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Molecular Basis of Disease > Mechanisms Of Oncogenesis > Flashcards

Mechanisms Of Oncogenesis Flashcards

1
Q

Name a few risks for cancer

A

Smoking, obesity and wight, workplace exposure to carcinogens, overexposure to UV, Infections e.g. HPV, air pollution and radiation, inherited genes

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2
Q

What is cancer?

A

GROUP of diseases characterised by:

  • abnormal cell proliferation
  • tumour formation
  • invasion of neighbouring normal tissue
  • metastasis to form new tumours at a distant sites
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3
Q

What are carcinomas?

A

Cancer in epithelial cells

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4
Q

What are sarcomas?

A

Cancers from mesoderm cells ie. bone and muscles

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5
Q

What are adenocarcinomas?

A

Cancers found in glandular tissue

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6
Q

Name 2 enabling characteristics of cancer

A

Genome instability and tumour inflammation

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7
Q

Name 2 emerging hallmarks of cancer

A

Avoiding immune destruction and reprogramming energy metabolism

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8
Q

Why is cancer more prevalent as lifespan increases?

A

The longer we live, the more time for DNA mutations to accumulate that may lead to cancer

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9
Q

How do carcinogens cause cancer?

A

Carcinogens cause mutations - alterations in the DNA including point mutations and deletions which accumulate

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10
Q

Why is cancer a disease of the genome?

A

Disease is caused by mutations to the DNA

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11
Q

Why do mutations accumulate?

A

Cell defense mechanism of DNA repair have been evaded. In some cases severe damage to a cell will lead to apoptosis instead

Cells escape surveillance due to burdening of systems that block carcinogenesis

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12
Q

What are the 2 types of mutations (where/when they happen)?

A

Germline (in sperm and egg so can heritable and can pass off to offspring) and somatic mutations (non inheritable so cannot be passed on as mutation only found in daughter cells not all cells)

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13
Q

How do germline mutations relate to developing cancer?

A

Only cause increased RISK of developing vancer, rarely causes cancer immediately inherited

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14
Q

Which type of mutation is more common in cancer?

A

Somatic mutations

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15
Q

How does a primary tumour arise? (first start)

A

From a single cell, initiation of development of cancer is CLONAL
- maligant transformation of single cell enough to give rise to tumour

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16
Q

Doe tumour cells in one tumour stay clonal?

A

Tumour cells evolve, sub clonal selection allows the growth of adavantageous cancer cells causing cancer cells to be HETEROGENEOUS

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17
Q

What does the sub clonal selection of cancer cells depend on?

A

Interactions with other tumour cells and tumour microenvironment

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18
Q

Why do cells need to proliferate and at what rate?

A

To self renew tissues to balance cell loss (apoptosis)

Proliferation must equal cell loss

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19
Q

What signals drive cell proliferation?

A

Growth factors e.g. EGF, PDGF
Cytokines e.g. growth hormone, interleukins
Hormones e.g. estrogen

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20
Q

When does apoptosis take place?

A

Irreparable damage to cells

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21
Q

What are the normal stages cells go through before from life to apoptosis?

A

Proliferation
Differentitation
Perfrom function
Apoptosis (programmed cell death)

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22
Q

In which stages of a cell’s life can mutations occur leading to carcinogenesis?

A

Mutations occurs in the DNA altering the function of normal genes involved in the differentiation stage or before the apoptosis stage both causing total cell numbers to increase (affecting the proliferation to apoptosis balance)

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23
Q

What are the control genes for canceriogenesis?

A

Oncogenes and tumour suppressor genes

24
Q

What are proto-oncogenes?

A

Normal genes that can be activated to be oncogenic

25
Q

What is an oncogene?

A

Proto-oncogene that has mutated leading to signals causing uncontrolled growth

26
Q

What are tumour suppressor genes?

A

Inhibit growth and tumour formation by giving braking signal during G1 phase before entering S phase
- brake mechanism - if mutated also leads to uncontrolled growth

27
Q

What are the 5 models of carcinogenesis?

A

Models can overlap, not one or the other

Model 1 - Chemical carcinogens
Model 2 - Familiality genome instability
Model 3 - Epigenetics and non genotoxic mechanisms
Model 4 - Clonal expansion/ cell selection (Darwinian)
Model 5 - Microenvironment and tissue organisation

28
Q

What are the classes of carcinogens? and examples of each

A

Chemical e.g. benzo(a)pyrene
Physical - radiation (ionisation or ultraviolent) or asbestos
Heritable - genetic predisposition
Viral - Hep B, Epstein Barr

29
Q

Examples of cancer causing carcinogens in tobacco and cigarrete smoke?

A 
Benzene
Arsenic
Formaldehyde
Chromium
Nickel
30
Q

What are the 4 main groups of chemical carcinogens?

A

Polycyclic aromatic hydrocarbons
Aromatic amines
Nitrosamines
Alkylating agents

31
Q

What do chemical carcinogens do on a molecular basis?

A

Add functional groups to DNA bases called DNA adducts

32
Q

What is benzo(a)pyrene?

A

Polycyclic hydrocarbon - pro-carcinogen (class of chemical carcinogen)

33
Q

Where is benzo(a)pyrene found?

A

Coal tar, cigarette smoke

34
Q

Why is benzo(a)pyrene efficiency carcingoen?

A

Enter cells easily

35
Q

How is benzo(a)pyrene activated?

A

Initially a pro-carcinogen

Microsomal enzymes convert G to T forming carcinogen benzo(a)pyrene epoxide

36
Q

How do you test for chemical carcinogen?

A

Ames test

- determines mutagenic activity of chemical by observing whether they cause mutations in sample bacteria

37
Q

Explain the steps in Ames test?

A

Salmonella that requires histidine mixed with possible antigen (half not as control) and both are put on separate dishes with media with minimal histidine.

If there are high number of cells in test and not in control dish, suggests mutagen caused mutations since only cancerous ones will grow in absence of histidine

38
Q

How do physical carcinogens cause mutations? + example

A

Alter bonding of molecules (not directly change the DNA itself like chemical carcinogens)
e.g. UV radiation breaks pyrimidine dimers, repair fails leading to translocation mutations

39
Q

Why do inherited germline mutations cause increased risk of developing cancer?

A

Affected genes usually involved in controlling cell cycle/repair of DNA damage. Impaired function = deficiency in DNA repair causing DNA damage to accumulate increasing risk for cancer

40
Q

What causes the risk of hereditary malignant syndromes?

A

Mutation of a single gene - monogenic hereditary disease

41
Q

What syndromes (inherited) predispose to cancer?

A 
DNA repair defects
- Ataxia Telangiectasia
- Bloom's syndrome
- Lynch Type 2
Chromosomal abnormalities
- Down's syndrome
- Klinefelter's syndrome
42
Q

What DNA repair defect causes ataxia telangiectasia?

A

Mutation in ATM gene which normally codes for serine/threonine kinase which in response to breaks in dsDNA causing cell cycle arrest and DNA repair/apoptosis if needed
- not repaired dsDNA break stays

43
Q

What are symptoms of ataxia telangiectasia?

A

Neuromotor dysfunction
Dilation of blood vessels
Telangiectasia (spider veins)

44
Q

What cancer does ataxia telengiectasia predispoe to?

A

Lymphoma, luekemia and breast cancer

45
Q

What DNA repair defect causes Bloom’s syndrom?

A

Mutation in BLM gene

BLM gene normally allows coding for RecQ helicase which maintains structure and integrity of DNA

46
Q

What are the symptoms of Bloom’s syndrome?

A

Short (rarely above 5 feet)

Skin rash after exposure to sun

47
Q

What cancer does Bloom’s syndrom predispose to?

A

Skin cancer, basal cell carcinoma, squamous cell carcinoma

48
Q

What mutation causes Lynch type 2?

A

Mutation in DNA mismatch repair (MMR) genes e.g. MLH1, MSH2, MSH6 and PMS2

49
Q

What are the symptoms of lynch type 2?

A

No symptoms, only sign is when bowel and womb cancer develops

50
Q

What cancer does lynch type 2 predispose to?

A

Colorectal cancer

51
Q

What properties do tumorigenic viruses have?

A

Stable association with cells (chromosomal integration)
Cells not killed (in non permissive hosts, suppress lytic cycle (normall killing of infected cell) and viral release by budding)
Evade immune surveillace of infected cells - immune suppression and viral antigens not expressed on cell surface

52
Q

Which viruses are associated with human cancer? (both categories of viruses within as well as the type of cancer it causes)

A

DNA viruses
- Epstein Barr - Burkitt’s lymphoma, nasopharyngeal carcinoma
- Papilloma virus - cervical carcinoma, warts
- Hep B and C - hepatoma
RNA retrovirus
HTLV-1 - adult T cell leukemia, lymphoma

53
Q

How many mutations need to take place for type 2 cancer model?

A

Genome instability
- 2 events for carcinogeneis and 1st event must last long enough in tissue to sustain 2nd event
Sporadic - both need to happen which is why happens with older age
Inherited - only one more needed so happens at younger age

54
Q

How do epigenetic changes put risk for cancer? + examples of factors

A

Not structural changes in DNA but functional changes

Risk factors e.g. diet, obesity, hormones

55
Q

Give examples of non genotoxic mechanisms? - model 3

A

Epigenetic changes - diet, obesity

Non genotoxic carcinogens (e.g. immunosuppressants - cyclosprine, tumour promoters - dichlorobenzene)

56
Q

What are the steps for carcinogeneis by clonal expansion and selection?

A

Sequential accumulation of mutations due to carcinogens giving growth advantage during clonal expansion. Cells no longer identical and tumour cells selected to ability to grow and invade.

Some mutations include resistance to therapy
Only few mutations is deleterious for tumour

57
Q

What is a tissue?

A

Groups of cells with similair function

Molecular Basis of Disease (29 decks)

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