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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
Q

tobacco can cause cancers of the

A

mouth, pharynx, larynx, esophagus, lung, pancreas, and bladder

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26
Q

some common carcinogens

A

radon gasses in brake linings, vinyl chloride used in plastics

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27
Q

diet thought to be associated with cancer

A

low fiber and cured meats associated with colon cancer - but remember correlation is NOT causation

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28
Q

cancer and weight

A

being more than 25% overweight leads to a higher death rate from cancer.

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29
Q

risk of cervical cancer is related to

A

age of first intercourse and number in sexual partners

30
Q

alcohol associated with

A

laryngeal and esophageal carcinoma

31
Q

age and cancer

A

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
Q

Causes of cancer

A

environment, occupation, age, heredity, unknown

33
Q

oocupation related cancer

A

formaldahyde can cause cancer, but is 20% of the GDP so it is seen in permissable amounts

34
Q

examples of common carcinogens

A

asbestos, vinyl chloride benzene, radon/radium, coaltars and soot

35
Q

asbestos associated with

A

mesothelioma

36
Q

vinyl chloride induces

A

liver angiosarcomas - malignant vessel cancer in the liver

37
Q

benzene

A

toxic to marrow causing leukemia

38
Q

radon

A

carcinoma of the tongue and lip bc brushes pere dipped in radon and then licked to hand paint dials on watches

39
Q

Sir Percivile potts

A

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
Q

Viruses that cause cancer

A

EBV, HPV, Hep B and C, HTLV, Herpes 8 (Kaposi)

41
Q

EBV associated cancer

A

burkitt’s and b-cell lymphoma, naso-pharyngeal cancer

42
Q

HPV associated with

A

cervical cancer

43
Q

Hep B and C associated with

A

hepatocellular cancer

44
Q

high carcinogen exposure

A

tumor formation

45
Q

low carcinogen exposure

A

no tumor formation

46
Q

low carcinogen exposure and wounding

A

tumor formation

47
Q

wounding

A

no tumor formation

48
Q

carcinogen after wounding

A

no tumor –sequence is important

49
Q

carcinogen and then wounding after 3 months causes tumors telling you

A

even though all the initially exposed cells are all sloughed off, they had progeny that are still affected

50
Q

factors affecting promutagenic DNA damage

A

structure, location, replication, and repair of damage

51
Q

promutagenic DNA

A

carcinogen exposed cells aquire

52
Q

invitro why do you need a liver homogenate to see a reaction with DNA and carcinogen

A

liver homogenate has p450 that produces the active reactants that act on the DNA

53
Q

P450 inducible and under genetic control so for example

A

if opiates or phenobarbitals are used there will be an increase in p450 enzymes and ER

54
Q

MMS

A

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
Q

MNU

A

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
Q

adjacent thymines can form

A

thymine dimers with lots of exposure to sunlight, and excision repair can fix it

57
Q

DNA mutations

A

point mutation, deletion, insertion

58
Q

sequence form DNA damage to key hit

A

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
Q

a key hit means

A

activation of a protooncogene, or inactivation of a tumor supressor

60
Q

when you irradite something where do you see tumor formation

A

the part around the dead area, but not the dead area bc dead things can’t replicate

61
Q

Effects of mutation

A

gene knockout (more common), alteration of gene function

62
Q

Promotion and promoters

A

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
Q

promoters increase

A

the rate of replication, many are inflammatory agens and increase secretion of oxidants

64
Q

Phorbol esters

A

increase inflammatory release of oxidants and bind and activate PKC to induce hyperplasia

65
Q

chronic osteomyelitis induces

A

squamous cell carcinoma

66
Q

hep B and C induce a high incidence of

A

hepatocellular carcinoma but contain no transforming genes

67
Q

Initiated cells

A

enhanced growht responses, decreased toxic responses (meaning less apoptosis more growth), comparative growth advantage under promotion

68
Q

need at least 2-5 steps to form a tumor

A

carcinogen –>promotion –> inflammation/secretion of oxidants –>adenoma(benign) –> carcinoma (malignant)

69
Q

Females are mosaics due to

A

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
Q

sequence from 1st hit

A

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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