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Semester 2 - Mechanisms of Disease > 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
What has to happen to tumour supressor genes in order to produce neoplasia?
Both alleles need to be mutated (2 hit hypothesis)
26
What is the two hit hypothesis?
Both alleles of a tumour supressor gene to be mutated in order for neoplasia to develop (suprresion rather than production)
27
How does the two hit hypothesis explain familial and sporadic cancers?
"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
Name three oncogenes
Ras C-myc HER-2
29
Discuss the role of RAS
- 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
Discuss the role of C-myc
- Binds to DNA, stimulates synthesis - Amplified (over-expressed) o Neuroblastoma, breast cancer - Translocation 8  14 o Burkitt’s lymphoma
31
Discuss the role of HER-2
- Encodes for a growth factor receptor - Amplified (over-expressed) - ~25% of breast cancers - Herceptin is a competitive antagonist at the HER-2 Receptor
32
Name two tumour supressor genes
pRb and P53
33
What does pRb control usually
- Passage beyond the R checkpoint at G1 | - S boundary is governed by the phosphorylation of pRb.
34
What does def3ect in both alleles of pRb lead to?
- Cell escaping cell cycle control. | - Retinoblastoma
35
What proportion of tumours have P53 mutations?
Approximately 50%
36
What does P53 do usually?
- Gene encodes a nuclear protein, which binds to and modulates expression of genes important for cell-cycle arrest, DNA repair and Apoptosis
37
What are the two main stages of carcinogenesis?
Initiator | Promoter
38
What occurs in initiation?
- 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
Name three promoters
Hormones, local tissue responses, immune responses
40
What happens in promotion?
- 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
What does radiation do to DNA? What does its effect depend on?
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
What does radiation need to do to cause cancer?
Overwhelm DNA repair mechanisms, leaving DNA damage unrepaired. Mutations in oncogenes/tumour supressor genes lead to cancer
43
Give two types of radiation and the types of cancer they cause
- 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
How do chemical carcinogens interact with DNA?
Directly, others require metabolic conversion to an active form
45
Name three chemical carcinogens
Polycyclic aromatic hydrocarbons - Aromatic Amines - Alkylating Agents
46
What are polycyclic aromatic hydrocarbons produced from? How do they have an effect? What types of cancer do they form?
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
What happens to aromatic amines to cause cancer? What cancer do they cause?
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
What kind of workers are exposed to aromatic amines?
Rubber and dye workers
49
What are three infective viruses which can cause cancer?
Hepatitis B Epstein Barr Human papilloma
50
Describe hepatitis B's action in the body, and the cancer it's associated wtih
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
What cancers is epstein barr implicated in?
pathogenesis of Burkitt’s Lymphoma, Some Hodgkin’s lymphoma, Nasopharyneal carcinoma
52
How does epstein barr have an effect
oInfects epithelial cells or oropharynx and B cells oViral genes dysregulate normal proliferative and survival signals oSets the stage for acquisition of mutations
53
How does human papilomma cuase cancer?
oHPV genes disrupt normal cell cycle - releases E6 (p53 inhibition) and E7 (pRb inhibition ) oViral genes incorporated into host cell genome, driving proliferation
54
Name five other agents which cause cancer and the cancers they cause
``` - 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
Name three conditions which predispose to tumours
Ulcerative colitis Cirrhosis Adenoma of colon/rectum
56
What cancer does ulcerative colitis cause and how?
- Colorectal carcinoma - DNA damage and microsatellite instability - May mask symptom of cancer
57
What cancer do cirrhosis cause and why?
hepatocellular carcinoma | Some of association due to chronic viral hepatitis
58
How does adenoma of colon/rectum cause cancer
Transforms to malignant neoplasia
59
What is the Ames test?
Bacteria homogenised with liver cells (p450 required) and mutagens, which allows them to grow in environments which would usually inhibit proliferation.
60
How can a pro-carcinogen cause cancer?
Converted to carcinogen by P450
61
What is a complete carcinoge?
Initiator + promoter
62
Where does radiation come from?
UV B Ionising - radon + medical tests
63
Three types if repair
``` Nucleotide excision repair (xeroderma pigmentosa - ub damage! Mismatch repair (HNPCC) Double strand break (breast/ovarian cancer) ```
64
Give type I DNA damage in each condition
Nucleotide excision repair (xeroderma pigmentosa - ub damage! Nucleotide instability ``` Mismatch repair (HNPCC) Micro satellite ``` Double strand break (breast/ovarian cancer) Chromosomal instability
65
Retinoblastoma mechanism?
RAS (gprotein, bound to GTP) Causes up regulation cyclic D Cycline dependent kinase activated Rb phosphorylated, so mitosis occurs (already deleted in retinoblastoma!)
66
Final model?
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

Semester 2 - Mechanisms of Disease (16 decks)

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