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BS3003 Cancer Cell and Molecular Biology > Tumour suppressor genes I > Flashcards

Tumour suppressor genes I Flashcards

1
Q

What is a tumour suppressor gene?

A

A gene that helps control or regulate cell growth.
A gene that protects a cell from one or more steps on the path to cancer.
A gene which, when mutated, predisposes an individual to cancer (cancer susceptibility gene).

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2
Q

Define a gatekeeper tumour suppressor gene

A

Prevent the growth of potential cancer cells (classic tumour suppressor genes)

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3
Q

Define a caretaker tumour suppressor gene

A

Genes that maintain the integrity of the genome (genetic instability)

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4
Q

Define a landscaper tumour suppressor gene

A

Genes that control the cellular microenvironment

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5
Q

Do tumour suppressor genes exclusively belong to a class of gatekeepers, caretakers or landscapers?

A

No, some tumour suppressor genes can perform more than one of these functions

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6
Q

Are mutations in oncogenes that cause cancer dominant or recessive?

A

Dominant

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7
Q

Are mutations in tumour suppressor genes that cause cancer dominant or recessive?

A

Recessive

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8
Q

Define dominant negative

A

Dominant interference of normal gene function

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9
Q

Define haploinsufficient

A

Reduced activity or lower quantity of tumour suppressor gene

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10
Q

Define recessive

A

Loss of activity or absence of tumour suppressor gene

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11
Q

What can dominant negative mutations, halpoinsufficieny and recessive mutations in tumour suppressor genes all lead to?

A

Cancer

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12
Q

What tumour suppressor gene was identified from the study of familial retinoblastoma?

A

Rb

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13
Q

What tumour suppressor gene was identified from the study of familial Li-Fraumeni syndrome?

A

p53

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14
Q

What tumour suppressor gene was identified from the study of familial adenomatous polyposis?

A

APC

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15
Q

What tumour suppressor gene was identified from the study of familial breast cancer?

A

BRCA

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16
Q

What tumour suppressor gene was identified from the study of familial neurofibromatosis?

A

NF1

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17
Q

What is retinoblastoma?

A

A rare childhood cancer of the eye

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18
Q

What percentage of retinoblastomas are sporadic?

A

60%

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19
Q

What percentage of retinoblastomas are familial?

A

40%

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20
Q

Who came up with Knudson’s two-hit hypothesis and when?

A

Alfred G. Knudson in 1971

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21
Q

When was Alfred G. Knudson born?

A

1922

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22
Q

What are the 7 mechanisms for loss of heterozygosity?

A 
Nondisjunction (chromosome loss)
Nondisjunction and duplication
Mitotic recombination
Gene conversion
Deletion
Point mutation
Promoter methylation
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23
Q

What is the need for promoter methylation?

A

Epigenetic silencing of gene expression

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24
Q

What enzyme catalyses the reaction of unmethylated transcriptionally active DNA to methylated DNA?

A

DNA methyl-transferase

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25
Q

What is promoter methylation an important mechanism for?

A

Inactivating tumour suppressor genes

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26
Q

What chromosome and band in particular do patients with retinoblastoma have visible alterations of?

A

Chromosome 13, particularly band 13q14.1

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27
Q

Deletions of the same region of chromosome 13 are detected in retinoblastoma tumour cells from patients of what form? Sporadic or familial?

A

Sporadic

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28
Q

In 1986, how many different laboratories clone and sequence the Rb gene using the known chromosomal location?

A

3

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29
Q

What is the size of the p105-RB gene?

A

> 200Kb

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30
Q

How many exons does the p105-RB gene contain?

A

27

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31
Q

How much mRNA does the p105-RB gene contain?

A

4.7kb

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32
Q

How many amino acids does the p105-RB gene make?

33
Q

What type of protein does the p105-RB gene encode and what two forms can it exist in?

A

Nuclear protein

Exists in phosphorylated and non-phosphorylated forms

34
Q

What are the two related proteins to p105-RB?

A

p107 and p130

35
Q

What type of protein are p107 and p130?

A

‘Pocket proteins’ as they have a pocket in their structure that allows binding to various cell proteins

36
Q

p105-Rb interacts with viral proteins that control what?

A

Cell division

37
Q

What happens to Rb during the cell cycle?

A

It gets phosphorylated

38
Q

What phase of the cell cycle does B:CDC2 act?

39
Q

What phase of the cell cycle does D:CDK4/6 act?

A

G1 up to the R point

40
Q

What phase of the cell cycle does E:CDK2 act?

A

G1 after the R point and a little way into S

41
Q

What phase of the cell cycle does A:CDK2 act?

A

First half of S

42
Q

What phase of the cell cycle does A:CDC2 act?

A

Second half of S and all of G2

43
Q

What cell cycle transition does Rb regulate?

A

The G1-S transition of the cell cycle

44
Q

What type of feedback loop makes cell cycle irreversible?

A

Positive feedback loop

45
Q

Give examples of E2F target genes involved in the cell cycle

A

p107

cdc25A

46
Q

Give examples of E2F target genes involved in DNA synthesis and replication

A

TYMS
MCM4
MCM5
MCM6

47
Q

Give examples of E2F target genes involved in metabolism

A

Thioether S-methyltransferase
Hydroxysteroid transferase
Carboxylesterase
Beta-lactamase

48
Q

Give examples of E2F target genes involved in DNA repair

A

Rad51
BRCA1
CtIP
Pir51

49
Q

Give examples of E2F target genes involved in mitosis

A

TTK

CDC25C

50
Q

Give examples of E2F target genes involved in apoptosis

A

TGFbeta

p14ARF

51
Q

Give examples of E2F target genes involved in transcription factors

A

ART27
Myc
c-Fos
JunB

52
Q

Give examples of E2F target genes involved in chromatin assembly

A

RbAp48
HP1alpha
H4F2
H2A/H2B

53
Q

Tumour suppressor genes protect cells from one or more steps on the path to cancer. What happens when these are mutated?

A

Predispose to cancer

54
Q

Mutations in tumour suppressor genes can be..

A

Recessive, haploinsufficient or dominant negative

55
Q

What do gatekeepers do?

A

Put a break on the cell cycle

56
Q

What do caretakers do?

A

Take care of the genome

57
Q

What doe landscapers do?

A

Regulate the microenvironment

58
Q

The first tumour suppressor genes were identified from studies of what?

A

Familial cancers

59
Q

What does Knudson’s two-hit hypothesis indicate?

A

Two genetic ‘hits’ are required to inactivate tumour suppressor genes, i.e. loss of heterozygosity

60
Q

Give examples of important tumour suppressor genes

A 
Rb
PTEN
p53
p16
ARF
61
Q

Where was Rb (p105) discovered?

A

In familial retionblastoma

62
Q

What do p105, p107 and p130 together form?

A

‘Pocket proteins’

63
Q

What does Rb control?

A

The G1-S transition of the cell cycle

64
Q

What is Rb regulated by?

A

Phosphorylation: hypophosphorylated blocks E2F, phosphorylated releases E2F

65
Q

What is a common way to inactivate tumour suppressor genes?

A

Promoter methylation

66
Q

Mutations in p53 are an example of..

A

A dominant negative mutation

67
Q

How is retinoblastoma normally cured?

A

By removal of the eye

68
Q

Are bilateral retinoblastoma tumours normally familial or sporadic cases?

69
Q

Are unilateral retinoblastoma tumours normally familial or sporadic cases?

A

Sporadic

First acquired mutation takes much longer

70
Q

Theoretically, how many ‘hits’ in a tumour suppressor gene is enough to cause cancer?

71
Q

Does loss of heterozygosity speed up or slow down the onset of cancer?

A

Causes cancers to happen faster

72
Q

Promoter methylation is an example of what type of change?

A

An epigenetic change

73
Q

Give an example of a gene that is well studied for promoter methylation

74
Q

Why are ‘pocket proteins’ given that name?

A

Because of their shape

75
Q

Once a cell has passed the R point in the cell cycle, can it be reversed?

A

No, it has to complete the cell cycle

76
Q

What point in the cell cycle is a critical point?

A

The R point

77
Q

Because the positive feedback loop makes the cell cycle irreversible, what is necessary to ensure proper regulation?

A

A balance of signals

78
Q

What are E2F1/2/3?

A

Transcription factors

79
Q

Is hyperphosphorylation normal during the cell cycle?

A

Yes, as long as it happens at the right time

BS3003 Cancer Cell and Molecular Biology (4 decks)

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