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?

A

Directly

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?

A

Indirect

24
Q

What effect can hepatitis B and C have?

A

Chronic liver cell injury and regeneration

25
Q

How does HIV potentially cause cancer?

A

HIV acts indirectly by lowering immunity and allowing other potentially carcinogenic infections to occur

26
Q

Can inherited pre-disposition to neoplasm occur?

A

Yes

27
Q

How are you genetically predisposed to neoplasm?

A

Through germline mutations

28
Q

Give an example of a neoplasm that you can have an inherited predisposition to?

A

Retinoblastoma - malignant retinal tumour

29
Q

What does the ‘two-hit’ hypothesis explain?

A

The differences between tumour occurring in families and those occurring in general population

30
Q

What is the ‘two-hit’ hypothesis?

A

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
Q

What genes inhibit neoplastic growth?

A

Tumour suppressor genes

32
Q

What genes enhance neoplastic growth?

A

Oncogenes

33
Q

What are proto-oncogenes?

A

Abnormally activates versions of normal oncogenes genes

34
Q

In order for neoplastic growth, what needs to happen to the tumour suppressor genes?

A

Both alleles need to be inactivated

35
Q

In order for neoplastic growth to occur, what needs to happen to proto-oncogenes?

A

Only one allele of each proto-oncogene needs to be activated

36
Q

What was the first oncogene to be discovered?

A

RAS

37
Q

How does the RAS proto-oncogene work?

A

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
Q

How does the RB gene work?

A

Restrains cell proliferation by inhibiting passage through R point.

39
Q

What does the inactivation of both RB alleles cause?

A

Allows unrestrained passage through the R point

40
Q

What causes xeroderma pigmentosa?

A

Due to mutations in DNA repair genes - mutation in DNA nucleotide excision repair

41
Q

What inheritance pattern does XP follow?

A

Autosomal recessive

42
Q

How does XP affect an individual?

A

Sensitive t UV damage and develop skin cancer at a young age

43
Q

What is HNPCC?

A

Hereditary non-polyposis colon cancer

44
Q

What is the inheritance pattern of HNPCC?

A

Autosomal dominant

45
Q

What causes HNPCC?

A

Germline mutation affects on of several DNA mismatch repair genes

46
Q

Which genes is familial breast cancer associated with?

A

BRCA1 or BRCA2

47
Q

Why are BRCA1 and BRCA2 important?

A

They are important for repairing double strand DNA breaks

48
Q

What are caretaker genes?

A

A class of tumour suppressor genes that maintain genetic stability

49
Q

What is progression?

A

The steady accumulation of multiple mutations