Session 9 Flashcards

1
Q

What causes neoplasm?

A

Combination of instrinsic host factors and extrinsic factors

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2
Q

Give example of some intrinsic factors that cause neoplasia?

A

Hereditary, age and gender

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3
Q

Give examples of extrinsic factors that cause neoplasia

A

Related to environment and behaviour (lifestyle)

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4
Q

Recently, what has caused the increased cancer incidence?

A

Prolonged life span

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5
Q

What behavioural and dietary risks cause neoplasia?

A

High body mass index, low fruit and veg intake, lack of physical activity, tobacco use and alcohol use.

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6
Q

Where does most of the evidence about cancer risk come from?

A

Epidemiological and animal studies

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7
Q

Which holds a greater risk for cancer - extrinsic or intrinsic factors?

A

Extrinsic - 85%

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8
Q

Which categories do extrinsic carcinogens fall into?

A

Chemicals, radiation and infection

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9
Q

Give an example of a chemical carcinogen

A

2-napthylamine is an industrial carcinogen used in the dye manufacturing industry

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10
Q

What do malignant neoplasms caused by chemical carcinogens show us?

A
  • Long delay between carcinogen exposure and malignant neoplasm onset
  • Risk of cancer depends on total carcinogen dosage
  • Organ specificity for particular carcinogens
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11
Q

What does the Ames test show?

A

Shows that initiators are mutagens, while promotes cause prolonged proliferation in target tissues

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12
Q

What is a complete carcinogen?

A

A carcinogen that have both initiator and promoter effects

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13
Q

How are pro-carcinogens converted to carcinogens?

A

By the cytochrome P450 enzymes in the liver

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14
Q

What is radiation?

A

Any type of energy travelling through space and some forms are mutagenic

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15
Q

How is radiation damaging?

A

Can damage DNA directly and also indirectly by generating free radicals

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16
Q

What is the most important type of radiation?

A

UV because we are exposed daily from sunlight leading to inc skin cancer risk

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17
Q

Infections are carcinogenic, so how do the act of cells?

A

Directly or indirectly

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18
Q

How do infections act directly to cause malignant neoplasia?

A

Affect genes that control cell growth

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19
Q

How do infections indirectly cause malignant neoplasm?

A

Causing chronic tissue injury where the resulting regeneration acts as either a promoter for any pre-existing mutations r else causes new mutations from DNA replication errors

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20
Q

Which cancer is Human Papiloma Virus (HPV) strongly linked with?

A

Cervical carcinoma

21
Q

Is HPV directly or indirectly carcinogenic?

22
Q

How does HPV cause cancer?

A

Expresses the E6 and E7 proteins that inhibit p53 and pRB protein function respectively, both of which are important in cell proliferation.

23
Q

Are hepatitis B and C direct or indirect carcinogens?

24
Q

What effect can hepatitis B and C have?

A

Chronic liver cell injury and regeneration

25
How does HIV potentially cause cancer?
HIV acts indirectly by lowering immunity and allowing other potentially carcinogenic infections to occur
26
Can inherited pre-disposition to neoplasm occur?
Yes
27
How are you genetically predisposed to neoplasm?
Through germline mutations
28
Give an example of a neoplasm that you can have an inherited predisposition to?
Retinoblastoma - malignant retinal tumour
29
What does the 'two-hit' hypothesis explain?
The differences between tumour occurring in families and those occurring in general population
30
What is the 'two-hit' hypothesis?
In familial cancers the first hit was delivered through the germline and affects all cells of the body and the second hit was a somatic mutation. In sporadic cancers, there was no germ line mutation
31
What genes inhibit neoplastic growth?
Tumour suppressor genes
32
What genes enhance neoplastic growth?
Oncogenes
33
What are proto-oncogenes?
Abnormally activates versions of normal oncogenes genes
34
In order for neoplastic growth, what needs to happen to the tumour suppressor genes?
Both alleles need to be inactivated
35
In order for neoplastic growth to occur, what needs to happen to proto-oncogenes?
Only one allele of each proto-oncogene needs to be activated
36
What was the first oncogene to be discovered?
RAS
37
How does the RAS proto-oncogene work?
Encodes a small G protein that relays signals into the cell that push cell past R point. Mutant RAS encodes a protein that is always active therefore constantly producing a signal.
38
How does the RB gene work?
Restrains cell proliferation by inhibiting passage through R point.
39
What does the inactivation of both RB alleles cause?
Allows unrestrained passage through the R point
40
What causes xeroderma pigmentosa?
Due to mutations in DNA repair genes - mutation in DNA nucleotide excision repair
41
What inheritance pattern does XP follow?
Autosomal recessive
42
How does XP affect an individual?
Sensitive t UV damage and develop skin cancer at a young age
43
What is HNPCC?
Hereditary non-polyposis colon cancer
44
What is the inheritance pattern of HNPCC?
Autosomal dominant
45
What causes HNPCC?
Germline mutation affects on of several DNA mismatch repair genes
46
Which genes is familial breast cancer associated with?
BRCA1 or BRCA2
47
Why are BRCA1 and BRCA2 important?
They are important for repairing double strand DNA breaks
48
What are caretaker genes?
A class of tumour suppressor genes that maintain genetic stability
49
What is progression?
The steady accumulation of multiple mutations