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Pathological Processes > Session 9 > Flashcards

Session 9 Flashcards

1
Q

What is carcinogenesis?

A

Causes of cancer

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2
Q

Name three intrinsic host factors that account for cancer risk

A

Hereditary
Age
Gender

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3
Q

Extrinsic factories related to… (2)

… account for cancer risk

A

Environment

Behaviour

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4
Q

Much of the increased cancer incidence over the last century is due to…

A

Prolonged life span

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5
Q

About 30% of cancer deaths are due to which 5 leading behavioural/dietary risks?

A 
Tobacco use
Alcohol use
Low fruit/vegetable intake 
High BMI
Lack of physical activity
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6
Q

Most of the evidence about cancer risk comes from…

A

Epidemiological and animal studies

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7
Q

Do intrinsic or extrinsic factors account for the majority of a population’s cancer risk?

A

Extrinsic - ~85%

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8
Q

Extrinsic carcinogens fall into which 3 main categories?

A

Radiation
Infection
Chemicals

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9
Q

Give an example of an industrial carcinogen used in the dye manufacturing industry

A

2-napthylamine

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10
Q

Malignant neoplasms caused by 2-napthylamine showed that there is… (3)

A

A long delay between carcinogen exposure and malignant neoplasm onset

The risk of cancer depends on total carcinogen dosage

There can be organ specificity for certain carcinogens

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11
Q

2-napthylamine has particular organ specificity. What cancer does it cause?

A

Bladder carcinoma

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12
Q

Industrial carcinogens (e.g. Asbestos, coal tars and vinyl chloride) have an effect primarily on the relevant workers. Tobacco smoke’s carcinogenic effect is largely limited to smokers.

What is the reason for this?

A

Due to the dependence on dosage (e.g. Non-smokers are not getting a sufficient dose of carcinogen from passive cigarette smoke)

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13
Q

Is the sequence in which carcinogens are administered critical?

A

Yes - chemical carcinogens called INITIATORS must be given first followed by carcinogens that are PROMOTERS

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14
Q

The Ames test showed that initiators are…

The Ames test showed that promoters cause…

A

Mutagens

Cause prolonged cell proliferation in tissues

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15
Q

Mutagenic chemical carcinogens (initiators) can be classified into which 5 categories?

Give an example of each

A

Polycyclic aromatic hydrocarbons - benzopyrene
Aromatic amines - 2-napthylamine
N-nitroso compounds - dimethylnitrosamine
Alkylating agents - vinyl chloride
Natural products - asbestos

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16
Q

Some chemical carcinogens are ‘pro-carcinogens’ and converted to carcinogens by…

A

Cytochrome P450 in the liver

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17
Q

What are complete carcinogens?

A

Carcinogens that act as both promoters and initiators

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18
Q

Give an example of a complete carcinogen

A

Cigarette smoke

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19
Q

What two main types of radiation can be mutagenic?

A

UV Radiation

Ionising radiation

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20
Q

Ionising radiation includes… (2)

A

X rays

Nuclear radiation

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21
Q

Nuclear radiation comprises… (3)

A

Alpha particles
Beta particles
Gamma rays

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22
Q

Ultraviolet light does not penetrate deeper than…

A

Skin

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23
Q

How can radiation damage DNA?

A

Directly

Indirectly through the production of free radicals

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24
Q

We are exposed daily to sunlight exposing us to more ____ radiation

This leads to an increased risk in which cancer?

A

UV

Skin cancer

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25
Q

How can radiation indirectly damage DNA?

A

Through the production of free radicals

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26
Q

For most people the main exposure to ionising radiation is…

A

Natural background radiation from radon - seeps from the Earth’s crust

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27
Q

How can ionising radiation directly damage DNA? (2)

A

Alters DNA bases

Causes single/double stranded DNA breaks

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28
Q

Some infections are carcinogenic and can act directly or indirectly.

How can infections directly be carcinogenic?

How can infections indirectly be carcinogenic?

A

Directly - affect the genes that control cell growth

Indirectly - chronic tissue injury - regeneration acts as a promoter for existing mutations/causes new mutations from DNA replication errors

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29
Q

Human papilloma virus is strongly linked to which cancer?

A

Cervical Carcinoma

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30
Q

Give an example of an infection that is directly carcinogenic

A

Infection by HPV (human papilloma virus)

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31
Q

How does HPV work as a direct carcinogen?

A

Expresses E6 and E7 protein.

E6 - inhibits p53

E7 - inhibits pRB

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32
Q

What is the function of p53 in cells?

A

Regulates apoptosis

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33
Q

What is the function of pRB in cells?

A

Allows entry of the cell into the cell cycle

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34
Q

The E6 protein expressed by HPV inhibits…

A

p53

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35
Q

The E7 protein expressed by HPV inhibits…

A

pRB protein

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36
Q

Give two examples of infections that act as indirect carcinogens

A

Hep B

Hep C

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37
Q

How can Hep B/Hep C act as indirect carcinogens?

A

Cause chronic liver cell injury and regeneration —> Mutations

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38
Q

Give an example of a bacteria that can act as an indirect carcinogen?

How does it work?

A

Helicobacter pylori

Causes chronic gastric inflammation —> Increased risk of gastric cancer

39
Q

How does HIV act as a carcinogen?

A

Indirectly by lowering the immunity and allowing other potentially carcinogenic infections to occur

40
Q

Give an example of a type of cancer that is more likely to occur due to HIV

A

Kaposi’s sarcoma - skin

41
Q

Inherited predisposition to neoplasia can occur through…

A

Germline mutations

42
Q

What does the two hit hypothesis of neoplasia explain? Describe it.

A

The differences between tumours occuring in families and those occuring in the general population. Says that a cell must acquire two ‘hits’ before becoming neoplastic - more likely in familial cases as a ‘hit’ is already provided in all cells due to germline mutations

43
Q

Give an example of a tumour that follows the two hit hypothesis of neoplasia

A

Retinoblastoma - malignant retinal tumour

44
Q

What is the inheritance pattern seen in retinoblastoma?

A

Dominant

45
Q

Describe the two hit hypothesis that retinoblastoma follows. Compare retinoblastoma running in families to sporadic retinoblastoma

A

Familial retinoblastoma - first hit delivered through germline affecting all cells in the body. Second hit is a somatic mutation in any retinal cell (all carry first hit)

Sporadic retinoblastoma - no germline mutation, two somatic mutations need to occur in the same cell to become neoplastic

46
Q

Invitation and promotion lead to neoplasm when they affect which genes? (2)

A

Proto-oncogenes

Tumour suppressor genes

47
Q

What are tumour suppressor genes?

A

Genes that inhibit neoplastic growth

48
Q

How are tumour suppressor genes inactivated?

A

By inactivation of both alleles - two ‘hits’

49
Q

What are oncogenes?

A

Abnormally activated versions of proto-oncogenes - enhance neoplastic growth

50
Q

How many alleles of each proto-oncogene need to be activated to favour neoplastic growth?

A

1 allele of each proto-oncogene

51
Q

What was the first human oncogene to be discovered that is mutated in ~1/3 of malignant neoplasms?

A

RAS

52
Q

What does the RAS proto-oncogene code for?

A

A small G protein that results in the cell being pushed past the cell cycle restriction point

53
Q

What is the normal function of the G protein coded for by RAS?

A

Results in the cell being pushed past the cell cycle restriction point

54
Q

What is the effect of mutant RAS?

A

A constant signal to push a cell through the cell cycle’s restriction point is produced

55
Q

Which gene restrains cell proliferation by inhibiting passage of a cell through the restriction point?

A

RB gene

56
Q

What is the function of the RB gene?

A

Restrains cell proliferation by inhibiting the passage of a cell through the restriction point

57
Q

Inactivation of how many RB alleles allows unrestrained passage through the restriction point of the cell cycle?

A

Both (2) RB alleles

58
Q

Inactivation of both RB alleles in a cells allows…

A

Unrestrained passage of the cell through the restriction point of the cell cycle

59
Q

In summary, the restriction point can be deregulated by either…

A

An activated/mutant RAS gene (proto-oncogene)

Inactivated pRB gene (tumour suppressor gene)

60
Q

Give an example of 7 things that proto-oncogenes can code for

TS genes code for which proteins?

A 
Growth factors 
Growth factor receptors 
Plasma membrane signal transducers 
Intracellular kinases
Transcription factors
Cell cycle regulators
Apoptosis regulators

Proteins in same pathways but with anti-growth effects

61
Q

How doe genetic instability affect mutation rate?

A

Increases mutation rate

62
Q

Xeroderma pigmentosum is due to mutations in which genes?

A

DNA repair genes - nucleotide excision repair (NER)

63
Q

In which pattern is xeroderma pigmentosum inherited?

A

Autosomal recessive

64
Q

Which DNA repair genes are affected by xeroderma pigmentosum?

A

Genes that affect DNA nucleotide excision repair

65
Q

What happens to patients with xeroderma pigmentosum?

A

They are very sensitive to UV light and develop skin cancer at a young age

66
Q

What does HNPCC stand for? In which pattern is it inherited?

A

Hereditary non-polypsis colon cancer syndrome

Autosomal dominant

67
Q

HNPCC is associated with which cancer?

A

Colon carcinoma

68
Q

The mutation seen in HNPCC affect which DNA repair genes?

A

DNA mismatch repair genes

69
Q

Familial breast carcinoma is associated with which two genes?

A

BRCA1

BRCA2

70
Q

What is the function of BRCA1/BRCA2?

A

They are important in repairing double stranded DNA breaks

71
Q

What mechanism AND genes of DNA repair are affected in…

I) xeroderma pigmentosum
II) HNPCC
III) familial breast cancer

A

XP - genes coding for nucleotide excision repair

HNPCC - DNA mismatch repair genes

Familial Breast Cancer - BRCA1/BRCA2 - double stranded break repair

72
Q

How is chromosome segregation in mitosis affected in malignant cells?

A

Can be abnormal

73
Q

The alterations that account for the accelerated mutation rate found in malignant neoplasms is known as…

A

Genetic instability

74
Q

What are caretaker genes?

A

Genes that maintain genetic stability (a class of tumour suppressor genes)

75
Q

Generally, is a single mutation in proto-oncogenes/tumour suppressor genes sufficient in making a malignant neoplasms?

A

No - alterations in a combination of multiple TS genes/proto-oncogenes is required

76
Q

What is cancer progression?

A

The steady accumulation of multiple mutations in malignant neoplasms

77
Q

What does colon carcinoma usually start as?

A

Colonic adenoma

78
Q

What is the adenoma-carcinoma sequence?

A

Refers to the accumulation of mutations in different TS genes/proto-oncogenes resulting in what started as a adenoma progressing to a carcinoma

79
Q

Give an example of a type of cancer that follows the adenoma-carcinoma sequence

A

Colon cancer

Colonic adenoma —> Colon carcinoma

80
Q

What is the typical timeframe for the accumulation of mutations seen in an adenoma-carcinoma sequence, from early adenoma to metastatic carcinoma?

A

Typically decades

81
Q

Cancer evolves by ___________ and _____________ and finally by _____________

A

Initiation

Promotion

Progression

82
Q

The exact number of mutations needed for a fully evolved malignant neoplasm is unknown but is thought to be approximately…

A

Ten or less

83
Q

It is believed that a fully evolved malignant neoplasms exhibits _____ hallmarks of cancer and ___ enabling feature

A

Six

One

84
Q

A malignant neoplasm exhibits which 6 hallmarks of cancer?

A

Self-sufficiency in growth signals
Resistance to growth stop signals
No limit on the number of times a cell can divide
Sustained ability to induce new blood vessels (angiogenesis)
Resistance to apoptosis
Ability to invade/produce metastases

85
Q

What is seen as the enabling characteristic of a malignant neoplasm?

A

Genetic instability

86
Q

Give an example of a molecular alteration in neoplasms related to self-sufficiency in growth signals

A

HER2 gene amplification in breast cancer

87
Q

Give an example of a molecular alteration in neoplasms related to resistance to anti-growth signals

A

CDKN2A gene deletion in melanoma

88
Q

Give an example of a molecular alteration in neoplasms related to indefinite growth/divisions

A

Telomerase gene activation in most cancers

89
Q

Give an example of a molecular alteration in neoplasms related to increased angiogenesis

A

VEGF expression in many cancers

90
Q

Give an example of a molecular alteration in neoplasms related to resistance to apoptosis

A

BCL2 gene translocation in lymphoma

91
Q

Give an example of a molecular alteration in neoplasms related to the ability of cancer cells to invade and produce metastases

A

E-cadherin mutation in gastric cancer

92
Q

Initiators cause…

Promoters cause…

A

Mutation

Prolonged cell proliferation

93
Q

Environmental carcinogens can be… (3)

A

Chemicals
Infections
Radiation

94
Q

Genetic instability refers to…

A

A high frequency of mutations in the genome of a cell

Pathological Processes (10 decks)

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