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MCD Cancer > Oncogenes and tumour suppressors > Flashcards

Oncogenes and tumour suppressors Flashcards

1
Q

What are the hallmarks of cancer (cancer cell phenotype)?

A 
Disregard of signals to stop proliferating
Disregard of signals to differentiate
Capacity for sustained proliferation
Evasion of apoptosis
Ability to invade 
Ability to promote angiogenesis
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2
Q

What do proto-oncogenes code for?

A

Essential proteins involved in maintenance of cell growth, division and differentiation

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3
Q

What can mutation of a protooncogene cause?

A

It converts the protooncogene into an oncogene whose protein product no longer responds to control influences

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4
Q

What is gene amplification?

A

Production of multiple gene copies- can occur due to problems with a polymerase protein

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5
Q

What does gene amplification lead to?

A

Overproduction of gene product

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6
Q

What are chimeric genes?

A

Genes that are formed by combinations of portions of one or more coding sequences to form new genes

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7
Q

When are chimeric genes a problem?

A

If one of the pieces of translocated DNA is a promoter leading to upregulation of the other gene portion- occurs in Burkitt’s lymphoma
Or if fusion gene formed produces an abnormal protein e.g. philadelphia chromosomes in CML

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8
Q

What is the Philadelphia chromosome formed by?

A

Translocation of chromosome segments from chromosomes 9 and 22, they 2 key areas are:
ABL- chromosome 9
BCR- chromosome 22
BCR-ABL fusion gene leads to development of cancer

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9
Q

In terms of signal transduction pathways, what effect can a protooncogene mutating to form an oncogene have?

A

It can lead to downstream activation of signalling pathways such that they no longer need to respond to upstream stimuli

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10
Q

What normally happens when GTP binds to Ras?

A

It becomes active and activates the kinase cascade leading to the production of gene regulatory proteins

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11
Q

How is active Ras switched off?

A

Dephosphorylation of GTP to GDP

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12
Q

What happens in mutant Ras?

A

It will fail to dephosphorylate GTP meaning that it persists so Ras remains active

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13
Q

What pathway does the Ras pathway belong to?

A

Complex signalling cascade called mitogen-activated protein kinase cascade (MAPK)

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14
Q

What does Ras code for?

A

Family of proteins such as Ki-Ras and Ha-Ras which are membrane bound GTPases that are important in stimulation of cell proliferation

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15
Q

What are tumour suppressor genes typically?

A

Proteins whose function is to regulate cellular proliferation and maintain cell integrity (e.g. retinoblastoma)

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16
Q

How many copies of each tumour suppressor gene does each cell have and what does this mean?

A

2
Mutation or deletion of just one gene copy is usually insufficient to promote cancer (mutation or loss of both copies means loss of control

17
Q

What are the features of inherited cancer susceptibility (has led to discovery of tumour suppressor genes)?

A 
Family history of related cancers
Unusually early onset
Bilateral tumours in paired organs
Synchronous or successive tumours
Tumours in different organ systems in same individual 
Mutation inherited through germline
18
Q

What is retinoblastoma?

A

Inherited malignant cancer of developing retinal cells

19
Q

What is retinoblastoma caused by?

A

Mutation of RB1 tumour suppressor gene on chromosome 13q14

20
Q

What does RB1 encode?

A

Nuclear protein that is involved in regulation of cell cycle

21
Q

What are the functional classes of tumour suppressor genes?

A 
Regulate cell proliferation 
Maintain cellular integrity
Regulate cell growth
Regulate cell cycle
Nuclear transcription factors
DNA repair proteins
Cell adhesion molecules
Cell death regulators
22
Q

What is the overall effect of tumour suppressor genes?

A

Suppress neoplastic phenotype

23
Q

What examples of tumour suppressor genes are there?

A 
p53
BRCA1
PTEN
APC
p16-INK4A
MLH1
24
Q

When is p53 inactive?

A

When bound to MDM2

25
Q

What is p53 important in?

A

Lots of stuff including regulation of p53 target genes and protein-protein interactions

26
Q

How is p53 activated?

A

Many different types of cellular stress

27
Q

What is different about p53 from other tumour suppressor genes?

A

Mutants of p53 act in a dominant way and mutation of a single copy is sufficient to get dysregulation of activity

28
Q

What does phosphorylation of p53 do?

A

Destabilises it so it isn’t degraded so quickly and can exert its effects- it is triggered by cellular stress

29
Q

What is the APC gene involved in?

A

Cell adhesion and cell signalling

30
Q

What causes loss of APC gene?

A

Deletion in 5q21

31
Q

What do people with APC mutation develop?

A

Multiple benign adenomatous polyps in the colon

32
Q

How does APC work?

A

It participate in WNT signalling pathway to alter transcription and growth
It helps control activity of beta-catenin and prevents uncontrolled growth

33
Q

In what type of cancer is mutation of APC common?

A

Colon

34
Q

How does colorectal cancer develop?

A

APC in normal epithelium gets mutated and becomes inactive (loss of TSG) leading to hyperprolifertion of epithelium
DNA hypomethylation (epigenetic change) combined with K-ras mutation (oncogene) will make polyps develop into adenomas
Mutation of P53 (guardian of genome) will result in development of carcinoma which can then go onto metastasise

35
Q

Compare oncogenes and tumour suppressor genes?

A 
Oncogene:
Gene active in tumour
Specific translocations/point mutations
Mutations rarely hereditary 
Dominant at cell level
Broad tissue specificity
Leukaemia and lymphoma
Tumour suppressor gene:
Gene inactive in tumour
Deletions or mutations
Mutations can be inherited
Recessive at cell level
Considerable tumour specificity
Solid tumours

MCD Cancer (15 decks)

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