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Pathology > 6.10 how does cancer develop > Flashcards

6.10 how does cancer develop Flashcards

1
Q

leading causes of pediatric cancer deaths

A

leukemia, brain and nervous system, endocrine

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2
Q

incidence of lung cancer is

A

lower than the death caused by cancer

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3
Q

what percent of all dealths of children under 15 is caused by cancer

A

10%

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4
Q

incidence of lung cancer in women has

A

increased

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5
Q

incidence of breast and cervical cancer in women has

A

decreased - improved screening

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6
Q

increase in deaths from lung cancer has shot up bc

A

there is about a 20 year lag period before lung cancer shows up

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7
Q

decline in stomach cancer due to

A

improved diet

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8
Q

highest rates of stomach cancer seen in

A

japanese due to smoking fish and meats –smoking introduces carcinogens into the food

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9
Q

decline in cervical cancer due to pap smers is higher in

A

white midddle class female due to access to good healthcare

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10
Q

carcinogens

A

chemicals and radiation that are capable of triggering the development of cancer -

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11
Q

how do carcinogens act

A

through a multistep process that initiates a series of genetic mutations and stimulates cells to proliferate

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12
Q

why is there a delay of years between exposure to a carcinogen and the onset of cancer

A

because several changes need to accumulate on top of the initial stimulation of cells by the carcinogen

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13
Q

canada

A

leukemia

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14
Q

US

A

colon cancer

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15
Q

Brazil

A

Cervical cancer

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16
Q

UK

A

lung cancer

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17
Q

China

A

liver cancer

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18
Q

Australia

A

skin cancer

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19
Q

japan

A

stomach cancer

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20
Q

cancer related to genetics and environment

A

cancer genese exist and can be inherited, however environment plays a big role in determining if one gets cancer —mor cancer in japanese man>japanese immigrant living in US>sons of japanese immigrant aprox=to white americans

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21
Q

gene important in cancer

A

cytochorme P450 in developing lung cancer - bc carcinogens are not metabolized properly?

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22
Q

suns rays and cancer

A

radiation are DNA damaging

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23
Q

afalatoxin in

A

peanuts - carcinogen but the amount is regulated such that you wont see cancer development

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24
Q

what is the single most important environmental factor contributing to premature death in the US

A

cigarette smoking

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25
tobacco can cause cancers of the
mouth, pharynx, larynx, esophagus, lung, pancreas, and bladder
26
some common carcinogens
radon gasses in brake linings, vinyl chloride used in plastics
27
diet thought to be associated with cancer
low fiber and cured meats associated with colon cancer - but remember correlation is NOT causation
28
cancer and weight
being more than 25% overweight leads to a higher death rate from cancer.
29
risk of cervical cancer is related to
age of first intercourse and number in sexual partners
30
alcohol associated with
laryngeal and esophageal carcinoma
31
age and cancer
most cancers increase with age and many may appear mainly after 55 (ex. Prostate cancer). Some are mainly pediatric and cancer is the second leading cause of death in children.
32
Causes of cancer
environment, occupation, age, heredity, unknown
33
oocupation related cancer
formaldahyde can cause cancer, but is 20% of the GDP so it is seen in permissable amounts
34
examples of common carcinogens
asbestos, vinyl chloride benzene, radon/radium, coaltars and soot
35
asbestos associated with
mesothelioma
36
vinyl chloride induces
liver angiosarcomas - malignant vessel cancer in the liver
37
benzene
toxic to marrow causing leukemia
38
radon
carcinoma of the tongue and lip bc brushes pere dipped in radon and then licked to hand paint dials on watches
39
Sir Percivile potts
found that chimeny sweepers where developing scrotal carcinoma causing a law to be passed forcing chimney sweeps to shower right after work and the rate of scrotal cancer dropped
40
Viruses that cause cancer
EBV, HPV, Hep B and C, HTLV, Herpes 8 (Kaposi)
41
EBV associated cancer
burkitt's and b-cell lymphoma, naso-pharyngeal cancer
42
HPV associated with
cervical cancer
43
Hep B and C associated with
hepatocellular cancer
44
high carcinogen exposure
tumor formation
45
low carcinogen exposure
no tumor formation
46
low carcinogen exposure and wounding
tumor formation
47
wounding
no tumor formation
48
carcinogen after wounding
no tumor --sequence is important
49
carcinogen and then wounding after 3 months causes tumors telling you
even though all the initially exposed cells are all sloughed off, they had progeny that are still affected
50
factors affecting promutagenic DNA damage
structure, location, replication, and repair of damage
51
promutagenic DNA
carcinogen exposed cells aquire
52
invitro why do you need a liver homogenate to see a reaction with DNA and carcinogen
liver homogenate has p450 that produces the active reactants that act on the DNA
53
P450 inducible and under genetic control so for example
if opiates or phenobarbitals are used there will be an increase in p450 enzymes and ER
54
MMS
methyl methane sulfate - methylating agent attachign a methyl group in aqueous and neutral pHs so if you mix it with DNA it will react and mostly methylates the N3 of guanine. This is a weak mutagen bc there is still a possiblity for the G to base pair correctly with a C.
55
MNU
methyl nitrosyl urea is a potent mutagen that methylates on the O6 on guanosine involved in base pairing so you have a higher rate of mispairing with thymine. There is a repair enzyme specifically for the O6 telling you how important this is. If the mismatch is not corrected it stays and goes to the progeny
56
adjacent thymines can form
thymine dimers with lots of exposure to sunlight, and excision repair can fix it
57
DNA mutations
point mutation, deletion, insertion
58
sequence form DNA damage to key hit
DNA dmage can be over come by DNA repair-->toxicity acts at the level of replication--->more replication can lead to mutation--->leads to either a lethal hit, key hit, or irrelevent hit
59
a key hit means
activation of a protooncogene, or inactivation of a tumor supressor
60
when you irradite something where do you see tumor formation
the part around the dead area, but not the dead area bc dead things can't replicate
61
Effects of mutation
gene knockout (more common), alteration of gene function
62
Promotion and promoters
not directly mutagenic, no binding to DNA, chronically aberantly activating signal transduction molecules like PKC, induction of cell replication, many infalmmatory agens, chemicals endogenous hormones, hormone like environmental agents, physical agents (trauma), infection
63
promoters increase
the rate of replication, many are inflammatory agens and increase secretion of oxidants
64
Phorbol esters
increase inflammatory release of oxidants and bind and activate PKC to induce hyperplasia
65
chronic osteomyelitis induces
squamous cell carcinoma
66
hep B and C induce a high incidence of
hepatocellular carcinoma but contain no transforming genes
67
Initiated cells
enhanced growht responses, decreased toxic responses (meaning less apoptosis more growth), comparative growth advantage under promotion
68
need at least 2-5 steps to form a tumor
carcinogen -->promotion --> inflammation/secretion of oxidants -->adenoma(benign) --> carcinoma (malignant)
69
Females are mosaics due to
x chormosome --> in heterozygous person individual cells will have one gene turned on but the entire tissue expresses both gene products. But in tumors they only show one type--->points to the fact tha tumors are monclonal
70
sequence from 1st hit
1st hit --> phenotypic change --> promotion leading to clonal expansion --> second hit leading to benign neoplasm --> further hits leading to malignant neoplasm

Pathology (26 decks)

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