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Saurin Flashcards

1
Q

Driving force of tumour evolution

A

Chromosomal instability

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2
Q

G1 checkpoints __________ conditions and G2 checkpoints __________ conditions.

A

G1 checkpoints external conditions and G2 checkpoints internal conditions.

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3
Q

External conditions

A

Cell-cell contact
Growth factors

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4
Q

Internal conditions

A

Cell size
Energy
DNA damage

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5
Q

____ levels remain high but _______ fluctuate depending on cell cycle stage.

A

CDK

Cyclins

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6
Q

CDK function

A

Phosphorylate proteins to progress cell cycle

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7
Q

Cyclin function

A

Bind to CDK to activate (releasing from inhibitor)

Substrate specificity

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8
Q

Which proteins induce cyclins?

A

Transcription factors

Ubiquitin ligases

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9
Q

How do cyclins overcome the threshold created by inhibitor proteins?

A

autophoshorylation and positive feedback

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10
Q

Cyclin D

A

Drives S phase entry with CKD4/6

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11
Q

Restriction point

A

Checkpoint

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12
Q

p53 activates p__ to cause inhibition and p__ to cause senesence.

A

21
16

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13
Q

Loss Of Heterozygocity

A

Losing a second allele when one is already mutated

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14
Q

LOH mechanisms

A

Gene loss
Chromosome loss (by aneuploidy)
Mutation duplication

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15
Q

How can a mutation be duplicated?

A

Template strand flips to other chromosome during replication

Mitotic recombination

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16
Q

Li-Fraumeni Syndrome

A

p53

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17
Q

Common tumour suppressor conditions

A

🦛☕️🍃

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18
Q

p53 drivers

A

hypoxia
ageing
ROS
DNA damage
infection
nutrient depletion
signals for hyperproliferation

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19
Q

Are p53 mutations recessive?

A

No, mostly missence

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19
Q

p53 structure

A

tetromer - 4 subunits each bind to DNA

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20
Q

___ is produced as biproduct of the cyclin pathway and activates p53.

A

ARF

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21
Q

How does p53 have 16 possible combinations?

A

Each subunit randomly gets a gene from one chromosome so a mutation on one chromosome can affect all subunits

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22
Q

How does p53 regress tumours?

A

Senscence

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23
Q

p53 and _______ operate within a negative feedback loop

A

MDM2

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24
MDM2
E3 ubiquitin ligase that promotes ubiquitylation and proteasomal degradation of p53
25
ARF binds to…
MDM2
26
p53 production
Constantly made and degraded
27
How does the APC gene organise the gut?
Cells proliferate at bottom of crypt, differentiate higher up
28
HIF1 drives transcription in hypoxia and is constantly degraded by…
VHL.
29
How does chromosomal instability drive tumour evolution?
Constant genome shuffling
30
Unattached kineticores in mitosis generate an inhibitor:
Mitotic checkpoint complex
31
What phosphorylates incorrectly attached kineticores?
Aurora B kinase
32
The mitotic spindle is __polar.
bi
33
What is cleaved in anaphase?
Cohesin complex
34
What does a multipolar mitotic spindle lead to?
Extra chromosomes pulled to one side
35
What does premature loss of cohesion mean?
Chromosomes cant match up
36
Describe proteotoxic stress
- chromosome imbalance - proteomic imbalance - constant degradation of unstable proteins that are produced in excess
37
WGD
Whole genome doubling
38
How else does aneuploidy benefit tumours?
Inflammation
39
Mis-segregation can create weak micronuclei, leading to…
chromothripsis – massive rearrangement/shattering of chromosomes.
40
Pieces of DNA can attach to other chromosomes. What problems can this cause?
Can contain oncogenes Can drive inflammation Can activate immune response in cytoplasm Can cause massive gene amplification on extrachromosomal DNA (ecDNA)
41
What senses DNA in the cytoplasm
cGAS pathway
42
How do aneuploid cells cause inflammation?
Constant senescence
43
Immune response to DNA in the cytoplasm
FN and NFKb
44
How does inflammation promote tumours?
Extracellular matrix remodelling Epithelial-Mesinchimal transition (EMT) Invasion and metastases Angiogenesis Mutagens release (e.g. ROS) Suppress apoptosis Growth factors
45
Chromosomal instability can reduce expression of proteins involved in…
antigen presentation.
46
Convergent evolution
Same selective pressure
47
Non-synonymous (dN): amino acid _________________ Synonymous (dS): amino acid _________________
Non-synonymous (dN): amino acid changes Synonymous (dS): amino acid doesn’t change
47
Which genes drive cancer?
Genes with high rates of change are positively selected
48
Degenerate nucleotide code
Many codon sequences for 1 amino acid
49
Types of genetic diversity
Gene level changes Chromosome level changes
50
Linear evolution
Stepwise evolution with driver mutation providing strong selective advantage so they outcome neighbouring clones (selective sweeps)
51
List the different models of tumour evolution
Linear Branched Neutral Punctuated
52
When does linear evolution occur?
Early tumourigenesis
53
Branched evolution
Clones diverge from common ancestor and evolve in parallel because they all offer increased fitness
54
Give an example of branched evolution
Glioblastoma
55
Neutral evolution
Extreme case of branching evolution, in which all individuals in the population have equal fitness
56
When does neutral evolution occur?
Different stages of tumourigenesis (e.g. in between the gain of beneficial traits)
57
Punctuated evolution
Rapid burst of change followed by stable clonal expansions Huge genetic diversity allows complex karyotypes to be selected
58
When does punctuated evolution occur?
copy number aberrations or chromosomal structural rearrangements
59
Give examples of punctuated evolution
Chromothripsis Genome doubling
60
What can be used to time “Most Recent Common Ancester” (MCRA)?
Clock mutations
61
Lethal cocktail
mutation + inflammation
62
dN/dS <1
deleterius
62

Bmsc (17 decks)

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