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BMS109 Pathobiology > Cancer > Flashcards

Cancer Flashcards

1
Q

What type of disease is cancer

A

evolutionary

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2
Q

What cancers have a high prevalence in asia

A

stomach, lung, liver and oesophagus

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3
Q

What are the causes of cancer

A

viral infection, radium, genetic instability, inherited factors, carcinogens

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4
Q

Name some inherited predispositions

A

retinoblastoma, Gorlin’s syndrome, wilm’s tumour, breast cancer

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5
Q

Describe Chronic myeloid leukaemia

A

sporadic cancer that is not inherited

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6
Q

Describe the genetics of chronic myeloid leukaemia

A

Philadelphia chromosome - chromosomal change causes genetic instability in cancer

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7
Q

What is ABL

A

proto-oncogene

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8
Q

What does ABL encode

A

nuclear tyrosine kinase

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9
Q

What is BCR/ABL

A

abnormal fusion protein

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10
Q

When does fusion of BCR/ABL occur

A

metaphase

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11
Q

What is the function of tyrosine kinases

A

use ATP to transfer phosphate

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12
Q

What does ABL regulate

A

positively regulates cell growth

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13
Q

What is the effect of BCR/ABL

A

increased tyrosine kinase activity & increased proliferation and malignant growth

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14
Q

What type of mutation is the fusion of BCR/ABL

A

gain of function

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15
Q

What happens to ABL when BCR/ABL fuse

A

turns into an oncogene

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16
Q

What are most cancers derived from

A

single abnormal cell - clonal origin

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17
Q

TRUE or FALSE - single mutations are enough to cause cancer

A

FALSE

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18
Q

What are some of the characteristics cells acquire before they become cancerous

A

evade apoptosis, limitless replication, tissue invasion, overcome immune system

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19
Q

Describe hyerplasia

A

tissue growth containing an excess number of cells

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20
Q

Describe metaplasia

A

tissue growth of normal cells in the wrong place

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21
Q

Describe dysplasia

A

tissue growth where cells appear abnormal

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22
Q

Describe neoplasia

A

invasive abnormal tissue growth

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23
Q

What mutations are associated with tumour suppressors

A

loss of function

24
Q

What mutations are associated with oncogenes

A

gain of function

25
Q

describe benign tumours

A

confined, defined structures, surrounded by basement membrane

26
Q

Describe the growth of benign tumours

A

grow locally, dont spread

27
Q

Who came up with the two hit cancer hypothesis

A

Knudson

28
Q

Describe the two hit cancer hypothesis

A

first hit inherited in germ cell, second hit in somatic cells during mitotic recombination

29
Q

Where do hits occur in people with sporadically occurring cancer

A

both in somatic cells

30
Q

How many mutated alleles in oncogenes are needed to exert effect

A

1

31
Q

Why do oncogenes only need one mutated allele to exert effect

A

dominant mutations in heteroyzgotes

32
Q

What is the effect of oncogenes on protein function

A

enhanced

33
Q

What inherited mutations are associated with tumour suppressors

A

p53, Rb, ptc

34
Q

What challenges does p53 respond to

A

hyper proliferative signals, DNA damage, telomere shortening and hypoxia

35
Q

Describe mutated p53

A

unstable protein

36
Q

What does p53 induce

A

cell cycle arrest, senescence and apoptosis

37
Q

What is the function of Rb

A

controls entry into S phase

38
Q

What happens if both Rb & p53 are mutated

A

increased cell division & decreased apoptosis

39
Q

What is p53

A

tumour suppressor gene

40
Q

Describe the active form of p53

A

stable, becomes a transcription factor

41
Q

Where is the process of apoptosis inherited from

A

mitochondria

42
Q

What does initiation of apoptosis involve

A

formation of pores in mitochondrial matrix - collapse of electrochemical gradient

43
Q

Describe the B cell leukemias on apoptosis

A

high levels of Bcl-2 - stops pores forming in mitochondria

44
Q

What is the major route for spread of cancer

A

blood stream or via lymphatic

45
Q

How do cancer cells create gaps in cell barriers

A

secrete enzymes

46
Q

What do lung and colon cancers secrete

A

decoy molecules that bind and inactivate MHC I receptors

47
Q

What is metastasis promoted by

A

decrease in adherence between cells, tumour angiogenesis, increased cell motility, evading host immune system

48
Q

What are some cancer treatments

A

surgery, radiotherapy, chemotherapy, immunotherapy

49
Q

what is her2/neu

A

receptor tyrosine kinase

50
Q

what do 1/3 of breast carcinomas have

A

her2 amplification

51
Q

what can be used to target breast carcinoma

A

her2 status

52
Q

How is her2 amplification treated in breast cancer

A

treated with herceptin

53
Q

What is herceptin

A

monoclonal antibody

54
Q

What does herceptin inhibit

A

receptor function

55
Q

What does herceptin suppress

A

angiogenesis

56
Q

What is the effect of herceptin

A

destroys over expression of Her2, causes cell cycle arrest

BMS109 Pathobiology (11 decks)

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