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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

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
What is a consequence of a stalled replication fork?
cell cannot finish S-phase
26
How do stalled replication forks occur? What is the solution to this?
due to chemical attaching onto strand before the fork= block DNA replication = need to get around it
27
What are alkylating agents?
chemical carcinogens that modify base structure and can cause stalled replication forks | (-CH3 or -CH2CH3)
28
What is Cisplatin effect on stalled replication forks?
contains Platinum which grabs onto DNA and doesn't allow DNA polymerase to get through the fork
29
What forms thymine dimers?
UV radiation
30
Which UV (A, B, or C) are strong enough to cause cancer?
B and C
31
What are the 2 repair mechanisms dealing with stalled replication forks?
chicken-foot model for repair | post-replication gap filling
32
What do RecQ helicases do? Are they used by tumors?
for repair, unwinds tangles and used for stalled replication forks | highly active in tumor cells
33
What are topoisomerases? What is significant about them in studying cancer?
gets rid of coils | target for cancer drugs, very used in tumors
34
What is Camptothecin? Which cells does it affect?
drug targeting and sticking to topoisomerase = keeps coils within DNA = cell dies | affects highly metabolic cells
35
What is ionizing radiation?
electromagnetic radiation strong enough to push electrons out of their orbits = breaks bonds
36
What are reactive oxygen species (ROS)?
products of production of ATP and other molecules
37
What is a break?
double strand DNA comes apart | can end up in lost genes
38
What is a nick?
only one of the DNA strands are broken
39
What is strand invasion?
broken strand on chromosome A invades sister chromatid A to fill in gap and continue synthesis
40
Which DNA polymerases are responsible for DNA synthesis?
delta and epsilon
41
What are lesions?
some kind of damage/break in the DNA
42
What are lesion-replication polymerases?
error-prone DNA polymerases that usually create errors with normal DNA but are efficient with damaged DNA
43
What are the functions of lesion-replication polymerases?
replicate the complementary strand best way possible and bypass the lesions (and then falls off) due to its bigger pockets
44
What are the 4 lesion-replication polymerases?
kappa, eta, zeta, iota (KEZI)
45
What is hyperploidy? What will it lead to?
accumulation of aneuploidy = overexpression of certain genes = increase gene expression by 50%
46
What do structural rearrangements refer to?
piecing together broken chromosomes
47
What are the 2 alternative mechanisms structural rearrangements exert their action by?
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
What are reciprocal translocations?
chromosome breakage with a subsequent reunion in a different configuration | pieces from 2 chromosomes switch out with each other
49
What causes reciprocal translocations? What is it's negative effect?
ionizing radiation | wrong promoter wrong gene
50
What is the difference between a weak and a strong promoter?
strong promoters are for genes that are constantly needed | weak promoters are for genes not always needed
51
What are the "hotspots" in the human genome commonly involved in translocating?
has to do with the sequence whether they are homologous to other sequences and recombination proteins
52
What are tumor suppressor genes?
keeps cell cycle from going too fast
53
How many mutations would a tumor suppressor gene need to be dysfunctional (one or both)?
BOTH
54
What are proto-oncogenes?
drives cell-cycle (in normal circumstances)
55
How many mutations would a proto-oncogene need to be dysfunctional (one or both)?
one = to lose growth control
56
Which chromosome mutation is the most dangerous and why?
deletion = results on losing a bunch of genes that may be part of the control system
57
What does "Loss of Heterozygosity" mean?
loss of gene function = bringing it down to one functional copy
58
What is "Break-fusion-bridge"?
chromosome has break on ends = telomeres >>> repair enzymes fuse ends of those sister chromatids (sees it as broken and unprotected) >>> separation of chromosomes during mitosis = fused parts create the bridge
59
What is "Break-fusion-bridge" due to?
telomere loss
60
What can "Break-fusion-bridge" lead to?
chromosomal rearrangement = cellular instability

Cancer Cell Biology (17 decks)

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