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Applied Biochemistry > Genetics of Cancer: Oncogenes and Tumor Suppressors > Flashcards

Genetics of Cancer: Oncogenes and Tumor Suppressors Flashcards

1
Q

types of genetic diseases (4)

A

chromosome disorders
single gene disorders
multifactorial or complex
sex linked and mitochondrial

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2
Q

chromosome disorders (4)

A

rearrangements/translocations
deletions
insertions
duplications

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3
Q

single gene disorders (3)

A

dominant
recessive
codominant

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4
Q

multifactorial or complex (2)

A

multiple genes

gene environment

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5
Q

Chronic Myelogenous Leukemia (CML)

A

Bone marrow produces excessive amounts of abnormal granulocytes at the expense of the other healthy white blood cells

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6
Q

The Philadelphia chromosome, creates a fusion of the (2) genes

A

BCR and ABL

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7
Q

BCR

A

break point cluster region

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8
Q

BCR + ABL =

A

oncogene

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9
Q

what lineages can the blood stem cell differentiate into?

A

myeloid

lymphoid

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10
Q

is a single mutation enough to cause cancer?

A

no

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11
Q

while cancer predisposing mutations can be (and often are) —, cancer or tumor formation is a — — involving other mutations and environmental factors

A

inherited

somatic event

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12
Q

most inherited mutations associated with cancer affect a persons

A

risk for developing cancer

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13
Q

can caner be inherited?

A

no, it is somatic. it can increase your risk of developing cancer, but that doesn’t mean you will get it because it takes multiple things to accumulate

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14
Q

tumor growth and progression generally involves

A

multiple, successive rounds of genetic changes with the end results of natural selection of a clonal cel that produces a tumor or cancer

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15
Q

rumors can arise from (2)

A

increased cel division

decreased apoptosis

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16
Q

normal cell division and normal apoptosis leads to

A

homeostasis

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17
Q

increase cell division and normal apoptosis leads to

A

tumor

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18
Q

normal cell division and decreased apoptosis leads to

A

tumor

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19
Q

tumors can arise from (2) changes

A

genetic

epigenetic

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20
Q

penetrance

A

how many people that inherit a genetic change experience the phenotype

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21
Q

we carry different variants of genes, with different

A

penetrance

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22
Q

higher relative risk associated with rare, high-penetrance genetic variants, such as mutations in the — genes associated with hereditary breast and ovarian cancer and the mismatch repair genes associated with Lynch syndrome

A

BRCA1/ BRCA2

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23
Q

how are malignant tumors classified

A

according to the tissue or cell type from which they originated

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24
Q

carcinomas

A

cancers arising from epithelial cells

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25
Q

sarcomas

A

arise from connective tissue or muscle cells

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26
Q

leukemias

A

derive from WBC and their precursors (hematopoietic cells)

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27
Q

gliomas

A

derive from glial cells of the CNS

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28
Q

benign tumors are

A

likewise classified

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29
Q

adenomas

A

benign epithelial tumors with glandular organization

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30
Q

chondromas

A

arise from cartilage

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31
Q

benign tumor

A

tumor contained within tissue they originated in

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32
Q

malignant tumor

A

tumor moves out of tissue it originated in to invade/metastasize

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33
Q

risk factors for cancer (5)

A

occupational exposure
tobacco related
diet (low in vegetables, high salt, high nitrate)
diet (high fat, low fiber, fried and broiled foods
tobacco and alcohol

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34
Q

top 2 % of total cases

A 
tobacco related (24)
diet (high fat, low fiber, fried and broiled foods) (37)
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35
Q

many cancers are maintained by a population of

A

cancer stem cells

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36
Q

cancer stem cells generally divide

A

more slowly

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37
Q

cancer stem cells may survive

A

radiate and or chemotherapy as these treatments generally target more rapidly dividing cells

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38
Q

tumors secrete — signals

A

angiogenic

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39
Q

tumor angiogenic signals promote the formation of new

A

blood vessels need to supply the nutrient needs of the growing tumor

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40
Q

these new blood vessels also provide a means by which — can colonize distant sites

A

metastasis

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41
Q

cancer cells are more — — than normal cells

A

self sufficient

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42
Q

cancer cells are relatively insensitive to

A

anti-proliferative extracellular signals

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43
Q

cancer cells are less prone to undergo

A

apoptosis

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44
Q

cancer cells are defective in the control mechanisms that normally

A

halt cell division

45
Q

cancer cells induce help from normal — cells in their microenvironment

A

stromal

46
Q

cancer cells induce

A

angiogenesis

47
Q

cancer cells can survive and proliferate in

A

foreign sites

48
Q

cancer cells are genetically

A

unstable

49
Q

cancer cells produce — or acquire another means of …

A

telomerase

stabilizing their telomeres

50
Q

classification of cancer genes (3)

A

genes that normally inhibit cellular proliferation
genes that activate proliferation
genes that participate in DNA repair

51
Q

Oncogenes

A

mutated forms of certain normal genes of the cell called proto-oncogenes

52
Q

Proto-oncogenes are often genes that normally control

A

what kind of cell it is and how often it grows and divides

53
Q

When a proto-oncogene mutates (changes) into an oncogene, it

A

turns on or activates when it is not supposed to be

54
Q

When this occurs, the cell can grow out of control, leading to —

A

cancer

55
Q

Tumor suppressor genes are normal genes that (3)

A

slow down cell division
repair DNA mistakes
tell cells when to die (apoptosis or programmed cell death)

56
Q

When tumor suppressor genes don’t work properly, cells can grow out of control, which can lead to —

A

cancer

57
Q

An important difference between oncogenes and tumor suppressor genes is that oncogenes result from the — of proto-oncogenes, but tumor suppressor genes cause cancer when they
are —

A

activation (turning on)

inactivated (turned off)

58
Q

RB1

A

Rb protein binds to E2F to brake cell cycle

59
Q

p16

A

CDK inhibitor

60
Q

p53

A

inhibits cell cycle arrest or apoptosis

61
Q

APC

A

intracellular component of degradation complex of beta-catenin signaling pathway

62
Q

BRCA1 interacts with — repair protein

A

RAD51

63
Q

BRCA2 interacts with — repair protein

A

RAD51

64
Q

what did Alfred Knutson invent

A

2 hit hypothesis of Rb

65
Q

Knudson’s original hypothesis was that

A

a person needed to acquire two mutant copies of the Rb gene

66
Q

This could be accomplished by a (2)

A

germline mutations inherited from one parent (carrier) and then a somatic second mutation/event in the normal allele

67
Q

The Rb protein is a “universal” cell cycle —

A

regulator

68
Q

Normal Rb protein functions as a

A

brake on cell cycle progression

69
Q

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

A

dominant

recessive

70
Q

other considerations (4)

A

type
hormone receptor status
ki-67 proliferation index
her2/neu status

71
Q

The somewhat paradoxical contradiction can be explained by realizing that

A

only a single tumor cell is required to produce a tumor, and in any individual who has inherited a mutant Rb allele it takes only a second hit in one cell to create a tumor

72
Q

Thus it is the strong predisposition to develop a tumor that is inherited as a — trait

A

dominant

73
Q

The Rb mutation also displays reduced —, only about –% of individuals who inherit the mutant allele experience a second hit and develop a tumor

A

penetrance

90

74
Q

The p16 protein (product of the INK4 gene) is produced when cells are — and is an
important component of the cell cycle — that should normally occur

A

stressed

arrest

75
Q

Mutations that inactivate the function of p16 or mutations in regulatory regions of the p16 gene that
— — can also contribute to cancer

A

shutdown expression

76
Q

one of the most common mutations in cancer

A

p53

77
Q

what can lead to activation of p53 (4)

A

hyper proliferative signals
DNA damage
telomere shortening
hypoxia

78
Q

types of breast cancer (2)

A

invasive

noninvasive

79
Q

noninvasive (2)

A
  • ductal carcinoma in situ (25% of all B.C)

* lobular carcinoma in situ

80
Q

invasive (3)

A

Usually epithelial
• Ductal (65-85% of Invasive)
• Lobular (5-10% of invasive)
• Other (10% of invasive)

81
Q

hormone receptor status (2)

A
  • ER + or –

* PR + or –

82
Q

-

A

wont respond

83
Q

+

A

drugs to treat tumors are more effective

84
Q

increased risk genes of breast cancer (3)

A

BRCA1 (breast cancer 1, early onset)
BRCA2 (breast cancer 2, early onset)
TP53 (p53)

85
Q

BRCA1/2 pedigree

A

autosomal dominant syndrome

86
Q

APC mutations give rise to

A

colon cancer

release of beta Catelin from degradation complex, goes to the nucleus, cell growth stimulation

87
Q

high % of colon cancers have mutations in (2)

A

APC

p53

88
Q

Unlike the genomes of all eukaryotic and prokaryotic cells, virus genomes can be found
either in the form of (2)

A

DNA or RNA

89
Q

Virus genomes can be (2)

A

single-stranded or double-stranded

linear or circular

90
Q

~15% of human cancers world-wide are thought to arise from mechanisms that
involve (3)

A

viruses, bacteria or parasites

91
Q

two types of viruses

A 
RNA viruses (RNA genome, retrovirus)
DNA viruses (DNA genome)
92
Q

first viral oncogene identified

A

from the avian rout sarcoma virus (RSV)

93
Q

oncogene=

A

cancer genes

94
Q

most oncogenes have normal cellular homologs called

A

porto-oncogenes

95
Q

protconcogenes function as

A

regulators of cell growth

96
Q

protooncogenes include (4)

A

growth factors
growth factor receptors
signal transduction molecules
transcription factors

97
Q

DNA virus examples (4)

A

HPV
hep B
hep C
herpesvirus family (Epstein Barr virus)

98
Q

RNA virus examples (2)

A

human T cell leukemia virus type 1

human immunodeficiency virus

99
Q

HIV infects (3)

A

CD+ T-cells, macrophages and microglial cells

100
Q

Virus particle consists of 2 identical copies of the

A

HIV positive single-

stranded RNA genome

101
Q

The RNA genome is bound to several proteins including key enzymes such as — —, which is needed to create a DNA copy of the HIV genome. Others include (3)

A

reverse transcriptase

proteases, ribonucleases and integrase

102
Q

The HIV genome consists of – structural landmarks (regions) and
generally – genes that encode – proteins

A

7
9 (sometimes 10)
19

103
Q

Upon entry into the cell, the reverse transcriptase copies the RNA genome into a — and eventually into a — that enters the nucleus and integrates into the host cell genome

A

ss-cDNA

ds-cDNA

104
Q

Because reverse transcriptase has a high error rate this results in a

A

high frequency of mutations in the cDNA copies

105
Q

influenza virus

A

8 segments of negative single-stranded RNA that exist in a complex
with various nucleoproteins.

106
Q

The 8 RNA strands code for – proteins

A

11

107
Q

The negative sense RNA is transcribed into a positive sense RNA (cRNA), which serves as a template for (2)

A

protein synthesis and for negative strands that are incorporated into new viral particles

108
Q

Influenza virus does not use a DNA copy and as RNA is much less stable than DNA and as such — at a faster rate than any other kind of virus

A

mutates

Applied Biochemistry (52 decks)

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