Chapter 23

Question 1

A cancer cell is a cell that ______.

Answer 1

has accumulated genetic changes that allow it to grow uncontrollably

Question 2

Normal cells stop dividing when they physically touch other cells. This normal cellular response is called [] []

Answer 2

contact inhibition

a cell-to-cell signaling mechanism that normally limits cell growth to a monolayer in culture.

Question 3

Unlike normal body cells, cultured tumor cells ______.

Answer 3

can often times divide indefinitely

normal cells can divide up to 20-50 times before they die

Question 4

cancer cells have the ability to burst through membranes and travel throughout the body, a process known as []

Answer 4

metastasis

the colonization of distant tissue by cancer cells that travel through the bloodstream.

Question 5

In the course of their growth, cancer cells often acquire mutations in genes related to DNA repair. What is a consequence of this?

Answer 5

Higher mutation rate

Question 6

What is the physiological effect of cancer that causes disease?

Answer 6

Uncontrolled cell growth

Question 7

Cancerous growths are clonal in origin because cancer cells ______.

Answer 7

originate from a single cell that has accumulated genetic changes during cell division

Question 8

Cancer scientists are able to study cancerous cells in culture, in large part because the cancer cells have the ability to

Answer 8

divide indefinitely.

Question 9

If a tumor in a woman originated from a single somatic cell, what would you expect to see in terms of X-inactivation?

Answer 9

The same X will be inactivated in each cell of the tumor.

Question 10

The fact that a cell may require 6-10 mutations to become malignant explains why _____.

Answer 10

cancer is more common with advanced age

Question 11

What is the main reason cancer cells have a higher mutation rate?

Answer 11

They often have mutations in DNA repair genes.

Question 12

A mutagen is _______.

Answer 12

a chemical that causes mutations in DNA

Question 13

What is the function of the BRCA1 and BRCA2 genes in normal, noncancerous cells?

Answer 13

They encode DNA repair proteins.

Question 14

Most cancer cells are descendants of an original cell that acquired genetic changes. Therefore, cancerous growths are considered to be ______ in origin.

Answer 14

clonal

Question 15

What evidence best supports the clonal origin of cancerous tumors from a single somatic cell?

Answer 15

In women, tumor cells all have the same X chromosome inactivated.

Question 16

Mutations in a cancer cell genome that cause the cancer phenotype are called [] mutations.

Answer 16

driver mutations

DNA alterations in cancerous cells that contribute to the cancer phenotype.

Question 17

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 ______.

Answer 17

tumor progression

the phenomenon where, over time, cancerous tumors grow faster and become more invasive.

Question 18

A growth factor is a _____.

Answer 18

signaling molecule that regulates cell division

Question 19

The large majority of mutations in the genome of a cancer cell are _____.

Answer 19

passenger mutations
DNA alterations in cancerous cells that occur due to the increased mutation rate of cancer cells but do not contribute to the cancer phenotype.

Question 20

Correct order of events in the normal pathway by which growth factors stimulate cell division

Answer 20

A growth factor binds to a specific receptor on the surface of the cell
a signal transduction pathway activates intracellular proteins amplifying the signal
Genes coding for proteins controlling cell division are activated

Question 21

The cytoplasmic proteins that relay signals received by growth factor receptors to initiate a cell response are called []

Answer 21

signal transducers

cytoplasmic proteins that relay signals inside the cell.

Question 22

stages of the cell cycle in the correct order starting with a cell that has just completed mitosis and cell division at the top.

Answer 22

G1, S, G2, M

Question 23

To stimulate the growth of epidermal cells, such as skin cells, which event would occur first?

Answer 23

An epidermal growth factor, EGF, binds to a receptor on the surface of a skin cell.

Question 24

The major cell cycle regulators are kinases called [] proteins that work in association with cyclins.

Answer 24

cyclins
a family of proteins that combine with cyclin-dependent kinases and thereby determine the substrate specificity of the kinases. By directing kinases to specific substrates, the cyclins help regulate passage of the cell through the cell cycle. Concentrations of the various cyclins rise and fall throughout the cell cycle.

Question 25

Hormones are ______.

Answer 25

extracellular signals

Question 26

Signal transducers are ______.

Answer 26

proteins inside the cell that relay information received by a growth factor receptor

Question 27

Cell proliferation and division is influenced by signaling molecules called growth factors. A growth factor that stimulates cell proliferation is also called a(n

Answer 27

mitogen | a growth factor that stimulates cell proliferation.

Question 28

Checking for DNA damage before S phase and checking for spindle attachment before anaphase are jobs carried out by cell cycle ______.

Answer 28

checkpoints mechanisms that prevent cells from continuing to the next phase of the cell cycle until a previous step has been completed successfully, thus safeguarding genomic integrity.

Question 29

DNA is replicated during the _____.

Answer 29

S phase of the cell cycle

Question 30

The role of the G1-to-S checkpoint is to ______.

Answer 30

prevent the replication of damaged DNA

Question 31

describe CDK proteins (3 things)

Answer 31

Phosphorylate other proteins Bind cyclins Major cell cycle regulators

Question 32

What role do CDK-cyclin complexes play in the G1-to-S transition?

Answer 32

They phosphorylate Rb, releasing E2F to allow transcription of synthesis genes.

Question 33

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

Answer 33

checkpoints

Question 34

In what way(s) has the budding yeast S. cerevisiae been useful for studying cell division?

Answer 34

Temperature-sensitive mutations allow study of critical genes. Bud size reveals the stage of the cell cycle. They are both haploid and diploid.

Question 35

What cell factor would most likely cause stalling at the G1-to-S checkpoint?

Answer 35

Damaged DNA

Question 36

The tumor-suppressor gene p53 has a significant role in _____.

Answer 36

responding to DNA damage in a cell

Question 37

The major cell cycle regulators are kinases called [] proteins that work in association with cyclins.

Answer 37

cyclin dependent kinase

Question 38

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?

Answer 38

By stimulating the expression of the p21 gene

Question 39

Homogeneously staining regions and double minutes are indicative of gene []

Answer 39

amplification

Question 40

homogeneously stained region (HSR)

Answer 40

a region of a chromosome that contains many tandem repeats of a gene due to gene amplification and is visible under a microscope as an enlarged area.

Question 41

two processes activated by p53 when DNA damage is detected during the G1 phase

Answer 41

It turns on expression of DNA repair genes. It turns on transcription of p21, a CDK inhibitor.

Question 42

A mutant allele that acts in a dominant fashion to promote cancer is called a(n) _____.

Answer 42

oncogene

Question 43

Tumor-causing viruses are often ______.

Answer 43

retroviruses

Question 44

If a cell has experienced DNA damage that cannot be properly repaired, the p53 protein turns on the expression of genes whose protein products initiate programmed cell [] also known as []

Answer 44

death; apoptosis

Question 45

double minutes

Answer 45

small chromosome-like bodies lacking centromeres and telomeres produced by gene amplification.

Question 46

An oncogene is a dominant mutant allele _____.

Answer 46

that promotes cancer

Question 47

Creation of a new transcription factor through the fusion of chromosomal segments from two different chromosomes describes how a proto-oncogene can become an oncogene due to a []

Answer 47

chromosomal translocation.

Question 48

mechanisms that explain the conversion of a proto-oncogene to an oncogene via an RNA tumor virus

Answer 48

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.

Question 49

A mutant allele that acts in a dominant fashion to promote cancer is called a(n) _____.

Answer 49

oncogene

Question 50

how a proto-oncogene can become an oncogene due to a chromosomal translocation

Answer 50

Creation of a new transcription factor through the fusion of chromosomal segments from two different chromosomes

Question 51

A cancer-causing change occurs when a tumor-suppressor gene is ______.

Answer 51

inactivated

Question 52

Most individuals who are born with an inherited form of cancer susceptibility are ______ for a defect in a ______.

Answer 52

heterozygous; tumor-suppressor gene

Question 53

Cancer can result from inactivation of which type of gene?

Answer 53

Tumor-suppressor gene

Question 54

Loss of heterozygosity is ______.

Answer 54

loss of function of a normal allele when the other allele was already inactivated

Question 55

Tumor-suppressor genes normally act to ______.

Answer 55

maintain genome integrity negatively regulate cell division

Question 56

The loss of function of a normal allele when the other allele for that gene was already inactivated is called ______.

Answer 56

loss of heterozygosity

Question 57

For the inherited tendency to develop retinoblastoma, which correctly describes inactivation of the RB tumor-suppressor alleles by the "two-hit" model?

Answer 57

One allele is inactivated prior to birth, the other becomes inactivated early in life.

Question 58

In which two ways have tumor-suppressor genes been shown to act within cells?

Answer 58

Regulating the rate of cell division and maintaining genomic integrity

Question 59

Normal, wild-type tumor-suppressor genes perform which the following functions

Answer 59

DNA repair Cell cycle checkpoints Inhibitor of the cell cycle

Question 60

Tumor-suppressor genes normally act to ______.

Answer 60

negatively regulate cell division maintain genome integrity