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carcinogens Flashcards

1
Q

What are the three stages for neoplastic development and progression?

A

Neoplastic cell
Differentiated neoplasm
Undifferentiated cancer

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2
Q

Property of chemical carcinogens

Carcinogens are _________ dependent.

A

Dose dependent

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3
Q

Property of chemical carcinogens

Is lag period for exposure and a tumor long or short.

A

Can be greater than 20 years

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4
Q

Property of chemical carcinogens

Carcinogens are subject to what two processes?

A

Activation and degradation

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5
Q

Property of chemical carcinogens

What are active carcinogens?

A

electrophiles

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6
Q

Most potent carcinogen known?

A

aflatoxins

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7
Q

Carcinogen that is a product of combustion?

A

Benzopyrene

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8
Q

Carcinogen used to make PVC plastic

A

Vinyl chloride

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9
Q

Carcinogen that is a coal tar derivative

A

Phenacetin

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10
Q

Carcinogen that is an immunosuppressant

A

Benzene

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11
Q

What type of estrogen is a carcinogen?

A

Conjugated estrogen

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12
Q

2 carcinogen that are alkylating agents

A

amine/amide
Cylophosphamide
Meclorethylamine

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13
Q

What are the 3 classes of carcinogens?

A

Direct acting carcinogen
Procarcinogen
Epigenic carcinogen

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14
Q

Examples of direct acting carcinogens

A

Mechlorethlamine+guanine

Results in depurination an abnormal base pairing

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15
Q

Examples of procarcinogens

A

Benzopyrene

Vinyl chloride

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16
Q

Examples of epigenic carcinogens

A

Immunosuppressor (Benzene)

Hormones (DES)

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17
Q

Gene that encodes for transforming proteins that cause cancer

A

Oncogenes

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18
Q

Genes in normal cells that encode for proteins involved in cellular regulations

A

Proto-oncogenes

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19
Q

Oncongens are derived from the mutation of what?

A

Proto-oncogenes

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20
Q

What are G proteins, tyrosine-specific kinase, kinases, growth factors and transcription regulators

A

Proteins involved in cellular regulation

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21
Q

What is an anti-oncogen? AKA?

A

Tumor suppressor gene

Growth suppressor genes

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22
Q

What does an anti-oncogen do?

A

Suppresses cell growth

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23
Q

what does the mutation of anti-oncogen lead to?

A

loss of ability to restrain cell growth and cell division…..the mutated anti-oncogen produces a mutant protein that is inactive as a growth suppressor

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24
Q 
what are these?
Acute lymphocytic leukemia
Burkitt's lymphoma
Ewings' sarcoma - bone tumor
Retinoblastoma
Wilms' tumor - kidney tumor
A

childhood tumors with high cure rates

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25
Q 
what are these?
Hodgkin's disease
Non-Hodgkin's lymphomas
Trophoblastic choriocarcinoma
Testicular and ovarian germ cell cancers
A

adult tumors with high cure rates

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26
Q

what is the mechanism through which chemotherapy drugs work?

A

inhibit cell proliferation

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27
Q

why are tumor cells sensitive to chemotherapy drugs?

A

they are rapidly proliferating

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28
Q

what healthy cells in the body are also affected by chemotherapy drugs and why?

A 
bone marrow
hair
GI
oral mucosa
also rapidly proliferating
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29
Q

what is Filgrastim (Neupogen)?

A

granulocyte colony stumilating factor used to increase WBCs

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30
Q

common side effect of chemo?

A

nausea and vomiting

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31
Q

what are Compazine, Marinol, and Zofran?

A

drugs used in chemo to reduce nausea/vomiting

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32
Q

can resistance occur with cancer drugs?

A

yes

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33
Q

what causes resistance to cancer drugs and where are they located?

A

G-glycoprotein pumps that reside in the cell membranes

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34
Q

what are two ways that drug resistance is combated?

A

-use of multiple agents that work on different parts of the cell
-use different agents that have different toxicities
Together this is known as:
COMBINATION THERAPY

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35
Q

what is the “ABVD regimen” used to treat? how often is the cycle repeated?

A

Hodgkin’s lymphoma

every 28 days

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36
Q 
what are these drugs:
doxorubicin
bleomycin
vinblastine
dacarbazine
A

the ABVD regimem for H. lymphoma

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37
Q

most anticancer drugs are what/do what 2 things?

A

cytotoxic
block cell proliferation
(send cell into G0 phase of mitosis)

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38
Q

what is the growth fraction?

A

proportion of cells actively proliferating

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39
Q

tumor growth rate is __________.

A

initially rapid (exponential)

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40
Q

why does tumor growth rate slow?

A
  • decrease in growth fraction

- cell loss due to hypoxia, poor nutrition supply, immunological defenses

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41
Q

how do alkylation agents work to treat cancer?

A

transfer alkyl groups to DNA which inhibits cell division

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42
Q

alkylating agents are cell-cycle _______.

A

non-specific

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43
Q

what are the adverse effects of alkylating agents?

A

bone marrow suppression

N and V

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44
Q

some alkylating agents are potent _________.

A

vesicants

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45
Q

what is a vesicant?

A

causes blistering or skin reactions

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46
Q

what are Mustargen and Iflex?

A

alkylating agents

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47
Q

what is a platinum coordination compound?

A

a metal complex

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48
Q

how do platinum coordination compounds work?

A

similar to alkylating agents

inhibits cell division

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49
Q

what type of drug in cisplatin and what is it used for?

A

platinum coordination compound

neoplasm of testes, lymph tissues, ovaries

50
Q

platinum coordination compounds are highly effective but limited by what?

A

nephrotoxicity

51
Q

what is Paraplatin?

A

platinum coordination compound

ovarian cancers

52
Q

how do antimetabolites work?

A

inhibit metabolic steps needed for DNA synthesis

sometimes used as an immunosuppressive

53
Q

what types of DNA synthesis are inhibited by antimetabolites?

A

folic acid
purine
pyrimidine

54
Q

methotrexate inhibits what?

A

folic acid synthesis

55
Q

mercaptopurine inhibits what?

A

purine synthesis

56
Q

fluorouracil inhibits what?

A

pyrimidine synthesis

57
Q

during what phase of the cell cycle do antimetabolites work?

A

S phase

58
Q

adverse effects of antimetabolites?

A 
immunosuppressive 
skin rash
bone marrow suppression
GI lesions
alopecia
59
Q

how do vinca alkaloids work?

A

inhibit M-phase of mitosis in cell cycle

60
Q

what are vinca alkaloids used to treat?

A

breast cancer

choriocarcinoma

61
Q

how are vinca alkaloids made?

A

from periwinkle plant

62
Q

what are the adverse effects of vinca alkaloids?

A

bone marrow suppression
GI lesions
alopecia
neurotoxicity

63
Q

what are vincristine and vinblastine

A

vinca alkaloids

64
Q

how do cytotoxic antibiotics and synthetics work?

A

bind to DNA

inhibit RNA synthesis (G2 growth phase)

65
Q

what is bleomycin? what is its serious side effect?

A 
cytotoxic antibiotic
lung fibrosis (impaired lung function)
66
Q

what types of cancers are treated with hormones?3

A

breast
prostatic
endometrial carcinoma

67
Q

fluoxymesterone and testalactone are examples of what type of hormone and are used to treat what?

A

androgens

breast cancer

68
Q

flutamide and bicalutmide are examples of what type of hormone and are used to treat what?

A

anti-androgens

prostatic cancer

69
Q

anti-androgen hormones used to treat prostatic cancer are often combined with what?

A

LHRH agonists (like Leuprolide)

70
Q

what are progestin used to treat?

A

advanced breast cancer

endometrial carcinoma

71
Q

what is tamoxifen and what is it used for?

A

an anti-estrogen

breast cancer

72
Q

what do tyrosine kinase inhibitors, monoclonal antibodies, cox-2 inhibitors, and thalidomide have in common?

A

all block cancer cell signaling

73
Q

tyrosine kinases receptors transduce signal that direct what 5 things in cells?

A 
growth
division
migration
synthesis
apoptosis
74
Q

what are tyrosine kinases?

A

enzymes that phosphorylate tyrosine residues

75
Q

how does tyrosine kinases and signal transduction work?

A
  1. ligand binds to 2 inactive receptors
  2. the ligand brings the 2 receptors together (called receptor dimerization)
  3. causes receptor autophosphorylation and activation to occur
76
Q

7 major tyrosine kinases receptor families

A 
Insulin Receptor and Family
Platelet-Derived GFR and F 
Fibroblast Growth Factor Receptor & Family. 
Hepatocyte GFR and F
Epidermal GFR and F
Vascular endothelial GFR and F
Ret Receptor (Orphan)
77
Q 
what is true of all of these tumors?
NSCLC (non-small cell lung cancer)
prostate
gastric
breast
colorectal
pancreatic
ovarian
A

these tumors show high epidermal growth factor receptor (EGFR) expression

78
Q

high epidermal growth factor receptor (EGFR) expression is associated with what 6 things?

A 
invasion
metastasis
late-stage
chemo resistance
hormone-therapy resistance
poor outcome
79
Q

Angiopoietin-1 (Ang-1) activates what, leading to what?

A

the VEGF receptor and leads to vessel stability

80
Q

angiopoietin-2 (Ang-2) binds to what, leading to what?

A

the VEGF receptor and competitively inhibits

Ang-1, leading to vessel instability.

81
Q

what is angiogenesis?

A

generation and growth of new blood vessels

82
Q

how will an absence of blood supply affect tumor growth?

A

will limit tumor growth to 1-2mm (cubed)

83
Q

what causes a tumor to secrete a growth factor and what effect does that have on blood vessels?

A 
secrete growth factor in response to hypoxia
promotes angiogenesis (vessel growth)
84
Q

what are VEGFs, EGF, FGFs, PDEGFs, and PIGF?

A

VEGF (Vascular endothelial growth factor)
EGF (Epidermal growth factor)
FGFs(Fibroblast growth factor, acidic or basic)
PDEGF (Platelet-derivate endothelial growth factor)
PIGF (placenta growth factor)

85
Q

for colorectal cancer, the metastasis of the cancer correlates with what two things?

A

number of blood vessels

VEGF levels

86
Q

how do tumors measuring less than 1 mm receive O2 and nutrients?

A

diffusion from vasculature

87
Q

large tumors require what (in relation to blood vessels)

A

new vessel network

88
Q

what is the sequence of new blood vessel generation in regards to tumors?

A
  1. tumor secretes angiogenic factors
  2. angiogenic factors stimulate migration, proliferation, and blood vessel development in adjacent blood vessels
  3. new blood vessels form and vascularize tumor
  4. facilitation of tumor growth
89
Q

TKR inhibitors (small molecules) work through what 5 strategies?

A 
Inhibits:
proliferation and maturation of tumor
chemotherapy resistance
angiogenesis
metastasis
anti-apoptosis
90
Q

what are Iressa, Tarceva, Gleevec?

A

Tyrosine Kinase Inhibitors

91
Q

Iressa and Tarceva target what receptors?

A

Her-1

92
Q

Gleevec targets what receptors?

A

Bcr-Abl (a Tyrosine kinase that is always active in CML)

93
Q

Iressa (gefitinib) is used to treat what kinds of cancer? AKA?

A

Non-small cell lung cancer

ZD1839

94
Q

how is Iressa administered and in what dose?

A

orally

250=500 mg daily

95
Q

Iressa adverse side effects? 4

A

Skin rash (72%)
Diarrhea (35%)
Nausea/vomiting
myelosuppression (i.e. bone marrow suppression)

96
Q

what is Tarceva used to treat?

A

advanced or metastatic non-small cell lung cancer
being investigated for use in:
head and neck squamous cell carcinoma
advanced ovarian cancer

97
Q

Tarceva adverse side effects? 1000

A 
Cutaneous toxicity (72-88%)
Diarrhea 
Nausea/vomiting
headache
fatigue
hyperbilirubinemia
myelosuppression
mucositis
98
Q

what was Gleevec designed to treat?

A

CML (chronic myeloid leukemia)

99
Q

what causes CML (chronic myeloid leukemia)?

A

a chromosomal rearrangement that fuses two genes together produces an oncogene that in turn produces an enzyme called BCR-ABL (type of tyrosine kinase)
BCR-ABL is always active and causes an overproliferation of WBCs

100
Q

what is the hallmark of CML (chronic myeloid leukemia)?

A

overproliferation of WBCs

101
Q

TKR inhibitors (monoclonal antibodies) work through what 5 strategies?

A 
same as small molecules
Inhibits:
proliferation and maturation of tumor
chemotherapy resistance
angiogenesis
metastasis
anti-apoptosis
102
Q

Herceptin, Erbitux, and Avastin are all example of what?

A

monoclonal antibodies

103
Q

Read this:
Fully humanized IgG monoclonal AB has been generated using XenoMouse technology, in which human immunoglobulin genes were introduced into mice engineered to lack functional mouse immunoglobulin genes. The full humanization would be expected to result in no immunogenicity and a slower clearance rate of the mAB, compared with mouse or mouse-derived mAbs, thus allowing repeated antibody administration in immunocompetent patients.

A

Read this:
Fully humanized IgG monoclonal AB has been generated using XenoMouse technology, in which human immunoglobulin genes were introduced into mice engineered to lack functional mouse immunoglobulin genes. The full humanization would be expected to result in no immunogenicity and a slower clearance rate of the mAB, compared with mouse or mouse-derived mAbs, thus allowing repeated antibody administration in immunocompetent patients.

104
Q

skin reactions to monoclonal antibodies are related to what?

A

prominent roles of erbB1 and EGF-like ligands in epidermal tissues

105
Q

Herceptin is FDA approved to treat what?

A

HER2 positive metastatic breast cancer

106
Q

adverse side effects of Herceptin?

A

Cardiomyopathy
Anemia/leukopenia
Rashes

107
Q

Erbitux is FDA approved to treat what? combined with what?

A

metastatic colorectal cancer

mono or irinotecan combination

108
Q

adverse side effects of Erbitux?

A

Acneiform rash

follicullitis (80% cases)

109
Q

Avastinis FDA approved to treat what? combined with what?

A

colorectal carcinoma

used in combination with 5FU

110
Q

Humanized MoAB may have what adverse effects?

A

Infusion associated symptoms, hypersensitivity reactions, including fatal anaphylaxis.

111
Q

Do fully humanized MoAB have immunogenesity reactions?

A

no

112
Q

how do cox-2 inhibitors and angiogenesis work?

A

Cox-2 inhibitors indirectly downregulate the activity of angioneogenic factors such as VEGF

113
Q

cox-2 inhibitors induce expression of what? how?

A

VEGF

through the production of PGE2

114
Q

cancer cells ______ Cox-2

A

overexpress

115
Q

how does thalidomide work?

A

Thalidomide inhibits angiogenesis by blocking VEGF which decreases the cells’ ability to induce Cox2 expression

116
Q

how does thalidomide affect an unborn fetus?

A

reduces angiogenesis in limbs causes deformation

117
Q

most of the data collected on thalidomide concerns what types of disorders?

A

plasma cell disorders (specifically refractory relapse multiple myeloma)

118
Q

what does antiangiogentic therapy do?

A

leads to inhibition of tumor growth rather than regression of established tumors

119
Q

Antiangiogenic therapy has the potential to do what?

A

convert an acute disease to a chronic disease (does not cause regression)
-this may extend a patients life more than traditional therapy because traditional therapy may completely fail and lead to death, while a person may be able live a long time with a tumor that is not growing

120
Q

Current anticancer therapy may cause what two things to happen?

A

either cause tumor regression or slow the progress of the tumor growth until failure of therapy

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