
C)regulate the progression of G1 to S in the cell cycle.
D)induce cyclin-CDK complex formation.
E)block the initiation of anaphase during the cell cycle.
A)inhibit p53 activity.
B)suppress transcription of tumor-suppressor genes.
C)regulate the progression of G1 to S in the cell cycle.
D)induce cyclin-CDK complex formation.
E)block the initiation of anaphase during the cell cycle.
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17
Which of the following chromosomal abnormalities is associated with chronic myelogenous leukemia?
A)A deletion
B)An inversion
C)A duplication
D)A reciprocal translocation
E)An aneuploidy involving one of the shorter autosomal chromosomes
A)A deletion
B)An inversion
C)A duplication
D)A reciprocal translocation
E)An aneuploidy involving one of the shorter autosomal chromosomes
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18
Genes that encode components of the cytoskeleton and extracellular matrix often contribute to which process?
A)DNA repair
B)Mutation
C)Metastasis
D)Primary tumor formation
E)Signal transduction
A)DNA repair
B)Mutation
C)Metastasis
D)Primary tumor formation
E)Signal transduction
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19
Mutations in proto-oncogenes are generally _____, whereas mutations in tumor-suppressor alleles are generally _____.
A)inversions; duplications
B)recessive; dominant
C)duplications; deletions
D)dominant; recessive
E)deletions; base-pair substitutions
A)inversions; duplications
B)recessive; dominant
C)duplications; deletions
D)dominant; recessive
E)deletions; base-pair substitutions
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20
Many tumors are BEST described by which of the following?
A)Abnormally high levels of telomerase expression
B)Abnormally high levels of tumor-suppressor gene expression
C)Translocations that move a tumor-suppressor gene to a new location that increases its normal expression
D)Deletions that remove an oncogene from the genome
E)Inhibition of DNA replication when it would normally occur
A)Abnormally high levels of telomerase expression
B)Abnormally high levels of tumor-suppressor gene expression
C)Translocations that move a tumor-suppressor gene to a new location that increases its normal expression
D)Deletions that remove an oncogene from the genome
E)Inhibition of DNA replication when it would normally occur
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21
Which of the following leads to the transcription of oncogenes that then stimulate cancer? Some evidence also suggests that this is the cause of chromosome instability, a hallmark of many tumors.
A)Hypomethylation
B)Hypermethylation
A)Hypomethylation
B)Hypermethylation
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22
Briefly describe the role that the genes APC, p53, and ras may have in the development of colorectal cancer.
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23
The development of colorectal cancer is relatively well understood.Describe the steps of the development of colorectal cancer, including any genetic components.
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24
List three ways in which proto-oncogenes can be converted to oncogenes by viruses.
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25
Explain how DNA sequencing studies can aid in our understanding of cancer formation.
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26
Which of the following statements is FALSE?
A)Tumors usually show a clonal evolution.
B)Some cancers are associated with reduced DNA repair.
C)Epigenetic changes in somatic cells may be associated with some cancers.
D)Most tumors arise from germ-line mutations that accumulate during our life span.
E)All of the above statements are true.
A)Tumors usually show a clonal evolution.
B)Some cancers are associated with reduced DNA repair.
C)Epigenetic changes in somatic cells may be associated with some cancers.
D)Most tumors arise from germ-line mutations that accumulate during our life span.
E)All of the above statements are true.
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27
If you were assigned to study a new form of cancer, you might want to determine whether it has a strong genetic basis or whether it is caused primarily by environmental factors.Propose some ways in which you could attempt to determine which hypothesis is correct.Which methods would be the easiest to use first?
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28
Briefly describe the relationship among cyclins, cyclin-dependent kinases (CDKs), and cancer.
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29
List three observations consistent with the idea that cancer arises through an accumulation of mutations in several genes that promote cellular proliferation in single cells.
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30
About 95% of all women with cervical cancer are infected with:
A)human papilloma viruses.
B)human T-cell leukemia virus.
C)Epstein-Barr virus.
D)human herpes virus.
E)Merkel cell polyomavirus.
A)human papilloma viruses.
B)human T-cell leukemia virus.
C)Epstein-Barr virus.
D)human herpes virus.
E)Merkel cell polyomavirus.
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31
Retinoblastoma (RB)protein is important in regulating the cell cycle.It must be completely phosphorylated before the cell can move from the G1 to the S phase of the cell cycle.Retinoblastoma is a type of cancer.Based on this information, what do you think goes wrong in retinoblastoma?
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32
What are oncogenes and tumor-suppressor genes? How are they involved in carcinogenesis?
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33
Explain briefly why changes in oncogenes result in more rapid progression of a cancer compared to changes in tumor-suppressor genes.Mention one situation in which changes in a tumor-suppressor gene have a similar likelihood of causing cancer as changes in an oncogene.
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34
A tumor-suppressor gene that is mutated in about 75% of all colon cancers is known as:
A)p53.
B)BRCA 1.
C)myc.
D)ras.
A)p53.
B)BRCA 1.
C)myc.
D)ras.
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35
What is one line of evidence supporting the idea that cancer is influenced by environmental factors?
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36
How can defects in DNA-repair mechanisms lead to the development of cancer?
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37
Burkitt lymphoma is caused by which of the following chromosomal rearrangements?
A)Duplication
B)Deletion
C)Inversion
D)Translocation
A)Duplication
B)Deletion
C)Inversion
D)Translocation
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38
Why is it more difficult for researchers to identify tumor-suppressor genes than oncogenes?
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39
Defects in _____ genes often increase the overall mutation rate of other genes.
A)oncogenes
B)proto-oncogenes
C)tumor-suppressor
D)DNA repair
A)oncogenes
B)proto-oncogenes
C)tumor-suppressor
D)DNA repair
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40
Describe an example in which environmental factors interact with a genotype to produce cancer.
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41
Which of the following features are associated with cancer?
A)Hypomethylation of DNA
B)Chromosome instability
C)Mutations in tumor-suppressor genes
D)Mutations in oncogenes
E)All of the answers are correct.
A)Hypomethylation of DNA
B)Chromosome instability
C)Mutations in tumor-suppressor genes
D)Mutations in oncogenes
E)All of the answers are correct.
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42
Select the statement that does NOT apply to tumor-suppressors and oncogenes gene categories.
A)These two categories are opposite in their normal function, with tumor suppressors acting to inhibit cell growth.
B)These two categories are opposite in their normal function, with oncogenes acting to promote cell growth.
C)These are synonymous names of the same gene category acting to facilitate cell division.
D)All of the answers are correct.
E)None of the answers is correct.
A)These two categories are opposite in their normal function, with tumor suppressors acting to inhibit cell growth.
B)These two categories are opposite in their normal function, with oncogenes acting to promote cell growth.
C)These are synonymous names of the same gene category acting to facilitate cell division.
D)All of the answers are correct.
E)None of the answers is correct.
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43
What is the possible sequence of events leading to cancer development?
A)Loss of heterozygosity of an oncogene, benign tumor growth, malignant tumor growth
B)Benign tumor growth, loss of heterozygosity of an oncogene, malignant tumor growth
C)Loss of heterozygosity of a tumor suppressor, benign tumor growth, malignant tumor growth
D)Loss of heterozygosity that converts oncogene into tumor suppressor, benign tumor growth, malignant tumor growth
E)All of these scenarios are plausible.
A)Loss of heterozygosity of an oncogene, benign tumor growth, malignant tumor growth
B)Benign tumor growth, loss of heterozygosity of an oncogene, malignant tumor growth
C)Loss of heterozygosity of a tumor suppressor, benign tumor growth, malignant tumor growth
D)Loss of heterozygosity that converts oncogene into tumor suppressor, benign tumor growth, malignant tumor growth
E)All of these scenarios are plausible.
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44
Which of the following are mechanisms by which viruses contribute to cancer development?
A)By modifications to cytoskeletal architecture
B)By mutating and rearranging host proto-oncogenes
C)By stimulating overexpression of proto-oncogenes
D)Both by mutating and rearranging host proto-oncogenes and by stimulating overexpression of proto-oncogenes
E)None of the answers is correct.
A)By modifications to cytoskeletal architecture
B)By mutating and rearranging host proto-oncogenes
C)By stimulating overexpression of proto-oncogenes
D)Both by mutating and rearranging host proto-oncogenes and by stimulating overexpression of proto-oncogenes
E)None of the answers is correct.
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45
Which of the following is NOT a reason we think that cancer is a genetic disease?
A)Exposure to mutagens such as chemicals or ionizing radiation often leads to cancer.
B)Some families have a disproportionally high number of family members with cancer compared to the general population.
C)All cancers develop due to changes during gametogenesis.
D)Certain types of cancer often share the same chromosomal abnormalities.
E)Most cancers result from accumulation of somatic mutations.
A)Exposure to mutagens such as chemicals or ionizing radiation often leads to cancer.
B)Some families have a disproportionally high number of family members with cancer compared to the general population.
C)All cancers develop due to changes during gametogenesis.
D)Certain types of cancer often share the same chromosomal abnormalities.
E)Most cancers result from accumulation of somatic mutations.
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46
Explain how retroviruses may cause cancers.
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47
Malignancy is related with changes in which parts of the cell?
A)Lysosomes
B)Nuclear membrane
C)Cytoskeleton
D)Peroxisomes
E)Ribosomes
A)Lysosomes
B)Nuclear membrane
C)Cytoskeleton
D)Peroxisomes
E)Ribosomes
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48
Which of the following sequence of events will likely lead to colorectal cancer?
A)Carcinoma develops, polyps form, cancer metastasizes.
B)Adenoma forms, polyps form, tumor-suppressor APC gene mutates, cancer metastasizes.
C)Tumor-suppressor APC gene mutates, polyps form, adenoma forms, carcinoma forms.
D)Proto-oncogenes mutate into tumor-suppressor genes, polyps form, cancer metastasizes.
E)Carcinoma becomes metastatic, polyps form, tumor-suppressor APC gene mutates.
A)Carcinoma develops, polyps form, cancer metastasizes.
B)Adenoma forms, polyps form, tumor-suppressor APC gene mutates, cancer metastasizes.
C)Tumor-suppressor APC gene mutates, polyps form, adenoma forms, carcinoma forms.
D)Proto-oncogenes mutate into tumor-suppressor genes, polyps form, cancer metastasizes.
E)Carcinoma becomes metastatic, polyps form, tumor-suppressor APC gene mutates.
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49
What is a possible effect of mutations in genes that influence chromosome segregation during division?
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50
What is haploinsufficiency?
A)It is a loss of one dominant allele due to deletion.
B)It is a loss of heterozygosity due to translocation.
C)It is a gain of a recessive allele due to duplication.
D)It is a result of dosage effect where the amount of product produced by the heterozygote is below optimal.
E)All of the answers are correct.
A)It is a loss of one dominant allele due to deletion.
B)It is a loss of heterozygosity due to translocation.
C)It is a gain of a recessive allele due to duplication.
D)It is a result of dosage effect where the amount of product produced by the heterozygote is below optimal.
E)All of the answers are correct.
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51
Haploinsufficiency may lead to cancer because:
A)it promotes angiogenesis.
B)it contributes to overexpression of oncogenes.
C)the cell produces only half of the required tumor-suppressor product.
D)it stimulates hypermethylation.
E)All of the answers are correct.
A)it promotes angiogenesis.
B)it contributes to overexpression of oncogenes.
C)the cell produces only half of the required tumor-suppressor product.
D)it stimulates hypermethylation.
E)All of the answers are correct.
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52
Deletions of what categories of genes are likely lead to cancer?
A)Tumor suppressors
B)Proto-oncogenes
C)Growth factors
D)All of the answers are correct.
E)None of the answers is correct.
A)Tumor suppressors
B)Proto-oncogenes
C)Growth factors
D)All of the answers are correct.
E)None of the answers is correct.
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53
Which of the following may result in conversion of proto-oncogenes into oncogenes?
A)Retroviral infection
B)Gene duplication
C)Promoter inhibition
D)Retroviral infection and gene duplication are both correct.
E)None of the answers is correct.
A)Retroviral infection
B)Gene duplication
C)Promoter inhibition
D)Retroviral infection and gene duplication are both correct.
E)None of the answers is correct.
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54
Mutations in what gene categories are unlikely to accelerate cancer progress?
A)DNA repair genes
B)Chromosome segregation genes
C)Lysosome-related genes
D)All of the answers are correct.
E)Only DNA repair genes and lysosome-related genes are correct.
A)DNA repair genes
B)Chromosome segregation genes
C)Lysosome-related genes
D)All of the answers are correct.
E)Only DNA repair genes and lysosome-related genes are correct.
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55
Mutations in what gene categories are unlikely to accelerate cancer progress?
A)DNA repair genes
B)Chromosome segregation genes
C)Cell wall-related genes
D)All of the answers are correct.
E)Only DNA repair genes and cell wall-related genes are correct.
A)DNA repair genes
B)Chromosome segregation genes
C)Cell wall-related genes
D)All of the answers are correct.
E)Only DNA repair genes and cell wall-related genes are correct.
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56
How do we know that cancer is a genetic disease?
A)For all individuals that carry a cancer gene, cancer will develop in every tissue in the body.
B)Cancer is a leading cause of mortality worldwide.
C)Only cells exposed to chemical mutagens, but not ionizing radiation, will develop cancer.
D)Certain types of cancer often share the same chromosomal abnormalities.
E)All of the answers are correct.
A)For all individuals that carry a cancer gene, cancer will develop in every tissue in the body.
B)Cancer is a leading cause of mortality worldwide.
C)Only cells exposed to chemical mutagens, but not ionizing radiation, will develop cancer.
D)Certain types of cancer often share the same chromosomal abnormalities.
E)All of the answers are correct.
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57
Which chromosomal abnormalities are often associated with cancer development?
A)Deletions
B)Inversions
C)Creation of fusion genes
D)Translocations
E)All of the answers are correct.
A)Deletions
B)Inversions
C)Creation of fusion genes
D)Translocations
E)All of the answers are correct.
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58
Which of the following occurs in familial retinoblastoma?
A)There are two subsequent gametic mutations in Retinoblastoma (Rb)gene.
B)A single mutation in the Retinoblastoma (Rb)gene leads to the loss of heterozygosity.
C)Tumors develop only after exposure to ionizing radiation.
D)Changes in the cytoskeleton lead to mutations in the Retinoblastoma (Rb)gene.
E)Multiple gametic cells mutate all at once.
A)There are two subsequent gametic mutations in Retinoblastoma (Rb)gene.
B)A single mutation in the Retinoblastoma (Rb)gene leads to the loss of heterozygosity.
C)Tumors develop only after exposure to ionizing radiation.
D)Changes in the cytoskeleton lead to mutations in the Retinoblastoma (Rb)gene.
E)Multiple gametic cells mutate all at once.
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59
Which of the following is NOT correct?
A)Mutations in oncogenes often act in a dominant manner.
B)Mutations in tumor-suppressor genes often act in a recessive manner.
C)In cancer, tumor-suppressor genes often convert to oncogenes following exposure to mutagens.
D)Normal action of proto-oncogenes is to stimulate cell proliferation.
E)All of the answers are correct.
A)Mutations in oncogenes often act in a dominant manner.
B)Mutations in tumor-suppressor genes often act in a recessive manner.
C)In cancer, tumor-suppressor genes often convert to oncogenes following exposure to mutagens.
D)Normal action of proto-oncogenes is to stimulate cell proliferation.
E)All of the answers are correct.
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60
Which of the following events may serve as a first step in cancer development?
A)Overexpression of angiogenesis-promoting factors
B)Duplication of an oncogene
C)Mutation of a tumor-suppressor gene
D)Both duplication of an oncogene and mutation of a tumor-suppressor gene
E)None of the answers is correct.
A)Overexpression of angiogenesis-promoting factors
B)Duplication of an oncogene
C)Mutation of a tumor-suppressor gene
D)Both duplication of an oncogene and mutation of a tumor-suppressor gene
E)None of the answers is correct.
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