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
give a list of some cancers that have a genetic predisposition
retinoblastoma, Li Fraimeini, Wilm's tumour, Gorlins sydrome, breast cancer (BRCA1+2), FAP these all involve tumour repressor genes
26
what was chronic myeloid Leukaemia the first cancer to show?
consistent chromosomal change (genetic instability)
27
what is the chromosome that is changed in C.M leukaemia called?
``` Philadelphia chromosome (karyotyping shows 95% sufferers have this chromosome) ```
28
how does the chromosomal change in chronic myeloid leukaemia cause cancer?
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
what is the ABL gene?
a proto-oncogene that encodes a nuclear tyrosine kinase which is a positive regulator of cell proliferation
30
why when karyotyping of the philadelphia chromosome would it appear as a yellow fluorescence on chromosome 22?
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
_/_ of individuals develop cancer
1/3 → linked to age
32
many changes in _______ _______ need to occur before a cell becomes ________
cellular function, malignant
33
many cancers display genomic instability. what does this term mean?
high frequency of mutations
34
clonal origin =
most cancers arise from a single cell
35
a single mutation is not enough to cause cancer. cells have to acquire a number of functions before they become cancerous. what are these?
``` → 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
what is genomic instability?
accumulation of DNA damage, mutations result in either cell death or tumourgenesis (tumour creation)
37
too much genomic instability =
cell death
38
optimum genomic instability =
cancer causing
39
normal cell division + normal apoptosis = increased cell division + normal apoptosis = normal cell division + decreased apoptosis =
homeostasis, tumour, tumour
40
most cancers are a combination of what 3 things?
increased cell division, decreased apoptosis, loss of ability to monitor integrity of DNA
41
errors can occur in what phases in the cell cycle?
S and M (when DNA is replicated and segregates)
42
what do checkpoints do in the cell cycle and what happens when they lose their function?
checkpoints → monitor DNA integrity loss of function in cell cycle checkpoints = genomic instability (accumulation of DNA damage)
43
what is P53?
'guardian of the genome' (DNA) stable active protein in the cell cycle that has short half life and is continually made and destroyed
44
what activates P53?
→ DNA damage → hyper proliferative signals → telomere shortening → hypoxia
45
what happens when P53 is activated?
→ 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
what is senescence?
loss of a cells power of division and growth
47
what gene do B cell leukaemia and lymphomas express a high level of to avoid apoptosis?
Bcl2 → anti apoptotic gene
48
how do lung and colon cancers avoid apoptosis?
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
metastasis of cancer cells is promoted by:
``` → 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
why is the aim of many cancer treatments to prevent metastasis?
makes cancers more deadly and harder to treat
51
what are the different treatments of cancer?
surgery, chemo/radiotherapy, endocrine hormone treatments, immunotherapy, molecular mechanism based therapies
52
what receptor is present on all breast carcinomas?
Her2
53
what is Her2 and what does it do?
receptor tyrosine kinase that regulates cell growth
54
what is the new drug called that works in breast cancer and how does it work?
Herceptin → monoclonal antibody binds to Her2 receptor site → inhibits its function → cell cycle stopped → G1 blocked → angiogenesis = suppressed
55
what should cancer screening be?
→ 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