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Carcinogenesis Flashcards

1
Q

abnormal cells with abnormal growth

A

Carcinogenesis

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2
Q

Abnormal cell differentiation and growth

A

Carcinogenesis

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3
Q

T/F: In all types of cancer, some of the body’s cells begin to divide without stopping and spread into surrounding tissues

A

True

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4
Q

Characteristics of Cancer:
_______________ in growth signals
Insensitivity to ____________
Evasion of ____________
Limitless ____________ potential
Tissue ____________ and ____________
Sustained ____________

A

Self-sufficiency; antigrowth signals; apoptosis; replicative; invasion and metastasis; angiogenesis

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5
Q

stages of carcinogenesis

A
  1. Initiation
  2. Proliferation
  3. Promotion
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6
Q

In this stage - cancer is already triggered (irreversible)

A

Initiation stage

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7
Q

proliferation happens in this stage

A

Promotion

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8
Q

Promotion is __________ (reversible/ireversible)

A

Reversible

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9
Q

stage where neoplasia happnes

A

Progression

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10
Q

Abnormal tissue growth in mucosal surface of colon (most common), ear canal, cervix

A

BENIGN TUMORS/POLY

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11
Q

Can Benign tumors/poly be removed?

A

Yes, they are not life threatening

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12
Q

Can Benign tumors/poly become malignant?

A

Yes

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13
Q

Non Cancerous cells

A

Benign turmors

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14
Q

Benign tumors are found in

A

mucosal surface of colon (most common), ear canal, cervix

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15
Q

types of malignant tumors

A

carcinoma
sarcoma

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16
Q

epithelial origin

A

carcinoma

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17
Q

superficial origin

A

carcinoma

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18
Q

Most common. Cancer of the skin or organ lining e.g., liver or kidneys

A

carcinoma

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19
Q

of mesenchymal origin

A

sarcoma

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20
Q

liquid type

A

sarcoma

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21
Q

connective tissues

A

sarcoma

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22
Q

loosely packed and can travel to new positions (e.g. blood vessels)

A

sarcoma

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23
Q

Cancer of connective tissue e.g., bones, muscles, cartilage, & blood vessels

A

sarcoma

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24
Q

Blood cancers

A

Leukemia
Hodgkin or non-hodgkin lymphoma, multiple myeloma

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25
Q

Bone marrow CA

A

Leukemia

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26
Q

CA of the immune system

A

Hodgkin or non-hodgkin lymphoma, multiple myeloma

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27
Q

with presence of Reed-Sternberg cells

A

Hodgkin

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28
Q

These are giant cells found in Hodgkin Lymphoma

A

Reed-Sternberg cells

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29
Q

Agents that causes change in the gene structure

A

Mutagens

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30
Q

Mutagens may result from misread DNA through __________ and __________,__________ or broken DNA stands

A

transitions; transversions; frame-shifting

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31
Q

alter transcription due to insertion/deletion leading to incorrect DNA sequence

A

Frame shifting

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32
Q

T/F: Frame shfiting may prodce malfunctioning cells

A

true

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33
Q

DIRECT-ACTING GENOTOXIC CARCINOGENS

A

Carbonium ions
Nitrenium Ions
Free radicals
Diazonium ions
Epoxides
Aziridinium ions
Episultonium ions
Strained lactones
Sulfonates
Halo ethers
Enals

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34
Q

T/F: The development of cancer following exposure to chemical
carcinogens is a relatively rare event because of a cell’s ability to recognize and repair DNA.

A

True

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35
Q

DNA Repair mechanism:

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

Cut-and-Patch by pol 1

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36
Q

According to Cut-and-Patch by pol 1, to be effective in restoring a cell to normal, repair of DNA must occur _____________ (before or after) cell division.

A

prior/before

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37
Q

In Cut-and-Patch by pol 1, the DNA region containing the adduct is __________ and a new patch of DNA is synthesized, using the ________________ as a template.

A

removed; opposite intact strand

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38
Q

Fragment translation by pol 1

A

nick translation by pol 1

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39
Q

Typically repairs chemically modified nucleobases

A

Base Excision or Mismatch Repair of Single-base Mispairs

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40
Q

Removes altered base in the Base Excision or Mismatch Repair of Single-base Mispairs DNA repair mechansim

A

DNA glycosylase

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41
Q

In Base Excision or Mismatch Repair of Single-base Mispairs DNA repair mechansim, _________ fills the gap created by DNA glycosylase

A

pol 1

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42
Q

Cut DNA near apurinic sites

A

Apurinic endonucleases

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43
Q

The cut by apurinic endonucleases is then extended by ____________, and the resulting gap is repaired by _____________ and ____________

A

exonucleases; DNA polymerase and ligase

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44
Q

In this repair mechanism, photolyase Binds T-T cyclobutane dimer → Individual pyrimidine bases

A

Photoreactivation Repair

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45
Q

In photoreactivation repair mechanism, photolyase binds to ____________ (________) resulting to an individual _________ bases

A

T-T cyclobutane dimer (Thymine-thymine); pyrimidine

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46
Q

The double-strand break on one chromosome is repaired using the information on the homologous, intact chromosome

A

Homologous Recombination

47
Q

In Homologous Recombination, the ____________break on one chromosome is repaired using the information on the homologous, intact chromosome

A

double-strand

48
Q

The predominant mechanism for double-stranded DNA repair

A

Nonhomologous End-joining Repair of DNA

49
Q

T/F: During Nonhomologous End-joining Repair of DNA, Several base pairs are lost at the joining point. This type of deletion may produce a possible mutagenic coding change

50
Q

CHEMICAL MUTAGENS

A

Polycyclic Aromatic Hydrocarbons (PAHs)
Alkylating agents (Electrophilic)
Aromatic amines and amides (Dyes)
Butylated Hydroxyanisole (BHA), Butylated Hydroxytoluene (BHT)

51
Q

example of Polycyclic Aromatic Hydrocarbons (PAHs)

A

Benzopyrene

52
Q

found in charcoal-broiled foods, tobacco, diesel exhaust

A

Benzopyrene

53
Q

Example of Alkylating agents (Electrophilic)

A

Nitrosamines (tocino/longganisa preservative)
Aflatoxin (nuts)
Alkyl sulfates
Cytotoxic Alkylating agents -

54
Q

Butylated Hydroxyanisole (BHA), Butylated Hydroxytoluene (BHT) may be found in

A

hotdog, potato chips

55
Q

PHYSICAL MUTAGENS

A

UVB radiation (Sun exposure)
Ionizing radiation (x and gamma rays)

56
Q

Only _______ and _______ can penetrate the ozone layer

57
Q

furochomarane that is used for psoriasis and vitiligo treatment and is photosensitizing

58
Q

Non genotoxic carcinogens includes chemicals that functions via:
1. _________ cytotoxicity → _________ DNA Mutations
2. _________-mediated
3. _________ perturbation
4. Induction of _________
5. Modulation/ Alteration of _________ status
6. _________

A
  1. Sustained cytotoxicity → Spontaneous DNA Mutations
  2. Receptor-mediated
  3. Hormonal perturbation
  4. Induction of oxidative stress
  5. Modulation/ Alteration of methylation status
  6. Immunosuppresion
59
Q

example of Sustained cytotoxicity → Spontaneous DNA Mutations

A

Chloroform

60
Q

these are Receptor-mediated chemicals

A

Constitutive Androstane Receptor (CAR)
Peroxisome proliferator–activated receptor alpha (PPARα)
Aryl hydrocarbon receptor (AhR) effects

61
Q

Phenobarbital

A

Constitutive Androstane Receptor (CAR)

62
Q

Fibrates

A

Peroxisome proliferator–activated receptor alpha (PPARα):

63
Q

Polychlorinated
biphenyls

A

Aryl hydrocarbon receptor (AhR) effects

64
Q

Biogenic amines

A

Hormonal perturbation

65
Q

Steroids Hormones: Phytoestrogens (Bisphenol A), Diethylstilbestrol

A

Hormonal perturbation

66
Q

Tamoxifen

A

Hormonal perturbation

67
Q

Peptide hormones: Chemical induce decrease in T3/ T4 levels and/ or increase in
TSH levels

A

Hormonal perturbation

68
Q

Phytoestrogens (Bisphenol A), Diethylstilbestrol

A

Steroid Hormones

69
Q

Chemical induce decrease in T3/ T4 levels and/ or increase in
TSH levels

A

Peptide hormones

70
Q

ROS formers [superoxide anion (O2-), hydroperoxyl radical (HO2), hydrogen peroxide (H2O2 ), and the hydroxyl radical (OH)]: Ethanol, Lindane, Dieldrin, Acrylonitrile

A

Induction of oxidative stress

71
Q

[superoxide anion (O2-), hydroperoxyl radical (HO2), hydrogen peroxide (H2O2 )

A

ROS formers

72
Q

Ethanol, Lindane, Dieldrin, Acrylonitrile

A

hydroxyl radical (OH)]

73
Q

Choline deficiency

A

Modulation/ Alteration of methylation status

74
Q

Phthalates, Atrazine

A

Immunosuppresion

75
Q

Inorganic Carcinogens

A

Metals (As, Be, Cd, Cr, Ni, Pb

76
Q

The carcinogenic manifestations of metals (inorganic carcinogens) vary and include increased risk for _____, _______, ________ tumors

A

skin, lung, liver

77
Q

Other Factors Affecting Carcinogenesis

A

Genes
Viral infection (Oncogenic viruses)
Environmental factors

78
Q

Gene has more than one allele

A

Genetic Polymorphism

79
Q

Gene mutations:

A

Proto-oncogenes
Tumor-suppressor genes

80
Q

Encodes a protein capable of transforming cells in culture or inducing cancer in animals

A

Proto-oncogenes

81
Q

involved in cell signaling cascades

A

Proto-oncogenes

82
Q

Retinoblastoma Gene (Rb1), Breast CA Gene 1 (BRCA1), Wilms Tumor Gene (WT-1), p16, p53

A

Tumor-suppressor genes:

83
Q

Rb1
Disorder: ________
Neoplasm: ________

A

Retinoblastoma; small-cell lung carcinoma

84
Q

p53
Disorder: ________
Neoplasm: ________

A

Li-Fraumeni syndrome
Breast, colon, lung cancers

85
Q

BRCA1
Disorder: ________
Neoplasm: ________

A

Unknown; Breast Carcinoma

86
Q

WT-1
Disorder: ________
Neoplasm: ________

A

Wilms tumor
Lung Cancer

87
Q

p16
Disorder: ________
Neoplasm: ________

A

Unknown; melanoma

88
Q

Retroviruses:_________________→Sarcoma

A

Rous Sarcoma Virus (RSV)

89
Q

7 DNA Tumor Viruses

A

Simian virus 40 (SV40), Polyoma virus, Hepatitis B virus, Human Papilloma viruses (HPV) , adenoviruses, herpes viruses, and Poxviruses

90
Q

Lifestyle, Poor diets or overnutrition

A

Environmental factors

91
Q

Assessing Carcinogenicity of Chemicals: In vitro

A

Ames Test
Mouse Lymphoma Assay
Chinese Hamster Ovary Test
Syrian Hamster Embryo
C3H/10T1⁄2 Cell Line Transformation Assay

92
Q

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

93
Q

In the presence of a mutagenic chemical, the defective histidine gene can be mutated back to a functional state (back mutation), resulting in a restoration of bacterial growth in medium lacking histidine.

94
Q

Used to determine whether a chemical is capable of inducing mutation in eukaryotic cells.

A

Mouse Lymphoma Assay

95
Q

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

96
Q

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

97
Q

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

A

Syrian Hamster Embryo (SHE)

98
Q

Originally derived from fibroblasts taken from the prostate of a C3H mouse embryo

A

C3H/10T1⁄2 Cell Line Transformation Assay

99
Q

Most frequently used endpoint (after exposure to carcinogen): Morphological transformation of mammalian cell fibroblasts in culture

A

C3H/10T1⁄2 Cell Line Transformation Assay

100
Q

Assessing Carcinogenicity of Chemicals: In vivo

A

ransgenic rodent mutation assay systems

101
Q

Take into account whole
animal processes such as ADME of chemicals and their metabolites.

A

Assessing Carcinogenicity of Chemicals: In vivo

102
Q

Based on the genes of the lac operon

A

Transgenic rodent mutation assay systems

103
Q

Transgenic rodent mutation assay systems

A

MutaMouse
Big Blue, and Pig-a Gene Mutation Assay

104
Q

Primarily performed in rats and is based on the X-linked Pig-a gene (phosphatidylinositol N- acetylglucosaminyltransferase, subunit A), which is involved in the production of glycosylphosphatidylinositol (GPI) anchor proteins on the cell surface

A

Pig-a gene mutation assay

105
Q

Currently, the assay is optimized for measuring the Pig-a mutant phenotype in peripheral blood erythrocytes by quantification of** CD59- negative reticulocytes **and red blood cells.

A

Pig-a gene mutation assay

106
Q

PIG-A meaning

A

phosphatidylinositol N- acetylglucosaminyltransferase, subunit A

107
Q

Pig-a gene mutation assay is based on the X-linked Pig-a gene (phosphatidylinositol N- acetylglucosaminyltransferase, subunit A), which is involved in the production of __________________ anchor proteins on the cell surface

A

glycosylphosphatidylinositol (GPI)

108
Q

Pig-a gene mutation assay is optimized for measuring the Pig-a mutant phenotype in _______________ blood erythrocytes by quantification of _________ reticulocytes and red blood cells.

A

peripheral ; CD59- negative

109
Q

Chronic Testing for Carcinogenicity: In vivo

A

Chronic (Two Year) Bioassay Two-year

110
Q

In Chronic Bioassay Two-year, ___________ levels of a test chemical (up to the __________ tolerated dose) and a ___________ are administered to 50 males and 50 females (mice and rats), beginning at ____________ of age, continuing throughout their lifespan

A

2-3 dose; maximum; vehicle control; 8 weeks

111
Q

During the study, food consumption and bodyweight gain 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

Chronic (Two Year) Bioassay Two-year

112
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.

113
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.

Toxicology (9 decks)

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