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human genetics > Week 5- Genetics of cancer > Flashcards

Week 5- Genetics of cancer Flashcards

(51 cards)

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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

Study These Flashcards
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

Study These Flashcards
A

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

23
Q

what are the classes of oncogenes

Study These Flashcards
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

Study These Flashcards
A
  • excessive amount of protein
  • abnormal protein
  • novel protein in excess
25
how were tumour suppressor genes understood
from the study of retinoblastoma
26
what is retinoblastoma
childhood cancer which occurs from transformation of immature neural cells in the retina
27
what happens in sporadic and familiar retinoblastoma
- sporadic: tumours form in only one eye - familial: tumours form in both eyes and often earlier, suggesting an underlying predisposition
28
what is Rb
a tumour suppressor which regulates G1-S phase cell-cycle checkpoint
29
what is p53
a major tumour suppressor described as the 'guardian of the genome'
30
what is the function of p53
arresting the cell cycle in response to DNA damage
31
what happen to p53 in normal cells
constantly degraded due to interaction with Mdm2 (an E3 ubiquitin ligase)
32
what happens to p53 and Mdm2 when DNA is damaged
response is activated where Mdm2 and p53 are phosphorylated
33
what happens to p53 after it has been phosphorylated
functions as a transcription factor where it transcribes p21
34
what does p21 protein do
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
what happens if DNA damage is catastrophic and cannot be repaired
p53 will induce a type of programmed cell death called apoptosis
36
what is Bax
a pro-apoptotic factor induced expression by p53
37
what does the phosphorylation state of p53 depend on
whether p53 induces cell-cycle arrest or apoptosis
38
what would the loss of 53 allow
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
who is more predisposed to a range of cancers
people with gremlin mutations in DNA repair genes
40
what are telomeres
sequences at the end of DNA which get shorter with each round of cell division
41
what do critically short telomeres trigger
cell to stop dividing
42
how do cancers continue to divide
cancers reactivate telomerase, an enzyme which extends telomeres during division, making the cell immortal
43
what is telomerase reverse transcriptase (TERT)
catalytic component of the enzyme telomerase
44
what do the mutations in TERT promote found in cancers create
new binding sites for ETS and GABP transcription factors
45
how do people get TERT promoter mutations
genetically inherited
46
what are micro RNAs (miRNAs)
type of non-coding RNA that control gene expression by degrading target mRNAs
47
how is a RISC complex formed
when miRNAs associate with proteins
48
what happens to mRNAs bound to the RISC complex
either cleaved and degraded or transitionally repressed
49
how can miRNAs be tutor suppressors
if they trigger deflation if oncogene mRNAs
50
how can miRNAs be oncogenes
if they trigger degradation of tumour suppressor mRNAs
51
how do normal cells become metastatic
when multiple mutations are needed in a range of genes

human genetics (9 decks)

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