Deck 24: Cancer Genetics

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Question
Why do cancer researchers study molecular events associated with mitosis?
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Question
In sporadic cases of retinoblastoma,only two gene mutations are thought to be necessary in the same cell for a tumor to develop.This happens when an organism inherits a mutant allele and a wild- type allele forms the parents.When the wild- type allele is mutated,resulting in tumorigenesis,this process is called,_______ .

A)gain of heterozygosity
B)loss of heterozygosity
C)recombination
D)metastasizing
E)attenuation
Question
Which three stages or transitions in the cell cycle seem to serve as points of control checkpoints)?
Question
Describe why cancer cells are more susceptible to chemotherapies and radiation therapies than normal cells.
Question
What is the name of the protein that appears to regulate the entry of cells into an S phase? This protein is also known as the "guardian of the genome."

A)cyclin
B)p34
C)phosphokinase
D)p102
E)p53
Question
Describe the general relationship that may exist between mutations and cancer.
Question
Which of the following general mechanisms appear to be involved in the formation of cancer cells?

A)transdetermination,mutation,allosteric interactions
B)suppression,tabulation,projection
C)genomic instability,DNA repair failure,chromatin modifications
D)inversions,operon formation,methylation
E)RNA failure,DNA phosphorylation,phosphorylation of adenyl cyclase
Question
Which of the following proteins function as a cell- cycle regulator and transcription factor that can result in cell death apoptosis)to a damaged cell?

A)p53
B)p102
C)p34
D)cyclin
E)phosphokinase
Question
What is the name of the protein that combines with cyclins to exert local control of the cell cycle?

A)cyclin- dependent kinase
B)integrase
C)ATPase
D)hexokinase
E)phosphatase
Question
Mutant versions of genes that are normally involved in promoting the development of cancer are known as_______ .

A)oncogenes
B)malignant genes
C)proto- oncogenes
D)attenuators
E)tumor suppressors
Question
Mutations in the ras gene family induce normally quiescent cells to proceed into the replication cycle.This converts the ras gene from a _______gene to a _______ gene.

A)proto- oncogene; oncogene
B)mutant; oncogene
C)oncogene; proto- oncogene
D)tumor suppressor; proto- oncogene
E)pseudooncogene; proto- oncogene
Question
Signal transduction is best described as_______.

A)communication between nuclei of two organisms
B)communication between cells through physical interaction
C)transmission of signals external to the cell to the nucleus
D)transmission of signals from cancer cells to normal cells
Question
What is the significance of CDK/cyclin interactions with respect to cancer cell proliferation?
Question
Chronic myelogenous leukemia appears to be associated with a chromosomal rearrangement.How is a chromosomal rearrangement responsible for this disease?
Question
Name two of the classes of proteins that combine to directly control progression through the cell cycle.
Question
Briefly describe what a passenger mutation is with respect to cancer genetics.
Question
Provide a definition of cancer at the genetic level.
Question
A loss- of- function mutation in BAX proteins could eliminate apoptotic response in cell.Describe why this type of mutation is a passenger mutation and not a driver mutation.
Question
Driver mutations provide a growth advantage to a tumor cell.Which type of mutation is known to accumulate in cancer cells but has no direct contribution to the cancer phenotype?

A)carrier mutations
B)indirect mutations
C)insignificant mutations
D)passenger mutations
E)alteration mutations
Question
Describe how tumor- suppressor genes keep cells in check.
Question
Chronic myelogenous leukemia is a cancer found in white blood cells.What is its supposed genetic basis of this disease?
Question
Describe the normal function of a tumor- suppressor gene.
Question
Describe the molecular nature of mutation,as related to cancer,in a ras gene.
Question
Describe the cellular and molecular function of the ras gene family and the consequences of mutations in ras.
Question
Many of the known cancers are a result of _____ .

A)the genetic stability of the human genome
B)the non- carcinogenic nature of our environment
C)the genetic instability of the human genome
D)exercising regularly
Question
What are two properties that various types of cancer cells share?
Question
Most cancer- causing animal viruses are RNA viruses called _____ .

A)neoviruses
B)retroviruses
C)DNA viruses
D)classic viruses
Question
Which category of genetic changes does not lead to the formation of oncogenes?

A)point mutations
B)copy number changes
C)translocations
D)correct DNA repair
Question
In what way can loss of heterozygosity lead to cancer?
Question
Briefly describe the following types of genes: tumor- suppressor gene,proto- oncogene,and oncogene.
Question
Describe three genetic mechanisms whereby proto- oncogenes can become overexpressed.
Question
As more is learned about cancer,it has become clear that cancer,with few exceptions, _____.

A)is only dependent on the inherited genetics
B)is a result of genetics and environmental factors
C)is 100% dependent on inherited genetics
D)has no genetic basis
Question
In what way might a virus contribute to cancer formation?
Question
Most cancers arise due to mutations in somatic cells,if someone has a predisposition to cancer,what genetic circumstance likely exists?
Question
Provide a simple definition of a carcinogen.
Question
Much has been written about p53 in terms of cancer biology.What is p53,and what is its significance?
Question
What is the name of a normal gene that serves to promote cellular division?

A)post- oncogene
B)cancer gene
C)proto- oncogene
D)oncogene
Question
The genetic difference between familial retinoblastoma and sporadic retinoblastoma appears to be based on those with the familial form starting out being _____,whereas those with the sporadic form start out being _____
.
Question
Most p53 mutations that result in cancer are a result of loss of function in p53.Describe one method through which a gain- of- function mutation in p53 could cause cancer.
Question
All of these are known to cause cancer EXCEPT _____.

A)chronic infections
B)some viruses
C)radiation
D)DNA repair
Question
All of the following are checkpoints in the cell cycle EXCEPT _____ .

A)G1/S
B)M
C)M/G1
D)G2/M
Question
Which virus type results in the immediate onset of cancer phenotype upon infection of a host?

A)adenovirus
B)acute transforming retrovirus
C)lentivirus
D)retrovirus
Question
Any agent that causes damage to DNA is a potential _____ .

A)pollutant
B)proto- oncogene
C)oncogene
D)carcinogen
Question
Examined cancer cells from the lungs of smokers demonstrate which of the following?

A)mutation rates that are similar to those in a smoker's heart
B)normal mutation rates compared to non- smokers
C)unregulated methylation patterns
D)the occurrence of tumor- suppressor mutations is less in the lung than the throat
Question
A tumor- suppressor gene normally functions to _____ .

A)induce cell division
B)create mutations forming cancer cells
C)repair cancer cells
D)suppress cell division
Question
A retrovirus uses _____to make a DNA copy of RNA.

A)cyclins
B)ras proteins
C)reverse transcriptase
D)CDKs
Question
The gene p53 is called the _____because it corrects mutations in the spindle apparatus before nondisjunction can occur.

A)M phase checkpoint monitor
B)tumor- suppressor monitor
C)guardian of the genome
D)S phase checkpoint monitor
Question
When considered as a root cause for cancer,which of the following is linked to at least 17 types of human cancer?

A)smoking
B)not exercising regularly
C)eating a low- fat diet
D)eating a high- fat diet
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Deck 24: Cancer Genetics
1
Why do cancer researchers study molecular events associated with mitosis?
While mitosis is a basic process related to genetic and general biological studies,it is also a significant event in the cell cycle.The cell cycle is regulated by a variety of gene products,which,when altered by mutation,may lead to cancer.
2
In sporadic cases of retinoblastoma,only two gene mutations are thought to be necessary in the same cell for a tumor to develop.This happens when an organism inherits a mutant allele and a wild- type allele forms the parents.When the wild- type allele is mutated,resulting in tumorigenesis,this process is called,_______ .

A)gain of heterozygosity
B)loss of heterozygosity
C)recombination
D)metastasizing
E)attenuation
loss of heterozygosity
3
Which three stages or transitions in the cell cycle seem to serve as points of control checkpoints)?
G1/S,G2/M,M
4
Describe why cancer cells are more susceptible to chemotherapies and radiation therapies than normal cells.
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
5
What is the name of the protein that appears to regulate the entry of cells into an S phase? This protein is also known as the "guardian of the genome."

A)cyclin
B)p34
C)phosphokinase
D)p102
E)p53
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6
Describe the general relationship that may exist between mutations and cancer.
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
7
Which of the following general mechanisms appear to be involved in the formation of cancer cells?

A)transdetermination,mutation,allosteric interactions
B)suppression,tabulation,projection
C)genomic instability,DNA repair failure,chromatin modifications
D)inversions,operon formation,methylation
E)RNA failure,DNA phosphorylation,phosphorylation of adenyl cyclase
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
8
Which of the following proteins function as a cell- cycle regulator and transcription factor that can result in cell death apoptosis)to a damaged cell?

A)p53
B)p102
C)p34
D)cyclin
E)phosphokinase
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
9
What is the name of the protein that combines with cyclins to exert local control of the cell cycle?

A)cyclin- dependent kinase
B)integrase
C)ATPase
D)hexokinase
E)phosphatase
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
10
Mutant versions of genes that are normally involved in promoting the development of cancer are known as_______ .

A)oncogenes
B)malignant genes
C)proto- oncogenes
D)attenuators
E)tumor suppressors
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
11
Mutations in the ras gene family induce normally quiescent cells to proceed into the replication cycle.This converts the ras gene from a _______gene to a _______ gene.

A)proto- oncogene; oncogene
B)mutant; oncogene
C)oncogene; proto- oncogene
D)tumor suppressor; proto- oncogene
E)pseudooncogene; proto- oncogene
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
12
Signal transduction is best described as_______.

A)communication between nuclei of two organisms
B)communication between cells through physical interaction
C)transmission of signals external to the cell to the nucleus
D)transmission of signals from cancer cells to normal cells
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
13
What is the significance of CDK/cyclin interactions with respect to cancer cell proliferation?
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k this deck
14
Chronic myelogenous leukemia appears to be associated with a chromosomal rearrangement.How is a chromosomal rearrangement responsible for this disease?
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k this deck
15
Name two of the classes of proteins that combine to directly control progression through the cell cycle.
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k this deck
16
Briefly describe what a passenger mutation is with respect to cancer genetics.
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17
Provide a definition of cancer at the genetic level.
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18
A loss- of- function mutation in BAX proteins could eliminate apoptotic response in cell.Describe why this type of mutation is a passenger mutation and not a driver mutation.
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
19
Driver mutations provide a growth advantage to a tumor cell.Which type of mutation is known to accumulate in cancer cells but has no direct contribution to the cancer phenotype?

A)carrier mutations
B)indirect mutations
C)insignificant mutations
D)passenger mutations
E)alteration mutations
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k this deck
20
Describe how tumor- suppressor genes keep cells in check.
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k this deck
21
Chronic myelogenous leukemia is a cancer found in white blood cells.What is its supposed genetic basis of this disease?
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Unlock Deck
k this deck
22
Describe the normal function of a tumor- suppressor gene.
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23
Describe the molecular nature of mutation,as related to cancer,in a ras gene.
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k this deck
24
Describe the cellular and molecular function of the ras gene family and the consequences of mutations in ras.
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
25
Many of the known cancers are a result of _____ .

A)the genetic stability of the human genome
B)the non- carcinogenic nature of our environment
C)the genetic instability of the human genome
D)exercising regularly
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
26
What are two properties that various types of cancer cells share?
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k this deck
27
Most cancer- causing animal viruses are RNA viruses called _____ .

A)neoviruses
B)retroviruses
C)DNA viruses
D)classic viruses
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
28
Which category of genetic changes does not lead to the formation of oncogenes?

A)point mutations
B)copy number changes
C)translocations
D)correct DNA repair
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Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
29
In what way can loss of heterozygosity lead to cancer?
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k this deck
30
Briefly describe the following types of genes: tumor- suppressor gene,proto- oncogene,and oncogene.
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Unlock Deck
k this deck
31
Describe three genetic mechanisms whereby proto- oncogenes can become overexpressed.
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Unlock Deck
k this deck
32
As more is learned about cancer,it has become clear that cancer,with few exceptions, _____.

A)is only dependent on the inherited genetics
B)is a result of genetics and environmental factors
C)is 100% dependent on inherited genetics
D)has no genetic basis
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
33
In what way might a virus contribute to cancer formation?
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k this deck
34
Most cancers arise due to mutations in somatic cells,if someone has a predisposition to cancer,what genetic circumstance likely exists?
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Unlock Deck
k this deck
35
Provide a simple definition of a carcinogen.
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Unlock Deck
k this deck
36
Much has been written about p53 in terms of cancer biology.What is p53,and what is its significance?
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Unlock Deck
k this deck
37
What is the name of a normal gene that serves to promote cellular division?

A)post- oncogene
B)cancer gene
C)proto- oncogene
D)oncogene
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
38
The genetic difference between familial retinoblastoma and sporadic retinoblastoma appears to be based on those with the familial form starting out being _____,whereas those with the sporadic form start out being _____
.
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
39
Most p53 mutations that result in cancer are a result of loss of function in p53.Describe one method through which a gain- of- function mutation in p53 could cause cancer.
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
40
All of these are known to cause cancer EXCEPT _____.

A)chronic infections
B)some viruses
C)radiation
D)DNA repair
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
41
All of the following are checkpoints in the cell cycle EXCEPT _____ .

A)G1/S
B)M
C)M/G1
D)G2/M
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
42
Which virus type results in the immediate onset of cancer phenotype upon infection of a host?

A)adenovirus
B)acute transforming retrovirus
C)lentivirus
D)retrovirus
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
43
Any agent that causes damage to DNA is a potential _____ .

A)pollutant
B)proto- oncogene
C)oncogene
D)carcinogen
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
44
Examined cancer cells from the lungs of smokers demonstrate which of the following?

A)mutation rates that are similar to those in a smoker's heart
B)normal mutation rates compared to non- smokers
C)unregulated methylation patterns
D)the occurrence of tumor- suppressor mutations is less in the lung than the throat
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
45
A tumor- suppressor gene normally functions to _____ .

A)induce cell division
B)create mutations forming cancer cells
C)repair cancer cells
D)suppress cell division
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
46
A retrovirus uses _____to make a DNA copy of RNA.

A)cyclins
B)ras proteins
C)reverse transcriptase
D)CDKs
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
47
The gene p53 is called the _____because it corrects mutations in the spindle apparatus before nondisjunction can occur.

A)M phase checkpoint monitor
B)tumor- suppressor monitor
C)guardian of the genome
D)S phase checkpoint monitor
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
48
When considered as a root cause for cancer,which of the following is linked to at least 17 types of human cancer?

A)smoking
B)not exercising regularly
C)eating a low- fat diet
D)eating a high- fat diet
Unlock Deck
Unlock for access to all 48 flashcards in this deck.
Unlock Deck
k this deck
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Unlock Deck
Unlock for access to all 48 flashcards in this deck.