Question 1

Chromosome mutations are common in tumor cells. Do these mutations cause cancer, or are they a result of cancer? What evidence is there for your conclusion?

Accepted Answer

Chromosome mutations can both cause cancer and be a result of cancer. These mutations can lead to the development of cancer by disrupting the normal functioning of genes that control cell growth and division. When these genes are altered, it can result in uncontrolled cell growth and the formation of tumors.

On the other hand, chromosome mutations can also occur as a result of the cancer itself. As tumor cells continue to divide and grow, they accumulate additional mutations, including chromosome mutations, which can further drive the progression of the cancer.

There is evidence to support both perspectives. Studies have identified specific chromosome mutations that are associated with an increased risk of developing certain types of cancer, indicating a causal relationship between these mutations and cancer development. Additionally, research has shown that the accumulation of chromosome mutations in tumor cells can contribute to the progression and aggressiveness of the cancer.

Overall, it is clear that chromosome mutations play a significant role in the development and progression of cancer, and they can both cause cancer and be a result of the disease.

Question 2

The overexpression of certain microRNAs, called oncomiRs, is associated with some types of cancer. What type of gene is the likely target of these oncomiRs in cancer cells?

Accepted Answer

A)  proto-oncogenes 
B)  tumor-suppressor genes 
C)  genes that promote angiogenesis 
D)  genes that allow the G1/S transition 
E)  genes involved in DNA repair 
A)  proto-oncogenes 
B)  tumor-suppressor genes 
C)  genes that promote angiogenesis 
D)  genes that allow the G1/S transition 
E)  genes involved in DNA repair B

Question 3

An abnormally low level of expression of a particular microRNA might facilitate the development of a cancer by which of the following methods?

Accepted Answer

A)  inducing the increased expression of a tumor-suppressor gene 
B)  inducing the increased expression of DNA-repair genes 
C)  promoting a decreased level of telomerase activity 
D)  inhibiting the G1 to M transition in the cell cycle 
E)  increasing the expression of an oncogene 
A)  inducing the increased expression of a tumor-suppressor gene 
B)  inducing the increased expression of DNA-repair genes 
C)  promoting a decreased level of telomerase activity 
D)  inhibiting the G1 to M transition in the cell cycle 
E)  increasing the expression of an oncogene E

Question 4

List three observations consistent with the idea that cancer arises through an accumulation of mutations in several genes that promotes cellular proliferation in single cells.

Accepted Answer

1. Tumor heterogeneity: Cancer cells wit

Question 5

Which of the following is a process whereby cancer cells travel to other sites in the body and establish secondary tumors?

Accepted Answer

A)  oncogenesis 
B)  angiogenesis 
C)  malignancy 
D)  secondary tumorigenesis 
E)  metastasis 
A)  oncogenesis 
B)  angiogenesis 
C)  malignancy 
D)  secondary tumorigenesis 
E)  metastasis

Question 6

A cancer cell line was identified as having inappropriate expression of telomerase. Which of the following would be the BEST treatment that could make this cell line mortal?

Accepted Answer

A)  a drug that increases the levels of telomerase expression 
B)  a drug that methylates the promoter of the telomerase gene 
C)  a drug that repairs the mutation within the coding region of the telomerase 
D)  a drug that allows the telomerase to be expressed but at lower levels 
E)  a drug that inhibits a tumor-suppressor gene in the cell line 
A)  a drug that increases the levels of telomerase expression 
B)  a drug that methylates the promoter of the telomerase gene 
C)  a drug that repairs the mutation within the coding region of the telomerase 
D)  a drug that allows the telomerase to be expressed but at lower levels 
E)  a drug that inhibits a tumor-suppressor gene in the cell line

Question 7

In cancer, mutations in stimulatory genes (such as in proto-oncogenes) are often dominant, whereas mutations in inhibitory genes (such as tumor-suppressor alleles) are often recessive. Why?

Accepted Answer

In cancer biology, the behavior of genes

Question 8

What specifically do most people inherit when they inherit a predisposition to a particular cancer such as retinoblastoma?

Accepted Answer

A)  a mutation that causes the overexpression of a DNA repair gene 
B)  a mutation that causes telomerase to have reduced expression in somatic cells 
C)  a deleterious mutation in one copy of a tumor-suppressor gene 
D)  a deletion that removes one copy of an oncogene 
E)  an extra X chromosome from the mother 
A)  a mutation that causes the overexpression of a DNA repair gene 
B)  a mutation that causes telomerase to have reduced expression in somatic cells 
C)  a deleterious mutation in one copy of a tumor-suppressor gene 
D)  a deletion that removes one copy of an oncogene 
E)  an extra X chromosome from the mother

Question 9

What is one line of evidence supporting the idea that cancer is influenced by environmental factors?

Accepted Answer

One line of evidence supporting the idea

Question 10

Consider the Ras signal-transduction pathway. Suppose a mutation occurred in the gene that encodes MEK that renders it nonfunctional. Which of the following effects would you see in this situation?

Accepted Answer

A)  Binding of the growth factor to the receptor would occur, but the receptor's conformational change that is needed for the pathway to go forward would not occur. 
B)  Activated Ras would no longer have the ability to activate Raf, and the signal-transduction pathway would be halted at this step. 
C)  Ras would lose the ability to bind GTP and thus could no longer become activated, and the signal-transduction pathway would be halted at this step. 
D)  MAP kinase would not be activated and thus could not move into the nucleus to activate transcription factors. 
E)  Inactive Ras would move into the nucleus and inactivate tumor-suppressor transcription factors, which could ultimately result in cancer. 
A)  Binding of the growth factor to the receptor would occur, but the receptor's conformational change that is needed for the pathway to go forward would not occur. 
B)  Activated Ras would no longer have the ability to activate Raf, and the signal-transduction pathway would be halted at this step. 
C)  Ras would lose the ability to bind GTP and thus could no longer become activated, and the signal-transduction pathway would be halted at this step. 
D)  MAP kinase would not be activated and thus could not move into the nucleus to activate transcription factors. 
E)  Inactive Ras would move into the nucleus and inactivate tumor-suppressor transcription factors, which could ultimately result in cancer.

Question 11

Most cancers are assumed to arise through which of the following?

Accepted Answer

A)  errors in transcription 
B)  the production of unbalanced gametes because of nondisjunction during meiosis 
C)  genetic or epigenetic changes in somatic cells 
D)  delayed cell division during early embryogenesis 
E)  No correct answer is provided. 
A)  errors in transcription 
B)  the production of unbalanced gametes because of nondisjunction during meiosis 
C)  genetic or epigenetic changes in somatic cells 
D)  delayed cell division during early embryogenesis 
E)  No correct answer is provided.

Question 12

Normal cellular genes whose products are involved in facilitating cell division to occur under appropriate conditions are called:

Accepted Answer

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.

Question 13

Distinguish between driver and passenger mutations in cancer genomes. Propose a strategy whereby "knock-in" technology (Chapter 19) could be used to distinguish between driver and passenger mutations. What might be a major limitation to this strategy?

Accepted Answer

Driver mutations are genetic alterations

Question 14

What are two processes that determine how quickly mutations accumulate within a cell?

Accepted Answer

Two processes that determine how quickly

Question 15

In Burkitt lymphoma, there is increased expression of the MYC gene. Which of the following statements BEST explains the reason for the increased expression of this gene?

Accepted Answer

A)  A chromosome deletion has removed a tumor-suppressor gene. 
B)  A chromosome deletion has removed an oncogene. 
C)  A chromosome duplication 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)  A chromosome duplication 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.

Question 16

List three ways in which proto-oncogenes can be converted to oncogenes by viruses.

Accepted Answer

Proto-oncogenes are normal genes that, w

Question 17

_____ and _____ are chromosomal mutations that may activate cellular oncogenes by moving them to new regulatory sequences where they become overexpressed.

Accepted Answer

A)  Duplications; deletions 
B)  Inversions; translocations 
C)  Duplications; inversions 
D)  Deletions; translocations 
E)  Aneuploidy; deletions 
A)  Duplications; deletions 
B)  Inversions; translocations 
C)  Duplications; inversions 
D)  Deletions; translocations 
E)  Aneuploidy; deletions

Question 18

Explain how DNA sequencing studies can aid in our understanding of cancer formation.

Accepted Answer

DNA sequencing studies can aid in our un

Question 19

The p53 gene is important in controlling apoptosis, but it also plays a role i:

Accepted Answer

A)  initiating mitosis. 
B)  controlling cell adhesion. 
C)  opening ion channels. 
D)  duplicating the centrosome. 
E)  preventing aneuploidy by regulating the spindle-assembly checkpoint. 
A)  initiating mitosis. 
B)  controlling cell adhesion. 
C)  opening ion channels. 
D)  duplicating the centrosome. 
E)  preventing aneuploidy by regulating the spindle-assembly checkpoint.

Question 20

The process by which genetic changes occur in tumors and allows them to become increasingly aggressive over time is called:

Accepted Answer

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.

Exam 23: Cancer Genetics

Chromosome mutations are common in tumor cells. Do these mutations cause cancer, or are they a result of cancer? What evidence is there for your conclusion?

The overexpression of certain microRNAs, called oncomiRs, is associated with some types of cancer. What type of gene is the likely target of these oncomiRs in cancer cells?

An abnormally low level of expression of a particular microRNA might facilitate the development of a cancer by which of the following methods?

List three observations consistent with the idea that cancer arises through an accumulation of mutations in several genes that promotes cellular proliferation in single cells.

Which of the following is a process whereby cancer cells travel to other sites in the body and establish secondary tumors?

A cancer cell line was identified as having inappropriate expression of telomerase. Which of the following would be the BEST treatment that could make this cell line mortal?

In cancer, mutations in stimulatory genes (such as in proto-oncogenes) are often dominant, whereas mutations in inhibitory genes (such as tumor-suppressor alleles) are often recessive. Why?

What specifically do most people inherit when they inherit a predisposition to a particular cancer such as retinoblastoma?

What is one line of evidence supporting the idea that cancer is influenced by environmental factors?

Consider the Ras signal-transduction pathway. Suppose a mutation occurred in the gene that encodes MEK that renders it nonfunctional. Which of the following effects would you see in this situation?

Most cancers are assumed to arise through which of the following?

Normal cellular genes whose products are involved in facilitating cell division to occur under appropriate conditions are called:

Distinguish between driver and passenger mutations in cancer genomes. Propose a strategy whereby "knock-in" technology (Chapter 19) could be used to distinguish between driver and passenger mutations. What might be a major limitation to this strategy?

What are two processes that determine how quickly mutations accumulate within a cell?

In Burkitt lymphoma, there is increased expression of the MYC gene. Which of the following statements BEST explains the reason for the increased expression of this gene?

List three ways in which proto-oncogenes can be converted to oncogenes by viruses.

_____ and _____ are chromosomal mutations that may activate cellular oncogenes by moving them to new regulatory sequences where they become overexpressed.

Explain how DNA sequencing studies can aid in our understanding of cancer formation.

The p53 gene is important in controlling apoptosis, but it also plays a role i:

The process by which genetic changes occur in tumors and allows them to become increasingly aggressive over time is called:

Introduction to Genetics

Chromosomes and Cellular Reproduction

Basic Principles of Heredity

Sex Determination and Sex-Linked Characteristics

Extensions and Modifications of Basic Principles

Pedigree Analysis, Applications, and Genetic Testing

Linkage, Recombination, and Eukaryotic Gene Mapping

Chromosome Variation

Bacterial and Viral Genetic Systems

DNA: the Chemical Nature of the Gene

Chromosome Structure and Organelle Dna

DNA Replication and Recombination

Transcription

Rna Molecules and Rna Processing

The Genetic Code and Translation

Control of Gene Expression in Prokaryotes

Control of Gene Expression in Eukaryotes

Gene Mutations and Dna Repair

Molecular Genetic Analysis and Biotechnology

Genomics and Proteomics

Epigenetics

Developmental Genetics and Immunogenetics

Quantitative Genetics

Population Genetics

Evolutionary Genetics

Filters

_ and _ are chromosomal mutations that may activate cellular oncogenes by moving them to new regulatory sequences where they become overexpressed.