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Block 9 Ellen > Carcinogenesis > Flashcards

Carcinogenesis Flashcards

1
Q

what do people with ataxia telangiectasia have a defect in

A

ATM protein defect

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2
Q

what does ATM do

A

detects DNA damage

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3
Q

what site do most endogenous mutations for p53 occur at

A

CpG (cytosine- guanine nucleotides next to each other)

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4
Q

what happens in cytosine deamination

A

gets turned into uracil

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5
Q

why can cytosine deamination be repaired

A

because uracil is a RNA base so seen as abnormal in DNA

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6
Q

what is deamination of 5-methylcytosine

A

it is deaminated into thymine

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7
Q

what is biotransformation

A

enzymatic process transforming chemicals into entities to be excreted from the body

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8
Q

3 exogenous things causing mutations of p53

A

UV light
Aflatoxin
Benzopyrene in tobacco smoke

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9
Q

what mutation in p53 does UV light cause

A

CC to TT

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10
Q

what cancer can aflatoxin (from diet) cause

A

liver cancer

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11
Q

mutation of p53 in aflatoxin damage

A

codon 249 AGG to AGT

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12
Q

why can deamination of 5-methylcytosine to thymine not be repaired

A

as thymine is a normal DNA base so is seen as normal

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13
Q

size of alkylation damage

A

a small change (not a bulky lesion)

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14
Q

what enzyme repairs alkylation damage

A

MGMT suicide enzyme

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15
Q

how does MGMT suicide enzyme repair alkylation damage

A

by removing the akyl group from the DNA and placing it into the cytosine residue on the enzyme

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16
Q

what tumours are responsive to treatment with alkylating agents

A

tumours with reduced MGMT expression

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17
Q

what 2 enzymes perform base excision repair

A

DNA glycosylases

AP endonuclease

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18
Q

what is DNA glycosylases job

A

removes base leaving empty AP site

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19
Q

what is AP endonuclease job

A

repairs AP site

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20
Q

what can reactive oxygen species cause thousands of per day in the human genome

A

“hits” creating AP sites

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21
Q

what kind of damage does UV cause

A

bulky lesions (e.g thymine dimers)

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22
Q

when is nucleotide excision repair (NER) used

A

when DNA damage is not recognised by DNA glycosylases (so base excision repair isn’t possible) -bulky lesions

23
Q

what does NER remove from DNA

A

oligonucleotide fragments containing the damaged bases

24
Q

what lesion is the primary cause of melanomas in humans

A

pyrimidine dimers

25
Q

in NER what replaces the gap

A

DNA polymerase

26
Q

what is xeroderma pigmentosum (XP)

A

genetic defect in NER (nucleoside excision repair) of UV damage

27
Q

what does XP lead to

A

1000x increased risk of skin cancer

28
Q

in a double strand break how is the DNA repaired

A

non-homologous end joining (NHEJ)

29
Q

a somatic mutations effect

A

only the individual

30
Q

a germ line mutation effects

A

inheritance

31
Q

what mutation can lead to familial melanoma

A

P16ink

32
Q

what transcription factor does Rb sequester

A

E2F

33
Q

what are lesions in colorectal adenoma called

A

polyps

34
Q

what are polyps precursors of

A

colorectal cancer

35
Q

2 types of inherited colorectal cancer

A
  • familial adenomatous polyposis (FAP)

- hereditary non polyposis colon cancer (HNPCC)

36
Q

inheritance pattern of FAP

A

autosomal dominant

37
Q

what is present in the colon in FAP

A

1000s of polyps

38
Q

what gene is mutated in FAP

A

APC gene

39
Q

what is the APC gene

A

negative regulator of beta catenin

40
Q

what signalling pathway is APC part of

A

APC-Wnt signalling pathway

41
Q

when there is no need for cell division what does APC do

A

sequesters beta-cat

42
Q

when beta-cat is not bound to APC what can it do

A

binds to DNA to activate Wnt target genes leading to cell proliferation

43
Q

what is the syndrome called of HNPCC

A

lynch syndrome

44
Q

what NOT present in HNPCC

A

polyps

45
Q

which inherited colorectal cancer is early onset

A

HNPCC

46
Q

which part of the colon is usually affected in HNPCC

A

right colon

47
Q

what can a defect in mismatch repair lead to (3)

A

-mutator phenotype

48
Q

what can mutator phenotype also be called

A

microsatellite instability

49
Q

two main sporadic colorectal cancer pathways

A

CIN

CIMP

50
Q

CIN=

A

chromosome instability pathway

51
Q

CIMP=

A

CpG island methylator phenotype

52
Q

which is the most common pathway for sporadic colorectal cancer

A

CIN (chromosome instability)

53
Q

which side of the colon does CIN effect

A

left

Block 9 Ellen (21 decks)

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