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Genetics Test 5 > 37 Cancer genetics > Flashcards

37 Cancer genetics Flashcards

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1
Q

Cancer cells have…

A
  1. uncontrolled cell division
  2. an alteration of the cell cycle leading to tumor development
  3. the ability to metastasize
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2
Q

What are the three cell regulation checkpoints

A
  • g1/S
  • g2/M
  • M
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3
Q

G1/S checkpoint

A

the cell is monitored for proper cell size and undamaged DNA

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4
Q

G2/M checkpoint

A

the cell cycle is paused if needed until the replication and DNA repair are complete

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5
Q

M checkpoint

A

the cell is monitored for proper spindle formation and attachment

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6
Q

what protein classes work at the cell regulation checkpoints

A

protein kinases

cyclins

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7
Q

protein kinases

A

phosphorylate proteins allowing changes in their activity

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8
Q

cyclins

A

structural proteins that interact to guide the progression through the cell cycle

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9
Q

cdc mutations

A

mutations that can result in errors in the cell division cycle

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10
Q

cancer

A

a mass of tissue or cells with an unlimited potential to divide and serve no useful purpose in the body

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11
Q

What are the major characteristics of cancer

A

hyperplasia
anaplasia
metastasis

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12
Q

hyperpolasia

A

uncontrolled cell division with cells that are immortal and invasive

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13
Q

loss of bottom shelf boundary

A

cancer cells with hyperplasia grow and sack on top of other cells and will downward into other tissues

allows them to invade body systems and kill good cells by robbing healthy tissue of nutrients

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14
Q

anaplasia

A

the structure and function of the cancer cells is undifferentiated compared to normal cells within the same tissue

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15
Q

metastasis

A

the ability to move to and establish tumors at other sites in the body

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16
Q

tumor

A

distinct mass of abnormal cells that do not have normal controls on cell division

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17
Q

benign

A

abnormal cells remain localized and do not invade surrounding tissue

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18
Q

malignant

A

cancer cells invade surrounding tissue

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19
Q

metastatic tumors

A

occur when cancer cells spread and establish secondary tumors in other sites in the body

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20
Q

genetic causes of cancer

A
  • single gene
  • polygenic
  • chromosome aberration
  • mutations in somatic cell or in gamete producing cell
  • viruses
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21
Q

environmental agents of cancer

A

carcinogens cause…
mutations
alteration in gene expression

ex. asbestos, lead, x-rays, UV light, tobacco chemicals

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22
Q

what does it mean that cancer is a multi-hit disease

A

several things go wrong over time and eventually a cancerous condition occurs

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23
Q

How is cancer a multi-hit disease

A
  • most are sporadic and influenced by environment

- they develop over time

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24
Q

example of how cancers are sporadic and influenced by the environment

A
  • siblings are rarely affected by the same cancer

- populations that migrate to new regions tend to get cancer rates typical of that region

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25
Q

example of how cancers develop over time

A

incidence rises with age

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26
Q

High incidence of cancer correlate with…

A

tissues that undergo more cell divisions as many mutations are due to errors in replication

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27
Q

tumor suppressor genes

A

prevent bad cells from dividing

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28
Q

proto-oncogenes

A

allow good cells to divide

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29
Q

loss of function in…

A

tumor suppressor gene

can no longer prevent bad cells form dividing leading to a tumor

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30
Q

gain of function in…

A

proto-oncogene

converts to an oncogene that is always on leading to inappropriate cell division and tumor development

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31
Q

oncogene

A

mutated proto-oncogene

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32
Q

compared to breaks of car

A

tumor suppressor gene

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33
Q

compared to gas of care

A

oncogenes

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34
Q

loss of function

A

complete or partial absence of protein function

recessive-acting mutation - needs mutation in both copies of gene to knock out protein function

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35
Q

gain of function

A

cell produces protein that is not normally present - either new gene product or gene product at new location or inappropriate time

normally dominant-acting mutation

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36
Q

example of gain of function mutation

A

mutation in gene that encodes a receptor for a growth factor might cause mutated receptor to stimulate growth in the absence of the growth factor leading to growth at the wrong time or place

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37
Q

about ___% of cancer causing genes are…

A

tumor suppressor genes

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38
Q

describe recessive nature of tumor suppressor gene

A

the normal alleles produce factors that inhibit division

if both alleles are mutant, the bad cells are not prevented form dividing

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39
Q

APC

A

tumor suppressor gene involved in colorectal cancer

40
Q

BRCA1

A

tumor suppressor genes

important in some breast and ovarian cancers

41
Q

P53

A

tumor suppressor gene

involved in many types of cancer

42
Q

RB

A

tumor suppressor gene
implicated in various cancers
was first correlated with retinoblastoma

43
Q

list some tumor suppressor gene

A

APC
BRCA1
P53
RB

44
Q

Knudson’s two hit hypothesis

A

hypothesis for the action of tumor suppressor gene based on studies of the RB gene

proposes that both copies need to be defective in the same cell to allow the tumor to develop

45
Q

RB protein

A

responsible for regulation at the G1/S checkpoint and regulates the action of a transcription factor

46
Q

Knudson’s two hit hypothesis and sporadic cancers

A

two mutations must occur in the same cell to lead to tumor formations

47
Q

Knudson’s two hit hypothesis and familial cancers

A

start with one mutated copy, only need one more mutation in same cell to lead to tumor formation

48
Q

BRCA1 and BRCA2 action

A

used to repair double strand breaks

when not functioning, broken DNA does not get repaired leading to mutations - these then divide and cause tumors

49
Q

P53

A

a tumor suppressor gene located on chromosome 17

functions at G1 checkpoint

50
Q

mutations of P53 can be found in…

A
  • colon, lung, breast, brain cancer

- found in altered form in 50% of human tumors

51
Q

fork in the road

A

action of p53 determines whether a damage cell is paused until repairs can be made or whether the damaged cell is too badly damaged to repair leading to apoptosis

52
Q

if p53 isn’t working properly…

A

cell division occurs even though the DNA is damaged and the cell division occurs in an unregulated manner

53
Q

p53 response to small DNA damage

A

p53 is activated, it is a DNA binding protein and can stimulate transcription of p21 which stops the cell cycle

54
Q

p53 response to lots of DNA damage

A

pt53 stimulations transcription of bcl2 which leads to apoptosis

55
Q

haploinsufficiency

A

a high susceptibility to cancer occurs when only one copy of the normal allele is present

a diploid organism has loss of function of one copy leaving only one functional copy which does not produce enough of the gene product to exhibit the wild-type phenotype

individuals can still be affected even if the have one normal allele

56
Q

example of haploinsufficiency

A

bloom syndrome

57
Q

bloom syndrome

A
  • due to defective DNA helicase important in repairing ds DNA breaks
  • individuals homozygous for mutated BLM have high rate of cancer
  • heterozygous have elevated risk of colon cancer
58
Q

How is bloom syndrome an example of haploinsuffiency

A

the heterozygote may never develop a mutation in the other copy. However, just the one copy leads not some nonfunctional helicase, leading to increased mutations

59
Q

example of oncogene

A

myc

60
Q

Burkitt’s lymphoma

A

abnormal B cell function

61
Q

c-myc

A

ongogene

normally present near end of chromosome #8
normally an antibody producing gene is near chromosome #14
translocation between the two places c-myc near enhancer for the antibody producing gene, leading to high function of c-myc gene resulting in tumors and Burkitt’s lymphoma

62
Q

Burkitt’s lymphoma is due to a ___ that puts an ___ next to ___

A

reciprocal translocation
enhancer
c-myc oncogene

63
Q

chronic myelogenous leukemia

A

fatal, uncontrolled replication of myeloid stem cells

results form reciprocal transloation of c-ABL gene and BCR gene

64
Q

Philadelphia chromosome

A

translocated cABL and BCR gene leading to CML

65
Q

CML involves chromosomes…

A

9 and 22

66
Q

Burkitt’s lymphoma involve chromosomes…

A

8 and 14

67
Q

the Philadelphia chromosome produces…

A

a fusion protein that affects cell cycle control leading to cancer associated with WBCs

68
Q

retroviruses

A

can cause cancer

they have RNA which they can convert into DNA which then integrates into host cell’s DNA

69
Q

HPV is associated with

A

cervical
penile
vulvar cancers

70
Q

Retroviruses can cause cancer by…

A
  • mutating and rearranging proto-oncogenes

- inserting strong promoter near proto-oncogenes

71
Q

strong promoters…

A

often in viruses

cause genes near the site of virus integration to be overexpressed

72
Q

what happens if a strong promoter is near a proto-oncogene

A

can overstimulate over-expression of the gene causing it to function as an abnormal oncogene

73
Q

HPV produces…

A

proteins that inactive p53 and RB allowing cells to overproliferate

74
Q

paladin gene codes for…

A

a cytoskeleton protein that is important in maintaining cell shape

implicated in metastasis

75
Q

cells that metastasize generally have…

A

poor cytoskeleton structure allowing them to easily detach from the tumor mass

76
Q

paladin gene was found in a family with a high frequency of…

A

pancreatic cancer

77
Q

colon cancer involves mutations in the…

A

APC gene, p53, ras and other

there is a progression from benign adenomas to malignant tumors to metastasis

78
Q

genetic testing of what gene is important to colon cancer

A

APC - a tumor suppressor gene

79
Q

clonal evolution

A

over time, tumor cells acquire more mutations that allow them to be progressively more aggressive in proliferation

80
Q

clonal evolution involves mutations that can affect…

A
  • cell cycle regulation
  • signal transduction
  • DNA repair
  • telomere length
  • chromosome segregation
  • vascularization
81
Q

signal transduction

A

external signal triggers a cascade of intracellular reactions to produce a specific response

ex. Ras signal-transduction

82
Q

Ras signal-transduction pathway

A

ras protein can be inactive or active to either allow or not allow external stimuli to start the cascade of events in the cell

if activated leads to MAP kinase activation which activates TF that stimulate genes leading to cell division

83
Q

mutation in ras pathway

A

the genes that code for Ras proteins are often oncogenes

mutations normally cause it to be stuck in active form leading to cell division

84
Q

repair mechanism in xeroderma pigmentosum

A

defective nucleotide excision repair

85
Q

defective mismatch repair

A

implicated in colorectal, endometrial, and stomach cancers

86
Q

defective double strand break repair

A

implicated in BRCA1 and BRCA2

87
Q

role of telomere length in cancer

A
  • normally telomeres shorten with age leading to cell death
  • telomerase works in germline but not somatic cells allowing somatic cells to die and be replaced
  • tumor cells often have telomerase expressed to give them “immortality”
88
Q

angiogenesis

A

growthof new blood vessels - important to tumor progression

growth factor and proteins involved are often overexpressed in tumor cells

inibitors may be inactivated or underexpressed

thought that prevention of this may fight cancer by decreasing metastasis

89
Q

classic cancer model

A

unregulated growth is due to a serial acquisition of genetic events leading to the expression of genes that promote cell proliferation while silencing the growth of inhibitory genes and blunting cell death

90
Q

cancer is a…

A

proliferative disease

91
Q

cancer therapy focuses on…

A

trying to shrink or destroy the tumors

92
Q

genes that can be tested

A

BRCA1 and 2
P53
APC
RB

93
Q

steps to decrease cancer risk

A
  • HPV vaccine
  • avoid environmental factors leading to cancer
  • get recommend screenings
94
Q

screenings for breast cancer

A

regular breast exams

mammograms

95
Q

screenings for colon cancer

A

colonoscopies

96
Q

screenings for prostate cancer

A

PSA test

Genetics Test 5 (5 decks)

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