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MOD 2 > Session 11 - Neoplase III > Flashcards

Session 11 - Neoplase III Flashcards

1
Q

What is carcinogenisis?

A

Study of causes of cancer

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2
Q

Three intrinsic factors which lead to canc

A

Age
Sex
Heredity

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3
Q

What two factors account for cancer risk?

A

A combination of intrinsic host factors such as heredity, age and gender (especially hormonal),and extrinsicfactors related to the environment and behaviour

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4
Q

What are extrinsic causes of cancer?

A

Environment and lifestyle

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5
Q

What are the three main categories of extrinsic cancer risk?

A

Chemicals, radiation and infection

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6
Q

What are the five leading behavuioural and dietary risks

A 
High BMI
Low fruit and vegetable intake
Tobbaco use
Alcohol use
Lack of physical activity
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7
Q

What are the two factors which are key to carcinogenesis?

A

The prescence of initators and promoters

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8
Q

What are initators?

A

Mutagens/carcinogens

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9
Q

What are promoters?

A

Substance which cause prolonged proliferation in target tissues

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10
Q

What does initiator and promoter action culminate in?

A

Amonoclonal expansion of mutant cells, and then become fully malignant via progression

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11
Q

Give three examples of inherited susceptibilty to the development of tumours

A

Retinitis (Xeroderma) Pigmentosum
Ataxia Telangiectasia
Fanconi’s Anaemia

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12
Q

What is retinitis (Xeroderma) pigmentosum

A

Increased risk of skin cancers when exposed to UV rays in sunlight

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13
Q

What is ataxia telangiectasia?

A

Defective response to radiation damage, profound susceptibility to lymphoid malignancies, usually die before age 20

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14
Q

What is fanconi’s anaemia?

A

Sensitivity to DNA cross-linking agents, marrow hypo function and multiple congenital anomalies, predisposition to cancer

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15
Q

Give three cancers and the genes they’re associated with

A

Familial Adenomatous Polyposis - APC
Breast Cancer - BRCA1/2
Li Fraumeni Syndrome - p53

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16
Q

What is a proto-oncogene?

A

A normal gene that can become an oncogene due to mutations or increased expression

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17
Q

What are the normal roles of proto-oncogene, and what about their DNA sequence makes them suspicous

A

Proto-oncogenes are present in all normal cells, and are involved in normal growth and differentiation.
They have a DNA sequence identical to viral oncogenes.

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18
Q

How can proto-oncogenes be modified to become oncogenes?

A

Mutation, amplification, translocation

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19
Q

What is the name of oncogene products?

A

Oncoproteins

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20
Q

What do oncoproteins from oncogenes allow the cell to do

A

To escape normal growth control, becoming self sufficient without external signals required to grow

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21
Q

Why are proto-oncogenes easily mutated to neoplasia? `

A

Only one allele of a proto-oncogene needs to be mutated to cause neoplasia

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22
Q

What is a tumour supressor gene?

A

A gene that encodes proteins that suppress growth and therefore cancer

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23
Q

What do tumour supressor genes do in cells?

A

Produce proteins which supress growth

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24
Q

What does loss or alteration of tumour supressor gene cuase to happen?

A

Loss of growth supression

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25
Q

What has to happen to tumour supressor genes in order to produce neoplasia?

A

Both alleles need to be mutated (2 hit hypothesis)

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26
Q

What is the two hit hypothesis?

A

Both alleles of a tumour supressor gene to be mutated in order for neoplasia to develop (suprresion rather than production)

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27
Q

How does the two hit hypothesis explain familial and sporadic cancers?

A

“First hit” can be inherited in families, increasing the incidence of the condition in related individuals. It can also occur sporadically in the population as a result of random first and second hits occuring.

28
Q

Name three oncogenes

A

Ras
C-myc
HER-2

29
Q

Discuss the role of RAS

A
  • Normally transmits growth-promoting signals to the nucleus
  • Mutant Ras is permanently activated resulting in continuous stimulation of cells
  • 15-20% of all Cancers
  • Colon and lung cancer
30
Q

Discuss the role of C-myc

A
  • Binds to DNA, stimulates synthesis
  • Amplified (over-expressed)
    o Neuroblastoma, breast cancer
  • Translocation 8  14
    o Burkitt’s lymphoma
31
Q

Discuss the role of HER-2

A
  • Encodes for a growth factor receptor
  • Amplified (over-expressed)
  • ~25% of breast cancers
  • Herceptin is a competitive antagonist at the HER-2 Receptor
32
Q

Name two tumour supressor genes

A

pRb and P53

33
Q

What does pRb control usually

A
  • Passage beyond the R checkpoint at G1

- S boundary is governed by the phosphorylation of pRb.

34
Q

What does def3ect in both alleles of pRb lead to?

A
  • Cell escaping cell cycle control.

- Retinoblastoma

35
Q

What proportion of tumours have P53 mutations?

A

Approximately 50%

36
Q

What does P53 do usually?

A
  • Gene encodes a nuclear protein, which binds to and modulates expression of genes important for cell-cycle arrest, DNA repair and Apoptosis
37
Q

What are the two main stages of carcinogenesis?

A

Initiator

Promoter

38
Q

What occurs in initiation?

A
  • Exposure of cells to a sufficient dose of initiator
  • Cell is altered, potentially capable of producing tumour
  • Permanent DNA damage (mutations)
  • Irreversible and has ‘memory’
  • Effect modified by genetic factors, DNA repair
  • Initiation alone is not sufficient for tumour formation

Extremely Agonising Pain Intrigues My Intellect

39
Q

Name three promoters

A

Hormones, local tissue responses, immune responses

40
Q

What happens in promotion?

A
  • Induce tumours in initiated cells
  • Non-tumourigenic on their own
  • Need exposure after initiation
  • Cellular changes are reversible
    o Remove promoter and cell should be okay and return to normal
  • Enhance proliferations, especially in mutated cells and increase incidence of further mutations – can result in cancer
    o Think of all the mutations necessary for metastasis… this makes it more likely
41
Q

What does radiation do to DNA? What does its effect depend on?

A

A whole range of damage

  • single/double strand breaks and base damage
  • DNA breaks

Indirectly - free radicals

The effect depend on the quality of radiation and the dose.

42
Q

What does radiation need to do to cause cancer?

A

Overwhelm DNA repair mechanisms, leaving DNA damage unrepaired. Mutations in oncogenes/tumour supressor genes lead to cancer

43
Q

Give two types of radiation and the types of cancer they cause

A
  • Ionising radiation
    o E.g. Hiroshima (Early leukaemia/lymphoma  Late Thyroid/breast)
  • Ultraviolet radiation
    oE.g. Squamous cell carcinoma, Basal cell carcinoma, Malignant melanoma
44
Q

How do chemical carcinogens interact with DNA?

A

Directly, others require metabolic conversion to an active form

45
Q

Name three chemical carcinogens

A

Polycyclic aromatic hydrocarbons

  • Aromatic Amines
  • Alkylating Agents
46
Q

What are polycyclic aromatic hydrocarbons produced from? How do they have an effect? What types of cancer do they form?

A

o Produced in combustion of tobacco and fossil fueld
o Hydroxylated to active form
o Lung Cancer, bladder cancer, skin cancer (scrotal skin in chimney sweeps)

47
Q

What happens to aromatic amines to cause cancer? What cancer do they cause?

A

o Hydroxylated in liver and conjugated with glucuronic acid (Phase 2 drug metabolism, non toxic)
oDeconjugated to active form in urinary tract by urinary glucuronidase
oActive form sits in bladder  Bladder cancer

48
Q

What kind of workers are exposed to aromatic amines?

A

Rubber and dye workers

49
Q

What are three infective viruses which can cause cancer?

A

Hepatitis B
Epstein Barr
Human papilloma

50
Q

Describe hepatitis B’s action in the body, and the cancer it’s associated wtih

A

o Associated with hepatocellular carcinoma
o Viral DNA integrated into host cell genome
o Virus causes liver cell injury –>Chronic inflammation causing regenerative hyperplasia
o Increased cell division gives increased risk of genetic changes

51
Q

What cancers is epstein barr implicated in?

A

pathogenesis of Burkitt’s Lymphoma, Some Hodgkin’s lymphoma, Nasopharyneal carcinoma

52
Q

How does epstein barr have an effect

A

oInfects epithelial cells or oropharynx and B cells
oViral genes dysregulate normal proliferative and survival signals
oSets the stage for acquisition of mutations

53
Q

How does human papilomma cuase cancer?

A

oHPV genes disrupt normal cell cycle
- releases E6 (p53 inhibition) and E7 (pRb inhibition )
oViral genes incorporated into host cell genome, driving proliferation

54
Q

Name five other agents which cause cancer and the cancers they cause

A 
-	Asbestos
o	Malignant mesothelioma, lung cancer
-	Aflatoxins
o	Hepatocellular carcinoma (collaborates with HBV)
-	Schistosoma
o	Bladder cancer
-	Helicobacter
o	Gastric cancer and lymphoma
-	Hormones
o	Androgens and hepatocellular carcinoma
55
Q

Name three conditions which predispose to tumours

A

Ulcerative colitis
Cirrhosis
Adenoma of colon/rectum

56
Q

What cancer does ulcerative colitis cause and how?

A
  • Colorectal carcinoma
  • DNA damage and microsatellite instability
  • May mask symptom of cancer
57
Q

What cancer do cirrhosis cause and why?

A

hepatocellular carcinoma

Some of association due to chronic viral hepatitis

58
Q

How does adenoma of colon/rectum cause cancer

A

Transforms to malignant neoplasia

59
Q

What is the Ames test?

A

Bacteria homogenised with liver cells (p450 required) and mutagens, which allows them to grow in environments which would usually inhibit proliferation.

60
Q

How can a pro-carcinogen cause cancer?

A

Converted to carcinogen by P450

61
Q

What is a complete carcinoge?

A

Initiator + promoter

62
Q

Where does radiation come from?

A

UV B

Ionising - radon + medical tests

63
Q

Three types if repair

A 
Nucleotide excision repair (xeroderma pigmentosa - ub damage! 
Mismatch repair (HNPCC)
Double strand break (breast/ovarian cancer)
64
Q

Give type I DNA damage in each condition

A

Nucleotide excision repair (xeroderma pigmentosa - ub damage!
Nucleotide instability

Mismatch repair (HNPCC)
Micro satellite

Double strand break (breast/ovarian cancer)
Chromosomal instability

65
Q

Retinoblastoma mechanism?

A

RAS (gprotein, bound to GTP)
Causes up regulation cyclic D
Cycline dependent kinase activated
Rb phosphorylated, so mitosis occurs (already deleted in retinoblastoma!)

66
Q

Final model?

A

Initiation - promotion - progression (additional mutations)

Intrinsic
Chronic inflammation can acts as promoter
Genetic activation of indicators abs promoters

Progression leads to deregulation of cell cycle

MOD 2 (16 decks)

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