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MCB II Block 1 > Cancer 5 > Flashcards

Cancer 5 Flashcards

1
Q

what is MOI for ataxia telangiectasia

A

AR

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2
Q

whre is mutation in ataxia telangiectasia

A

mutation of ATM

one from each parent

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3
Q

draw pathway for ATM

A

pg 160

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4
Q

what does ATM phosphoryalate

A

kinase that can phoshporylate p53

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5
Q

where is mutation for bloom syndrom

A

BLM

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6
Q

what does BLM code for

A

DNA helicase

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7
Q

what kind of disorder is bloom syndrome

A

chromosome instability

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8
Q

what is characteristic of blooms yndrome regarding chromosomes

A

hundred s of sister chromatid exchanges

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9
Q

symptoms of bloom

A

sun senstivie
dwarfism
immune dfeicience
etc

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10
Q

werner syndrome is caused by mutation in

A

WRN

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11
Q

WRN codes for

A

DNA helicase & exonuclease

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12
Q

what distinguishes werner syndrome from other chromosome instability disease

A

premature aging

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13
Q

premature aging starting at puberty, short stature, cancer is what disease

A

werner syndrome

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14
Q

why premature aging in werner syndrome

A

the DNA helicase (that WRN codes for) is involved in telomere maint.

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15
Q

fanconi anaemia have mutations where

A

FA complex

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16
Q

pancytopenia is

A

bone marrow failure

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17
Q

fanconi anaemia are at risk of developing what

A

AML, lymphoma, hepatic carcinoma

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18
Q

pancytopenia, skeletal (upper limb) abnormalities is what disease

A

fanconi anaemia

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19
Q

Where do FA genes work

A

BRCA pathway

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20
Q

what is FA gene important for

A

DNA repair

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21
Q

how can viruses cause cancer

A

oncogenic virus expresses oncogene, so viral genes are expressed when go into cell
viral genome insert or integrate into host cell and the insertion could disrupt tumor suppressor or oncogene

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22
Q

EBV

A

ebson bar virus

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23
Q

EBV (virus) associated with what cancers

A

burkitt lymphoma

B-cell lymphoma

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24
Q

B-cell lymphoma is particularilly associated with

A

HIV or pts at low immunity

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25
Q

hepatitis B & C virus associated with what cancer

A

hepatic cancer

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26
Q

why do hepatitis B & C cause hepatic cancer

A

due to the chronic infection

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27
Q

HTLV

A

human t cell leukemia virus

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28
Q

HTLV-1 retrovirus is responsible for wht cancer

A

T-cell leukemia

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29
Q

HPV responsible for what cancer

A

cervical

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30
Q

oppostunistic neoplasms that infect because of HIV

A 
kaposis sarcoma ( HHV-8)
non-hodgkin lymphoma (EBV)
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31
Q

whwhere does non-hodgkin lymphoma usually occur

A

in brain

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32
Q

what viruses are directly oncogenic and take opportunity from HIV

A

HHV-8

EBV

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33
Q

papalloma viruses are responsible for

A

warts

cervical cancer starts as a wart

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34
Q

hepatitis viruses associated with what kind of cancer

A

liver cancer

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35
Q

EBV associated with

A

burkitt lypmphoma

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36
Q

HPV & Cervical cancer draw pathway

A

pg 171

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37
Q

hpv stands for

A

human papaloma virus

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38
Q

HPV is transmitted

A

sexual

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39
Q

different strains/grades of HPV describe

A

some are more highly oncogenic than others. so female infected wtith some type could lead to higher risk

40
Q

what are add’l risk factors to HPV to getting cancer

A

smoking

oral contraceptives

41
Q

what are high risk strains of HPV

A

16 18 31 45

42
Q

HPV virus encodes for (how does it work, what is initial step)

A

viral oncogenes that inhigibt p53 and Rb in cell it infects

43
Q

acetic acid does what (gynecology, if pap smear comes out abnormal)

A

stain any cell infected with virus white

44
Q

CIN stands for

A

cervical intraepithelial neoplasia

45
Q

what are steps of CIN

A

CIN I to II to II to cervical cancer

46
Q

Rb is inhibiting

A

E2F

47
Q

what does E2F normally transcribe

A

cyclin E

48
Q

P53 activated it can do what

A

block cell cycle
induce apoptosis
help repair

49
Q

HPV genome encodes for what

A

hpv genome encodes for E6 and E7

50
Q

what do E6 and E7 inhibit

A

p53 and Rb

51
Q

draw out HPV oncogenes E6 and E7 and how they affect p53 and rb

A

pg 173

52
Q

at later stages of cancer, you will see what

A

massive cytogenetic changes

VERY unstable

53
Q

when will you see massive cytogenetic changes

A

at end of cancer

54
Q

what sequence is repeated at end of chromosome that makes telomere

A

TTAGGG

55
Q

what is function of telomere

A

protect end of chromosomes
permit complete replication of chromosomal DNA
regulate chromosomal integrity
regulate life span
keep chromosomal integrity during cell division

56
Q

what does it mean that it protects the ends of chromosome

A

they form a loop at the end of the linear chromosomes, without that, if they are just straight ends, chrom. will fuse together. so they prevent chrom. from fusing together

57
Q

what does it mean that telomeres regulate chromosomal integrity during cell devision & determine life span

A

t loop - the loop that forms is protectin chrom. from fusing

also determines lifespan - only stem cells express telomerase

58
Q

length of telomeres at end of chromosome tells what

A

number of times particular cell can proliferate

59
Q

telomerase is enzyme tha does what

A

elongates telomeres

60
Q

telomerase is active in what kind of cell

A

germ cell and stem cells

61
Q

in cancer what is reactivated regarding telomeres

A

telomerase

62
Q

without telomerase activity, what happens

A

once cells replicate certain # of times they die

63
Q

how do telomeres protect against DNA repair mechanisms

A

loop at end of linear chromosomes, when p53 is activated it would think there was a break and would fuse different chromosomes together, so it prevents repair mechanisms from doing taht

64
Q

each cell division chrom. loses what

A

10-20 TTAGGG repeats

65
Q

end replication problem

A

in adult cell the telomere repeats will be lost b/c of end of replication problem b/c most cells do not express telomerase. telomerase only expressed in stem cells that need to keep proliferating (germ cells have telomerase). b/c of end replication problem cell will eventually go to senescence

66
Q

senescent cell

A

can never again go into cell cycle

67
Q

in germline and embryonic cells how much telomeric repeat at end

A

15 KB telomeric repeat

68
Q

G0 is what

A

senescence, inactive stage of cell cycle, it will never be able to replicate again
telomeres are too short

69
Q

what causes G0

A

telomeres are too short

70
Q

if cell continue proliferating after G0 what happens

A

DNA damage which should result in cell death

71
Q

having telomeres is a way of protecting what?

determining what?

A

ends of chromosomes

determining the lifespan of a cell

72
Q

what is telomerase

A

enzyme that contains two components

73
Q

what two components are in telomerase

A

TERC

TERT

74
Q

what is TERC

A

RNA template

75
Q

what is TERT

A

reverse transcriptase

76
Q

TERC + TERT form

A

telomerase

77
Q

what is function of TERC

A

synthesising telomere DNA repeats

78
Q

what is function of TERT

A

synthesises telomere DNA
by copying the telomere
repeat sequences encoded
in the RNA template

79
Q

describe how telomerase works

A

RNA component base pairs at end and uses rest of template to insert DNA using the reverse transcriptase capability. it slides along inserting new DNA bases

80
Q

what is required for cancer progression regarding telomerase

A

reactivation

81
Q

in immortal cancer how much has reactivation of telomeres

A

90%

82
Q

why is there 90% found for reactivation of telomeres in cancer, what happens to other 10%?

A

independent pathway of telomere elongation - not fully understood

83
Q

will telomerase activiation initiate tumor formation

A

no

but it allows for tumor proliferation

84
Q

what is one protein involved in checkpoint when telomere gets too short

A

p53

85
Q

inhibition of telomerase as a treatment for cancer

A

hasn’t been very successful.

86
Q

dyskeratosis congenita where is mutation

A

pt has mutation in telomerase - prematurely shortening telomeres

87
Q

why do chrom. fuse together in dyskeratosis congenita

A

defect in telomerase, cells that should normally be able to express telomerase (like hematopoetic stem cells) are not expressing it, if checkpoints are bipassed and cell still replicates will end up with chrom. fusion events.

88
Q

pts with defect in telomerase are at risk for devloping what

A

cancer

89
Q

why do pts with dyskeratosis congenita at risk for developing cancer

A

telomeric repeats are very short very quickly, sometimes checkpoint is bipassed and keeps going through cycle, chrom. fuse together, the fusion is oncogenic. when chrom. fuse together then the alternative pathway could be activated

90
Q

what does tricentric and dicentric chrom mean

A

they have fused together

91
Q

what happens from metaphase into anaphase when there are tricentric and dicentric chrom

A

there is a break - which could disrupt tumor suppressor or proto-oncogene, increased instability which could mean activation of alternative pathway and telomeres become partially restabilized

92
Q

what mutation needs to happen to have pt get cancer due to dyskeratosis congenita or other similar disease

A

alternative pathway for telomerase needs to be activated

93
Q

what are some symptoms in dyskeratosis congenita

A

defects in cells that proliferate rapidly, hair teeth, nails, etc

94
Q

if there is failure of checkpoint to go to G0 what could happen

A

cell continues replicating, can lose T loop, end up with chrom. instability (chrom fusion events)
if telomerase activity is not reactivated, cell could die b/c of all the rearrangements and breakages
if telomerase is reactivated or alternative pathway is activated and cell is stabilized then the cell will go on and the tumor will carry on and more mutations

95
Q

draw out checkpoint failure for telomeres

A

pg 192

96
Q

what is a dicentric chromosome

A

fusion of 2 chromosomes

MCB II Block 1 (12 decks)

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