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pathobiology > cancer > Flashcards

cancer Flashcards

1
Q

in 2008, how many deaths were due to cancer?

A

157,000

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2
Q

oesophageal =

larnyx =

A

more females,
more males,

biological reasons for gender differences are poorly understood

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3
Q

cancer mortality is

A

decreasing

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4
Q

what is cancer?

A

group of diseases characterised by uncontrolled cell division

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5
Q

what does the severity of a cancer depend on?

A

site of cancer and character of malignancy

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6
Q

what type of cancer is easier to treat?

A

a static primary tumour compared to metastasis of a secondary tumour

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7
Q

migration of cancer to a secondary site =

A

metastasis

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8
Q

what are the features of transformed cancer cells?

A

→ more round
→ uncontrolled proliferation
→ anchor independent growth (can grow through and away from anchoring tissue)
→ can grow on other cells

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9
Q

tissue growth containing excessive cell numbers =

A

hyperplasia

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10
Q

tissue growth containing displaced but normal cells =

A

metaplasia

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11
Q

tissue growth with abnormal cells =

A

dysplasia (dys=abnormal)

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12
Q

invasive abnormal tissue growth =

A

neoplasia

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13
Q

cells revert to undifferentiated state (no longer resemble tissue) =

A

anaphasia

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14
Q

what is the difference between benign and malignant tumours?

A

benign:
→ grows locally
→ well differentiated cells surrounded by basement membrane
→ does not spread to secondary site

malignant:
→ breaks through basement membrane
→ cells are usually poorly differentiated
→ metastatises to different parts of body
→ cell interactions remain but in an altered form

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15
Q

give an example of a benign tumour

A

pituitary adenoma → blindness by compressing optic nerve

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16
Q

what is the general progression of a malignant tumour?

A

dysplasia → anaplasia → invasion → metastasis

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17
Q

discuss cancer stages

A

the higher the stage of cancer the more advanced and difficult to treat it
(stage 4 = higher death rate than 1,2&3)

earlier cancer detection stage = better survival rate

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18
Q

cancer cells =

A

undifferentiated and proliferative

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19
Q

in what country is digestive organ cancers high and why?

A

eastern Asia, diet

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20
Q

what cancer is most common in south Africa and why?

A

Kaposi’s sarcoma, due to HIV prevalence

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21
Q

what are the causes of cancer?

A

→ exposure to carcinogens and mutagens
→ occupational exposure
→ tobacco and alcohol
→ poor diet

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22
Q

when are environmental factors most impactive?

A

most impactive on the likelihood of development and which kind of cancer

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23
Q

what was the first tumour virus discovered in 1910 by Peyton Rous?

A

rous sarcoma virus

24
Q

what are a few viral cancers?

A

HPV 16-18, EBV, Kaposi’s sarcoma

HPV now has a vaccination program to reduce rates of cervical cancer

25
Q

give a list of some cancers that have a genetic predisposition

A

retinoblastoma, Li Fraimeini, Wilm’s tumour, Gorlins sydrome, breast cancer (BRCA1+2), FAP

these all involve tumour repressor genes

26
Q

what was chronic myeloid Leukaemia the first cancer to show?

A

consistent chromosomal change (genetic instability)

27
Q

what is the chromosome that is changed in C.M leukaemia called?

A 
Philadelphia chromosome
(karyotyping shows 95% sufferers have this chromosome)
28
Q

how does the chromosomal change in chronic myeloid leukaemia cause cancer?

A

TRANSLOCATION from chromosome 9 to chromosome 22
→ fusion of 2 genes occur (ABL and BCR)

ABL - encodes tyrosine kinase → helps cell proliferation

BRC/ABL → abnormal fusion protein that increases tyrosine kinase activity → increases proliferation and malignant growth

29
Q

what is the ABL gene?

A

a proto-oncogene that encodes a nuclear tyrosine kinase which is a positive regulator of cell proliferation

30
Q

why when karyotyping of the philadelphia chromosome would it appear as a yellow fluorescence on chromosome 22?

A

normal BCR and ABL are marked with green and red fluorescent probes

yellow appears as red and green overlap due to abnormal fusion protein

31
Q

/ of individuals develop cancer

A

1/3 → linked to age

32
Q

many changes in _______ _______ need to occur before a cell becomes ________

A

cellular function, malignant

33
Q

many cancers display genomic instability. what does this term mean?

A

high frequency of mutations

34
Q

clonal origin =

A

most cancers arise from a single cell

35
Q

a single mutation is not enough to cause cancer. cells have to acquire a number of functions before they become cancerous. what are these?

A 
→ self sufficiency in growth signals
→ insensitivity to anti growth signals
→ tissue invasion and metastasis
→ limitless replication potential
→ sustained angiogenesis 
→ evading apoptosis
→ overcoming immune surveillance
36
Q

what is genomic instability?

A

accumulation of DNA damage, mutations result in either cell death or tumourgenesis (tumour creation)

37
Q

too much genomic instability =

A

cell death

38
Q

optimum genomic instability =

A

cancer causing

39
Q

normal cell division + normal apoptosis =
increased cell division + normal apoptosis =
normal cell division + decreased apoptosis =

A

homeostasis,
tumour,
tumour

40
Q

most cancers are a combination of what 3 things?

A

increased cell division, decreased apoptosis, loss of ability to monitor integrity of DNA

41
Q

errors can occur in what phases in the cell cycle?

A

S and M (when DNA is replicated and segregates)

42
Q

what do checkpoints do in the cell cycle and what happens when they lose their function?

A

checkpoints → monitor DNA integrity

loss of function in cell cycle checkpoints = genomic instability (accumulation of DNA damage)

43
Q

what is P53?

A

‘guardian of the genome’ (DNA)

stable active protein in the cell cycle that has short half life and is continually made and destroyed

44
Q

what activates P53?

A

→ DNA damage
→ hyper proliferative signals
→ telomere shortening
→ hypoxia

45
Q

what happens when P53 is activated?

A

→ apoptosis
→ cell cycle arrest when DNA is damaged
→ turning on of DNA repair genes and the gene that stops the cell cycle
→ senescence

mutated P53 results in an inactive protein

46
Q

what is senescence?

A

loss of a cells power of division and growth

47
Q

what gene do B cell leukaemia and lymphomas express a high level of to avoid apoptosis?

A

Bcl2 → anti apoptotic gene

48
Q

how do lung and colon cancers avoid apoptosis?

A

by overcoming immune surveillance:

secrete decoy molecules → bind and inactivate MHC-1 receptors

these receptors normally present antigens to cytotoxic T cells (CD8+)

by binding, this prevents cytotoxic T lymphocytes and natural killer cells from identifying and killing cancer cells

49
Q

metastasis of cancer cells is promoted by:

A 
→ decreased adherence between cells
→ synthesis of defective basement membrane
→ tumour angiogenesis
→ increased cell motility
→ secretion of growth factors 
→ secretion of alternative extracellular matrix 
→ secretion of proteinases
→ evasion of hosts immune system
50
Q

why is the aim of many cancer treatments to prevent metastasis?

A

makes cancers more deadly and harder to treat

51
Q

what are the different treatments of cancer?

A

surgery, chemo/radiotherapy, endocrine hormone treatments, immunotherapy, molecular mechanism based therapies

52
Q

what receptor is present on all breast carcinomas?

A

Her2

53
Q

what is Her2 and what does it do?

A

receptor tyrosine kinase that regulates cell growth

54
Q

what is the new drug called that works in breast cancer and how does it work?

A

Herceptin → monoclonal antibody binds to Her2 receptor site → inhibits its function → cell cycle stopped → G1 blocked → angiogenesis = suppressed

55
Q

what should cancer screening be?

A

→ affordable to health care system
→ be appropriate to all social groups
→ have good discrimination between benign + malignant
→ show a reduction in mortality from the cancer

pathobiology (10 decks)

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