1
Q
- What distinguishes benign from malignant neoplasms?
A) Benign tumors metastasize; malignant do not
B) Malignant tumors grow expansively; benign infiltrate
C) Benign neoplasms do not invade surrounding tissues
D) Malignant neoplasms are non-autonomous
A
C - Benign tumors grow without invading nearby tissues, unlike malignant tumors that infiltrate and metastasize.
2
Q
- What is the significance of metastases in cancer development?
A) They are the primary growths that remain localized
B) They are benign outgrowths of mesenchymal origin
C) They are clonal expansions from the primary neoplasm
D) They are secondary growths derived from malignant cells
A
D - Metastases are secondary tumors derived from malignant cells of the primary neoplasm.
3
Q
- Which of the following defines a chemical carcinogen?
A) Any compound that interacts with proteins to cause inflammation
B) A substance that increases the incidence of neoplasms compared to control
C) Only substances that cause benign tumors
D) A substance that exclusively causes DNA methylation
A
B - Carcinogens are identified by their ability to increase tumor incidence compared to controls.
4
Q
- Which mode of action defines a genotoxic carcinogen?
A) Promotes increased mitosis without DNA interaction
B) Interacts with membrane receptors to stimulate growth
C) Directly alters DNA structure
D) Indirectly modifies RNA function
A
C - Genotoxic carcinogens cause direct DNA damage, often leading to mutations.
5
Q
- What type of carcinogens increase cell division without directly damaging DNA?
A) Genotoxic
B) Initiators
C) Mutagens
D) Non-genotoxic carcinogens
A
D - Non-genotoxic carcinogens promote cell division without interacting with DNA directly.
6
Q
- What is an example of a complete carcinogen?
A) One that causes inflammation but not mutation
B) One that only induces benign neoplasms
C) One that has both genotoxic and non-genotoxic properties
D) One that requires a promoter for action
A
C - Complete carcinogens both initiate (genotoxic) and promote (non-genotoxic) tumor formation.
7
Q
- Who first linked occupational exposure to cancer and in what context?
A) Bruce Ames with liver cancer in mice
B) Percivall Pott with bladder cancer and dye exposure
C) Percivall Pott with scrotal cancer in chimney sweeps
D) James Miller with asbestos-related lung cancer
A
C - Percivall Pott identified scrotal cancer in chimney sweeps, linking cancer to occupational exposure.
8
Q
- What is the first stage of multistage carcinogenesis?
A) Promotion
B) Initiation
C) Progression
D) Transformation
A
B - Initiation involves irreversible DNA changes that can start tumor development.
9
Q
- What defines a direct-acting initiator in chemical carcinogenesis?
A) Requires metabolic activation
B) Reacts covalently with DNA without activation
C) Interacts with cytoplasmic RNA
D) Is detoxified before cellular entry
A
B - Direct-acting initiators bind DNA without needing metabolic activation.
10
Q
- What is a DNA adduct?
A) A protein that binds DNA during transcription
B) A reversible covalent bond between a carcinogen and DNA
C) A mutated protein formed during mitosis
D) An RNA complex with a transcription factor
A
B - DNA adducts are carcinogen-DNA complexes that may cause mutations if unrepaired.
11
Q
- What is required for tumor promotion to occur?
A) One-time exposure to a mutagen
B) Continuous exposure to tumor-promoting agents
C) A mutation in a tumor suppressor gene
D) A complete carcinogen
A
B - Tumor promotion requires sustained exposure to agents that expand initiated cells.
12
Q
- What is true about tumor promotion in chemical carcinogenesis?
A) It is irreversible
B) It requires only one exposure
C) It is a threshold and dose-dependent process
D) It only occurs in the presence of oxidative stress
A
C - Promotion has a dose threshold and is reversible when the promoting agent is removed.
13
Q
- Which term describes the final stage of chemical carcinogenesis?
A) Promotion
B) Fixation
C) Progression
D) Initiation
A
C - Progression is the final stage with irreversible changes leading to malignancy.
14
Q
- Which stage of carcinogenesis is reversible?
A) Initiation
B) Progression
C) Transformation
D) Promotion
A
D - Promotion can be reversed if the promoting chemical is withdrawn.
15
Q
- What type of carcinogens typically drive the progression stage?
A) Non-genotoxic
B) Hormonal
C) Genotoxic
D) Indirect-acting
A
C - Genotoxic carcinogens cause the additional mutations characteristic of progression.
16
Q
- What defines a direct-acting (activation-independent) carcinogen?
A) Requires microsomal activation
B) Forms DNA adducts via indirect binding
C) Tests positive in Ames test without microsomes
D) Requires Phase II metabolism to activate
A
C - Direct-acting carcinogens are already reactive and test positive in Ames test without requiring metabolic activation (microsomes).
17
Q
- What is a procarcinogen?
A) A compound that is directly mutagenic
B) A genotoxic agent that acts without activation
C) An inactive compound requiring metabolic activation
D) A type of tumor suppressor gene
A
C - Procarcinogens are compounds that require metabolic activation to form a DNA-reactive ultimate carcinogen.
18
Q
- What is a transition mutation?
A) Purine replaced by pyrimidine
B) Pyrimidine replaced by purine
C) Purine replaced by purine or pyrimidine by pyrimidine
D) A shift in reading frame
A
C - A transition mutation is when a purine is swapped with another purine or a pyrimidine with another pyrimidine.
19
Q
- What is the most common biomarker for oxidative DNA damage?
A) 6-methylguanine
B) 8-hydroxyguanine
C) Thymine dimers
D) Uracil-DNA glycosylase
A
B - 8-hydroxyguanine is the most commonly recognized marker of oxidative DNA damage.
20
Q
- What is the role of oncogenes in cancer development?
A) Encode proteins that slow cell division
B) Result from mutations of tumor suppressors
C) Promote cell proliferation after mutation
D) Code for DNA repair enzymes
A
C - Oncogenes are mutated proto-oncogenes that can drive unregulated cell growth and cancer.
21
Q
- What is the function of tumor-suppressor genes?
A) Stimulate apoptosis in all healthy cells
B) Promote mitosis in cancer cells
C) Encode proteins that inhibit cell proliferation
D) React with DNA to form adducts
A
C - Tumor-suppressor genes produce proteins that inhibit excessive cell division, maintaining cell cycle control.
22
Q
- What chemical class includes benzo[a]pyrene?
A) Alkylating agents
B) Aromatic amines
C) Polyaromatic hydrocarbons
D) Vinyl compounds
A
C - Benzo[a]pyrene is a well-known polyaromatic hydrocarbon linked to combustion products and cancer.
23
Q
- Which mode of action is characteristic of non-genotoxic carcinogens?
A) Direct DNA mutation
B) Clonal expansion via cytotoxicity
C) Frameshift mutation
D) DNA cross-linking
A
B - Non-genotoxic carcinogens often promote tumors via cytotoxicity and stimulation of cell division rather than DNA damage.
24
Q
- What receptor is activated by phenobarbital to promote liver tumors in rodents?
A) AhR
B) PPARα
C) CAR (Constitutive Androsterone Receptor)
D) EGFR
A
C - Phenobarbital activates CAR, leading to liver cell proliferation and tumor promotion in rodents.
25
10. What is the key mechanism of PPARα agonists in liver tumor formation?
A) Inhibit DNA repair
B) Increase liver oxidative stress
C) Promote peroxisome proliferation and decrease apoptosis
D) Induce immune suppression
C - PPARα agonists enlarge liver size and tumor risk by increasing peroxisomes, cell proliferation, and reducing apoptosis.
26
11. Which environmental compound is a classic agonist for AhR?
A) Vinyl chloride
B) Dioxin (TCDD)
C) Clofibrate
D) Bisphenol-A
B - Dioxin (TCDD) is a potent AhR agonist and a known rodent tumor promoter.
27
12. What is a known effect of estrogen-mimicking chemicals?
A) DNA alkylation in muscle tissue
B) Tumor formation in estrogen-dependent tissues
C) Induction of apoptosis in neurons
D) DNA repair enhancement
B - Estrogenic chemicals induce tumors in hormone-sensitive tissues such as mammary glands and ovaries.
28
13. What epigenetic modification is associated with decreased transcription?
A) Histone acetylation
B) DNA methylation
C) RNA silencing
D) Phosphorylation
B - DNA methylation on cytosines represses gene transcription and can silence tumor suppressor genes.
29
14. What are microRNAs primarily responsible for?
A) Direct protein synthesis
B) Enhancing DNA replication
C) Gene expression repression and mRNA degradation
D) Histone deacetylation
C - MicroRNAs regulate gene expression post-transcriptionally by degrading mRNA or blocking translation.
30
15. What does 8-OHdG indicate?
A) Apoptosis
B) Protein misfolding
C) Oxidative DNA damage
D) Mitotic slippage
C - 8-OHdG is a biomarker of oxidative damage to DNA, often resulting from reactive oxygen species.
31
1. Which Salmonella strains in the Ames test detect point mutations?
A) TA98, TA1537, TA1538
B) TA100, TA1535
C) TA1537, TA100
D) TA1538, TA1535
B - TA100 and TA1535 strains detect point mutations in the Ames test.
32
2. Which Salmonella strains in the Ames test detect frame shift mutations?
A) TA98, TA1537, TA1538
B) TA100, TA1535
C) TA1535, TA1537
D) TA100, TA98
A - TA98, TA1537, and TA1538 strains detect frame shift mutations.
33
3. What is the purpose of adding S9 mix in the Ames test?
A) Provide cofactors for DNA repair
B) Supply histidine for bacterial growth
C) Mimic mammalian metabolic activation
D) Maintain pH balance in the medium
C - The S9 mix simulates metabolic activation of procarcinogens by adding microsomal enzymes.
34
4. What type of mutation does the Mouse Lymphoma Assay detect?
A) Frame shift mutation
B) Forward mutation at thymidine kinase locus
C) Point mutation at lacZ gene
D) Deletion of HGPRT gene
B - The Mouse Lymphoma Assay detects forward mutations at the thymidine kinase gene locus.
35
5. What cells are used in the Mouse Lymphoma Assay?
A) CHO cells
B) L5178Y cells
C) HepG2 cells
D) MutaMouse fibroblasts
B - L5178Y cells are the mammalian cells used in this assay.
36
6. What is measured in the Mouse Lymphoma Assay to detect mutation?
A) Resistance to trifluorothymidine
B) DNA strand breaks
C) β-galactosidase activity
D) GPI-anchor protein loss
A - Resistance to trifluorothymidine indicates mutation in the thymidine kinase gene.
37
7. What gene is analyzed in the CHO test for mutagenicity?
A) lacZ
B) P53
C) HGPRT
D) G6PD
C - HGPRT gene is the target of mutational analysis in the CHO cell test.
38
8. What does the Pig-a gene assay detect?
A) DNA methylation changes
B) Micronucleus formation
C) Loss of GPI-anchor proteins on red blood cells
D) Apoptosis in hepatocytes
C - Loss of GPI-anchor proteins on RBCs indicates Pig-a gene mutation.
39
9. What is the main advantage of the Pig-a assay?
A) Only used in vitro
B) Detects tumor suppressor mutations
C) Applicable to mice, rats, monkeys, and humans
D) Measures gene expression changes
C - Pig-a assay is versatile and used across multiple species for in vivo gene mutation analysis.
40
10. What does the micronucleus test evaluate?
A) Gene mutations
B) Chromosomal damage
C) DNA methylation
D) Oxidative stress
B - The micronucleus test identifies chromosomal alterations like fragments or missegregated chromosomes.
41
11. What is UDS in mutagenicity testing?
A) Unscheduled DNA synthesis
B) Uniform DNA suppression
C) Ubiquitin degradation score
D) Unregulated DNA signal
A - UDS measures DNA synthesis outside the normal replication cycle, often due to DNA repair.
42
12. What does the Comet assay detect?
A) Cell proliferation
B) DNA strand breaks
C) RNA fragmentation
D) Transcriptional activity
B - The Comet assay evaluates single and double-strand DNA breaks using gel electrophoresis.
43
13. What is the duration of a chronic bioassay for carcinogenicity?
A) 30 days
B) 6 months
C) 1 year
D) 2 years
D - Chronic bioassays are conducted over 2 years to assess long-term carcinogenicity.
44
14. How many male and female rodents are used per dose group in chronic bioassays?
A) 20
B) 30
C) 50
D) 100
C - 50 males and 50 females are included per dose level group for statistical power.
45
15. What is the MTD in chronic testing?
A) Median toxicity dose
B) Maximum tolerable dose with no toxicity in 90-day study
C) Minimal therapeutic dose
D) Mutagenic test dose
B - MTD is the highest dose that causes no toxicity in a 90-day study and helps set safe upper limits.
46
16. What is a commonly used promoter in skin carcinogenicity testing?
A) Cyclophosphamide
B) Croton oil/TPA (12-O-tetradecanoylphorbol-13-acetate)
C) Phenobarbital
D) Clofibrate
B - Croton oil and TPA are standard promoters used in skin cancer promotion models.
47
17. What liver biomarker indicates pre-neoplastic foci?
A) GSH-P (glutathione S-transferase pi)
B) CYP2E1
C) Albumin
D) Histone H3
A - GSH-P is a biomarker enzyme used to stain liver pre-neoplastic lesions.
48
18. Which mouse models are used in genetic carcinogenicity assessment?
A) B6C3F1, F344
B) rasH2, TgAC, P53
C) Big Blue, MutaMouse
D) BALB/c, A/J
B - Transgenic models such as rasH2, TgAC, and P53 knockouts are useful in short-term cancer testing.
49
19. What modern method complements traditional carcinogenicity testing?
A) ELISA kits
B) PCR screening
C) High-throughput in vitro assays and computational models
D) Southern blotting
C - High-throughput and computational assays are newer, efficient methods in carcinogenicity screening.
50
20. What organization classifies carcinogens into groups?
A) NIH
B) FDA
C) IARC (International Agency for Research on Cancer)
D) CDC
C - IARC categorizes carcinogens into groups (1–4) based on their carcinogenic evidence in humans and animals.
51
1. What defines a benign neoplasm?
A) Invasive and metastatic
B) Rapidly growing and mutagenic
C) Expansive growth without invasion
D) Derived from multiple tissues
C - Benign tumors exhibit slow, expansive growth and do not invade surrounding tissues.
52
2. What is the definition of metastases?
A) Benign tumors that grow slowly
B) Secondary growths from the primary malignant neoplasm
C) Non-neoplastic cellular changes
D) Primary tumors that invade skin
B - Metastases are secondary tumors derived from primary malignant neoplasms that spread.
53
3. What type of carcinogen directly interacts with DNA to cause mutations?
A) Non-genotoxic
B) Hormonal
C) Genotoxic
D) Epigenetic
C - Genotoxic carcinogens interact directly with DNA to induce mutations and initiate cancer.
54
4. What is a non-genotoxic carcinogen?
A) Causes direct DNA breaks
B) Promotes tumors via increased cell division
C) Always acts as a mutagen
D) Binds to DNA to form adducts
B - Non-genotoxic carcinogens promote cancer through mechanisms like increased proliferation, not DNA interaction.
55
5. Who first linked occupational exposure to cancer?
A) Ames with nitrosamines
B) Miller with aromatic amines
C) Pott with chimney sweeps and scrotal cancer
D) Watson with asbestos
C - Percivall Pott first linked scrotal cancer to occupational soot exposure in chimney sweeps.
56
6. What is a direct-acting initiator in carcinogenesis?
A) Requires metabolic activation
B) Binds DNA without activation
C) Acts only through cell receptors
D) Causes protein degradation
B - Direct-acting initiators can bind to DNA without requiring metabolic activation.
57
7. What is an indirect-acting initiator?
A) Reacts directly with DNA
B) Requires enzymatic activation to form DNA-binding species
C) Is non-carcinogenic
D) Prevents mutations
B - Indirect-acting initiators must be metabolically activated into reactive DNA-binding compounds.
58
8. What defines tumor promotion?
A) Involves irreversible genetic damage
B) Requires continuous or repeated exposure to promoting agents
C) Is initiated by radiation
D) Acts only on healthy cells
B - Tumor promotion requires prolonged or repeated chemical exposure to expand initiated cells.
59
9. What type of carcinogen typically drives tumor promotion?
A) Genotoxic
B) Non-genotoxic
C) Hormonal
D) Viral
B - Non-genotoxic carcinogens typically drive promotion by increasing mitogenesis and cell turnover.
60
10. What is the final stage of multistage carcinogenesis?
A) Initiation
B) Promotion
C) Reversion
D) Progression
D - Progression is the final stage marked by irreversible genetic changes leading to malignancy.
61
11. What is the nature of progression in carcinogenesis?
A) Reversible cellular damage
B) Involves additional genotoxic events and is irreversible
C) Initiated by inflammation
D) Suppressed by antioxidants
B - Progression involves additional mutations and chromosomal damage, making it an irreversible step.
62
12. What are direct-acting carcinogens also known as?
A) Procarcinogens
B) Receptor ligands
C) Ultimate carcinogens
D) Tumor suppressors
C - These are highly reactive species capable of directly damaging DNA and causing mutations.
63
13. Which test do direct-acting carcinogens typically test positive in?
A) UDS test
B) Ames test without microsomes
C) Comet assay
D) ELISA
B - They test positive in the Ames assay without requiring S9 metabolic activation.
64
14. What is a transition mutation?
A) Purine to pyrimidine switch
B) Purine to purine or pyrimidine to pyrimidine
C) Duplication of a codon
D) Insertion of a base
B - A transition is the replacement of a purine with another purine or a pyrimidine with another pyrimidine.
65
15. What is the most common biomarker of oxidative DNA damage?
A) 8-hydroxyguanine
B) Thymine dimer
C) Uracil mismatch
D) DNA crosslink
A - 8-hydroxyguanine is a key biomarker for oxidative stress-related DNA damage.
66
16. What gene type, when mutated, promotes cancer by increasing cell division?
A) Tumor suppressor
B) DNA repair
C) Oncogene
D) Ribosomal
C - Oncogenes are mutated proto-oncogenes that promote uncontrolled cell proliferation.
67
17. What is the function of tumor suppressor genes?
A) Enhance mitosis
B) Promote DNA damage
C) Inhibit cell proliferation
D) Block protein synthesis
C - Tumor suppressor genes produce proteins that slow cell cycle progression or promote apoptosis.
68
18. What class of carcinogens includes benzo[a]pyrene?
A) Alkylating agents
B) Aromatic amines
C) Polyaromatic hydrocarbons
D) Phenols
C - Benzo[a]pyrene is a polycyclic aromatic hydrocarbon (PAH) found in combustion products.
69
19. What is the mechanism of receptor-mediated non-genotoxic carcinogens?
A) Interact with transcription factors
B) Activate nuclear receptors like CAR and PPARα
C) Cause DNA strand breaks
D) Enhance methylation of all genes
B - These chemicals activate nuclear receptors like CAR and PPARα to promote tumorigenesis without DNA mutation.
70
20. Which receptor does phenobarbital activate to induce liver tumors in rodents?
A) AhR
B) EGFR
C) CAR (Constitutive Androsterone Receptor)
D) PXR
C - CAR is activated by phenobarbital, which increases liver size, proliferation, and tumor formation in rodents.
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