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Bmsc > Saurin > Flashcards

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
Q

MDM2

A

E3 ubiquitin
ligase that promotes ubiquitylation and proteasomal degradation of p53

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25
Q

ARF binds to…

A

MDM2

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26
Q

p53 production

A

Constantly made and degraded

27
Q

How does the APC gene organise the gut?

A

Cells proliferate at bottom of crypt, differentiate higher up

28
Q

HIF1 drives transcription in hypoxia and is constantly degraded by…

A

VHL.

29
Q

How does chromosomal instability drive tumour evolution?

A

Constant genome shuffling

30
Q

Unattached kineticores in mitosis generate an inhibitor:

A

Mitotic checkpoint complex

31
Q

What phosphorylates incorrectly attached kineticores?

A

Aurora B kinase

32
Q

The mitotic spindle is __polar.

A

bi

33
Q

What is cleaved in anaphase?

A

Cohesin complex

34
Q

What does a multipolar mitotic spindle lead to?

A

Extra chromosomes pulled to one side

35
Q

What does premature loss of cohesion mean?

A

Chromosomes cant match up

36
Q

Describe proteotoxic stress

A
  • chromosome imbalance
  • proteomic imbalance
  • constant degradation of
    unstable proteins that are produced in excess
37
Q

WGD

A

Whole genome doubling

38
Q

How else does aneuploidy benefit tumours?

A

Inflammation

39
Q

Mis-segregation can create weak micronuclei, leading to…

A

chromothripsis – massive rearrangement/shattering of chromosomes.

40
Q

Pieces of DNA can attach to other chromosomes. What problems can this cause?

A

Can contain oncogenes

Can drive inflammation

Can activate immune response in cytoplasm

Can cause massive gene amplification on
extrachromosomal DNA (ecDNA)

41
Q

What senses DNA in the cytoplasm

A

cGAS pathway

42
Q

How do aneuploid cells cause inflammation?

A

Constant senescence

43
Q

Immune response to DNA in the cytoplasm

A

FN and NFKb

44
Q

How does inflammation promote tumours?

A

Extracellular matrix remodelling

Epithelial-Mesinchimal transition (EMT)

Invasion and metastases

Angiogenesis

Mutagens release (e.g. ROS)

Suppress apoptosis

Growth factors

45
Q

Chromosomal instability can reduce expression of proteins
involved in…

A

antigen presentation.

46
Q

Convergent evolution

A

Same selective pressure

47
Q

Non-synonymous (dN): amino acid _________________
Synonymous (dS): amino acid _________________

A

Non-synonymous (dN): amino acid changes
Synonymous (dS): amino acid doesn’t change

47
Q

Which genes drive cancer?

A

Genes with high rates of change are positively selected

48
Q

Degenerate nucleotide code

A

Many codon sequences for 1 amino acid

49
Q

Types of genetic diversity

A

Gene level changes
Chromosome level changes

50
Q

Linear evolution

A

Stepwise evolution with driver mutation providing strong selective advantage so they outcome
neighbouring clones (selective sweeps)

51
Q

List the different models of tumour evolution

A

Linear
Branched
Neutral
Punctuated

52
Q

When does linear evolution occur?

A

Early tumourigenesis

53
Q

Branched evolution

A

Clones diverge from common ancestor and evolve in parallel because they all
offer increased fitness

54
Q

Give an example of branched evolution

A

Glioblastoma

55
Q

Neutral evolution

A

Extreme case of branching evolution, in which all individuals in the population have equal fitness

56
Q

When does neutral evolution occur?

A

Different stages of tumourigenesis (e.g. in between the gain of beneficial traits)

57
Q

Punctuated evolution

A

Rapid burst of change followed by stable clonal expansions

Huge genetic diversity allows complex karyotypes to be selected

58
Q

When does punctuated evolution occur?

A

copy number aberrations or chromosomal structural
rearrangements

59
Q

Give examples of punctuated evolution

A

Chromothripsis
Genome doubling

60
Q

What can be used to time “Most Recent Common Ancester” (MCRA)?

A

Clock mutations

61
Q

Lethal cocktail

A

mutation + inflammation

62
Q

dN/dS <1

A

deleterius

62
Q
A

Bmsc (15 decks)

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