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Biology of Cancer SSC > Tumour Suppressors > Flashcards

Tumour Suppressors Flashcards

1
Q

What is a tumour suppressor? (1)

A

A gene that protects a cell from one or more steps on the path to cancer

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2
Q

What is a tumour suppressor? (2)

A

A gene which, when mutated, predisposes an individual to cancer

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3
Q

What are the 3 classes of TSGs?

A

Gatekeepers
Caretakers
Landscapers

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4
Q

What do gatekeeper TSGs do?

A

Prevent growth of potential cancer cells

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5
Q

What do caretaker TSGs do?

A

Maintain the integrity of the genome

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6
Q

What do landscaper TSGs do?

A

Control the cellular microenvironment

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7
Q

What are the 10 hallmarks of cancer?

A 
Resisting cell death
Avoiding immune destruction
Enabling replicative immortality
Evading growth suppressors
Sustaining proliferative signalling
Genome instability and mutation
Inducing angiogenesis
Activating invasion and metastasis
Tumour-promoting inflammation
Deregulating cellular energetics
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8
Q

What 2 kinds of retinoblastoma are there?

A

Familial (40%) and sporadic (20%)

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9
Q

When do familial retinoblastomas appear compared to sporadic?

A

At a younger age

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10
Q

Where can familial retinoblastomas develop?

A

Often in both eyes, can also be accompanied by tumours in other organs

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11
Q

What was Knudson’s two-hit hypothesis?

A

Cancer is a multi-hit disease i.e. it is the result of accumulated mutations.

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12
Q

Why does a familial mutant Rb allele mean the carrier will develop bilateral disease much earlier than in sporadic case?

A

The first somatic mutation in a familial Rb mutation case leads to two mutant Rb gene copies. The chances of this happening on both sides is much higher. In sporadic cases, 2 somatic mutations must occur to reach the same stage.

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13
Q

Name the 7 ways of eliminating normal Rb function

A
  • Non-disjunction (Chromosome)
  • Non-disjunction and replication
  • Mitotic recombination
  • Gene conversion
  • Deletion
  • Point mutation
  • Promoter methylation
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14
Q

Name 2 key tumour suppressor genes

A

p53

PTEN

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15
Q

How was p53 originally identified?

A

By its interaction with viral proteins

SV40, Adenovirus and Papillomavirus

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16
Q

What do p53 mutations do?

A

Some don’t stop cancer developing, some actively help cancer develop.

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17
Q

What proportion of human cancers is p53 mutated in?

A

~50%

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18
Q

What happens in the majority of cancers that don’t have p53 mutations?

A

There are other mutations that affect the p53 activation pathway or other indirect ways to inactivate p53.

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19
Q

In which rare, autosommal dominant condition do patients have a germline TP53 mutation?

A

Li-Fraumeni Syndrome - develops early and aggressively

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20
Q

What is the protein structure of p53?

A

Nuclear phosphoprotein. Acts in tetrameric form.

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21
Q

What is the function of p53?

A

Transcription factor that recognises a 10bp consensus sequence in promoters

22
Q

Where are p53 mutations clustered?

A

Exons 5-8

23
Q

Where are the p53 mutation hotspot?

A

Amino acids 175, 248, and 273 - DNA binding domains.

24
Q

What do mutant p53 do to normal p53?

A

Interfere with normal p53 function.

25
Q

Why does mutant p53 interfere with normal p53 function?

A

Because p53 exists as a tetramer, if even one of the units is mutated the protein will not function.

26
Q

How is p53 expressed in the absence of damage?

A

At very low levels. T1/2 = 20 minutes

27
Q

What functions does p53 have?

A

It depends on what the specific cell needs at any one time, both in response to stress and in normal conditions.

28
Q

Can these functions be antagonistic and spontaneous?

A

Yes

29
Q

What does p53 need to exert its effect?

A

Some require gene transcription (transactivation), some don’t.

30
Q

Where are the functions of p53 performed?

A

Some in the nucleus, some in the cytosol.

31
Q

What can p53 do as the guardian of the genome?

A
  • Cell cycle arrest
  • DNA repair
  • Block angiogenesis
  • Apoptosis
32
Q

What can cell cycle arrest lead to?

A
  • Senescence

- Return to proliferation

33
Q

How is p53 activated?

A

By post-translational modifications

34
Q

How do the post translational modifications give p53 their specific function?

A

Via a mixture of modifications at different combinations of sites along p53

35
Q

What is MDM2?

A

The chief cellular antagonist of the p53 tumour suppressor gene

36
Q

How is MDM2 induced?

A

By p53 to moderate itself

37
Q

What does MDM2 do?

A

Degrades p53

38
Q

What happens to MDM2 if a mutation is detected?

A

It is stopped so p53 function can be upregulated

39
Q

What is the Warburg effect?

A

p53s effect on metabolism - cancer cells mostly use aerobic glycolysis to obtain energy instead of oxidative phosphorylation. This leads to lactic acid build up in the cytosol.

40
Q

What are the 2 pathways to senescence?

A
  • Replicative senescence

- Stress induced premature senescence

41
Q

What is replicative senescence?

A

Occurs physiologically with age. Telomere shortening with each division as duplication is incomplete.

42
Q

What is PTEN?

A

A tumour suppressor with phosphatase activity

43
Q

What does PTEN do?

A

Dephosphorylates PIP3 to block cell proliferation.

44
Q

What can induce PTEN?

A

p53

45
Q

What is the oathway that normally activates PIP3?

A

PI(membrane bound, intracellular molecule) -(PI Kinases)-> PIP2 -(Phospholipase C) -> IP3 or
PI(membrane bound, intracellular molecule) -(PI Kinases)-> PIP2 -(PI3 kinase) -> PIP3

46
Q

What is PIP3 normally used for?

A

To signal division and growth

47
Q

What does PTEN convert PIP3 to?

A

PIP2

48
Q

What percentage of prostate carcinomas have a PTEN mutation?

A

40-50%

49
Q

What percentage of glioblastomas have a PTEN mutation?

A

25-50%

50
Q

What percentage of endometrial carcinoma have a PTEN mutation?

A

35%

51
Q

p53 + PTEN =

A

Apoptosis

52
Q

p53 - PTEN =

A

Senescence

Biology of Cancer SSC (16 decks)

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