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Toxicology Final > Chemical Carcinogenesis > Flashcards

Chemical Carcinogenesis Flashcards

1
Q

When mutation occurs what two groups can it be subdivided into?

A

Reproductive cells and Somatic Cells.

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2
Q

What occurs when there is alteration in somatic cells?

A

cell death, cancer, aging, heart disease, and other diseases. (Most important is cancer)

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3
Q

What occurs in the alteration of Reproductive cells?

A

birth defects and genetic diseases.

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4
Q

What is cancer?

A

disease of cellular mutation, proliferation, and aberrant cell growth.

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5
Q

What are multiple causes of cancer?

A

infectious agents, radiation, and chemicals.

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6
Q

What percent of human cancers are linked to environmental, dietary, and behavioral factors?

A

70-90%

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7
Q

Estimated 70-90% of human cancers are linked to what?

A

environmental, dietary, and behavioral factors.

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8
Q

What is unknown about cancers?

A

aspects of causes, prevention, and treatment.

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9
Q

in 1775 what did Percival Pott discover?

A

linkage between increased occurrence of scrotal and nasal cancer among chimney sweeps.

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10
Q

In 1875 What did Karl Thiersch discover?

A

sunlight exposure and skin cancer.

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11
Q

In 1879 what did Harting and Hesse discover?

A

Lung cancer and uranium mining.

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12
Q

What was discovered in the early 1900s?

A

role of chemical mixtures and individual chemicals in mixtures in animal models.

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13
Q

What is neoplasia?

A

new growth or autonomous growth of tissue.

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14
Q

What is neoplasm?

A

lesion resulting from neoplasia.

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15
Q

What is benign?

A

expansive growth, frequently exhibiting slow rates of proliferation that do not invade surrounding tissues.

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16
Q

What is malignant?

A

Lesion with invasive growth, capable of metastasis to other tissues and organs.

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17
Q

What is Metastasis?

A

secondary growths derived from a primary malignant neoplasm.

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18
Q

What is a tumor?

A

Lesion characterized by swelling or increase in size that may or may not be neoplastic.

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19
Q

What is the mechanism for cancer?

A
  1. Cells grow as a benign tumor in epithelium —> 2. Break through basal lamina —>3. Invade capillary —> 4. Travel through bloodstream (less than 1 in 1000 cells will survive to form metastases) —>5. Adhere to blood vessel wall in liver. —>6. Escape from blood vessel (extravasation) —>7. Proliferate to form metastasis in liver.
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20
Q

What is cancer?

A

Malignant neoplasm

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21
Q

What is a carcinogen?

A

a physical or chemical agent that causes or induces neoplasia.

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22
Q

What does genotoxic mean?

A

Carcinogens that interact with DNA resulting in mutation.

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23
Q

What is non-genotoxic?

A

carcinogens that modify gene expression but do not alter DNA sequence.

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24
Q

What are epigenetic modifications?

A

non genotoxic.

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25
Q

What are the 3 stages of Carcinogensis?

A

Initiation, promotion and Progression

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26
Q

What is initiation in the first stage of cancer?

A

Stable DNA change

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27
Q

What is promotion in the stages of carcinogenesis?

A

Selective clonal expansion of initiated cells to produce a preneoplastic lesion.

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28
Q

What is progression in the 3rd stage of carcinogensis?

A

conversion of benign preneoplastic lesion into neoplastic cancer.

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29
Q

What are multiple outcomes of “Initiation”? (3)

A

Remain in static non-dividing state, cell deleted through apoptosis, undergo cell division resulting in the growth and the proliferation of the initiated cell.

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30
Q

In “initiation” what is needed to lock in a mutation?

A

on cell division.

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31
Q

What are intiators for the “initiation” of Carcinogensis?

A

Chemical and physical agents.

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32
Q

What is the detailed definition of carcinogenesis initiation?

A

Rapid, irreversible process resulting in carcinogen-induced mutation or epigenetic alteration (DNA change).

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33
Q

What is the detailed definition of the promotion of carcinogenesis?

A

selective clonal expansion of initiated cells to produce a preneoplastic lesion.

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34
Q

What are agents are tumor promoters?

A

exogenous and endogenous agents.

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35
Q

What are tumor promoters?

A

Not mutagenic and not able to induce tumors by themselves but act through gene expression changes to sustain cell proliferation.

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36
Q

What does it mean to not be mutagenic?

A

no DNA sequence alteration.

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37
Q

What does it mean to be clinically cancer free?

A

5 years w/o reoccurance.

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38
Q

Why was scrotal cancer big in 1775?

A

chimney sweeps worked naked so clothes wouldn’t get caught.

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39
Q

In promotion of carcinogenesis what is required?

A

multiple cell division and non genotoxic carcinogens.

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40
Q

What is progression in carcinogenesis?

A

conversion of benign preneoplastic lesion into neoplastic cancer.

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41
Q

In progression additional modifications may occur when?

A

with increased cell proliferation.

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42
Q

What are hallmarks of progression in carcinogenesis?

A

accumulation of nonrandom chromosomal aberrations and karyotypic instability.

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43
Q

What are clastogenic agents?

A

hallmarks.

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44
Q

Is progression irreversible?

A

NO!

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45
Q

What is important to know about chemical agents and all the stages of carcinogenesis?

A

chemical agents can act at all stages.

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46
Q

What are the anti-initiation strategies?

A

normal –> initiated –> Preneoplastic –> neoplastic

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47
Q

What are two mechanisms of action of chemical carcinogens?

A

Genotoxic and non genotoxic.

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48
Q

What does genotoxic mean??

A

DNA sequence alteration (Mutagents and DNA repair)

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49
Q

What does non-genotoxic mean?

A

Non-DNA sequence alteration (epigentic alteration).

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50
Q

What does non-genotoxic consists of?

A

Receptor mediated, altered methylation, and altered miRNA expression.

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51
Q

What is generally clonal in nature?

A

Tumors

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52
Q

Many carcinogens are or can be metabolized to what?

A

electrophilic intermediates.

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53
Q

What happens when carcinogens are/can be metablized to electrophilic intermediates?

A

can covalently bind to DNA

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54
Q

What can be mutagens?

A

Many carcinogens

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55
Q

Autosomal dominant inherited cancers provide what?

A

direct evidence for a genetic component in the origin of cancer.

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56
Q

Autosomal recessive-inherited cancers are associated with what?

A

chromosomal fragility or decreased DNA repair.

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57
Q

What predisposes affected individuals to cancer?

A

Autosomal recessive inherited cancers.

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58
Q

What displays chromosomal abnormalities?

A

cancers

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59
Q

What is MAJOR supporting genetic mechanism of carcinogensis?

A

the transformed phenotype can be transferred from a tumor cell to non-tumor cells by DNA transfection.

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60
Q

What can cells be transformed by?

A

oncogenes

61
Q

Proto-Oncogenes are what?

A

activated by mutation in cancer cells.

62
Q

Tumor suppresser genes are what?

A

inactivated by mutation in cancer cells.

63
Q

When do oncogenes originate?

A

when proto-oncogenes involved in normal cellular growth and development are altered.

64
Q

What is an example of an oncogene?

A

when growth factors, PDGF (platelet derived growth factor)

65
Q

Tumor suppressor genes inhibit what?

A

cellular proliferation

66
Q

What is an example of Tumor suppressor genes?

A

P53- Checkpoint control and arrests the cell cycle in G1

67
Q

What occurs when tumor suppressor genes are altered?

A

deletion of tumor suppressor occurs

68
Q

What occurs to oncogenes?

A

upregulation of proto-oncogene.

69
Q

What occurs in the cell cycle checkpoint for P53?

A

no more stop sign in between G1 phase and S phase.

70
Q

Direct acting carcinogens have no what?

A

metabolic activation or chemical modification.

71
Q

Direct- Acting carcinogens are highly reactive electrophiles that do what?

A

can interact with and bind to nucleophiles such as cellular macromolecules including DNA.

72
Q

What are examples of Direct-Acting Carcinogens?

A

Free radicals and Epoxides

73
Q

Direct Acting Carcinogens form what at the site of chemical exposure?

A

tumor formation.

74
Q

Direct acting carcinogens are positive in what assay?

A

in Ames assay WITHOUT bioactivation (S9)

75
Q

What is S9?

A

in vitro liver function, is the factor metabolizing mixture added to Ames Assay to account for bioactivation.

76
Q

What did Millers discover in 1970s?

A

Indirect Acting Carcinogens.

77
Q

What do indirect-Acting carcinogens require?

A

metabolic activation to be carcinogenic.

78
Q

What are examples of Indirect-Acting Carcinogens?

A

Benzyo(a)pyrene two step epoxidation.

79
Q

Where does tumor formation occur in Indirect-Acting carcinogens?

A

not generally at site of exposure but at target tissue.

80
Q

What is Benzoyo(a)pyrene?

A

it is an indirect acting carcinogen

81
Q

Indirect acting carcinogens yield what in the ames assay?

A

positive in ames assay ONLY with biocativation (s9)

82
Q

Mutagens are what?

A

Carcinogens

83
Q

What was introduced by Theodor Boveri in 1914?

A

Somatic Mutation Theory

84
Q

What does the Somatic mutation theory suggest?

A

Cancer was related to chromosome abnormalities in somatic cells.

85
Q

What did Bruce Ames and Colleagues say in first papers in mid 1790s?

A

demonstrating that 90% of carcinogens known at that time were mutagens.

86
Q

Major mutagenic changes in somatic cells lead to what?

A

a total disruption in DNA- directed cellular organization.

87
Q

Major mutagenic changes in somatic cells yield what?

A

may lead to cell death and also lead to inability to grow and divide.

88
Q

What type of interactions do mutagens have?

A

Direct or indirect interaction with DNA to form adduct or damage.

89
Q

What are two mechanisms for mutagens?

A
  1. Base pair substitutions and modifications.

2. Frameshift mutations (deletion or insertion)

90
Q

How DOES DNA repair or the lack of cause cancer?

A

persistence of mutation or adduct is major determinant of outcome and whether cell is able to repair damage.

91
Q

What are DNA repair mechanisms?

A
  1. Direct reversal of DNA damage
  2. Excision Repair Systems
  3. Post-Replication Repair (recombination repair)
  4. Non-homologous-end joining
92
Q

What is non-homologous -end joining?

A

double strand break repair

93
Q

What are the excision repair systems?

A

Base excision repair, nucleotide excision repair, and mismatch repair.

94
Q

What does DNA repair?

A

Both spontaneous alterations and chemical induced alterations

95
Q

What do X-rays yield to as a damaging agent?

A

oxygen radicals, alkylating agents, and spontaneous reactions.

96
Q

What does the Base Excision repair in X-ray damages?

A

uracil, abasic site, and single strand break.

97
Q

Damaging agent is X-rays and what repair process is used?

A

Base Excision Repair (BER)

98
Q

What does UV produce as a damaging agent?

A

Polycyclic aromatic hydrocarbons.

99
Q

What is the repair process for UV light?

A

Nucleotide Excision Repair (NER)

100
Q

What is the repair mechanisms for X-rays anti-tumor agents?

A

Recombinational repair.

101
Q

What is the repair process for replication errors?

A

Mismatch repair

102
Q

What are epigenetic carcinogens?

A

do not involve the mutation of DNA sequence.

103
Q

What lacks genotoxicity?

A

Epigenetic Carcinogens

104
Q

Epigenetic carcinogens involve the alteration in the expression of genes that do what?

A

function in important cellular processes such as proliferation, differentiation and apoptosis.

105
Q

What is cancer associated with?

A

Altered differentiation

106
Q

The cancerous state of tumors is said to sometimes be what?

A

reversible

107
Q

Carcinogenesis is induced by what?

A

non-mutagenic agents.

108
Q

Not all carcinogens are what?

A

mutagens

109
Q

Carcinogenesis is associated with what?

A

Chances in DNA methylation

110
Q

Cell transformation can occur when?

A

at very high frequencies in vitro.

111
Q

What is receptor mediated?

A

Epigenetic Carcinogens

112
Q

What is PPAR alpha?

A

Peroxisome Proliferator Activated Receptor Alpha

113
Q

What are PPAR alpha?

A

Chemicals that increase number and volume of peroxisomes in cell cytoplasm.

114
Q

What are examples of PPAR alpha?

A

Herbicides and plasticizers (phthalates).

115
Q

What are indications of PPAR alpha occurrence?

A

Liver enlargement and hepatocellular carcinoma in rodent models.

116
Q

What is the current MOA?

A

Agonist binding to PPAR alpha which induces cell proliferation and suppression of apoptosis

117
Q

Has PPAR alpha been confirmed to effect humans?

A

no

118
Q

What is AhR?

A

Aryl Hydrocarbon Receptor

119
Q

Receptor mediated cells are what?

A

Agonsits

120
Q

What is TCDD and Select PCBs linked to?

A

Tumor development = increase in gene expression.

121
Q

AhR is a potential function as what?

A

a hepatic tumor promoters that is AhR-dependent.

122
Q

Estrogen receptor is a receptor mediated epigenetic carcinogen that disrupts what?

A

endocrine chemicals that bind to estrogen receptors.

123
Q

What is the agonist of the estrogen receptor?

A

17 Beta- estradiol and BPA (Bisphenol A)

124
Q

What is an antagonist of Estrogen receptor?

A

Tamoxifen

125
Q

Estrogen receptor disruption of hormonal control can result in what?

A

tumor development.

126
Q

Altered methylation is an example of what?

A

epigenetic methylation

127
Q

What is DNA methylation?

A

Promoter CpG islands

128
Q

What are the general assumptions of increased DNA methylation?

A

Decrease in Gene expression.

129
Q

What are the general assumptions of decreased DNA methylation?

A

Increased gene expression.

130
Q

What is tumorigenesis?

A

Alteration in normal site

131
Q

In normal cells what occurs when CpG island TSG promoters are unmethylated?

A

Transcriptionally active open chromatin structure.

132
Q

What occurs in normal cells in CpG island TSG promoters methylated?

A

Transcriptionally silent chromatin state.

133
Q

What is a tumor risk?

A

Methylated TSG promoter

134
Q

Change in MiRNA expression yields to what?

A

Disrupted gene regulation

135
Q

Depending on target gene and modulation, disrupted gene regulation will yield to what?

A

Cancer

136
Q

what is miRNA?

A

Short RNA

137
Q

What is the length of miRNA?

A

22 Nucleotides in length

138
Q

What are post transcriptional regulators?

A

miRNA

139
Q

What does miRNA bind to??

A

sequences of mRNA

140
Q

single miRNA may target multiple mRNA transcripts including what?

A

oncogenes and TSGs

141
Q

Indirect gene expression alterations include what? (3)

A
  1. Translation repression
  2. Target Degradation
  3. Gene silencing.
142
Q

Which genotoxic assays indicate tumor/cancerous growth?

A

chronic bioassays: in vivo

143
Q

What are the genotoxic mutation assays?

A

Ames assay, in vitro mammalian mutation assays (MLA assay), and in vivo gene mutation assays.

144
Q

What are the 3 general genotoxic assays?

A

Mutation assays, chromosomal aberration assays, and chronic bioassays.

145
Q

What are the 3 epigenetic assays?

A

Receptor binding assays, DNA methylation assays, and miRNA expressions assays.

146
Q

What are DNA methylation assays?

A

targets and genome wide

147
Q

What are miRNA expression assays?

A

targeted and genome wide

148
Q

What is the proposed mechanism for Hormesis and Carcinogenesis?

A

adaptive responses that overcompensate for damage

149
Q

What occurs in alteration in DNA?

A

Mutation occurs

Toxicology Final (7 decks)

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