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Chapter 23

Terms in this set (80)

A cancer cell is a cell that ______.
has accumulated genetic changes that allow it to grow uncontrollably
Contact inhibition is the ability of _____.
normal cells to stop dividing when they touch other cells
A series of events leading to programmed cell death is called _.
apoptosis
Select all of these that are unique features of cancer cells.
They produces their own growth factors.
They do not undergo apoptosis.
They keep growing when they contact other cells.
Unlike normal body cells, cultured tumor cells ______.
can often times divide indefinitely
What is the physiological effect of cancer that causes disease?
Uncontrolled cell growth
Cancer cells are "immortal," that is, they can divide indefinitely. One reason for that is that they have expression of ______.
telomerase
Normal cells stop dividing when they physically touch other cells. This normal cellular response is called _.
contact; inhibition
What are three ways that cancer cells evade the normal controls on cell division?
Produce their own growth factors
Fail to undergo apoptosis
Lose contact inhibition
Cancer scientists are able to study cancerous cells in culture, in large part because the cancer cells have the ability to
divide indefinitely.
One reason why cancer cells are "immortal" is that they can preserve their DNA ends through expression of the enzyme _.
telomerase
In the course of their growth, cancer cells often acquire mutations in genes related to DNA repair. What is a consequence of this?
Higher mutation rate
Cancerous growths are clonal in origin because cancer cells ______.
originate from a single cell that has accumulated genetic changes during cell division
If a tumor in a woman originated from a single somatic cell, what would you expect to see in terms of X-inactivation?
The same X will be inactivated in each cell of the tumor.
What best explains why cancer is more common among older people than among younger people?
Multiple mutations must occur in the same cell
What is the main reason cancer cells have a higher mutation rate?
They often have mutations in DNA repair genes.
Chemicals that cause mutations and can lead to cancer are called _____.
mutagens
Most cancer cells are descendants of an original cell that acquired genetic changes. Therefore, cancerous growths are considered to be ______ in origin.
clonal
What evidence best supports the clonal origin of cancerous tumors from a single somatic cell?
In women, tumor cells all have the same X chromosome inactivated.
The fact that a cell may require 6-10 mutations to become malignant explains why _____.
cancer is more common with advanced age
A mutagen is _______.
a chemical that causes mutations in DNA
What is the function of the BRCA1 and BRCA2 genes in normal, noncancerous cells?
They encode DNA repair proteins.
Mutations in a cancer cell genome that cause the cancer phenotype are called _ mutations.
driver
Over time, tumors tend to grow faster and become more invasive of other tissues, a phenomenon known as tumor _.
progression
A growth factor is a _____.
signaling molecule that regulates cell division
The large majority of mutations in the genome of a cancer cell are _____.
passenger mutations
As tumors grow, they increase rates of proliferation and suffer more genomic instability. This causes them to grow faster and become more invasive. This increase in malignancy is known as ______.
tumor progression
Cell proliferation and division is influenced by signaling molecules called growth factors. A growth factor that stimulates cell proliferation is also called a(n) _.
mitogen
To stimulate the growth of epidermal cells, such as skin cells, which event would occur first?
An epidermal growth factor, EGF, binds to a receptor on the surface of a skin cell.
Which of the following accurately describe CDK proteins?
Phosphorylate other proteins
Major cell cycle regulators
Bind cyclins
Checking for DNA damage before S phase and checking for spindle attachment before anaphase are jobs carried out by cell cycle ______.
checkpoints
What cell factor would most likely cause stalling at the G1-to-S checkpoint?
Damaged DNA
The major cell cycle regulators are kinases called _ proteins that work in association with cyclins.
cyclin dependent kinase (CDK)
To prevent errors in the cell cycle, the cell uses multiple systems to check for problems before progressing to each new stage, known as cell cycle _.
checkpoints
The role of the G1-to-S checkpoint is to ______.
prevent the replication of damaged DNA
What is the normal role of Rb protein during the process of cell division?
Unphosphorylated Rb protein prevents progress through the cell cycle by binding to transcription factor E2F.
The tumor-suppressor gene p53 has a significant role in _____.
responding to DNA damage in a cell
How does the p53 transcription factor arrest a cell whose DNA is damaged at the G1-to-S checkpoint, so that DNA repair can occur?
By stimulating the expression of the p21 gene
An oncogene is a dominant mutant allele _____.
that promotes cancer
Which event speeds up the cell cycle?
Phosphorylation of Rb protein so that it no longer binds to transcription factor E2F.
A gene that must be mutated in both copies to promote cancer is called a _ gene.
tumor; suppressor
f DNA is damaged during the G1 phase, the p53 pathway is activated. Which of the following are ways in which p53 acts?
It turns on transcription of DNA repair genes.
It turns on transcription of p21.
Choose two processes activated by p53 when DNA damage is detected during the G1 phase.
It turns on transcription of p21, a CDK inhibitor.
It turns on expression of DNA repair genes.
A mutant allele that acts in a dominant fashion to promote cancer is called a(n) _____.
oncogene
A tumor-suppressor gene is one that ________.
promotes cancer when both copies are mutated
Which gene plays a significant role in responding to DNA damage in a cell?
p53
An oncogene is formed by mutation that increases the activity of a normal gene called a(n) ______.
proto-oncogene
Cancer cells may carry gain-of-function mutations that increase the activity of a proto-oncogene. In which of the following ways could the expression of the protein encoded by the proto-oncogene be altered by this type of mutation?
- The protein is expressed in a cell type where it is not normally found.
- The amount of protein produced from the proto-oncogene is significantly increased.
- The structure of the protein is altered so that it is overly active.
A cancer-causing mutation in a proto-oncogene will ______ its activity; a cancer-causing mutation in a tumor-suppressor gene will ______ its activity.
increase; decrease
Viruses that cause tumors are often _ which have an RNA genome.
retroviruses
An oncogene is formed when a proto-oncogene gains a ______.
mutation that causes its expression to be abnormally active
Choose all mechanisms that explain the conversion of a proto-oncogene to an oncogene via an RNA tumor virus?
- A virus can carry a proto-oncogene which can mutate into an oncogene as the virus replicates inside of cells.
- A virus can integrate in the genome of a cell near a proto-oncogene and affect its expression.
- Strong viral enhancers can increase expression levels of a proto-oncogene carried by the virus.
The ERBB2 receptor normally plays a role in promoting cell division. Cells from many breast cancer patients show an increase in the number of ERBB2 receptors available on the plasma membrane. The type of mutation that contributed to cancer development in these cases would be called a ______-of-function mutation in a(n) ______.
gain; proto-oncogene
The normal job of a wild-type proto-oncogene is to ______ progression through the cell cycle; the normal job of a wild-type tumor-suppressor gene is to ______ progression through the cell cycle.
accelerate; slow
Which two genes are fused due to a translocation between chromosomes 9 and 22 in patients with chronic myelogenous leukemia?
bcr
c-abl
Tumor-causing viruses are often ______.
retroviruses
A cancer-causing change occurs when a tumor-suppressor gene is ______.
inactivated
Chronic myelogenous leukemia is caused by a _ between chromosomes 9 and 22 which fuses the gene c-abl with the gene bcr. In the newly produced hybrid protein, the c-Abl part acts as a protein tyrosine _ which regulates certain growth-factor-induced signal transduction pathways.
translocation; kinase
Most individuals who are born with an inherited form of cancer susceptibility are ______ for a defect in a ______.
heterozygous; tumor-suppressor gene
An individual who is heterozygous for a defect in a tumor-suppressor gene ______.
has inherited an increased susceptibility to develop cancer
Children of parents with retinoblastoma often develop retinoblastoma tumors as well. In those children's cancer cells, both copies of the ______ gene are missing due to deletions in the long arm of the 13th chromosome.
RB
Retinoblastoma is associated with inactivation of the RB+ allele to RB—. Suppose a woman whose genotype is RB+ RB— develops retinoblastoma. What is the genotype of her cancer cells?
RB- RB-
The cancer cells of many people suffering from retinoblastoma are missing both copies of the RB gene because _____.
both copies of chromosomes 13 have experienced a deletion in a particular region of the long arm
The loss of function of a normal allele when the other allele for that gene was already inactivated is called ______.
loss of heterozygosity
At the cellular level, retinoblastoma development is _______.
recessive because the cell must become homozygous for a loss-of-function allele
Retinoblastoma can be either inherited or sporadic and noninherited. You could predict that in general, the patients with the sporadic, noninherited form will be _____.
older
In which two ways have tumor-suppressor genes been shown to act within cells?
Regulating the rate of cell division and maintaining genomic integrity
Loss of heterozygosity is ______.
loss of function of a normal allele when the other allele was already inactivated
For the inherited tendency to develop retinoblastoma, which correctly describes inactivation of the RB tumor-suppressor alleles by the "two-hit" model?
One allele is inactivated prior to birth, the other becomes inactivated early in life.
A man acquires a single retinoblastoma tumor late in life. His family has no history of the disease. What is the most likely explanation?
A single retinal cell acquired two RB— mutations in succession.
Tumor-suppressor genes normally act to ______.
negatively regulate cell division
maintain genome integrity
Normal tumor-suppressor genes generally act to repair DNA or to ______ the cell cycle, either as part of a checkpoint or as a component of the cell proliferation machinery.
slow
Antibody therapy for cancer is possible when _____.
cancer cells overexpress a receptor on their surface
Normal, wild-type tumor-suppressor genes are likely to perform which the following functions?
Inhibitor of the cell cycle
DNA repair
Cell cycle checkpoints
The two types of genes that can contain driver mutations causing cancer are proto-oncogenes and tumor-suppressor genes, however, development of drugs to treat cancer is focused mainly on proto-oncogenes. Why?
Cancer cells have mutations in both copies of a specific tumor-suppressor gene, so no functional protein is made that can be targeted by a drug.
Even when cancer therapy seems successful initially, cancer sometimes recurs because many tumors are _ - that is, they are a mixture of cells with slightly different genomes.
heterogeneous
Breast tumors that overexpress the Her2 growth factor receptor have been successfully treated by injecting Herceptin© monoclonal _.
antibodies
Cancer cells lack both functional copies of one or more tumor-suppressor genes. For that reason, the development of drugs to treat cancer ______.
focuses more often on proto-oncogenes
What can explain why cancers often recur after treatment?
Tumors are often heterogeneous.
What can explain why cancers often recur after treatment?
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