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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
describe benign tumours
confined, defined structures, surrounded by basement membrane
26
Describe the growth of benign tumours
grow locally, dont spread
27
Who came up with the two hit cancer hypothesis
Knudson
28
Describe the two hit cancer hypothesis
first hit inherited in germ cell, second hit in somatic cells during mitotic recombination
29
Where do hits occur in people with sporadically occurring cancer
both in somatic cells
30
How many mutated alleles in oncogenes are needed to exert effect
1
31
Why do oncogenes only need one mutated allele to exert effect
dominant mutations in heteroyzgotes
32
What is the effect of oncogenes on protein function
enhanced
33
What inherited mutations are associated with tumour suppressors
p53, Rb, ptc
34
What challenges does p53 respond to
hyper proliferative signals, DNA damage, telomere shortening and hypoxia
35
Describe mutated p53
unstable protein
36
What does p53 induce
cell cycle arrest, senescence and apoptosis
37
What is the function of Rb
controls entry into S phase
38
What happens if both Rb & p53 are mutated
increased cell division & decreased apoptosis
39
What is p53
tumour suppressor gene
40
Describe the active form of p53
stable, becomes a transcription factor
41
Where is the process of apoptosis inherited from
mitochondria
42
What does initiation of apoptosis involve
formation of pores in mitochondrial matrix - collapse of electrochemical gradient
43
Describe the B cell leukemias on apoptosis
high levels of Bcl-2 - stops pores forming in mitochondria
44
What is the major route for spread of cancer
blood stream or via lymphatic
45
How do cancer cells create gaps in cell barriers
secrete enzymes
46
What do lung and colon cancers secrete
decoy molecules that bind and inactivate MHC I receptors
47
What is metastasis promoted by
decrease in adherence between cells, tumour angiogenesis, increased cell motility, evading host immune system
48
What are some cancer treatments
surgery, radiotherapy, chemotherapy, immunotherapy
49
what is her2/neu
receptor tyrosine kinase
50
what do 1/3 of breast carcinomas have
her2 amplification
51
what can be used to target breast carcinoma
her2 status
52
How is her2 amplification treated in breast cancer
treated with herceptin
53
What is herceptin
monoclonal antibody
54
What does herceptin inhibit
receptor function
55
What does herceptin suppress
angiogenesis
56
What is the effect of herceptin
destroys over expression of Her2, causes cell cycle arrest

BMS109 Pathobiology (11 decks)

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