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SSC- Biology of Cancer > Carciogenesis > Flashcards

Carciogenesis Flashcards

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1
Q

What is cancer?

A

A group of diseases all sharing similar characteristics

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2
Q

What are the characteristics that all cancers share?

A

They are all abnormal, uncontrolled growths of cells. They all show inappropriate proliferation, invasion, and metastasis

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3
Q

What are the characteristics of a benign tumour?

A
  • Slow growth
  • Non-invasive
  • No metastasis
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4
Q

What are the characteristics of a malignant tumour?

A
  • Rapid growth
  • Invasive
  • Potential for metastasis
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5
Q

What is the increase in incidence of cancer due to?

A
  • Lifestyle changes
  • Increased screening
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6
Q

What is carciogenesis?

A

The process of transformation of a ‘normal’ cell to a cancer cell

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7
Q

What are the stages in carciogenesis?

A
  1. Initiation
  2. Promotion
  3. Progression
  4. Transformation
  5. Evolution
  6. Metastasis
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8
Q

What happens in initiation?

A

A mutation in stem cells is acquried when they are exposed to a carcinogen, and you get unrepaired DNA damage

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9
Q

What happens in promotion?

A

There is induction of cell division, where the cancer starts from a single cell that has a selective advantage over other cells within the same tissue

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10
Q

How does promotion lead to progression?

A

Increased proliferation means increased mutations and therefore an increased advantage

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11
Q

What happens in progression?

A
  • Conversion
  • Propagation
  • Dedifferentiation
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12
Q

What is there a potential for in transformation?

A

Regression

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13
Q

What can be produced in cancer evolution?

A

A drug resistant clinical tumour

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14
Q

What happens in cancer metastasis?

A

Spread of transformed cells

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15
Q

What stages of carciogenesis can be used to treat cancer?

A

Can enter at any stage to try and prevent disease

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16
Q

What does mutation lead to in colorectal carciogenesis?

A

Inactivation of the APC gene

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17
Q

What will an inactivation of the APC gene in colorectal carcinogenesis cause?

A

May cause a change in frequency in division, which leads to an increase in stem cells. This will develop over time into a cluster of APC-less cells with stem cell properties

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18
Q

What might the ‘second hit’ be in colorectal carcinogenesis?

A

Inactivation of Ras

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19
Q

What is the result of the inactivation of Ras in colorectal carcinogenesis?

A

Increased selective advantage

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20
Q

What might the third hit be in colorectal carcinogenesis?

A

Inactivation of p53

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21
Q

What happens after the third hit in colorectal carcinogenesis?

A

Increased growth, starts to form an adenoma

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22
Q

What does the forth hit in colorectal carcinogenesis lead to?

A

The rapid development of cancer

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23
Q

What extracellular/environmental factors can cause genes to mutate?

A
  • Binding of ultimate carcinogens
  • Ionising radiation/UV
  • DNA translocation
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24
Q

What do ultimate carcinogens do?

A

Bind to DNA and alter the sequence

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25
Q

What effect does ionising radiation and UV have on DNA?

A

Causes strand breaks and cross links

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26
Q

When may DNA translocation cause mutations?

A

When it is translocation to transcriptionally active regions

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27
Q

What intracellular factors can cause mutations?

A
  • Misinterpretation of code
  • Polymerase slippage/base misalignment
  • Ineffective repair
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28
Q

What can all mutations potentially affect?

A

Cellular signalling

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29
Q

What can act as initiating stimuli in carcinogenesis?

A
  • Chemical carcinogens
  • Oncogenic viruses
  • Radiation
  • UV light
  • Oxygen free radicals
  • Replication errors
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30
Q

When can oxygen free radicals act as an initiating stimuli for carcinogenesis?

A

When there is an imbalance between their production (which happens naturally) and their removal

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31
Q

What are the categories of directly acting carcinogens?

A
  • Alkylating and acylating agents
  • Weak carcinogens
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32
Q

Give three examples of alkylating or acylating agents that can act as carcinogens

A
  • Dimethylsulphate
  • Chlorambucil
  • Dichloromethane
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33
Q

What can act as a weak carcinogen?

A

Cytotoxic drugs

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34
Q

Give an example of a class of procarcinogens

A

Polycyclic aromatic hydrocarbons

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35
Q

When might polycyclic aromatic hydrocarbons be produced?

A

During the combusion of organic compounds, e.g coal, petrol, cooked foods, tobacco, smoke

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36
Q

What does exposure to polycyclic aromatic hydrocarbons typically cause tumours?

A

Lung and colon

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37
Q

Where is aflatoxin found?

A

In fungus found on peanuts and other foodstuffs

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38
Q

What are the steps in the metabolic toxification of aflatoxin?

A

Aflatoxin B1 + Mfo –> Aflatoxin-2,3-epoxide

Alfatoxin-2,3-epoxide is highly reactive, so will react with DNA to form a DNA adduct

39
Q

What does exposure to aflatoxin correlate to?

A

The risk of liver cancer

40
Q

Where is liver cancer related to aflatoxin prevalent?

A

In hot regions

41
Q

How can you determine aflatoxin exposure?

A
  • Can measure content in food
  • Can measure DNA adduct
42
Q

What happens to genes in cancer?

A
  • Oncogenes are activated
  • Tumour supressor genes are inactivated
43
Q

What mutations can occur to a gene?

A
  • Alteration of bases
  • Strand break
  • Base oxidation
  • Deletion of bases
  • Adducts of carcinogens and base
  • Chromosomal translocation/rearrangement
  • Gene amplification
44
Q

Describe the severity of different DNA strand breaks?

A

If it’s a single strand break, the body can normally repair it. Double strand breaks normally can’t be repaired

45
Q

How does an adduct mutation cause cancer?

A

A chemical binds to the base, and so repair mechanisms either can’t get part that point on the DNA, or don’t know what base to replicate

46
Q

What mechanisms are in place to prevent mutations causing cancer?

A
  • Repair mechanisms
  • Mismatch and excision repair
  • p53
47
Q

What causes single point mutations?

A

Mutagens

48
Q

What are the type of single point mutations?

A
  • Transitions
  • Transversions
49
Q

What is a transition mutations?

A
  • Purine -> purine (A -> G, G -> A)
  • Pyrimidines -> pyrimidines (C -> T, T -> C)
50
Q

What is a transversion mutation?

A
  • Purine -> Pyramidine
  • Pyramidine -> Purine
51
Q

What causes structural chromosomal abberations?

A

Clastogens

52
Q

What structural chromosomal aberrations can occur?

A
  • Translocations
  • Inversions
  • Deletions
  • Insertions
  • Chromatid interchanges
53
Q

What causes genome mutations?

A

Aneugens

54
Q

What is aneuploidy?

A

An increase in the number of chromosomes in the cell

55
Q

What is the most common nucleophilic binding site on DNA?

A

N7

56
Q

Is N7 on guanine highly mutagenic or not?

A

No, it is easily repaired

57
Q

What is the guanine N7 commonly used for?

A

Monitoring

58
Q

What guanine nucleophilic binding sites are highly mutagenic?

A

N2 and N3

59
Q

How does mutagenesis by adduct formation occur?

A
  1. An adduct binds to the base
  2. After the first replication, the adduct is maintained in the sequence for one copy
  3. After replication of the copy with the adduct, you get a different amino acid, resulting in a different protein and therefore different structure
60
Q

What proportion of base changes result in pernament mutation?

A

Fewer than 1:1000

61
Q

What are the DNA repair pathways?

A
  • Excision repair
  • Error-prone repair
  • Mismatch repair
  • Defects in DNA replication
62
Q

What can be removed in excision repair?

A
  • Base
  • Nucleotide
63
Q

What enzymes perform base excision?

A

DNA glycosylases

64
Q

What does nucleotide excision remove?

A

Bases with bulky adducts

65
Q

Is excision repair error prone or error free?

A

Error free

66
Q

What is error-prone repair a response to?

A

Severe DNA damage

67
Q

What happens in error-prone repair?

A

Low fidelity DNA polymerases recognise specific lesions, and restore the original sequence

Accepts error, but fixes gross changes

68
Q

What is mismatch repair?

A

Proofreading by exonuclease part of DNA polymerase

69
Q

How does repair occur in mismatch repair?

A
  • Correcting mismatched bases in new strand during DNA replication
  • Genetic recombination
70
Q

How are defects in DNA replication used in repair?

A
  • Genome rearrangements
  • Chromosome loss
71
Q

What things can act as promoting agents?

A
  • Chemical promoters
  • Hormones
  • Inflammation
  • Microbial infection
72
Q

Give 4 classes of chemical promoters

A
  • Phorbol esters
  • Phenols
  • Xenoestrogens
  • Saccharin
73
Q

Give three examples of where inflammation and infection can act as promoters

A
  • Chronic irritation
  • Endoparasites
  • Bacterial infection
74
Q

Give an example of an endoparasite that can act as a promoter

A

Schistosoma haematobium

75
Q

Give an example of a bacterial infection that can act as a promoter

A

Helicobacter pylori

76
Q

What factors increase the risk of breast cancer?

A
  • Older age at menopause
  • Post-menopausal hysterectomy
  • Oral contraceptives
  • Alcohol
  • Obesity
  • Younger age at menarche
77
Q

What factors decrease the risk of breast cancer?

A
  • More children
  • Breastfeeding
  • Pre-menopausal hysterectomy
78
Q

What factors increase the risk of getting cancer?

A
  • Hereditary
  • Carcinogens
  • Radiation
  • Chemicals
  • Viruses
  • Diet
79
Q

How can food act as carcinogens?

A
  • Can contain carcinogens/mutagens
  • Can contain toxins
  • Calories can alter the hormone balance
  • Inflammation/oxidative stress inducers
  • Hot drinks/food can cause inflammation in mouth and oesophagus
80
Q

What foods increase the risk of cancers?

A
  • Alcohol
  • Red meat intake
  • Animal fat
  • Salted fish
  • BBQ and chargrilled foods
  • Salt-preserved foods
  • Contaminated foods
81
Q

What evidence is there for the link between certain foods and cancer?

A
  • Migration studies
  • Intervention trials
82
Q

What are the components of the diet?

A
  • Macronutrients
  • Micronutrients
  • Other compounds; procarcinogens, promoters, alcohol
83
Q

What are the categories of macronutrients?

A
  • Fats
  • Carbohydrates
  • FIbres
84
Q

What are the categories of micronutrients?

A
  • Antioxidants
  • Carotenoids
  • Polyphenols
85
Q

What does red meat consumption increase the risk of?

A

Colon cancer

86
Q

What effect does cooking red meat have on its carcinogenic risk?

A

It increases the heterocyclic amine concentration by 50-100x. HA’s are mutagenic.

87
Q

What happens to heterocyclic amines in the liver?

A

They are metabolised to genotoxic metabolites

88
Q

What has shown heterocyclic amines to be mutagenic?

A

Ames test

89
Q

What has shown heterocyclic amines to be carcinogenic?

A

In vivo models

90
Q

What can increase the HA levels in food?

A

Increasing the cooking time

91
Q

What can reduce the HA levels in food?

A

Marinating

92
Q

What are the sources of acrylamide?

A
  • Used as drinking water clarifier
  • Found in cigarette smoke
93
Q

What is the problem with acrylamide?

A

It is a genotoxic metabolite, which adducts with DNA in vivo

However, the human evidence for cancer is scarce

SSC- Biology of Cancer (11 decks)

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