Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine Year 1 - Semester 2 - Part 2 > Carcinogenesis > Flashcards

Carcinogenesis Flashcards

1
Q

State the major categories of carcinogens

A

Chemicals (smoking)
Radiation (e.g. UV, ionising radiation)
Viruses

Some parasites - fungal toxins (e.g. aflatoxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

State the mechanism of chemical carcinogenesis

A

Initiation (by a carcinogen)

Promotion - (by an accelerator) [reversible]

Progression [irreversible]

Malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the mechanism of chemical carcinogenesis

A

Normal tissue
(addition of carcinogen)
Altered genotype of an ‘initiated’ cell

New phenotype emerges resulting in clonal expansion of initiated cell (pre-neoplastic focal lesion)

Malignant metastases (neoplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are promotors also known as ?

A

Accelerators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Carcinogen

A

A carcinogen is a substance, organism or agent capable of causing cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Initiator

A

Compounds capable of initiating tumour development may act directly to cause genetic damage.

OR

They may require metabolic conversion by an organism to become reactive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Promoter

A

Tumor promoters are substances that enhance tumorigenicity when administered after a carcinogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Latent period

A

Time between initiation of exposure/ dose of carcinogen to the presentation of the tumours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does an initiation event involve ?

A

Initiation (mutagenic) event involves cellular genome mutations in tumour suppressor genes and oncogenes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Promotion

A

Reversible, Not Mutagenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does promotion involve ?

A

Stimulates proliferation and causes both mutated and normal cells to proliferate.

e.g. TPA, dioxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Progression

A

Irreversible enhancement
Repression of gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does progression involve ?

A

Selection of neoplastic cells for optimal growth of the genotype / phenotype in response to the cellular environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Feature of carcinogenesis

A

Multi-stage process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

High dose of carcinogen

A

Tumours develop
(carcinogen acts as both initiator and promoter/accelerator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Low dose of carcinogen

A

No tumours develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Multiple doses of promoter

A

No tumours develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Low dose of carcinogen + promoter

A

Tumours develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chemical carcinogenesis of the bladder

A

Bladder cancer - common in workers in the dye industry

Carcinogenic compound was: 2-napthylamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Function of 2-napthylamine

A

Used as an intermediate in the manufacture of dyes and as an anti-oxidant in the rubber industry.

Carcinogenic compound in bladder cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe 2-napthylamine

A

Aromatic compounds such as 2-napthylamine are PRE-CARCINOGENS requiring activation.

  • Processed in different parts of the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Action of the liver on 2-napthylamine

A

Convertes 2NTA to carcinogenic metabolite 2-amino-napthol

Detoxified to glucuronide

Excreted by the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Action of the bladder on 2-napthylamine

A

Glucoronide collects in the bladder

Human urothelial cells express Beta-glucuronidase

This converts glucoronide to a carcinogen (o-aminophenol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does the latent period of onset and risk of bladder cancer depend on ?

A

Length of carcinogen exposure.

Short onset (latent) –> high risk of cancer

Longer onset (latent) –> reduced risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Asbestosis

A

Formation of scar tissue in the lung as a result of exposure.

Commonly pre-disposes to bronchogenic carcinomas, increasing the risk by a factor of 5.

26
Q

Result of Asbestos exposure

A

Mesothelioma

Risk depends on the duration and intensity of exposure

27
Q

Latent period of mesothelioma

A

25-45 year

Rare tumour - mesothelioma

28
Q

Asbestos fibres

A

Asbestos is a fibrous silicate substance

When inhaled, the needle like fibres become coated in proteins and their presence excites a macrophage and giant cell response, rather like silicosis.

29
Q

Features of Mesothelioma

What is the problem ?

A

Metastatic spread is uncommon

Problem is local spread, changes in the lung tissue, which destroys the lungs.

30
Q

What is mesothelioma ?

A

A bulky tumour that can fill the chest cavity.

31
Q

Statistic relating to cigarette smoking an cancer risk

A

IN comparison with a non-smoker, a smoker is subject to a 22 fold increase in lung cancer risk.

Stopping smoking reduces risk of cancer

32
Q

Changes in DNA causing lung cancer to form - due to smoking

A

K-Ras and p53 are the 2 genes most frequently mutated in smoking-related lung cancers.

33
Q

Causes of guanine mutations in K-Ras and p53

A

(3,4) Benz(o)pyrene

Binds to DNA leading to guanine mutations.

34
Q

Active carcinogen in tobacco smoke

A

Polycyclic Aromatic Hydrocarbon 3,4-benzpyrene

This is converted by AHH into Benzopyrene diol that binds to DNA forming damaging adducts.

35
Q

What is upregulated in smokers ?

A

AHH

36
Q

What detoxifies carcinogens ?

A

Glutathione S transferase (GSTM1) detoxifies carcinogens.

37
Q

Why may some heavy smokers not develop lung cancer ?

A

AHH may not be expressed

DNA binding epoxies are therefore not generated.

38
Q

Cigarette smoking and cancer risk

A

IN addition to the risk of lung cancers, there is an increased risk of other cancers.

e.g. oesophagus, bladder, kidney and pancreas

39
Q

TCC

A

Transitional cell carcinoma

Arises in the urothelium - bladder
Multifocal and has a tendency to recur.

40
Q

Passive smoking and cancer risk

A

Increased risk of lung cancer

Most potentially toxic gases are present in higher concentrations in side stream smoke than in mainstream smoke.

Nearly 85% of smoke in a room results from side stream smoke.

41
Q

Chemical carcinogenesis following chemotherapy

A

Secondary carcinogenesis can occur from the use of alkylating agents in chemotherapy.

42
Q

What causes an increased risk of secondary tumours following cancer treatment ?

A

DNA damage inflicted on surviving normal somatic cells during treatment.

DNA strand-breakage and base damage induced.

43
Q

Risk from carcinogens in diet

A

Risk involved with nitrites and nitrates

Food additives / Fertilisers that enter drinking water –>

Nitrosamines - carcinogens that can lead to cancers of gastro-intestinal tract and liver.

44
Q

Aflatoxins

A

Naturally occurring carcinogens
- poisoning of the liver
- results in ingestion of aflatoxins from contaminated food

45
Q

What produces aflatoxins ?

A

Fungi Aspergillus Flavus
A. parasiticus

46
Q

What is a potent carcinogen in both human and animal species ?

A

Aflatoxin B1
Liver cancer

  • p53 mutations in liver cancer
47
Q

What predisposes to liver cancer ?

A

A combination of aflatoxins and hepatitis B infections.

48
Q

Influence of rate of carcinogenesis

GI tract

A

Expression of genes in different regions of the GI tract.

Large intestine has a much larger incidence than in the small intestine.

49
Q

Function of BcL2 expression

A

Increased BcL2 expression suppresses apoptosis, which increases cell survival.

BcL2 expressed in the large intestine.

BcL2 NOT expressed in the small intestine.

50
Q

BcL2 expression in the large intestine function

A

BcL2 expressed in the crypts of the large intestine.

BcL2 protects damaged cells from dying.

Thus, these cells survive and accumulate mutations, leading to carcinogenesis.

51
Q

What causes BcL2 over-expression ?

A

Gene Amplification

52
Q

Effect of BcL2 knockout on small / large intestine

A

Small - No effect on apoptosis

Large - Large effect on apoptosis

53
Q

UV-light carcinogenesis

A

Malignant Melanoma Incidence

54
Q

UV radiation

A

Non-ionising (causes excitation of atoms)

Damage DNA

Form pyrimidine dimers but can also break DNA by indirect mechanisms.

55
Q

Xeroderma pigmentosum

A

Rare autosomal recessive disease

Inherited deficiency of endonuclease - an enzyme in the pathway of thymine dimer removal.

Hence repair of damage is ineffective.

56
Q

Radiation carcinogenesis

A

Radiation induced skin cancer

  • Necroses and skin cancer most common amongst early radiologists
57
Q

Latent period of radiation induced leukaemia

A

Latent period is age dependent

Higher age group, longer the latent period

58
Q

Radiation induced bone cancer in radium dial patients

A

Radium follows calcium into the bone during calcium turnover.

Radium is radioactive.

59
Q

Chernobyl radiation

A

Thyroid cancer in children after Chernobyl.

60
Q

Controllable factors contributing to cancer

A

UV light
Alcohol
Diet/ Weight/ Activity
Tobacco

Medicine Year 1 - Semester 2 - Part 2 (53 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions