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Cancer Cell Biology > 2 - Genomic Stability and DNA Replication and Repair > Flashcards

2 - Genomic Stability and DNA Replication and Repair Flashcards

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1
Q

How do cancer cells find blood vessels?

A

by using the nutrient concentration gradient

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2
Q

When do secondary tumors begin to deconstruct the organ it is in?

A

when it becomes big enough

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3
Q

What will happen if the secondary tumor is in the bone marrow?

A

disrupts physiology in BM = disrupts blood cells = affects O2 delivery to organs

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4
Q

What are examples of selection barriers?

A

connective tissue and tumor suppression genes

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5
Q

What will happen if the DNA repair gene is mutated?

A

ability to fix damage decreases = mutation rate increases

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6
Q

What happens if the mutation rate is too high in cancer cells? What does this mean?

A

loses its basic functions = may die | needs to be a balance, should not mutate too fast

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7
Q

What % of genes in human genome encodes for protein and what is the advantage of this percentage?

A

1.5% | small chance that nutation will occur in one of the protein-encoding genes

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8
Q

What causes DNA mismatches?

A

DNA polymerase gets confused and mismatches DNA

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9
Q

What is a mismatch due to deamination?

A

amine substituent on base gets replaced by oxygen

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10
Q

What is the error rate of DNA polymerase?

A

1 in 10 billion

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11
Q

What does DNA polymerase have that RNA polymerase doesn’t?

A

proofreading and exonuclease ability

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12
Q

What does exonuclease do within DNA polymerase?

A

kicks out mismatch

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13
Q

What is the DNA Mismatch Repair (DNA MMR)?

A

recognizes mispairings of nucleotides

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14
Q

What are the functions of DNA MMR?

A

maintains genomic stability | signals cells to die if error not repaired | recognizes DNA damage

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15
Q

What are the 3 critical steps in DNA MMR?

A

Recognition | Removal | Re-synthesis

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16
Q

What proteins are involved in the Recognition step of DNA MMR and how does it recognize the damage site?

A

MutL/homologs dimer rides DNA like rollercoaster until it runs into a kink

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17
Q

What proteins are involved in the Removal step of DNA MMR?

A

MutH and exonuclease

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18
Q

How do the proteins in the Removal step of DNA MMR remove the damage?

A

MutH makes loop with DNA+kink &raquo_space;> pull strand thru to look for GATC sequence &raquo_space;> MutH clips one side of GATC &raquo_space;> exonuclease breaks apart base pairs on daughter strand

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19
Q

What proteins are involved in the Re-synthesis step of DNA MMR and how does it re-synthesize the damage site?

A

DNA polymerase fills in gap

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20
Q

What cancer is linked with mutations in DNA MMR genes?

A

colon cancer

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21
Q

What is a major reason why we start getting errors in our genome?

A

chemicals attach to DNA directly and react with nucleic acid

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22
Q

How can DNA polymerase get confused with adducts?

A

alters the H-bonding sites of nucleic acids so DNA polymerase puts compliment base that would match the available H-binding sites

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23
Q

What are the 2 fates of a DNA with an adduct undergoing MMR?

A

apoptosis or increased mutation if not fixed

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24
Q

What is a DNA adduct?

A

something added/attached to DNA

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25
Q

What is a consequence of a stalled replication fork?

A

cell cannot finish S-phase

26
Q

How do stalled replication forks occur? What is the solution to this?

A

due to chemical attaching onto strand before the fork= block DNA replication = need to get around it

27
Q

What are alkylating agents?

A

chemical carcinogens that modify base structure and can cause stalled replication forks | (-CH3 or -CH2CH3)

28
Q

What is Cisplatin effect on stalled replication forks?

A

contains Platinum which grabs onto DNA and doesn’t allow DNA polymerase to get through the fork

29
Q

What forms thymine dimers?

A

UV radiation

30
Q

Which UV (A, B, or C) are strong enough to cause cancer?

A

B and C

31
Q

What are the 2 repair mechanisms dealing with stalled replication forks?

A

chicken-foot model for repair | post-replication gap filling

32
Q

What do RecQ helicases do? Are they used by tumors?

A

for repair, unwinds tangles and used for stalled replication forks | highly active in tumor cells

33
Q

What are topoisomerases? What is significant about them in studying cancer?

A

gets rid of coils | target for cancer drugs, very used in tumors

34
Q

What is Camptothecin? Which cells does it affect?

A

drug targeting and sticking to topoisomerase = keeps coils within DNA = cell dies | affects highly metabolic cells

35
Q

What is ionizing radiation?

A

electromagnetic radiation strong enough to push electrons out of their orbits = breaks bonds

36
Q

What are reactive oxygen species (ROS)?

A

products of production of ATP and other molecules

37
Q

What is a break?

A

double strand DNA comes apart | can end up in lost genes

38
Q

What is a nick?

A

only one of the DNA strands are broken

39
Q

What is strand invasion?

A

broken strand on chromosome A invades sister chromatid A to fill in gap and continue synthesis

40
Q

Which DNA polymerases are responsible for DNA synthesis?

A

delta and epsilon

41
Q

What are lesions?

A

some kind of damage/break in the DNA

42
Q

What are lesion-replication polymerases?

A

error-prone DNA polymerases that usually create errors with normal DNA but are efficient with damaged DNA

43
Q

What are the functions of lesion-replication polymerases?

A

replicate the complementary strand best way possible and bypass the lesions (and then falls off) due to its bigger pockets

44
Q

What are the 4 lesion-replication polymerases?

A

kappa, eta, zeta, iota (KEZI)

45
Q

What is hyperploidy? What will it lead to?

A

accumulation of aneuploidy = overexpression of certain genes = increase gene expression by 50%

46
Q

What do structural rearrangements refer to?

A

piecing together broken chromosomes

47
Q

What are the 2 alternative mechanisms structural rearrangements exert their action by?

A

gene over/underexpression of a gene at one of the break-points | creation of a hybrid gene via fusion of two genes’ parts at the breakpoint

48
Q

What are reciprocal translocations?

A

chromosome breakage with a subsequent reunion in a different configuration | pieces from 2 chromosomes switch out with each other

49
Q

What causes reciprocal translocations? What is it’s negative effect?

A

ionizing radiation | wrong promoter wrong gene

50
Q

What is the difference between a weak and a strong promoter?

A

strong promoters are for genes that are constantly needed | weak promoters are for genes not always needed

51
Q

What are the “hotspots” in the human genome commonly involved in translocating?

A

has to do with the sequence whether they are homologous to other sequences and recombination proteins

52
Q

What are tumor suppressor genes?

A

keeps cell cycle from going too fast

53
Q

How many mutations would a tumor suppressor gene need to be dysfunctional (one or both)?

A

BOTH

54
Q

What are proto-oncogenes?

A

drives cell-cycle (in normal circumstances)

55
Q

How many mutations would a proto-oncogene need to be dysfunctional (one or both)?

A

one = to lose growth control

56
Q

Which chromosome mutation is the most dangerous and why?

A

deletion = results on losing a bunch of genes that may be part of the control system

57
Q

What does “Loss of Heterozygosity” mean?

A

loss of gene function = bringing it down to one functional copy

58
Q

What is “Break-fusion-bridge”?

A

chromosome has break on ends = telomeres &raquo_space;> repair enzymes fuse ends of those sister chromatids (sees it as broken and unprotected) &raquo_space;> separation of chromosomes during mitosis = fused parts create the bridge

59
Q

What is “Break-fusion-bridge” due to?

A

telomere loss

60
Q

What can “Break-fusion-bridge” lead to?

A

chromosomal rearrangement = cellular instability

Cancer Cell Biology (17 decks)

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