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MIMS > Cancer > Flashcards

Cancer Flashcards

1
Q

Where is the incidence of cancer highest and lowest

A

Highest generally more developed countries (it is the 2nd largest cause of death after cardiovascular disease)
Lowest in developing countries, lowest in Africa as a continent

4 fold difference between them

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2
Q

What is the largest cause of cancer

A

Smoking (~30%)

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3
Q

What does metastasis mean

A

Spreading to other organs from the site of origin (primary tumour) to other sites (secondary tumours)

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4
Q

What are carcinomas

A

Malignant rumours of epithelial cells

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5
Q

What is carcinoma in situ

A

A pre-malignant change in which the epithelium shows malignant changes but does not invade underlying tissue

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6
Q

What are sarcomas

A

Tumours of tissue derived from the mesenchymal layer

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7
Q

What sí leukaemia

A

Abnormal proliferation of circulating white blood cells

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8
Q

How do the hallmarks of cancer arise

Why is it an old age disease

A

Through accumulation of mutations in the genome

There is an accumulation of mutations

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9
Q

How many bases and genes in the human genome

A

3x10^9

~ 20,000 genes

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10
Q

How close to a blood vessel must a cell be to avoid hypoxia

Why

A

~10 cells distance

Inadequate diffusion over long distances

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11
Q

What is angiogenesis

A

Growth of new blood vessels

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12
Q

What does bevacizumab target

A

It is A monoclonal antibody that targets VEGF

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13
Q

What is the vasculature in tumours like and what does this mean

A

Tumour neo-vasculature is usually leaky and tortuous with unstable blood flow patterns, leading to hypoxia and thus necrosis in the core

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14
Q

Are tumours clonal?

A

Yes but mutations result in them being heterogenous with multiple clones co-existing in the tumour. The predominant clone at any point will comprise superior fitness compared to the other clones

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15
Q

Which mutations give rise to cancer

A

Mutations in key signalling molecules that control cell fate

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16
Q

Give the 4 hallmarks of cancer

A

Mutation
Angiogenesis
Tumour expression
Invasion and metastasis

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17
Q

How many deaths in 2014 were caused by cancer

A

29%

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18
Q

True or false: the increased cancer incidence may be accounted for by increased longevity

A

True
More than a third of deaths from cancer were in people aged 75 or over
Cancer is mainly a disease of old age due to the accumulation of genetic changes over time

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19
Q

What are the top 3 environmental causes of cancer

A

Smoking (33%)
Obesity (20%)
Diet (5%)

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20
Q

Name an infection that causes cancer

A

Helicobacter pylori

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21
Q

Name 2 kinds of transmissible cancer

A

Tasmanian devil facial tumours

Canine transmissible venereal tumours

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22
Q

True or false: the most common cancers have a good survival rate

A

False

Several of the most common cancers have a very poor survival rate

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23
Q

Which are the four most common causes of cancer mortality

A

Lung
Bowel
Breast
Prostate

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24
Q

What is the largest preventable cause of cancer

A

Smoking

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25
Q

Why may large dog breeds be more susceptible to osteosarcomas

What evidence further backs this up

A

Highly active growth plates at these sites?

Primary osteosarcomas are generally restricted to children and young adults

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26
Q

What does mastinib do

A

It is a small molecule inhibitor that targets the c-Kit growth factor receptor in dogs

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27
Q

What are the key differences between benign and malignant tumours?

A

Benign: slow growing
Encapsulated
Non-invasive/ -metastatic
Differentiated

Malignant: fast growing
Invasive/ metastatic
Poorly differentiated

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28
Q 
Which of the following are benign and which are malignant:
Adenoma 
Sarcoma
Fibroma
Hyperplasia 
Carcinomas in situ 
Carcinoma
Dysplasia 
Metaplasia
A

Only carcinoma and sarcoma are malignant

The rest (including carcinoma in situ) are benign

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29
Q

What is a sarcoma

A

Tumours of mesenchymal layer (connective tissue and blood vessels)

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30
Q

What is leukaemia

A

Abnormal proliferation of white blood cells

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31
Q

What is a neuroectodermal tumour

A

Tumours of the PNS or CNS

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32
Q

What kind of tumour are astrocytomas and meningiomas

A

Neuroectodermal tumours

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33
Q

Give the 6 cell intrinsic hall marks of cancer

A 
Growth signal autonomy 
Resistance to inhibitory growth signals
Unlimited replicative capacity
Reprogramming of cell metabolism
Resistance to apoptosis 
Genetic instability
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34
Q

Discuss the first 4 hallmarks of cancer

A

These are the major characteristics of tumour cells - uncontrolled proliferation

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35
Q

Discuss the hallmark of apoptosis resistance

A

Most incipient tumours die by apoptosis

Mutations that render cells resistant to apoptosis contribute to cancer

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36
Q

Why is the hall mark of genetic instability important in cancer

A

It can contribute to rapid accumulation of further mutations

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37
Q

What are the 3 cell extrinsic hallmarks of cancer

A

Induction of angiogenesis
Metastatic potential
Evasion from immune system

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38
Q

Why is angiogenesis important in cancer

A

Solid tumours need to develop a vasculature that supplies oxygen and nutrients

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39
Q

How does metastasis occur

A

Tumour cells invade surrounding tissue, enter the blood, or lymphatic system and lodge in distant sites

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40
Q

How do tumours avoid the immune system

A

Tumour cells and recruited normal cells produce cytokines that dampen the immune response to the tumour

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41
Q

How big are benign dormant micro tumours

A

~10^5 cells

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42
Q

What limits the growth of a microtumour

A

Growth requires a blood supply

Oxygen can diffuse 10 cells from source
This limits the size of an avascular tumour to 1-2mm

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43
Q

Angiogenesis is a cancerous process. True or false?

A

No it is a normal process as new vessels are always needed, eg in wound healing

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44
Q

Give an example of a tumour hijacking the angiogenic process

A

Some tumour cells secrete VEGF

VEGF binds to specific receptors on endothelial cells that line blood vessels and stimulates secretion of MMPs, allowing tissue remodelling
The activated endothelial cells proliferate and migrate towards the source of the VEGF
these activates endothelial cells also secrete PDGF, a chemo attractant for smooth muscle cells

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45
Q

Is tumour vasculature stable?

A

No the neo-vasculature of tumours is often leaky and tortuous with unstable blood flow patterns

46
Q

What does the unstable neo vasculature of tumours usually lead to

A

The centre of the tumour becoming hypoxic, forming a necrotic core

47
Q

What are the 6 stages of angiogenesis in tumours

A 
Hypoxia
Proteolytic degradation 
Tip cell migration
Tube formation
Regulation of vessel size
Tumour vascularisation
48
Q

Why is hypoxia important for angiogenesis

A

Hypoxia induces HIF-1 expression and the consequent release of VEGF

49
Q

What is the angiogenic switch

A

When the careful regulation of stimulants and inhibitors of angiogenesis is disrupted

50
Q

Name 2 angiogenic inhibitors

A

Angiostatin

Endostatin

51
Q

What is Avastin

A

A monoclonal antibody to VEGF

It is an anti-angiogenic drug with complicated side effects

It is no longer approved by the FDA

52
Q

Other than VEGF, name 4 angiotensin activators

A

PDGF-BB

FGF

IGF

HGF

53
Q

What does IGF stand for

A

Insulin like Growth Factor

54
Q

What does HGF stand for

A

Hepatocyte Growth Factor

55
Q

Name a cancer that does not require angiogenesis

Why does this present complications

A

PDAC

It is a tumour that is largely avascular and hypoxic

Lack of vasculature compromises the effective delivery of therapeutic drugs into the tumour

56
Q

What is the most frequent characteristic of a malignant tumour

A

Invasion of surrounding normal tissue

57
Q

What mechanism allows local tissue invasion of cancer

A

Tumour cells express proteases that degrade the basement membrane that defines the boundary of the tissue/ organ in which they originate

58
Q

What do you call entering tissues that are distant from the primary tumour

A

Extravasate

59
Q

True or false: metastic tumours possess the same genetic changes as the primary tumour from which they are derived

What does this suggest

A

True

Mutations conferring metastatic potential occur early and are not acquired

60
Q

What kind of phenotype do both primary tumours and metastatic tumours exhibit

A

A de-differentiated phenotype

61
Q

What is the Ames test

A

A test of the ability of a chemical to mutate the genome of salmonella

62
Q

What correlation shows cancer is due to genetic mutation

A

There is a good correlation between the ability of a chemical to mutate DNA and chase tumourigenic transformation of cells

63
Q

How do dietary carcinogens affect DNA

A

They react with nucleophilic sites in purines and Pyrimidine rings to form DNA adducts

64
Q

Only mutations in which kind of gene lead to cancer?

A

Proto-oncogenes

Genes that control cell fate such as cell proliferation, survival etc

65
Q

What genes are associated with HNPCC

A

MSH 2
MLH 1

HNPCC tends to occur when these are non functional

66
Q

What are tumour suppressors

A

Genes whose inactivation promotes the incidence of cancer
OR
A gene whose protein product inhibits cancer

DNA repair genes are tumour suppressors

67
Q

Why are tumours heterogenous

A

They are constantly evolving in response to intrinsic (eg hypoxia) or extrinsic factors (therapy)

68
Q

Why do familial cancers require only 1 hit to a tumour suppressor

A

Patient already has 1 inactivated tumour suppressor allele

69
Q

Why do sporadic cancers occur at lower frequency

A

Requires 2 independent hits to deactivate both copies of the tumour suppressor

70
Q

What is a loss of heterozygosity often associated with

A

An inherited predisposition to cancer

71
Q

3 epigenetic causes of cancer

A

Changes in chromatin
Post translational modification of proteins
Control of transcription or translation

72
Q

What are epigenetic changes

Can these be heritable

A

Ones that do not involve mutation of the DNA itself

Yes they can pass from parent cell to daughter cell

73
Q

Are miRNAs oncogenes or tumour suppressors

A

Different ones can be either

If there are increased miRNAs in a tumour it is an oncogene
Whereas increased miRNA in normal cells compared to the tumour suggests it is a tumour suppressor

74
Q

What mediates the transformation from normal cell to tumour cells

A

The counter balance activities of oncogenes and tumour suppressors

75
Q

How do tumours rise with oncogenes vs tumour suppressor genes

A

Oncogene: gain of function

Tumour suppressor: loss of function

76
Q

Who discovered the first oncogene

How did he do it

What oncogene was it

A

Peyton Rous

Removed a chicken breast sarcoma and ground it up with sand. He passed this through a fine pore filter
He injected the filtrate into a young chicken and observed a sarcoma in the injected chicken

Rous Sarcoma Virus

77
Q

How does the RSV cause cancer

A

It inserts a gene into the DNA leading to a replication defect

78
Q

Does it take a single RSV cell to cause cancer

A

No

Transformation by RSV requires continuous maintenance by sarcoma gene activity

79
Q

Transformation by RSV requires continuous maintenance by sarcoma gene activity. Give experimental evidence of this

A

Infect normal cells with RSV mutant at 37 degrees C
Cells transform
Shift temperature to 41 degrees C and the cells return to normal
Shift temperature back to 37 degrees C and the cells become cancerous again

80
Q

What does retroviruses integration result in

A

The insertion of a potent LTR promoter at each end

81
Q

What are the 2 general mechanisms to turn cellular genes cancerous ?

A
  1. Deregulated activity

2. Deregulated/ elevated expression

82
Q

What does the c-src protein kinase look like in its inactive form

A

C-terminal Tyr is bound by internal SH2 domain, locking Src into inactive conformation

83
Q

How does the c-src protein kinase become activated

A

Upstream signals displace SH2 domain, allowing adoption of active conformation

84
Q

What do Ras proteins do

A

Connect receptors to the internal effectors of the cell

85
Q

How are Ras proteins deactivated

A

Hydrolysis of GTP

86
Q

Which Ras αα are mutated in many human cancers

A

12, 13, 61

87
Q

Why is RSV unusual

A

In retains all the viral genes in addition to transducing the cellular src gene

88
Q

What are the 2 ways of oncogene activation

A
  1. Mutation of the normal coding sequence

2. Gene amplification, chromosome duplication or truncation or promoter region mutation

89
Q

Give an example of gene amplification causing cancer

A

Abnormal expression of MYC promotes cell proliferation

90
Q

Lower levels of MYC correlate with a worse prognosis. True or false?

A

False

Higher levels of MYC lead to poor prognosis

91
Q

Give an example of when c-MYC is deregulated

A

Non AIDS Burkitt’s lymphoma

92
Q

What kinda of transcription factor is myc

A

Pleiotropic

93
Q

Oncogenesis is a result of persistence. True or false?

A

True

Requires persistent deregulation

94
Q

Is a single oncogenic mutation enough for cancer

A

No

Eg Land et al showed in Vitro that high levels of both Ras and Myc were needed for tumour growth

95
Q

What is intrinsic tumour suppression

Give examples of intrinsic tumour suppression

A

A fail safe mechanism for high levels of a single oncogene activity

High levels of myc stimulate apoptosis
High levels of Ras stimulate cell cycle arrest

96
Q

Normal cell + tumour cell=

A

Normal cell usually

97
Q

What do Simian Virus, HPV, and Adenovirus 5 all do

A

Bind to p53 and p105^RB

Eg E6 binds to p53 and destroys It

98
Q

What does p105^RB do

A

It is a pocket protein that binds and inactivated the E2Fs transcription factors that drive expression of cell cycle genes

It is A cell cycle inhibitor

99
Q

What does p53 do

A

It is a transcription factor that responds to stress/ damage/ oncogenic signalling and induces cell cycle arrest or cell death

100
Q

Why is cancer much more common in people with heterozygous Rb alleles

A

They have a high frequency of LOH (loss of heterozygosity)

There is exchange of genetic information between homologous chromosomes in the Rb heterozygote meaning the mutated and non functional copy becomes dominant

101
Q

What kind of exchange of genetic information occurs in the Rb heterozygote

A

Mitotic recombination
Chromosomal non disjunction
Gene conversion

102
Q

What does Rb do

A

In non phosphorylated state it sequesters E2F proteins, which stops cell cycle proliferation

Phosphorylation stops Rb
However, HPV and Adenovirus inhibit Rb but not by phosphorylating it

103
Q

High levels of myc stimulate what to cause apoptosis?

A

p53

104
Q

What does high levels of Ras stimulate

A

p16

p53

105
Q

What do p53 mutations do

A

Inhibit DNA binding

106
Q

What does p53 have to do to become active

A

It must bind with other p53 molecules to become a homo tetramer

DNA binds in the centre of the tetramer

107
Q

What happens if p53 is a hetero tetramer

What does this mean

A

It is inactive

A mutant p53 would act as a dominant negative as only one mutation is needed to knock it out

108
Q

What do oncogenes do that their normal counterparts don’t?

A

Nothing but their activity is no longer regulated

109
Q

What will happen if a tumour suppressor is hypo-methylated

A

It is silenced and cancer can occur

110
Q

Name a protein made active by a point mutation in its proto-oncogene

A

RAS

111
Q

What activates cyclin B/ CDK1

A

CDK24

112
Q

What is APC gene product involved in

A

G1/S checkpoint

MIMS (12 decks)

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