Question 1

Cancer is sometimes viewed as a disease of stem cells. What is the evidence?

Accepted Answer

In the cancer stem cell model the cancer

Question 2

The progression of normal colonic epithelium to colon cancer has been viewed as a multi-stage progression. What is known about how the cancer develops and which are the genes that are most frequently involved?

Accepted Answer

At the phenotype level, the progression

Question 3

The number of mutations in a cancer cell can vary. Match the different types of tumors listed in
a) to
e) with one of the three ranges for numbers of somatic substitutions per tumor given in i) to iii).

Accepted Answer

a) iii)
b)

Question 4

The range of different point mutation classes and their locations within coding DNA are major features that differentiate oncogenes from tumor suppressor genes. Explain.

Accepted Answer

Point mutations in tumor suppressor gene

Question 5

Which, if any, of the following statements is false?

Accepted Answer

A)  p53 acts as a brake on the cell cycle. 
B)  p53 and RB1 are mutually antagonistic. 
C)  p53 is normally inhibited by being bound to the MDM2 protein, but when phosphorylated, it changes conformation and is released from MDM2. 
D)  At high concentrations p53 stimulates the transcription of various genes that inhibit apoptosis. 
A)  p53 acts as a brake on the cell cycle. 
B)  p53 and RB1 are mutually antagonistic. 
C)  p53 is normally inhibited by being bound to the MDM2 protein, but when phosphorylated, it changes conformation and is released from MDM2. 
D)  At high concentrations p53 stimulates the transcription of various genes that inhibit apoptosis.

Question 6

How are MSI-positive tumors recognized and what does the MSI-positive property signify?

Accepted Answer

MSI-positive tumors mean tumors that sho

Question 7

Match cancers
a) to
d) with one of the descriptions i) to iv)

Accepted Answer

a) iii)
b)

Question 8

What are double minute chromosomes and homogeneously staining regions, and why do they occur in some cancer cells?

Accepted Answer

Oncogene activation usually occurs by so

Question 9

Distinguish between driver mutations and passenger mutations in cancer. How many driver mutations might be expected in cancers?

Accepted Answer

As normal cells evolve to become cancer

Question 10

Tumors gradually acquire mutations to evolve from benign to malignant lesions. Because that takes some time, cancer is primarily a disease of aging. So, how can childhood cancers be explained?

Accepted Answer

In self-renewing tissues the cells conta

Question 11

Recent studies have shown that non-classical cancer genes link metabolism to the epigenome. Explain the connection.

Accepted Answer

The IDH1 and 1DH2 genes make cytosolic a

Question 12

With reference to cancer spreading what is involved in intravasation and extravasation?

Accepted Answer

Cancer spreading involves both local inv

Question 13

Describe three classes of activation mechanism whereby normal cellular oncogenes are activated to become oncogenes.

Accepted Answer

1) Activation by gene amplification. Tum

Question 14

What is the Philadelphia chromosome and why is it a cause of cancer?

Accepted Answer

The Philadelphia chromosome is a recurri

Question 15

The biological hallmarks of cancer are regulated by partially redundant signalling pathways and that can pose very significant challenges to therapeutic approaches that seek to inhibit a specific biological hallmark of cancer. Explain the challenges posed when using inhibitors of telomerase and of angiogenesis.

Accepted Answer

The problem here is that using one appro

Question 16

List three classes of stromal cell that support the tumor microenvironment.

Accepted Answer

1) Infiltrating immune cells (

Question 17

Which, if any, of the following statements is false?

Accepted Answer

A)  Mismatch repair is dedicated to repairing errors made during DNA replication. 
B)  MutS $\alpha$ is responsible for recognizing single base mismatches during DNA replication. 
C)  MutS$\beta$ is responsible for recognizing all short insertion and deletion errors made during DNA replication. 
D)  MutL $\alpha$ contributes an endonuclease activity that is required to nick the DNA during DNA repair. 
A)  Mismatch repair is dedicated to repairing errors made during DNA replication. 
B)  MutS $\alpha$ is responsible for recognizing single base mismatches during DNA replication. 
C)  MutS$\beta$ is responsible for recognizing all short insertion and deletion errors made during DNA replication. 
D)  MutL $\alpha$ contributes an endonuclease activity that is required to nick the DNA during DNA repair.

Question 18

Which, if any, of the following statements is false?

Accepted Answer

A)  Chromothripsis is an extraordinary event in which multiple chromosomes within a cell are shattered into many pieces. 
B)  Chromothripsis is much more like to occur in cells where the TP53 gene has received loss-of-function mutations. 
C)  Kataegis is a type of somatic hypermutation. 
D)  The mutations involved in a kataegis event are clustered in one subchromosomal region. 
A)  Chromothripsis is an extraordinary event in which multiple chromosomes within a cell are shattered into many pieces. 
B)  Chromothripsis is much more like to occur in cells where the TP53 gene has received loss-of-function mutations. 
C)  Kataegis is a type of somatic hypermutation. 
D)  The mutations involved in a kataegis event are clustered in one subchromosomal region.

Cancer is sometimes viewed as a disease of stem cells. What is the evidence?

The progression of normal colonic epithelium to colon cancer has been viewed as a multi-stage progression. What is known about how the cancer develops and which are the genes that are most frequently involved?

The number of mutations in a cancer cell can vary. Match the different types of tumors listed in a) to e) with one of the three ranges for numbers of somatic substitutions per tumor given in i) to iii).

The range of different point mutation classes and their locations within coding DNA are major features that differentiate oncogenes from tumor suppressor genes. Explain.

Which, if any, of the following statements is false?

How are MSI-positive tumors recognized and what does the MSI-positive property signify?

Match cancers a) to d) with one of the descriptions i) to iv)

What are double minute chromosomes and homogeneously staining regions, and why do they occur in some cancer cells?

Distinguish between driver mutations and passenger mutations in cancer. How many driver mutations might be expected in cancers?

Tumors gradually acquire mutations to evolve from benign to malignant lesions. Because that takes some time, cancer is primarily a disease of aging. So, how can childhood cancers be explained?

Recent studies have shown that non-classical cancer genes link metabolism to the epigenome. Explain the connection.

With reference to cancer spreading what is involved in intravasation and extravasation?

Describe three classes of activation mechanism whereby normal cellular oncogenes are activated to become oncogenes.

What is the Philadelphia chromosome and why is it a cause of cancer?

List three classes of stromal cell that support the tumor microenvironment.

Which, if any, of the following statements is false?

Which, if any, of the following statements is false?

Fundamentals of Dna, Chromosomes, and Cells

Fundamentals of Gene Structure, Gene Expression, and Human Genome Organization

Principles Underlying Core Dna Technologies

Principles of Genetic Variation

Single-Gene Disorders: Inheritance Patterns, Phenotype Variability, and Allele Frequencies

Principles of Gene Regulation and Epigenetics

Genetic Variation Producing Diseasecausing Abnormalities in Dna and Chromosomes

Identifying Disease Genes and Genetic Susceptibility to Complex Disease

Genetic Approaches to Treating Disease

Genetic Testing From Genes to Genomes, and the Ethics of Genetic Testing and Therapy

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Exam 10: Cancer Genetics and Genomics

Cancer is sometimes viewed as a disease of stem cells. What is the evidence?

The progression of normal colonic epithelium to colon cancer has been viewed as a multi-stage progression. What is known about how the cancer develops and which are the genes that are most frequently involved?

The number of mutations in a cancer cell can vary. Match the different types of tumors listed in a) to e) with one of the three ranges for numbers of somatic substitutions per tumor given in i) to iii).

The range of different point mutation classes and their locations within coding DNA are major features that differentiate oncogenes from tumor suppressor genes. Explain.

Which, if any, of the following statements is false?

How are MSI-positive tumors recognized and what does the MSI-positive property signify?

Match cancers a) to d) with one of the descriptions i) to iv)

What are double minute chromosomes and homogeneously staining regions, and why do they occur in some cancer cells?

Distinguish between driver mutations and passenger mutations in cancer. How many driver mutations might be expected in cancers?

Tumors gradually acquire mutations to evolve from benign to malignant lesions. Because that takes some time, cancer is primarily a disease of aging. So, how can childhood cancers be explained?

Recent studies have shown that non-classical cancer genes link metabolism to the epigenome. Explain the connection.

With reference to cancer spreading what is involved in intravasation and extravasation?

Describe three classes of activation mechanism whereby normal cellular oncogenes are activated to become oncogenes.

What is the Philadelphia chromosome and why is it a cause of cancer?

List three classes of stromal cell that support the tumor microenvironment.

Which, if any, of the following statements is false?

Which, if any, of the following statements is false?

Fundamentals of Dna, Chromosomes, and Cells

Fundamentals of Gene Structure, Gene Expression, and Human Genome Organization

Principles Underlying Core Dna Technologies

Principles of Genetic Variation

Single-Gene Disorders: Inheritance Patterns, Phenotype Variability, and Allele Frequencies

Principles of Gene Regulation and Epigenetics

Genetic Variation Producing Diseasecausing Abnormalities in Dna and Chromosomes

Identifying Disease Genes and Genetic Susceptibility to Complex Disease

Genetic Approaches to Treating Disease

Genetic Testing From Genes to Genomes, and the Ethics of Genetic Testing and Therapy

Filters