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hallmarks of cancer > genome instability and mutation part 1 > Flashcards

genome instability and mutation part 1 Flashcards

1
Q

what is genome instability?

A

an increased acquisition of genome alterations

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2
Q

what is DNA damage?

A

anything structurally abnormal in DNA

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3
Q

exogenous damage + 3 examples

A

from environment, UV, Xrays, chemicals

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4
Q

endogenous damage + 3 examples

A

from cellular processes, metabolism, DNA rep, fork stalling

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5
Q

what does metabolism produce which is harmful to cells

A

reactive oxygen species (ROS)

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6
Q

what are ROS

A

highly reactive molecular species with unpaired e-

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7
Q

how can ROS be induced?

A

chemicals, radiation, inflammation

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8
Q

how is DNA protected from damage?

A

its in nucleus and packaged around histones

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9
Q

pumps as a detoxification mechanism

A

pumps in cell membrane pump out harmful agents

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10
Q

enzymes as a detoxification mechanism

A

break down harmful agents into safe products

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11
Q

proteins as a detoxification mechanism

A

conjugate chemicals, bind and take out of cell

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12
Q

what does loss of base result in?

A

apurinic/ apyrimidinic site (purine or pyrimidine lost)

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13
Q

example of a small adduct

A

addition of an oxygen or methyl group to DNA

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14
Q

what is a bulky adduct

A

addition of a larger chemical group to the DNA

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15
Q

what is a single strand break

A

1 strand breaks

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16
Q

what are cross-links

A

bases in same or opposite strands pair

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17
Q

consequence of unrepaired small adduct

A

mismatch during DNA rep

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18
Q

small adducts: e.g. 8-oxoguanine

A

when there is oxidative stress on guanine an O is added, changing chemical structure and therefore there is no G-C bond

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19
Q

what do bulky adducts do to the helix

A

distort it

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20
Q

consequence of bulky adducts

A

blocks DNA replication and stall transcription

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21
Q

bulky adducts: e.g. benzopyrene

A

added to guanine causing distortion (change in chemical structure) and so the enzymes in DNA rep cant get past bulky adduct

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22
Q

what happens with single strand DNA break

A

base lost so enzymes cant get past break

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23
Q

consequence of single strand break

A

DNA rep blocked, stalls trascription

24
Q

consequence of double strand DNA break

A

loss of genetic material

25
Q

consequence of cross links

A

loss of genetic material

26
Q

intrastrand cross link

A

bases next to each other bond

27
Q

interstrand cross link

A

opposite bases bond (not as they are meant to though)

28
Q

what happens to DNA damage in non-dividing cells

A

accumulates

29
Q

what happens to DNA damage in dividing cells

A

blocks DNA rep, can be fixed as a mutation (mismatch), mutations passed onto daughter cells

30
Q

what 3 cell types arise from DNA damage which is unrepaired?

A

senescent cell, apoptotic cell, cancerous cell

31
Q

what is a senescent cell

A

a cell that goes to sleep and doesn’t wake up again

32
Q

what is cell cycle arrest

A

checkpoints tell cycle to stop or apoptosis

33
Q

what does cell cycle arrest allow for

A

more time for DNA damage repair, cells can determine if the damage is too great (apoptosis)

34
Q

how are bulky adducts and pyrimidine dimers repaired

A

nucleotide excision repair

35
Q

how are single strand breaks and abasic sites repaired

A

Base excision repair

36
Q

how are double stranded breaks and interstand cross links repaired?

A

Homologous recombination repair/ non-homologous end-joining

37
Q

how is base pair mismatch repaired

A

mismatch repair pathway

38
Q

how is guanine alkylation repaired

A

MGMT

39
Q

what is strand slippage

A

the wrong base is put on the partner strand (insertions/deletions)

40
Q

what is the first line repair

A

proof reading

41
Q

what is the second line repair

A

mismatch repair

42
Q

how does mismatch repair work

A

MutS-alpha recognises mistake on newly synthesised strand, binds to mismatch, recuits MutL-alpha, exonucleases chops away faulty strand, RPA binds to ssDNA to stabilise it, polymerase puts correct DNA back in again and the ligase seals ends

43
Q

how are small insertion or deletion loops corrected

A

similarly by MutS-beta protiens

44
Q

how is O^6-MeG repaired (direct reversal repair)

A

methylguanine DNA methyltransferase has a thiol group which binds to methyl group and takes it out of the DNA

45
Q

base excision repair - e.g. 8-oxoguanine

A

damaged base is recognised and removed by OGG1 (DNA glycosylase), AP site (apurinic or apyrimidinic)
is incised by AP endonuclease (APE 1), PARP1 binds to this intermediate (which is a single strand break) and recruits other DNA repair factors, DNA polymerase beta puts correct DNA and then ligase seals for short patch BER

46
Q

what happens in long patch BER

A

if ends are structurally complex then a different DNA polymerase is recruited, FEN1 excises the additional flap on DNA, ligase seals

47
Q

5 core steps of BER

A
  1. recognition and excision by glycosylase
  2. incision of the strand by AP endonuclease
  3. end processing
  4. repair synthesis, including gap filling
  5. ligation
48
Q

important thing with NER

A

cell knows which strand of DNA is important (strand being transcribed)

49
Q

Transcription coupled NER

A

recognised by CSA and CSB proteins, chunk of DNA excised by ERCC1 complex, polymerases add new DNA and ligases seal end

50
Q

global genome NER

A

recognised by XPC, ERCC1 complex excises the DNA, polymerases add correct DNA and ligases seal ends

51
Q

when does non homologous end joining occur

A

throughout whole cell cycle

52
Q

non homologous end joining

A

Ku proteins recognise break and bind to ends, Ku recruit DNA PKcs which process the ends (so they can be rejoined) it then pulls the ends together and sticks them with ligase. sometimes there can be additions or deletions but thats okay

53
Q

what is DNA PKcs

A

DNA protein kinase catalytic subunit

54
Q

when is homologous recombination active

A

S and G2 phases as a copy of DNA is synthesised

55
Q

homologous recombination

A

MRN complex recognises the break but is only present in S and G2 phases, 1 stand of DNA is resected by RPA protein, RAD51 binds to the end and invades the sister chromatid and goes along until it finds the matching homologous sequence that you’ll have once you synthesise the DNA, it copies the info exactly.

hallmarks of cancer (17 decks)

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