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SSC- Biology of Cancer > Tumour Suppressors > Flashcards

Tumour Suppressors Flashcards

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1
Q

What is a tumour suppressor gene?

A

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

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

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2
Q

What are the different classifications for tumour suppressor genes?

A
  • Gatekeepers
  • Caretakers
  • Landscapers
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3
Q

What do gatekeeper tumour supressor genes do?

A

Prevent growth of potential cancer cells

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4
Q

What do caretaker tumour suppressor genes do?

A

Maintain the integrity of the genome

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5
Q

What does failure of the caretaker tumour suppressor genes lead to?

A

Genetic instability, which is one of the hallmarks of cancer

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6
Q

What do landscaper tumour suppressor genes do?

A

Control the cellular microenvironment

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7
Q

Why is the cellular microenvironment important in cancer?

A

Cells around can have a positive or negative effect on cancers .

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8
Q

Which of the hallmarks of cancer do tumour suppressor genes stop?

A
  • Deregulating cellular energetics
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Tumour-promoting inflammation
  • Activating invasion and metastasis
  • Inducing angiogenesis
  • Genome instability and mutation
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9
Q

What hallmarks of cancer do tumour suppressor genes encourage?

A
  • Avoiding immune destruction
  • Enabling replicative immortality
  • Resisting cell death
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10
Q

What are the two types of retinoblastomas?

A
  • Sporadic (60%)
  • Familial (40%)
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11
Q

How do sporadic and familial retinoblastomas differ?

A
  • Familial retinoblastomas appear at a younger age
  • Familial retinoblastomas often develop in both eyes, and can be accompanied by tumours in both organs
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12
Q

What can be deduced from the differences between sporadic and familial retinoblastomas?

A

Something predisposes the familial patients to cancer

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13
Q

What is Knudson’s two hit hypothesis?

A

That cancer is a multi-hit disease.

In the case of familial retinoblastoma, one hit is hereditary, and one is acquired

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14
Q

What are the mechanisms for loss of heterozygosity (the second hit)?

A
  • Non-disjunction (chromosome loss)
  • Nondisjunction and duplication
  • Mitotic recombination
  • Gene conversion
  • Deletion
  • Point mutation
  • Promoter methylation
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15
Q

What are human tumour supressor genes normally involved in?

A

Cell cycle and DNA damage control

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16
Q

How was p53 originally identified?

A

By interactions with viral proteins

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17
Q

Which viral proteins did p53 interact with, leading to its initial discovery?

A
  • Large T antigen of SV40
  • E1B of adenovirus
  • E6 of papillomavirus
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18
Q

What was p53 first thought to be?

A

An oncogene

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19
Q

In what % of human cancers is p53 mutated?

A

50%

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20
Q

What must be true of cancer cells that do not have mutated p53?

A

p53 must have undergone some form of inactivation

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21
Q

What is Li-Fraumeni syndrome?

A

A rare, dominant-inherited cancer syndrome where patients have germline mutation in TP53

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22
Q

What kind of protein is p53?

A

A nuclear phosphoprotein

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23
Q

What is meant by a nuclear phosphoprotein?

A

Nuclear - found in nucleus

Phosphoprotein - regulated by phosphorylation

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24
Q

What is the function of p53?

A

It is a transcription factor

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25
Q

In what form does p53 act?

A

In its tetrameric form

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26
Q

How does p53 act as a transcription factor?

A

It recognises a 10bp consesus sequence in promoters

27
Q

Where in the molecule do p53 mutations occur?

A

They are clustered in exons 5-8

Amino acids 175, 248, and 273 are hotspots

28
Q

Describe the expression of p53?

A

It is expressed at very low levels in the absense of damage

29
Q

What is the half life of p53?

A

20 minutes

30
Q

What is the role of p53?

A
  • Main role is to define the cellular response to differnet kinds of damage
  • Has many other dunctions, both in response to stress and in normal conditions - some of these functions are antagonistic and simultaneous
31
Q

Do the functions of p53 require the transcription of genes?

A

Some do (transactivation), some do not

32
Q

Where do the functions of p53 occur?

A

Some in the nucleus, some in the cytosol

33
Q

What kinds of stress does p53 protect against?

A
  • Lack of nucleotides
  • UV radiation
  • Ionising radiation
  • Oncogene signalling
  • Hypoxia
  • Blockage of transcription
34
Q

What actions can p53 take to ensure the integrity of the genome?

A
  • Cell cycle arrest
  • DNA repair
  • Block of angiogensis
  • Apoptosis
35
Q

What can happen to the cell after p53 has induced cell cycle arrest?

A
  • Senescence
  • Return to proliferation
36
Q

What is senescence?

A

Pernament cell arrest

37
Q

How is p53 activated?

A

Post-translational modifications

38
Q

How is p53 activated?

A

p53 induces mdm2, which then blocks p53

39
Q

What are the cellular responses to p53 induction?

A
  • Apoptosis
  • Cell cycle arrest, and senescence if prolonged
  • DNA repair
  • Antiangiogenesis
  • Metabolism
  • Pro-survival (goes against other functions)
40
Q

What genes are involved in the p53 apoptotic pathways?

A
  • Bax
  • PUMA
  • Noxa
  • PERP
  • Fas
41
Q

What genes are involved in p53 induced cell cycle arrest and sensecence?

A
  • p21
  • GADD45
  • Reprimo
42
Q

How do basal levels of p53 act to aid survival?

A

They are an anti-oxidant

43
Q

What is the Warburg effect?

A

Cancer cells mostly use aerobic glycolysis to obtain energy, instead of oxphos pathway

44
Q

What kind of energy production do normal cells use?

A
  • Oxidative phosphorylation
  • Fatty acid oxidation
45
Q

What kind of energy production does p53 induce?

A
  • Glycolysis
  • Fatty acid oxidation
  • Oxidative phosphorylation
46
Q

What are the types of senescence?

A
  • Replicative senescence
  • Stress-induced premature sensecence
47
Q

What causes replicative senesence?

A

Short or damaged telomeres

48
Q

What causes stress-induced premature senescence?

A
  • Oxidative stress
  • Activated oncogenes
  • Other stresses
49
Q

What are telomeres?

A

Repetitive DNA sequences that cap the chromosomes and protects their ends from erosion

50
Q

What happens to the telomeres with each duplication?

A

Their ends shorten because duplication is not complete

51
Q

What effect does telomerase have on telomeres?

A

They elongate them

52
Q

What kind of cells possess telomerase?

A
  • Cancer cells
  • Stem cells
53
Q

Draw a diagram illustrating the pathway to senesence

A
54
Q

What is the problem with the accumulation of senescent cells?

A

They disrupt the tissues and so decrease function

55
Q

What is antagonistic pleiotrophy?

A

When one gene controls more than one phenotypic trait in an organism (pleitropy), at least one of them is beneficial, and at least one is detrimental to the organisms fitness

56
Q

What is PTEN?

A

A tumour suppressor with phosphatase activity

57
Q

What does PTEN do?

A

Dephosphorylates PIP3,, and so blocks cell proliferation

58
Q

What is PIP3?

A

A signalling molecular of many pro-growth pathways

59
Q

Where is the PI3K/PTEN pathway commonly inactivated/downregulated?

A

In many cancers - prostate, lung, brain

60
Q

What can induce PTEN?

A

p53

61
Q

What does p53 and PTEN together lead to?

A

Apoptosis

62
Q

What does p53 without PTEN lead to?

A

Senescence

63
Q
A

SSC- Biology of Cancer (11 decks)

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