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2nd shift lecs > CANCER > Flashcards

CANCER Flashcards

1
Q

Is a collection of related diseases

A

cancer

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2
Q

In ALL type of cancer, some of the body’s cells begin to divide without stopping and spread into surrounding tissues

A

cancer

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3
Q

Characteristics of cancer

A
  • Self- sufficiency in growth signals
  • Sustained angiogenesis
  • Tissue invasion and metastasis
  • Limitless replicative potential
  • Evasion of apoptosis
  • Insensitivity to antigrowth signals
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4
Q

Features of Genotoxic Carninogens

A
  • Mutagenic
  • Can be complete carcinogens
  • Tumorigenicity is dose responsive
  • No theoretical threshold
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5
Q

Features of Non-genotoxic carcinogens

A
  • Nonmutagenic
    -Threshold, reversible
  • Tumorigenicity is dose responsive
  • May function at tumor promotion stage
  • No direct DNA damage
  • Species, stain, tissue specificity
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6
Q

Stages of carcinogenesis

A

initiation, promotion, and progression

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7
Q

Once a ________ is formed, additional intracellular and extracellular changes occur in the process of the development of a malignant cancer

A

neoplasm

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8
Q

Under initiation stage:

A
  • DNA modification
  • Mutation
  • Genotoxic
  • One cell division necessary to lock-in mutation
  • Modification is not enough to produce cancer
  • Non-reversible
  • Single treatment can induce mutation
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9
Q

Once initiated cells are formed:

A

can remain in static non-dividing state through influences by growth control either via normal surrounding cells or through endocrine influence

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10
Q

Once initiated cells are formed:

A

may posses mutations incompatible with viability or normal function and be deleted through apoptotic mechanisms

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11
Q

Once initiated cells are formed:

A

the cell, through stimuli such as intrinsic factors or from chemical exposure, may undergo cell division resulting in the proliferation of the initiated cell

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12
Q

First step of carcinogenesis

A

initiation

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13
Q

Caused by irreversible genetic changes which predispose susceptible normal cells to malign evolution and immortality

A

initiation

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14
Q

the initiated cell is not a neoplastic cell (t or f)

A

T - has taken its first step towards this state

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15
Q

Under Promotion:

A
  • No direct DNA modification
  • non-genotoxic
  • no direct mutation
  • multiple cell divisions necessary
  • clonal expansion of the initiated cell population
  • increase in cell proliferation where decrease in cell death (apoptosis)
  • reversible
  • multiple treatments (prolonged treatment) necessary
  • threshold
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16
Q

(under promotion) Involves the _________________ of initiated cells to produce a preneoplastic lesion

A

Selective clonal expansion

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17
Q

(under promotion) ______________ is a dose-dependent and _______________ process; with removal of the promotional agent, focal cells cease proliferation and may return to single initiated cells.

A

Tumor promotion; reversible

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18
Q

(under promotion) Carcinogens that function at the tumor promotion stage in general are organ specific. For example, phenobarbital functions at the tumor promotion stage selectively in _________

A

Liver

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19
Q

(under promotion) exogenous and endogenous agents that function at this stage are frequently referred to as __________ , which are not mutagenic and generally are not able to induce tumors by themselves.

A

tumor promoters

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20
Q

Under progression:

A
  • DNA modification
  • Genotoxic event
  • Mutation chromosome disarrangement
  • Changes from preneoplasia to neoplasia benign/malignant
  • Irreversible
  • Number of treatments needed with compound unknown may require only single treatment
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21
Q

Involves conversion of preneoplastic lesion into a neoplasm

A

Progression

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22
Q

Additional genotoxic events may further DNA damage including chromosomal damage such as aberrations and translocations.

A

Progression

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23
Q

Cells accumulate mutations and epigenetic changes that cause cells to lose normal growth control

A

Neoplastic state

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24
Q

Progression is irreversible, whether the formed neoplasm is benign or malignant, and autonomous growth and/or lack of growth control is achieved (t or f)

A

T

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25
Q

Can occur from spontaneous karyotypic changes that occur in mitotically active initiated cells during promotion

A

Spontaneous progression

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26
Q

Hallmarks of progression

A

accumulation of nonrandom chromosomal aberrations and karyotypic instability

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27
Q

Characteristics of a Neoplasm as it progresses into malignant state

A
  • sustaining cell proliferation
  • resisting cell death (apoptosis)
  • inducing angiogenesis
  • enabling replicative immortality
  • activating invasion and metastasis
  • evading growth suppressors
  • reprogramming of energy metabolism
  • evading immune destruction
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28
Q

Is a multistage, multistep process that involves the ultimate release of the neoplastic cells from normal growth control processes and creating a tumor microenvironment

A

Formation of neoplasm

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29
Q

Normal stromal and inflammatory cells

A

contributes to the growth and development of neoplasm

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30
Q

Interacts with nuclear DNA of a target cell producing DNA damage that, if not repaired, is inherited in subsequent daughter cells

A

Genotoxic compounds

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31
Q

DNA-reactive carcinogens can be further subdivided according to:

A

Active in their parent form (direct-acting) or those that require metabolic activation (indirect-acting)

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32
Q

Relative carcinogenic strength depends in part of the relative rates of interactions between the chemical and genomic DNA, as well as competing reactions with chemical and other cellular nucleophiles

A

Direct-acting

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33
Q

Chemical stability, transport, and membrane permeability, determine the carcinogenic activity of the chemical. ______________are typically carcinogenic at multiple sites and in all species examined

A

Direct-acting

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34
Q

Majority of the DNA-reactive carcinogens are found as parent compounds, or procarcinogens that require subsequent metabolism to be carcinogenic

A

Indirect-acting

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35
Q

Procarcinogen

A

Parent compound

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36
Q

Proximate carcinogen

A

Intermediate

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37
Q

Ultimate carcinogen

A

Final

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38
Q

Most likely the chemical species that result in mutation and neoplastic transformation

A

Ultimate form

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39
Q

Usually produce their neoplastic effects at the target tissue where the metabolic activation of the chemical occurs

A

Indirect-acting genotoxic carcinogens

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40
Q

effects of mutation depend on when in the cell cycle the DNA adducts are formed, where the adducts are formed, and the type of repair process used in the response to the damage

A

Mutagenesis

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41
Q

Result from the misread DNA through transitions and transversions, frame-shifting or broken DNA strands

A

Mutagenesis

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42
Q

Most chemical carcinogens require ___________ to exert a carcinogenic effect (damage by alkylating electrophiles)

A

Metabolic activation

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43
Q

The ultimate carcinogenic forms of these chemical are frequently ______________ that can readily form covalent adducts with nucleophilic targets (damage by alkylating electrophiles)

A

strong electrophiles

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44
Q

_________________ display a greater range of nucleophilic target (attack weak and strong nucleophiles) ________________ whereas are only capable of alkylating strong nucleophiles (atoms in amino acids)

A

The stronger electrophiles; weak electrophiles

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45
Q

Relative rates or persistence of particular DNA adducts may bee an important determinant of carcinogenicity

A

DNA repair

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46
Q

DNA region containing the adduct is removed and a new patch of DNA is synthesized, using the opposite intact strand as a template

A

DNA repair

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47
Q

The new DNA segment is then spliced into the DNA molecule in place of the defective one. To be effective in restoring a cell to normal, repair of DNA must occur prior to cell division

A

DNA repair

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48
Q

Exposure to chemicals can increase the probability of acquiring mutations that ultimately lead to cancer development (t or f)

A

T

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49
Q

DNA repair mechanisms

A
  • Mismatch repair of single-base mispairs
  • Excision repair
  • Homologous Recombination and Nonhomologous End-joining repair DNA
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50
Q

may occur through normal cellular DNA replication mistakes such as point mutations, a chance in a single base pair in the DNA sequence, or a small insertion or deletion or a frame shift mutation of some modest size (under mismatch repair of single-base mispairs)

A

Spontaneous mutation

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51
Q

Is a fairly common occurrence and spontaneous event in mammals, and results in the formation of apurinic sites (under mismatch repair of single-base mispairs)

A

Depurination

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52
Q

all mammalian cells prosses __________ that function to cut DNA near apurinic sites. Cut is extended by exonucleases, and the resulting gap repaired by DNA polymerases and ligase

A

apurinic endonucleases

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53
Q

DNA regions containing chemically modified bases, or DNA chemical adducts, are typically repaired by ____________ processes

A

Excision repair

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54
Q

Proteins that slide along the surface of a double-stranded DNA molecule recognize the irregularities in the shape of the double helix and affect the repair of the lesion

A

Excision repair

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55
Q

A cell that has double-stranded breaks can be repaired by _________________

A

joining the free DNA ends

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56
Q

The joining of broken ends from different chromosomes, however will lead to the _________________ pieces from one chromosome to another

A

translocation of DNA

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57
Q

Have the potential to enable abnormal cell growth by placing the proto-oncogene next to, and, therefore, under the control of another gene promoter

A

Translocations

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58
Q

Is one of two mechanisms responsible for the repair of double -strand break on one chromosome is repaired using the information on the homologous, intact chromosome

A

Homologous recombination

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59
Q

The predominant mechanism for double-stranded DNA repair in multicellular organisms is non-homologous repair and involves

A

rejoining the ends of the two DNA molecules

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60
Q

Although the process yields a continuous double-stranded molecules, ___________________ at the joining point. This type of deletion may _______________________

A

several base pairs are lost; produce a possible mutagenic coding change

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61
Q

Classes of Genotoxic Carcinogens

A

Polyaromatic Hydrocarbons (PAH), Alkylating agents, Aromatic amines and amides

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62
Q

Are found at high levels in charcoal-broiled foods, cigarettes, smoke, and in diesel exhaust

A

Polyaromatic Hydrocarbons (PAH)

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63
Q

Readily reacts with DNA at more than 12 sites. The N7 position of guanine and the N3 position of adenine are the most reactive sites for alkylating chemicals to bind to DNA

A

Alkylating agents

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64
Q

Encompass a class of chemical with varied structures. Exposure to these chemicals was through use in the dye industry. Today, exposure still occurs through cigarette smoke and environmental sources

A

Aromatic amines and amides

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65
Q

yield hydroxylated metabolites that are often associated with adduct formation in proteins and DNA and produce liver and bladder carcinogenicity

A

Phase I cytochrome P450-mediated reactions

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66
Q

Induced by non-genotoxic carcinogens are often in tissues where a significant incidence of background, spontaneous tumors is seen in the animal model

A

Organ and tissue targets

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67
Q

___________ to relatively high levels of chemicals is usually necessary for tumor production by this mechanism

A

Prolonged exposure

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68
Q

Proposed modes of action for selected non-genotoxic chemical carcinogens

A
  • Cytotoxicity
  • a2U-Globulin binding
  • Receptor mediated
    > CAR
    > PPARa
    > AHR
  • Hormonal
  • Altered Methylation
  • Immunosuppression
  • Oxidative stress inducers
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69
Q

Cytotoxicity

A
  • Chloroform
  • Melamine
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70
Q

a2U-Globulin binding

A
  • D-Limonene
  • 1,4-Dichlorobenzene
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71
Q

CAR

A
  • Phenobarbital
  • Toxaphene
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72
Q

PPARa

A
  • Trichloroethylene
  • Perchloroethylene
  • Diethylhexylphthalate
  • Fibrates (e.g. clofibrate)
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73
Q

Hormonal

A
  • Biogenic amines
  • Phenobarbital
  • Steroid and peptide hormones
  • Diethylstilbestrol (DES)
  • Phytoestrogens (Bisphenols-A)
  • Tamoxifen
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74
Q

Altered methylation

A
  • Phenobarbital
  • Choline deficiency
  • Diethanolamine
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75
Q

Immunosuppression

A
  • Atrazine
  • Bisphenol A
  • Phthalates
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76
Q

Oxidative stress inducers

A
  • Ethanol
  • TCDD
  • Lindane
  • Dieldrin
  • Acrylonitrile
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77
Q

Chemicals functions through this mechanism produce sustained cell death that is accompanied by persistent regenerative growth, resulting in the potential for the acquisition of spontaneous DNA mutations and allowing mutated cells to accumulate and proliferate

A

Cytotoxicity

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78
Q

This process gives rise to preneoplastic focal lesions that upon further expansion can lead to tumor formation

A

Cytotoxicity

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79
Q

Induction of cytotoxicity may be observed with many carcinogens both genotoxic and non-genotoxic when high toxic exposure occur (t or f)

A

T

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80
Q

Induction of cytotoxicity with compensatory hyperplasia may contribute to the observed tumorigenicity of many carcinogenic chemicals at high-dose levels (t or f)

A

T

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81
Q

Receptor mediated

A

CAR, PPARa, AHR

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82
Q

Is a commonly studied non-DNA-reactive compound that is known to cause tumors by a non-genotoxic mechanism involving liver hyperplasia

A

Phenobarbital

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83
Q

Induction of ___________ is mediated by activation of the constitutive androstane receptor (CAR), a member of the nuclear receptor family.

A

Cyp2b

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84
Q

Other CAR-dependent phenobarbital responses that are critical for tumor formation include

A
  • increased cell proliferation
  • inhibition of apoptosis
  • inhibition of gap junctional communication
  • hypertrophy
  • development of preneoplastic focal lesions in the liver
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85
Q

CAR can be activated by both direct ligand binding and ligand-independent (indirect) mechanisms (t or f)

A

T

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86
Q

Phenobarbital activates CAR indirectly by inhibiting __________ binding to EGF and preventing downstream events leading to increased gene expression

A

epidermal growth factor receptor (EGFR)

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87
Q

A wide array of chemicals increase the number and volume of peroxisomes in the cytoplasm of cells

A

PPARa (peroxisome proliferator activator receptor a)

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88
Q

Peroxisome proliferators include

A
  • lipid lowering fibrate drugs
  • herbicides
  • chlorinated solvents
  • per fluorinated compounds
  • plasticizers
  • natural products
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89
Q

Lipid lowering fibrate drugs

A

ciprofibrate, clofibrate

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90
Q

Herbicides

A

2,4- dichlorophenoxyacetic acid

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91
Q

Chlorinated solvents

A

trichloroethylene and perchloroethylene

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92
Q

Perfluorinated compounds

A

perfluorooctane sulfonate and perfluorooctanoic acid

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93
Q

Plasticizers

A

diethylhexylphthalate and other phthalates

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94
Q

PPARa is highly expressed in cells that have active fatty acid oxidation capacity (site)

A

hepatocytes, cardiomyocytes, enterocytes

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95
Q

Plays a central role in lipid metabolism and acts as a transcription factor to modulate gene expression following ligand activation

A

PPARa

96
Q

TCDD and selected polychlorinated and brominated-biphenyl (PCBs and PBBs0 compounds bind to the AhR, the ligand bound AHR translocate to the nucleus, dimerizes with the Ah receptor nuclear transporter (ARNT) and binds to aryl hydrocarbon response elements

A

Aryl Hydrocarbon Receptor activators

97
Q

AREs are also known as

A

dioxin repsonse elements (DRE) and xenobiotic response elements (XRE)

98
Q

AhR-ARNT-dependent genes

A
  • cytochrome P450 family members
  • NAD(P)H: quinone oxidoreductase
  • cytosolic aldehyde dehydrogenase 3
  • UDP-glucuronosyltransferase
  • glutathione transferase
99
Q

Hormonally active chemicals include _______________________ that produce tissue-specific changes through interaction with a receptor

A

steroids, peptide hormones

100
Q

Induce cell proliferation at their target organs, which may lead to tumor development when the mechanisms of hormonal control are disrupted

A

Trophic hormones

101
Q

Hormonal mode of action

A
  • estrogenic agents
  • thyroid hormone
102
Q

Can induce tumors in estrogen-dependent tissues

A

Estrogen and estrogen-mimetic chemicals

103
Q

Individuals with higher circulating estrogen levels and those with exposure to the potent estrogenic chemical diethylstilbestrol (DES) are at increased risk for cancer development (t or f)

A

T

104
Q

DES has been causally associated with the higher incidence of

A

adenocarcinomas of the vagina and cervix in daughters of women treated with the hormone during pregnancy

105
Q

Mechanism of DES

A

induce changes in the cell cycle and microtubule function, which may lead to an abnormal number of chromosomes in a cell

106
Q

Estrogenic substances in plants (phytoestrogens)

A

genistein, daidzein, glycitein, equol, and their metabolites found in soy products, and various lignan derivatives

107
Q

A ________ of thyroid hormone concentrations (T4 and /or T3) and _______ thyroid-stimulating hormone (TSH) have been shown to induce neoplasia in the rodent thyroid

A

reduction; increased

108
Q

____ Increases proliferative activity in the thyroid. After chronic treatment chemical-induced increased in ____ lead to follicular cell hypertrophy, hyperplasia, and eventually neoplasia

A

TSH

109
Q

_______ of the five position of cytosine (5-methylcytosine; 5mC) is a naturally occurring modification to DNA in higher eukaryotes that influence gene expression. Under normal conditions, DNA is methylated symmetrically on both strands

A

Post-DNA synthetic methylation

110
Q

Immediately following DNA replication, the newly synthesized double-stranded DNA contains ____________________

A

Hemimethylated sites

111
Q

Signals DNA maintenance methylases to transfer methyl groups from S-adenosylmethionine to cytosine residues on the new DNA strand

A

Hemimethylated sites

112
Q

The degree of methylation within a gene __________ correlates with the expression of that gene

A

inversely

113
Q

hypermethylation of genes is associated with _________, whereas hypomethylation results in ________________

A

gene silencing; enhanced expression of genes

114
Q

During carcinogenesis, both hypomethylation and hypermethylation are observed (t or f)

A

T

115
Q

Can also modify DNA methylation through interfering with the ability of methyltransferases to interact with DNA resulting in changes in DNA methylation profiles.

A

Reactive oxygen species

116
Q

______________ of CpG sites allows the expression of normally quiescent genes. Also, the abnormal methylation pattern observed in cells transformed by chemical oxidants may contribute to an overall aberrant gene expression and promote the tumor process

A

Hypomethylation

117
Q

Are small noncoding RNAs usually consisting of 21 to 25 nucleotides, that typically regulate gene expression through repression or degradation of targeted messenger RNAs (mRNAs) controlling gene involved in multiple cellular processes

A

MicroRNAs

118
Q

Has been implicated in the development of initiation, promotion, and progression of cancer

A

dysregulation of mRNAs

119
Q

Many _________ functions as anti tumor agents ( or tumor suppressor genes ), others behave as oncogenes, commonly known as onco _______

A

miRNAs

120
Q

May potentially be used as indicators of the carcinogenic process, biomarkers for carcinogen exposure, and for the identification of potential chemical carcinogen

A

miRNA profiles and miRNAs specific to carcinogen exposure

121
Q

Is an essential host protection mechanism that inhibits carcinogenesis by identifying and removing early preneoplastic cells from the body and to maintain cellular homeostasis

A

Cancer immune surveillance

122
Q

is one hallmark of cancer

A

Evading immune recognition and destruction

123
Q

Has also been proposed as a possible mode of action of non-genotoxic carcinogens

A

Immune suppression

124
Q

can destroy immune cells leading to immune suppression

A

Prolonged inflammation

125
Q

Immunosuppression is suggested to be involved in the carcinogenesis of environmental immune disruptors such as

A

bisphenol A, atrazine, phthalates, and PBDEs

126
Q

includes superoxide anion (O2), hydroperoxyl radical (HO2), hydrogen peroxide (H2O2), the the hydroxyl radical (OH) produced from both endogenous and exogenous sources which are typically counterbalanced by antioxidants

A

Reactive oxygen species

127
Q

Endogenous sources of ROS includes:

A

oxidative phosphorylation, P450 metabolism, peroxisomes, and inflammatory cell activation

128
Q

An increase is H2O2 production often accompanies exposure to chemicals that stimulate the number and activity of peroxisomes (t or f)

A

T

129
Q

left unbalanced by antioxidants can
result in damage to cellular macromolecules

A

ROS

130
Q

can produce single or double-stranded
DNA breaks, purine, pyrimidine, or deoxyribose modifications, and DNA cross-links

A

ROS

131
Q

can result in either arrest or induce
transcription, induce signal transduction pathways, replication errors, and genomic instability: these events are potentially involved in carcinogenesis.

A

Persistent DNA Damage

132
Q

Reasons why mitochondrial genome is susceptible to oxidative base damage

A
  • close proximity to the electron transport system, a major source of reactive oxygen species
  • lack of mitochondrial DNA protection by histones
  • limited DNA repair capacity in the mitochondria
133
Q

High concentrations of reactive oxygen species can initiate apoptosis, whereas low levels influence signal transduction pathways and alter gene expression. (t or f)

A

T

134
Q

Xenobiotics alter gene expression through activation of:

A
  • cAMP-mediated cascades
  • calcium-calmodulin pathways
  • transcription factors such as AP-1, Nrf2, Hif1, and NF-κB
  • mitogen-activated protein (MAP) kinases
  • extracellular signal-regulated kinases [ERK]
  • c-Jun N-terminal kinases [JNK], and the p38 kinases)
135
Q

Cells within an organism communicate variously including through _________, which are aggregates of connexin proteins that form a conduit between two adjacent cells

A

gap junctions

136
Q

communication is important in the regulation of cell growth and cell death, in part, through the ability to exchange small molecules (<1 kDa) between cells

A

Gap junctional intercellular

137
Q

Inorganic carcinogens

A

Metals: arsenic, beryllium, cadmium, chromium, nickel, and lead.

138
Q

Modifiers of Chemical Carcinogenic Effects: have a significant impact on the way in which individuals and/or organisms respond to carcinogen exposure

A

Genetic and environmental factors

139
Q

As with most genes, enzymes that metabolize carcinogens are expressed in a ________ manner, and the enzymatic profile can vary with tissue or cell type or display differential localization within cells.

A

tissue-specific

140
Q

Polymorphisms in Carcinogen Metabolism and DNA Repair: where a gene has more than one allele arise from human genetic variability

A

Genetic polymorphism

141
Q

Base variations occurred approximately once in every ________base pairs

A

1000

142
Q

is a variant in DNA sequence found in greater than 1% of the population

A

single nucleotide polymorphism (SNP)

143
Q

encode a wide array of proteins that function to control cell growth and proliferation

A

Proto-oncogenes and tumor-suppressor genes

144
Q

Proto-oncogenes

A
  • dominant
  • Broad tissue specificity for cancer development
  • germline inheritance rarely involved in cancer
    developmen
  • Analogous to certain viral oncogenes
  • Somatic mutations activated during all stages of carcinogenesis
145
Q

Oncogenes

A
  • dominant
  • broadspecificity for cancer development
  • Germline inheritance rarely involved in cancer
    development
  • No known analogues in oncogenic viruses
  • Somatic mutations activated during all stages of carcinogenesis
146
Q

Tumor suppressor genes

A
  • Recessive
  • Considerable tissue specificity for cancer development
  • Germline inheritance frequently involved in cancer development
  • No known analogues in oncogenic viruses
  • Germline mutations may initiate, but mutation to neoplasia occurs only during progression stage
147
Q

RSV can produce sarcomas

A

Rous sarcoma virus

148
Q

The genome of RSV and other retroviruses consists of:

A

two identical copies of mRNA, which is then reverse transcribed into DNA and incorporated into the host-cell genome

149
Q

Oncogenic transforming viruses such as RSV contain the_______, a gene required for cancer induction.

A

v-src gene

150
Q

_________ contains a gene closely related to v-src in RSV

A

Normal cells

151
Q

This discovery highlighted that cancer may be induced by the action of normal, or nearly normal, genes. (T or F)

A

T

152
Q

Six major classes of DNA tumor viruses have been identified:

A
  • simian virus 40 SV40
  • polyoma virus
  • hepatitis B virus
  • papilloma viruses
  • adenoviruses
  • herpes viruses
  • poxviruses
153
Q

Retroviral oncogenes are derived from normal cellular genes and have no functions for the virus (t or f)

A

T

154
Q

encodes a protein that is capable of transforming cells in culture or inducing cancer in animals

A

Oncogene

155
Q

the majority appear to have been derived from normal genes and are involved in cell signaling cascades.

A

proto-oncogenes

156
Q

Activation arises through mutational events occurring within proto-oncogenes

A

Proto-oncogenes

157
Q

In contrast to oncogenes, the proteins encoded by most tumor- suppressor genes act as inhibitors of cell proliferation or cell survival

A

Tumor-suppressor genes

158
Q

Prototype tumor-suppressor gene

A

Rb gene

159
Q

Loss or mutational inactivation of Rb contributes to the development of many human cancers (t or f)

A

T

160
Q

In its unphosphorylated form, Rb binds to the ___________ preventing E2F-mediated transcriptional activation of several genes whose products are required for DNA synthesis.

A

E2 factor (E2F) transcription factor

161
Q

When Rb becomes phosphorylated during late ______ and dissociates from E2F, E2F induces synthesis of DNA replication enzymes resulting in a commitment into the cell cycle

A

G1

162
Q

Tumor suppressors

A
  • Rb1
  • p53
  • BRCA1
  • WT-1
  • p16
163
Q

Rb1 disorder

A

Retinoblastoma

164
Q

Rb1 neoplasm

A

Small-cell lung carcinoma

165
Q

p53 disorder

A

Li-Fraumeni syndrome

166
Q

p53 neoplasm

A

Breast, colon, lung cancers

167
Q

BRCA1 disorder

A

Unknown

168
Q

BRCA1 neoplasm

A

Breast carcinoma

169
Q

WT-1 disorder

A

Wilms tumor

170
Q

WT-1 neoplasm

A

Lung cancer

171
Q

p16 disorder

A

Unknown

172
Q

p16 neoplasm

A

Melanoma

173
Q

is a tumor-suppressor that is essential for
checkpoint control and arrests the cell cycle in cells with damaged DNA in G1

A

p53

174
Q

Cells with __________ arrest in G1 when exposed to DNA-damaging agents such as irradiation

A

functional p53

175
Q

whereas cells lacking
functional p53 are unable to block the cell cycle. (T or f)

A

T

176
Q

p53 is activated by a wide array of stressors including

A

UV light, γ-irradiation, heat, and many carcinogens

177
Q

In most cells, accumulation of p53 also leads to induction of proteins that promote__________, thereby preventing proliferation of cells that are likely to accumulate multiple mutations

A

apoptosis

178
Q

Genetic analysis of breast tumors has revealed a hereditary predisposition for breast cancer linked to…

A

BRCA1

179
Q

Mutation of a single BRCA1 allele results in a % probability of developing breast cancer by age 50

A

60% probability

180
Q

lead to loss of function of the BRCA1 gene,
perhaps by acting as a transcription factor through binding at a zinc finger domain. However, no mutations have been observed in sporadic breast cancers, suggesting that BRCA1 gene silencing may occur through non-mutational mechanisms

A

Germ-line mutations

181
Q

occurs in the developing kidney at a rate of
approximately one per 10,000 children

A

WT-1 gene

182
Q

The proteins that function as cyclin-kinase inhibitors are important in cell cycle regulation

A

p16

183
Q

would mimic cyclin D1 overexpression, leading to Rb hyperphosphorylation and release of active E2F transcription factor

A

Loss of p16

184
Q

is a U, J, or inverted U-shaped dose–response with low-dose exposures often resulting in beneficial rather than harmful effects

A

Hormesis

185
Q

usually involve actions of the chemical on cellular signaling pathways that lead to changes in gene expression, resulting in enhanced detoxification and excretion of the chemical as well as preserving the cell cycle and programmed cell death

A

Adaptive response

186
Q

A common feature of chemical carcinogens for which hormetic effects have been proposed is the formation of

A

ROS and induction of cytochrome P450 isoenzyme

187
Q

The study of chemicals that prevent, inhibit, or slow down the process of cancer is referred to as

A

Chemoprevention

188
Q

are typically of the duration of days to a few weeks, intermediate-term tests last from weeks up to a year, whereas chronic long-term tests usually encompass 6 months to 2 years.

A

Short-term tests

189
Q

tests for mutagenicity were developed to identify potentially carcinogenic chemicals based on their ability to induce mutations in DNA

A

Short-term

190
Q

Therefore, although they are usually very predictive of indirect (if a metabolic source is provided) and direct acting agents, these tests routinely fail to detect non-genotoxic carcinogens.

A

Short-term tests

191
Q

most widely used short-term test is:

A

Ames test

192
Q

Salmonella typhimurium strains, deficient in DNA repair and unable to synthesize histidine, are treated with several doses of the test compound.

A

Ames test

193
Q

is used to determine whether a chemical is capable of inducing mutation in eukaryotic cells. The ability of cells in culture to acquire resistance to trifluorothymidine (the result of forward mutation at the thymidine kinase locus) is quantified.

A

mouse lymphoma assay

194
Q

is commonly used to assess the potential mutagenicity of chemicals with the hypoxanthine–guanine phosphoribosyltransferase (HGPRT) gene as the endpoint.

A

Chinese hamster ovary (CHO) test

195
Q

In vitro gene mutation assays

A
  • Ames test
  • Mouse lymphoma assay
  • Chinese hamster ovary (CHO) test
196
Q

disadvantages over the in vitro test systems in
that they take into account whole animal processes such as absorption, tissue distribution, metabolism, and excretion of chemicals and their metabolites. (t or f)

A

F

197
Q

commonly used in vivo models include

A

transgenic rodent mutation assay systems, base on genes of lac operon (MutaMouse, Big Blue, and Pig-a gene mutation assay)

198
Q

is primarily performed in rats and is based on the X-linked ________ which is involved in the production of glycosylphosphatidylinositol (GPI) anchor
proteins on the cell surface.

A

Pig-a gene mutation assay

199
Q

the assay is optimized for measuring the Pig-a
mutant phenotype in peripheral blood erythrocytes by
quantification of ______________________

A

CD59- negative reticulocytes and red blood cells

200
Q

is highly conserved in humans, rats, mice, and
monkeys, allowing comparison of mutation induction across multiple species.

A

Pig-a gene

201
Q

are quite common in malignant neoplasms. Both in vivo and in vitro assays are available.

A

Chromosomal alterations

202
Q

To assess induction of chromosomal alterations, cells are
harvested in their ___________ after the initiation of
chemical exposure. Cells are stained with _______ and scored for completeness of karyotype (21 ± 2 chromosomes).

A

first mitotic division; Giemsa

203
Q

represents possible pre-mutational events that can be detected, either directly or indirectly, using mammalian cells in culture or using rodent tissue.

A

Primary DNA damage

204
Q

is a commonly used assay that measures the ability of a test article to induce DNA lesions by quantifying the increase in DNA repair.

A

Unscheduled DNA synthesis (UDS)

205
Q

has been widely used for the transformation assay; It was originally derived from fibroblasts taken from the prostate of a C3H mouse embryo.

A

C3H/10T½ cell line

206
Q

this assay assesses carcinogenic potential based on the percentage of colonies that are transformed.

A

transformation assays

207
Q

a diploid cell transformation assay, measures carcinogenic potential of xenobiotics by assessing transformed colonies based on morphological criterion.

A

Syrian Hamster Embryo cell assay (SHE)

208
Q

____________ studies in laboratory rodents remain the primary method by which chemicals or physical agents are identified as having the potential to be hazardous to humans.

A

Chronic (Two Year) Bioassay Two-year

209
Q

In the chronic bioassay, two or three dose levels of a test
chemical (up to the maximum tolerated dose) and a vehicle control are administered to _______________ , _______________, continuing throughout their lifespan.

A

50 males and 50 females (mice and rats); beginning at 8 weeks of age

210
Q

During the study (chronic bioassay), ______________ are monitored and the animals are observed clinically on a regular basis; at necropsy, the tumor number, location, and diagnosis for each animal are thoroughly assessed.

A

food consumption and bodyweight gain

211
Q

It has been estimated that nearly half of the
chemicals tested in the two-year chronic bioassay by the National Toxicology Program showed an increased incidence of liver cancer. (t or f)

A

T

212
Q

have been developed to study and distinguish chemicals that affect the initiation or promotion stage of hepatocarcinogenesis.

A

Liver carcinogenesis assays

213
Q

this model exploits many of the unique properties of mouse skin, one major advantage being that the development of neoplasia can be followed visually. In addition, the number and relative size of papillomas and carcinomas can be quantified as the tumors progress.

A

Carcinogenicity Testing in Skin: mouse skin model

214
Q

In this model, carcinogenicity is typically assessed as an
acceleration of tumor development rather than an increase in tumor incidence.

A

Carcinogenicity Testing in Lung Strain: mouse lung tumor assay

215
Q

mice are genetically susceptible to the development of lung tumors, with lung tumors being observed in control animals as _______________ with a steady increase to nearly 100% by _____________.

A

early as 3 to 4 weeks of age; 24 months of age

216
Q

The strain A mouse lung tumor assay is sensitive to chemicals, such as.

A

PAHs, nitrosamines, nitrosoureas, carbamates, aflatoxin, certain metals, and hydrazines

217
Q

the component that contributes the most to human
cancer induction and progression is:

A

lifestyle: tobacco use, alcohol use, and poor diet

218
Q

is estimated to be responsible for 25% to 40% of all human cancers

A

tobacco usage

219
Q

____________ consumption also contributes anywhere from 2% to 4% of cancers of the esophagus, liver, and larynx.

A

Alcohol

220
Q

whether high-fat, low-protein, high-calories or diets
lacking in needed antioxidants and minerals account for
anywhere from 10% to 70% of human cancers.

A

poor diet

221
Q

excess calories and/or high-fat diets contributes to breast,
colon, and liver cancer in humans

A

overnutrition

222
Q

are formed during broiling and grilling of meat

A

carcinogenic heterocyclic amine and PAHs

223
Q

a suspected human carcinogen, has been found in
fried foods at low concentrations.

A

Acrylamide

224
Q

Carcinogenic factors associated with Lifestyle

A

chemicals:
- alcohol
- alfatoxins
- betel chewing
- dietary intake (fat, protein, calories)
- tobacco smoking

225
Q

Neoplasm(s) from alcohol beverage

A

Esophagus, liver, oropharynx, and larynx

226
Q

Neoplasm(s) from aflatoxins

A

liver

227
Q

Neoplasm(s) from betel chewing

A

mouth

228
Q

Neoplasm(s) from dietary intake

A

breast, colon, endometrium, gallbladder

229
Q

Neoplasm(s) from tobacco smoking

A

Mouth, pharynx, larynx, lung, esophagus, bladder

230
Q

Agent is carcinogenic to humans
- Evidence: Human data strong Animal data strong

A

IARC Classification of the Evaluation of Carcinogenicity for
Human Beings: GROUP 1

231
Q

Agent is probably carcinogenic to humans
- Evidence: Human epidemiology data
suggestive Animal data positive

A

IARC Classification of the Evaluation of Carcinogenicity for
Human Beings: GROUP 2A

232
Q

Agent is possibly carcinogenic to humans
- Evidence: Human epidemiology data weak Animal data positive

A

IARC Classification of the Evaluation of Carcinogenicity for
Human Beings: GROUP 2B

233
Q

Agent is not classifiable as to carcinogenicity to humans
- Evidence: Human and animal data inadequate

A

IARC Classification of the Evaluation of Carcinogenicity for
Human Beings: GROUP 3

234
Q

Agent is probably not carcinogenic to humans
- Evidence: Human and animal data negative

A

IARC Classification of the Evaluation of Carcinogenicity for
Human Beings: GROUP 4

235
Q

is a multistage process that involves initial mutational
events followed by changes in gene expression leading to the selected clonal proliferation of the precancerous cell.

A

Cancer

236
Q

appears to exhibit multiple characteristics including
increased selective lesion growth (through sustained cell
proliferation and/or resistance to apoptosis), the induction of angiogenesis, enabling replicative immortality, activation of factors that influence invasion and metastasis, evasion of normal growth suppression, modulation of energy metabolism, and the avoidance of attack by the immune system.

A

Neoplasia

2nd shift lecs (21 decks)

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