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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
What is promoter methylation an important mechanism for?
Inactivating tumour suppressor genes
26
What chromosome and band in particular do patients with retinoblastoma have visible alterations of?
Chromosome 13, particularly band 13q14.1
27
Deletions of the same region of chromosome 13 are detected in retinoblastoma tumour cells from patients of what form? Sporadic or familial?
Sporadic
28
In 1986, how many different laboratories clone and sequence the Rb gene using the known chromosomal location?
3
29
What is the size of the p105-RB gene?
>200Kb
30
How many exons does the p105-RB gene contain?
27
31
How much mRNA does the p105-RB gene contain?
4.7kb
32
How many amino acids does the p105-RB gene make?
928
33
What type of protein does the p105-RB gene encode and what two forms can it exist in?
Nuclear protein | Exists in phosphorylated and non-phosphorylated forms
34
What are the two related proteins to p105-RB?
p107 and p130
35
What type of protein are p107 and p130?
'Pocket proteins' as they have a pocket in their structure that allows binding to various cell proteins
36
p105-Rb interacts with viral proteins that control what?
Cell division
37
What happens to Rb during the cell cycle?
It gets phosphorylated
38
What phase of the cell cycle does B:CDC2 act?
M phase
39
What phase of the cell cycle does D:CDK4/6 act?
G1 up to the R point
40
What phase of the cell cycle does E:CDK2 act?
G1 after the R point and a little way into S
41
What phase of the cell cycle does A:CDK2 act?
First half of S
42
What phase of the cell cycle does A:CDC2 act?
Second half of S and all of G2
43
What cell cycle transition does Rb regulate?
The G1-S transition of the cell cycle
44
What type of feedback loop makes cell cycle irreversible?
Positive feedback loop
45
Give examples of E2F target genes involved in the cell cycle
p107 | cdc25A
46
Give examples of E2F target genes involved in DNA synthesis and replication
TYMS MCM4 MCM5 MCM6
47
Give examples of E2F target genes involved in metabolism
Thioether S-methyltransferase Hydroxysteroid transferase Carboxylesterase Beta-lactamase
48
Give examples of E2F target genes involved in DNA repair
Rad51 BRCA1 CtIP Pir51
49
Give examples of E2F target genes involved in mitosis
TTK | CDC25C
50
Give examples of E2F target genes involved in apoptosis
TGFbeta | p14ARF
51
Give examples of E2F target genes involved in transcription factors
ART27 Myc c-Fos JunB
52
Give examples of E2F target genes involved in chromatin assembly
RbAp48 HP1alpha H4F2 H2A/H2B
53
Tumour suppressor genes protect cells from one or more steps on the path to cancer. What happens when these are mutated?
Predispose to cancer
54
Mutations in tumour suppressor genes can be..
Recessive, haploinsufficient or dominant negative
55
What do gatekeepers do?
Put a break on the cell cycle
56
What do caretakers do?
Take care of the genome
57
What doe landscapers do?
Regulate the microenvironment
58
The first tumour suppressor genes were identified from studies of what?
Familial cancers
59
What does Knudson's two-hit hypothesis indicate?
Two genetic 'hits' are required to inactivate tumour suppressor genes, i.e. loss of heterozygosity
60
Give examples of important tumour suppressor genes
``` Rb PTEN p53 p16 ARF ```
61
Where was Rb (p105) discovered?
In familial retionblastoma
62
What do p105, p107 and p130 together form?
'Pocket proteins'
63
What does Rb control?
The G1-S transition of the cell cycle
64
What is Rb regulated by?
Phosphorylation: hypophosphorylated blocks E2F, phosphorylated releases E2F
65
What is a common way to inactivate tumour suppressor genes?
Promoter methylation
66
Mutations in p53 are an example of..
A dominant negative mutation
67
How is retinoblastoma normally cured?
By removal of the eye
68
Are bilateral retinoblastoma tumours normally familial or sporadic cases?
Familial
69
Are unilateral retinoblastoma tumours normally familial or sporadic cases?
Sporadic | First acquired mutation takes much longer
70
Theoretically, how many 'hits' in a tumour suppressor gene is enough to cause cancer?
2
71
Does loss of heterozygosity speed up or slow down the onset of cancer?
Causes cancers to happen faster
72
Promoter methylation is an example of what type of change?
An epigenetic change
73
Give an example of a gene that is well studied for promoter methylation
p16
74
Why are 'pocket proteins' given that name?
Because of their shape
75
Once a cell has passed the R point in the cell cycle, can it be reversed?
No, it has to complete the cell cycle
76
What point in the cell cycle is a critical point?
The R point
77
Because the positive feedback loop makes the cell cycle irreversible, what is necessary to ensure proper regulation?
A balance of signals
78
What are E2F1/2/3?
Transcription factors
79
Is hyperphosphorylation normal during the cell cycle?
Yes, as long as it happens at the right time

BS3003 Cancer Cell and Molecular Biology (4 decks)

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