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human genetics > Week 5- Genetics of cancer > Flashcards

Week 5- Genetics of cancer Flashcards

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Biology 101 flashcards
1
Q

what is differentiation

A

during embryogenesis, tissues and organs are formed in a regulated process

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2
Q

what is terminal differentiation

A

when cells are not programmed to divide

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3
Q

what does it meant have undergone transformation

A

if a cell lose control of their own division giving rise to abnormal cell masses called tumours

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4
Q

what is a benign tumour

A

if the tumour is not invasive

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5
Q

what are malignant tumours

A

if the tumour is invasive

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6
Q

what is metastasis

A

when the tumour spreads to other organs by the blood or lymphatic vessels

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7
Q

what are the 4 phases f the cell cycle

A
  1. gap (G1)
  2. synthesis (S)- DNA replication occurs
  3. gap 2 (G2)
  4. mitosis (M)- dividing cells separate
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8
Q

what does the gap phases allow

A

cell time needed to replicate proteins and organelles

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9
Q

what happens at cell-cycle check points

A

internal and external environments are monitored to ensure conditions are favourable for divisions

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10
Q

what are cell-cycle check points regulated by

A

cyclins and cyclin-dependant kinases (CDK)

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11
Q

what is the role of CDKs

A

they are activated when they bind to cyclins and then phosphorylate proteins required for cell progression

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12
Q

what happens to cyclins to ensure the cell cycle goes in one direction

A

thet are rapidly degraded after they have completed their job

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13
Q

how is cell cycle entry regulated in complex organisms

A

via an intracellular signalling system that responds to extracellular signals

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14
Q

what do extracellular signals include

A

growth factors produced by other cells (paracrine) or by the cells itself (autocrine)

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15
Q

what do extracellular signals tigger

A

the activation of signal transduction pathways that ultimately switch on the genes required for cell cycle progression

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16
Q

what are cancer critical genes

A

defects in genes required to regulate cell division causing cancer

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17
Q

what are the 2 types of cancer critical genes

A
  • proto-oncogenes
  • tumor suppressor genes
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18
Q

what are proto-oncogenes

A

genes which cause cancer from gain of function mutations. when mutated to cause cancer they are called oncogenes

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19
Q

what are tumour suppressor genes

A

genes which cause cancer from loss of function mutations

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20
Q

what is sous tacoma virus (RSV)

A

a retrovirus- must convert its RNA genome into DNA to be integrated

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21
Q

what is c-src

A

a proton-oncogene which activates cellular pathways involved in cell growth and division

22
Q

what happens if c-src is mutated to become oncogenic

A

signalling pathways become hyperactive, resulting in increased proliferation, survival, and invasion leading to transformation

23
Q

what are the classes of oncogenes

A
  • growth factors (EGF)
  • growth factors receptors (EGF receptors)
  • membrane associated G proteins (RAS)
  • cytoplasmic signal transducers (MEK)
  • nuclear transcription factors (MYC)
24
Q

how can the gain of function in proto-oncogenes arise

A
  • excessive amount of protein
  • abnormal protein
  • novel protein in excess
25
Q

how were tumour suppressor genes understood

A

from the study of retinoblastoma

26
Q

what is retinoblastoma

A

childhood cancer which occurs from transformation of immature neural cells in the retina

27
Q

what happens in sporadic and familiar retinoblastoma

A
  • sporadic: tumours form in only one eye
  • familial: tumours form in both eyes and often earlier, suggesting an underlying predisposition
28
Q

what is Rb

A

a tumour suppressor which regulates G1-S phase cell-cycle checkpoint

29
Q

what is p53

A

a major tumour suppressor described as the ‘guardian of the genome’

30
Q

what is the function of p53

A

arresting the cell cycle in response to DNA damage

31
Q

what happen to p53 in normal cells

A

constantly degraded due to interaction with Mdm2 (an E3 ubiquitin ligase)

32
Q

what happens to p53 and Mdm2 when DNA is damaged

A

response is activated where Mdm2 and p53 are phosphorylated

33
Q

what happens to p53 after it has been phosphorylated

A

functions as a transcription factor where it transcribes p21

34
Q

what does p21 protein do

A

prevents binding of cyclin D to CDK4, inactivating the complex.
This results in loss of Rb phosphorylation and arrest at G1.
This arrest allows the cell to repair the damaged DNA.

35
Q

what happens if DNA damage is catastrophic and cannot be repaired

A

p53 will induce a type of programmed cell death called apoptosis

36
Q

what is Bax

A

a pro-apoptotic factor induced expression by p53

37
Q

what does the phosphorylation state of p53 depend on

A

whether p53 induces cell-cycle arrest or apoptosis

38
Q

what would the loss of 53 allow

A

cell division to occur without repairing DNA, can lead to further genetic instability, allowing further mutations to accumulate and cancer to develop and increases survival of cancer cells

39
Q

who is more predisposed to a range of cancers

A

people with gremlin mutations in DNA repair genes

40
Q

what are telomeres

A

sequences at the end of DNA which get shorter with each round of cell division

41
Q

what do critically short telomeres trigger

A

cell to stop dividing

42
Q

how do cancers continue to divide

A

cancers reactivate telomerase, an enzyme which extends telomeres during division, making the cell immortal

43
Q

what is telomerase reverse transcriptase (TERT)

A

catalytic component of the enzyme telomerase

44
Q

what do the mutations in TERT promote found in cancers create

A

new binding sites for ETS and GABP transcription factors

45
Q

how do people get TERT promoter mutations

A

genetically inherited

46
Q

what are micro RNAs (miRNAs)

A

type of non-coding RNA that control gene expression by degrading target mRNAs

47
Q

how is a RISC complex formed

A

when miRNAs associate with proteins

48
Q

what happens to mRNAs bound to the RISC complex

A

either cleaved and degraded or transitionally repressed

49
Q

how can miRNAs be tutor suppressors

A

if they trigger deflation if oncogene mRNAs

50
Q

how can miRNAs be oncogenes

A

if they trigger degradation of tumour suppressor mRNAs

51
Q

how do normal cells become metastatic

A

when multiple mutations are needed in a range of genes

human genetics (9 decks)

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