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Biochemistry > Genetics of Cancer Oncogenes and Tumor Suppressors > Flashcards

Genetics of Cancer Oncogenes and Tumor Suppressors Flashcards

1
Q

A ____ mutation enable proto-oncogenes to become oncogenes.

A

gain-of-function

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2
Q

When ___ or ___ don’t work properly, they can allow cells to grow out of control and cause cancer.

A

proto-oncogenes; tumor suppressor genes

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3
Q

The transcription of RNA to DNA is done through the enzyme ____.

A

reverse transcriptase

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4
Q

What is one of the main pathways that gives rise to colon cancer?

A

Wnt/B-catenin signaling pathway

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5
Q

Tobacco use can lead to what types of cancers?

A

mouth
lung
kidney
bladder

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6
Q

What happens if there is a gene amplification mutation in a proto-oncogene?

A

a normal protein may be greatly overproduced

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7
Q

When cells are stressed, what do they not want to do?

A

divide

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8
Q

What type of cancers arise from epithelial cells?

A

carcinomas

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9
Q

____ are normal genes that slow down cell division, repair DNA mistakes, and tell cells when to die.

A

Tumor suppressor genes

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10
Q

The ___ protein is produced when cells are stressed.

A

p16

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11
Q

When do tumors become malignant?

A

once they escape their site of origin

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12
Q

What happens if there is a regulatory mutation of a proto-oncogene?

A

a normal protein may be greatly overproduced

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13
Q

What was the first viral oncogene discovered and identified?

A

Rous Sarcoma Virus (RSV)

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14
Q

What happens if there are reduced levels of Rb in the cell?

A

there won’t be enough Rb protein to control the actions of E2F, but p16 will be at normal levels in a stressed cell, inhibiting cyclin-CDK as it should, but because the Rb brake isn’t there, the cell will divide in a stressed environment

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15
Q

The chromosomal translocation associated with Chronic Myelogenous Leukemia (CML) is known as the ____.

A

Philadelphia chromosome

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16
Q

The oncogenic mutation from valine to ____ on the Her2 receptor causes dimerization and formation of a ligand-independent receptor oncoprotein.

A

glutamine

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17
Q

The control mechanisms of cancer cells are ____, in that they are unable to halt or control cell division.

A

defective

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18
Q

DNA tumor viruses tend to target the ____.

A

tumor suppressor genes

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19
Q

What happens to B-catenin when the Wnt ligand is not bound to the receptor?

A

B-catenin is sequestered and phosphorylated inside the cell and DEGRADED by the proteasome

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20
Q

How is the paradoxical contraindication of Rb explained?

A

only one single tumor cell is required to produce a tumor, so any individual who has inherited a mutant Rb allele takes only one more “hit” to create a tumor

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21
Q

Are Apc, p53, TGFB receptor II, Smad4, and MLH1 oncogenes or tumor suppressors?

A

tumor suppressors

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22
Q

Are cancer cells less prone to undergo apoptosis?

A

YES

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23
Q

What happens to B-catenin when the Wnt ligand is bound to the receptor?

A

GSK-3B is phosphorylated and inactivated, allowing B-catenin to build up in the cytoplasm and translocate to the nucleus

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24
Q

____ are benign cancers that arise from cartilage.

A

Chondromas

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25
Q

What happens if there is a deletion or point mutation in the coding sequence of a proto-oncogene?

A

a hyperactive protein may be made in normal amounts

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26
Q

What type of benign tumor is from epithelial cells and have a glandular organization?

A

adenomas

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27
Q

The ____ creates a fusion gene of the BCR and ABL genes.

A

Philadelphia chromosome

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28
Q

Ligand-independent cell division gives rise to ___.

A

tumors

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29
Q

The myeloid stem cell lineage gives rise to what types of blood cells?

A

red blood cells
platelets
myeloblasts
granulocytes (N, E, B)

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30
Q

How is breast cancer classified?

A
  • Primary Tumor (TX - T4)
  • Lymph Node Status (NX - N3)
  • Metastases (MX - M1)
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31
Q

____ tumors develop invasiveness.

A

Malignant

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32
Q

When cells are stressed they don’t want to divide. Which protein is produced?

A

p16

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33
Q

The Rb mutation displays a ___ penetrance.

A

reduced

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34
Q

What keeps cells from dividing and expressing S-phase genes when stressed?

A

p16 inactivates the cyclin-CDK kinase which in turn prevents active Rb surrounding E2F from being phosphorylated and deactivated, thereby preventing E2F from being released and activated to allow DNA synthesis

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35
Q

Is a high-grade intraepithelial neoplasia considered benign or malignant?

A

benign - hasn’t progressed into connective tissue yet

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36
Q

Influenza is a ____ virus. Why does this cause us to create a new flu vaccine each year?

A

RNA; due to reverse transcriptase, the flu mutates very quickly

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37
Q

One mutant Rb allele is considered ____ at the level of the individual, but ____ at the level of the cell.

A

dominant; recessive

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38
Q

Breast cancer is an ____ syndrome.

A

autosomal dominant

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39
Q

Cancer stem cells generally divide more ____ and may survive radiation and chemotherapy.

A

slowly

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40
Q

What cells normally control what kind of cell it is and how often it grows and divides?

A

proto-oncogenes

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41
Q

____ is tightly packed DNA; ____ is DNA that has been unwound.

A

Heterochromatin; euchromatin

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42
Q

Estrogen receptors, Her2 receptors, and EGF receptors are all involved in ___.

A

breast cancer

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43
Q

What is cancer maintained by?

A

a population of cancer stem cells

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44
Q

Active ___ protein provides a safety brake on cell proliferation.

A

p53

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45
Q

What type of growth factor do cancer cells secrete a lot of? Why is this significant?

A

VEGF; VEGF is very important in angiogenesis

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46
Q

What cells do we extract DNA from if we are using blood?

A

white blood cells

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47
Q

The ligand-____ dimerization of the receptor, therefore activating the intracellular signaling WITHOUT the ligand present.

A

independent

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48
Q

How might a normal Rb gene be eliminated?

A
  • nondisjunction causes chromosome loss
  • chromosome loss, then duplication
  • mitotic recombination
  • gene conversion
  • deletion
  • point mutation
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49
Q

ABL is a ___ that becomes activated and leads to CML.

A

proto-oncogene

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50
Q

Why can’t we extract DNA from red blood cells?

A

red blood cells don’t have a nucleus

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51
Q

___ changes are changes in the DNA sequence, such as a nucleotide change.

A

Genetic

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52
Q

What type of tumor remains contained in the tissue from which they originated?

A

benign tumors/growths

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53
Q

Viral protein ___ can expose E2F and allow cell proliferation.

A

E7

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54
Q

Can you still develop a tumor if normal cell death is taking place?

A

YES - if there is increased cell division with normal apoptosis

55
Q

Why are there often cancer relapses or long, complicated therapies?

A

because radiation and chemotherapy target rapidly dividing cells and not the slowly-dividing cancer stem cells

56
Q

___ protein binds to E2F to brake the cell cycle.

A

Rb

57
Q

What type of cancer arises from the glial cells of the CNS?

A

gliomas

58
Q

Blood stem cells give rise to the ___ and ___ stem cell lineages.

A

myeloid; lymphoid

59
Q

A diet high in fat, low in fiber, and containing fried and broiled foods is associated with what kinds of cancer?

A

bowel
pancreas
prostate
breast

60
Q

It is the strong ____ to develop a tumor that is inherited as a dominant trait.

A

predisposition

61
Q

Is cancer inherited?

A

NO - but cancer-predisposing mutations can be

62
Q

Most inherited mutations associated with cancer affect a person’s ___.

A

risk for developing cancer

63
Q

____ induce help from normal stromal cells in their microenvironment.

A

Cancer cells

64
Q

What happens if there is a chromosomal rearrangement in a proto-oncogene?

A

a normal protein may be overproduced or fusion to a transcribed gene produces a hyperactive fusion protein

65
Q

___ are derived from lymphatic tissue.

A

Lymphomas

66
Q

____ are derived from white blood cells and their precursors (hematopoietic cells).

A

Leukemias

67
Q

When p16 is bound to CDK, can the cyclin bind?

A

NO

68
Q

___, when stable and active, is involved in cell cycle arrest, senescence, and apoptosis.

A

p53

69
Q

Is a single mutation enough to cause cancer?

A

NO

70
Q

What happens to a cell when p16 is not present or has been mutated and inactivated?

A

the cyclin-CDK complex will form and phosphorylate the Rb protein, which will allow E2F to express S-phase genes

71
Q

What happens if there is a mutation in any of the B-catenin degradation complex components?

A

there is unopposed, un-ligand activated B-catenin signaling, which can lead to cancer

72
Q

Tobacco use and alcohol use are associated with ___ and ___ cancer.

A

mouth; throat

73
Q

What happens when there are mutations to the p16 gene?

A

cell cycle arrest does not occur normally; the function of p16 and its regulatory regions do not function normally and can lead to cancer

74
Q

Are K-ras and B-catenin oncogenes or tumor suppressors?

A

oncogenes

75
Q

What are some other considerations when assessing breast cancer?

A

if it is noninvasive or invasive and hormone receptor status

76
Q

How can a proto-oncogene become activated?

A
  • deletion or point mutation
  • regulatory mutation
  • gene amplification
  • chromosome rearrangment
77
Q

Skin tags and moles are examples of ____.

A

benign growths

78
Q

What type of cancer cells do radiation and chemotherapy typically target?

A

rapidly dividing cells

79
Q

Normally, _____ receptor proteins are monomers, single path transmembrane-spanning proteins that have a binding receptor on the extracellular side that bind one ligand.

A

proto-oncogene

80
Q

If p53 is knocked out, what would happen to the cell?

A

none of the signals that would normally induce cell death would be detected, so the damaged cells would continue to proliferate

81
Q

In this type of cancer, bone marrow produces excessive amounts of abnormal granulocytes at the expense of other healthy white blood cells.

A

Chronic Myelogenous Leukemia (CML)

82
Q

___ have a high penetrance and contain a high risk of cancer.

A

Rare variants

83
Q

DNA being inappropriately packaged into heterochromatin rather than euchromatin is an example of a ____ change.

A

epigenetic

84
Q

RNA tumor viruses tend to target the ____.

A

oncogenes

85
Q

With Wnt signal, what happens to the Wnt-responsive genes?

A

they are transcribed or “turned on”

86
Q

Cancer or tumor formation is often a ____ event involving other mutations and environmental factors.

A

somatic

87
Q

The Hepatitis viruses can promote the development of ___ cancer.

A

liver

88
Q

A ___ mutation functionally eliminate the tumor suppressor genes to stimulate cell survival and proliferation.

A

loss-of-function

89
Q

Can cancer cells survive and proliferate in foreign sites?

A

YES

90
Q

___ induces cell cycle arrest or apoptosis.

A

p53

91
Q

What gene is the intracellular component of the degradation complex of the B-catenin signaling pathway?

A

APC

92
Q

At what level is control lost in the cell when the Her2 or EGF receptors dimerize and allow activation without the ligand actually present?

A

at the receptor level

93
Q

If p16 is bound to CDK and cyclin cannot bind, what protein is not able to be activated?

A

inactive E2F

94
Q

The ___ receptor can lose its extracellular domain, dimerize and its intracellular domains can activate signaling.

A

EGF

95
Q

___ infects CD+ T-cells, macrophages, and microglial cells.

A

HIV

96
Q

The ___ protein is a universal cell cycle regulator.

A

Rb

97
Q

What are some things that can cause gene inactivation?

A
  • accidental nucleotide change
  • euchromatin into heterochromatin
  • methylation of nucleotides
98
Q

A diet low in vegetables, high in salt, and high in nitrate can lead to what kinds of cancers?

A

stomach

esophagus

99
Q

___ is a CDK inhibitor.

A

p16

100
Q

What signals can be detected by p53 that would lead to cell cycle arrest or apoptosis?

A
  • hyperproliferative signals
  • DNA damage
  • telomere shortening
  • hypoxia
101
Q

What are the 3 ways cancer genes are classified?

A

1) genes that normally inhibit cellular proliferation
2) genes that activate proliferation
3) genes that participate in DNA repair

102
Q

Do cancer cells stabilize their telomeres? How so?

A

YES - they produce telomerase or acquire other means to stabilize their telomeres

103
Q

How do cancer cells induce help in their microenvironment?

A

by secreting hormones and factors via autocrine and paracrine fashion to induce the desired effects

104
Q

Oncogenes occur as a result of ____; tumor suppressor genes that cause cancer occur as a result of ____.

A

activation; inactivation

105
Q

Viral protein ___ can inactivate p53 and remove the “brake” on cell proliferation.

A

E6

106
Q

Most oncogenes have normal cellular homologs called ___ that function as cell growth regulators.

A

proto-oncogenes

107
Q

What cells are in the white blood cell population?

A 
Neutrophils
Eosinophils
Basophils
B lymphocytes
T lymphocytes
Natural killer cells
108
Q

Are cancer cell genetically stable?

A

NO - they are unstable

109
Q

Can children inherit changes that occur in somatic cells?

A

NO

110
Q

Do cancer cells induce angiogenesis?

A

YES

111
Q

Most tumors seem to go through the ___ pathway.

A

p53

112
Q

Tumors secrete angiogenic signals which promote the formation of new ____.

A

blood vessels

113
Q

What type of cancers arise from connective tissue or muscle cells?

A

sarcomas

114
Q

Without Wnt signal, the Wnt-responsive genes are ___.

A

off

115
Q

____ are more self-sufficient than normal cells.

A

Cancer cells

116
Q

New blood vessels prompted by cancerous cells do 2 things. What are they?

A
  • supply the tumor with more nutrients

- provide a means of metastasis which can colonize distant sites

117
Q

Rb protein binds the cell proliferation factor ___.

A

E2F

118
Q

How many polymorphisms do we have in our genome? Are they dangerous?

A

thousands; NO

119
Q

What molecule gives rise to colon cancers?

A

APC

120
Q

Cancer cells are relatively ____ to anti-proliferative extracellular signals.

A

insensitive

121
Q

HIV’s RNA genome is bound to key enzymes, such as ____.

A

reverse transcriptase
protease
ribonuclease
integrase

122
Q

____ are the mutated form of certain normal genes of the cell called proto-oncogenes.

A

Oncogenes

123
Q

What happens when a proto-oncogene mutates?

A

it turns into an oncogene that activates when it shouldn’t and can allow proliferative growth and cancer

124
Q

How are malignant tumors classified?

A

according to the tissue or cell type from which they originated

125
Q

Can viruses have a DNA or RNA genome?

A

EITHER

126
Q

___ growth and progression generally involves multiple, successive rounds of genetic changes, ending with clonal selection of a cell that produces cancer.

A

Tumor

127
Q

What cells does the lymphoid stem cell lineage give rise to?

A

B lymphocytes
T lymphocytes
Natural killer cells

128
Q

What causes a malignant tumor from a viral DNA fragment?

A

when it accidentally gets incorporated into the host genome (and not just within the cell)

129
Q

What type of cell can lead to the cancerous stem cell population?

A

normal stem cells that become afflicted

130
Q

___ changes are alterations outside the genetic sequence, such as issues with regulation.

A

Epigenetic

131
Q

What does activated E2F allow for?

A

progression into the S phase

132
Q

What are the two mechanisms in which tumors arise?

A
  • increased cell division with normal apoptosis

- normal cell division with decreased apoptosis

133
Q

____ have a low penetrance and have a low risk of developing cancer.

A

Common variants

Biochemistry (17 decks)

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