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Path Gen 1 > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

expression mutated gene, abnormal expression quiescent gene, gene amplification, loss growth inhibitory genes

A

expression mutated gene, abnormal expression, quiescent gene, gene amplification, loss growth inhibitory genes

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2
Q

nuclear regulatory proteins

A

myc, myb, jun, fox

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3
Q

nuclear regulatory protein in Burkitt’s lymphoma

A

c-myc

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4
Q

nuclear regulatory protein in neuroblastoma

A

N-myc

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5
Q

tumor supressor genes -> must have loss of BOTH copies

A

RB, p53, NF-1, DCC (deleted in colon cancer)

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6
Q

cancers with high correlation of ras mutation

A

colon, pancreas, thyroid (glandular)

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7
Q

single most common abnormality of dominant oncogenes in human tumors

A

ras

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8
Q

two hit hypothesis of retinoblastoma (40% familial cases, malignant retinal tumor)

A

one mutated from parent, other does somatic mutation

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9
Q

single most common target for genetic alterations in human cancer (RECESSIVE also)

A

p53

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10
Q

this oncogene acts as “policeman” to inhibit division of genetically damaged cells to allow for repair (quiescence, senescence, or apoptosis) -> typically UV light damage and carcinogenesis

A

p53

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11
Q

p53 can cause this: temporal cell cycle arrest that allows for repair

A

quiescence

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12
Q

p53 can cause this: induction of permanent cell cycle arrest (if repair doesn’t happen)

A

senescence

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13
Q

what mediates cell cycle arrest in p53 action?

A

CDK inhibitor p21

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14
Q

what mediates apoptosis from p53 activation?

A

BAX

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15
Q

these tumors are more susceptible to chemotherapy and radiation

A

normal p53

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16
Q

what is a complete carcinogen?

A

carcinogen that induces initiation and promotion

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17
Q

what can carcinogens (reactive electrophiles) attack?

A

DNA, RNA, proteins

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18
Q

chemical carcinogen associated with angiosarcoma of the liver

A

vinyl chloride (PVC)

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19
Q

fungus that infects peanuts -> has aflatoxin B1

A

aspergillus flavus

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20
Q

Aspergillus flavus is associated with this cancer

A

hepatocellular carcinoma

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21
Q

malignant forms of HPV have these proteins that cause cancer; what do they inactivate?

A

E6 and E7; p53, Rb (respectively)

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22
Q

ways you can look for clonality (expression of specific alleles in daughter cells)

A

methylation patterns, indicators identical gene RAR (like Ig and T cell isotype)

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23
Q

primary target for genetic damage in neoplasm formation

A

growth regulatory elements

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24
Q

4 classes of normal regulatory proteins that are targets for alteration causing autonomous proliferation

A

growth promoting oncogenes, growth inhibiting tumor suppressor genes, genes regulating apoptosis, genes regulating DNA repair

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25
Q

non-altered gene present in normal cells that can then become altered or expressed

A

proto-oncogene

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26
Q

oncogenes that promote growth are these kind -> only need one allele mutated; what are some examples?

A

dominant; RAS, GF, GFR

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27
Q

oncogenes that inhibit growth are these kind -> BOTH alleles must be mutated; what are some examples?

A

recessive; p53, Rb

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28
Q

what is necessary for total unregulated growth to occur in oncogenesis?

A

constitutive expression multiple positive growth signals and loss inhibitory signals

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29
Q

when does the first restriction point occur in cell cycle?

A

after G1

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30
Q

regulates orderly progression through the cell cycle phases

A

cyclins and CDKs

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31
Q

these phosphorylate critical regulatory proteins in the cell cycle

A

CDKs

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32
Q

this activates CDK, which then activates Rb; what phase is it present in?

A

cyclin D; mid G1 (disappears in S due to ubiquitin-proteasome)

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33
Q

EF2 transcription

A

E2F transcription

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34
Q

this cyclin/CDK permits DNA replication (through the S phase)

A

cyclin E/CDK2

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35
Q

this regulates mitotic prophase

A

cyclin A/CDK2

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36
Q

this regulates nuclear division

A

cyclin B/CDK1

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37
Q

class of CDK inhibitors -> p21 is part of it (which is activated by p53)

A

CIP/WAF

38
Q

two check-points to prevent duplication of damaged cells

A

G1/S, G2/M

39
Q

what does G1/S checkpoint act through?

A

p53

40
Q

four key regulators of cell cycle -> dysregulated in majority of human cancers

A

p16/INK4a, cyclin D, CDK4, Rb

41
Q

this inhibits transcription of proteins required for S phase -> prevents entry into G1

A

Rb

42
Q

growth inhibition of damaged cells and apoptosis

A

p53

43
Q

how does a cell differentiate?

A

going through successive cell divisions

44
Q

Xeroderma pigmentosum is caused by this

A

loss of nucleotide excision repair pathway, can’t excise pyrimidine dimers (DNA repair)

45
Q

mechanisms by which oncogene can be activated

A

change in structure (point mutation) or regulating element (translocation, other oncogene), gene amplification, viral transformation, epigenetic methylation

46
Q

mutation in this can cause increased gene expression of growth factors -> forming oncogene

A

RAS

47
Q

how can GFRs become oncogene?

A

constitutive activation, overexpression (gene amplification, translocation)

48
Q

how can signal-transducing proteins be oncogenes?

A

constitutive activation ras/g proteins or activation regulatory kinases

49
Q

this protein prevents programmed cell death -> overexpression allows damaged cells to survive and mutations to be expressed

A

bcl-2

50
Q

this acts as break to prevents cell from moving from G0 to G1

A

Rb

51
Q

does phosphorylation activate or inhibit Rb?

A

inactivates (inhibits the inhibitor…dissociates from EF2 and allows replication)

52
Q

protein/oncogene involved in malignant melanoma

A

p16(INK4a)

53
Q

this phosphorylates Rb (inactivating it)

A

cyclin D/CDK4

54
Q

does loss of p53 usually occur late or early in stepwise progression of DNA changes?

A

late (allows for duplication of DNA-damaged cells)

55
Q

this syndrome is related to inheritance of mutated allele of p53 (similar to two-hit hypothesis) -> greatly increases chance of developing malignant tumor by age 50

A

Le Fraumeni syndrome

56
Q

this virus (among others) can inhibit p53 function

A

papilloma

57
Q

Bcl overexpression (associated with translocation) is seen in this condition

A

B cell lymphoma

58
Q

potential oncogenes that induce pores in mitochondrial membrane to release cytochrome C

A

BAX, BAK

59
Q

defective mismatch repair resulting in microsatellite instability

A

Hereditary non-polyposis cancer syndrome

60
Q

these diseases are associated with improper activation of p53 due to strand breaks

A

ataxia-telangiectasia, Bloom syndrome, Fanconi anemia

61
Q

BRCA1, BRCA2 normally have this role in DNA repair

A

repair DNA breaks

62
Q

this enzyme is upregulated in 85-95% of cancers

A

telomerase (active normally only in germ cell and stem cells)

63
Q

examples of promoters of transformation

A

hormones, cytokines, GF (any mitogenic stimulus)

64
Q

induction of oncogenic DNA changes by environmental agent -> most cause initiation

A

carcinogenesis

65
Q

mechanisms of gene alteration in carcinogenesis

A

mutagenesis, translocation, gene amplification, insertion transcription element (viral)

66
Q

what metabolizes most carcinogens

A

p-450 dependent mono-oxygenase

67
Q

vast majority of initiating chemicals are these

A

mutagens

68
Q

primary target of carcinogens

A

DNA

69
Q

these chemical carcinogens require metabolic activation -> tobacco smoke, broiling animal fats, smoked meat/fish

A

polycyclic aromatic hydrocarbons

70
Q

these chemical carcinogens have been associated with bladder cancer

A

B-naphthylamine, aniline dyes

71
Q

chemical promoters (carcinogens)

A

phorbol esters, saccharin and cycylamates, estrogens, dietary fat

72
Q

ionizing radiation types

A

electromagnetic, particle

73
Q

mechanism of action for xray/gamma ray radiation

A

indirect (free radical)

74
Q

MOA for radiant energy radiation damage

A

indirect and direct

75
Q

MOA for particulate radiation damage

A

direct

76
Q

these are formed due to radiation damage of DNA

A

pyrimidine dimers and crosslinks, single and double strand breaks, RAR

77
Q

UV light affects these layers/can cause these cancers; what forms as a result of UV damage?

A

squamous cell, basal cell, melanoma; pyrimidine dimers

78
Q

what bands of UV light radiation are most dangerous/harmful?

A

middle B bands

79
Q

ca associated with miners of radioactive elements

A

lung cancer

80
Q

ca associated with atomic bomb survivors (ionizing radiation)

A

leukemia

81
Q

ca associated with therapeutic exposures (ionizing radiation)

A

thyroid

82
Q

ca associated with radium dial painters

A

mouth, throat (because licked paint brush)

83
Q

this radiation often causes leukemia (except chronic lymphocytic)

A

ionizing

84
Q

cells are sensitive to radiation directly proportional to this level, inversely to this

A

reproductive/mitotic activity, level of specialization

85
Q

what is HPV oncogene associated with -> stable integration of viral DNA into host DNA

A

squamous cell ca cervix

86
Q

integration of malignant HPV subtypes involves alterations in these proteins

A

Rb and p53

87
Q

malignant cancers associated with EBV infection

A

Burkitt’s lymphoma, B cell lymphomas (immunosuppressed), Hodgkin’s disease, nasopharyngeal carcinoma

88
Q

what cells are infected by EBV?

A

epithelial and B cells

89
Q

what occurs due to HBV oncogene -> chronic liver cell injury with regenerative hyperplasia

A

expression HBx protein, increase protein kinase C

90
Q

this virus causes cancer from chronic inflammation (not direct oncogene/insertion)

A

HCV

91
Q

human herpes type 8 is associated with this cancer

A

Kaposi’s sarcoma

92
Q

this has tropism for CD4, transmission is same as HIV -> see T cell proliferation plus 2nd mutagenic event (latent 20-30 years)

A

human T cell leukemia/lymphoma

Path Gen 1 (6 decks)

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