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Q2. All of the following are true regarding rate of growth of a neoplasm except?
Q3. Which of the following is the appropriate term for a rest of normal tissue in an
abnormal location?
A. Teratoma
B. Adenoma
C. Normoma
D. Choristoma
E. Hamartoma
Q4. Marked dysplastic changes involving the entire thickness of the epidermis but
confined to the normal tissue boundaries is termed:
A. Carcinoma
B. Carcinsarcoma
C. Carcinoma in situ
D. Carcinoma in vivo
E. Squamous cell carcinoma
A. Leiomyoma
B. Rhabdomyoma
C. Musculosarcoma
D. Leiomyosarcoma
E. Rhabdomyosarcoma
A. Increased mitosis
General pathology 2008-2009
Compiled by Bhupinder Bawa
B. Hyperchromatic nuclei
C. Loss of normal polarity
D. Cellular and nuclear pleomorphism
E. Increased production of normal secretory product
Q7. Which feature can typically be used to distinguish neoplastic from dysplastic
cells?
A. Disorderly architecture
B. Hyperchromatic nuclei
C. Cellular pleomorphism
D. Abnormal mitotic figures
E. Nuclear:cytoplasmic ratios
A. Mitoses
B. Loss of polarity
C. Pleomorphism
D. Tumor giant cells
E. Abnormal nuclear morphology
Q9. By the time a tumor is clinically detectable, most cells are in which stage of the
cell cycle?
A. S
B. M
C. G0
D. G1
E. G2
Q10. Next to the development of distant metastasis, what is the most reliable feature
that differentiates a malignant from a benign neoplasm?
A. Mitotic rate
B. Rate of growth
C. Tissue invasiveness
D. Size of primary tumor
E. Cellular differentiation
Q11. Which of the following cellular or tissue changes would least likely lead to
malignant transformation?
A. Atrophy
B. Dysplasia
C. Metaplasia
D. Hyperplasia
General pathology 2008-2009
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E. Regeneration
Q12. Which of the following regulatory genes can be involved with malignant
cellular transformation when mutated?
A. Protooncogenes
B. DNA repair genes
C. Tumor suppressor genes
D. Genes regulating apoptosis
E. All of the above
Q13. Mutations in all of the following genes can lead to inherited cancer syndromes
EXCEPT?
A. p53
B. APC
C. BRCA1
D. p14ARF
E. p161NK4A
Q14. The most important factors that determine the rate of tumor growth are:
A. 1, 2
B. 1, 3, 4
C. 1, 4, 5
D. 3, 4, 5
E. 4, 5
A. Lymphatic spread
B. Seeding into a body cavity
C. Hematogenous dissemination
D. Implantation into surrounding tissues following biopsy
E. All of the above are equally likely
A. Local expansion
B. Lymphatic spread
General pathology 2008-2009
Compiled by Bhupinder Bawa
C. Hematogenous spread
D. Seeding of body cavities
E. None of the above
A. Evasion of apoptosis
B. Defects in DNA repair
C. Sustained angiogenesis
D. Limitless replicative potential
E. Insufficency in self-growth signals
Q18. Which of the following is not a target of genetic damage in tumor formation
Q19. Which of the following serves as a marker for clonality in B-cell lymphoma?
A. RB
B. p53
C. p16INK4A
D. a and b
E. a, b and c
A. Cyclin D/cdk4
B. Cyclin D/cdk6
C. Cyclin E/cdk2
D. A only
E. All of the above
General pathology 2008-2009
Compiled by Bhupinder Bawa
Q22. p16INK4a can cause cell cycle arrest by one of following ways?
A. p53 activation
B. p53 degradation
C. inhibiting cyclin D/cdk4 complex
D. inhibiting cyclin E/cdk 2 complex
E. all of the above
Q23. A defect in DNA before replication is detected and repaired at which of the
following checkpoints?
A. S phase
B. M phase
C. G1/S transition
D. G2/M transition
E. All of the above phases
Q24. Which of the following is needed to progress through both the G1/S and G2/M
checkpoints?
A. CDK 2
B. CDK 1
C. Cyclin D
D. Cyclin E
E. Cyclin A
A. E2F/DP1/Histone deacetylase
B. Histone deacetylase/E2F
C. DP1/ Histone deacetylase
D. E2F/DP1
E. E2F
Q26. Cell cycle inhibitor p161NK4 functions by which of the following mechanisms?
A. Binds to RB
B. inhibits MDM2
C. Inhibits Cyclin E/CDK2
D. Binds to Cyclin D/ CDK4
E. inactivates Cyclin B/ CDK 1
1. CDK2
2. CDK4
General pathology 2008-2009
Compiled by Bhupinder Bawa
3. Cyclin A
4. Cyclin D
5. Cyclin E
A. 1, 2
B. 1, 2, 3
C. 2, 4
D. 3, 4, 5
E. 4, 5
Q28. The cyclin-CDK complex required to drive the cell through the G1/S restriction
point is:
A. Cyclin A-CDK2
B. Cyclin B-CDK1
C. Cyclin D-CDK4
D. Cyclin E-CDK2
E. Cyclin F-CDK3
Q29. Place in order the sequence of events that leads to activation of the cell cycle:
1. Transcription of cyclin D
2. Activation of transcription factor E2F
3. Stimulation of the cell by growth factors
4. Cyclin D binds CDK4 and phosphorylates RB
5. Removal of histone deacetylase from chromatin
A. 1, 3, 2, 4, 5
B. 3, 1, 4, 5, 2
C. 3, 2, 1, 5, 4
D. 3, 2, 1, 4, 5
E. 3, 5, 4, 1, 2
Q31. Which of the following cyclins is first detectable in G1 of the cell cycle?
A. Cyclin A
B. Cyclin B
C. Cyclin C
D. Cyclin D
E. Cyclin E
General pathology 2008-2009
Compiled by Bhupinder Bawa
Q32. Which of the following is the transcription factor activated by phosphorylation
of retinoblastoma susceptibility protein (RB)?
A. DP1
B. EF2
C. CDK-4
D. CDK-2
E. p16INK4
Q33. Which of the following would not likely result from a mutation leading to a
decreased production of p14ARF?
A. Decreased levels of p21
B. Decreased levels of p53
C. Increased levels of MDM2
D. Increased activation of EF2
E. All of the above would likely result
Q34. Which of the following is the correct progression of the cell cycle
1. Formation of Cyclin D/cdk4
2. Formation of Cyclin E/cdk2
3. Formation of Cyclin A/cdk2
4. Formation of Cyclin B/cdk1
5. Phosphorylation of RB
A. 1,2,3,4,5
B. 1,5,2,3,4
C. 1,2,5,3,4
D. 1,2,3,5,4
E. 5,4,3,2,1
A. Phosphorylation of RB
B. The G1/S phase transition
C. Formation of Cyclin D/cdk 4
D. Inactivation of Cip/Kip family
E. Inhibition of INK4/ARF family
A. GAP
B. GTP
C. RAF-1
D. MAP kinases
E. Farnesyl transferase
General pathology 2008-2009
Compiled by Bhupinder Bawa
Q37. Dysregulation of which of the following transcription factor is seen in Burkitt
lymphoma?
A. MYC
B. MYB
C. FOS
D. JUN
E. Cyclin D
A. p21
B. BAX
C. BCL-2
D. MDM2
E. GAAD45
A. p53
B. p21
C. p27
D. cip/kip
E. P16INK4a
Q41. If DNA damage is repaired successfully cell cycle progression continues by?
Q44. Which of the following mutations would most likely lead to uncontrolled RAS
activity?
A. ATPase
B. GTPase
C. ADP kinase
D. GTP kinase
E. all of the above
A. SIS
B. RAS
C. MYC
D. ECFR
E. BCL-2
A. RB
B. p53
C. RAS
D. INK4a
E. APC/β-catenin
A. “two-hit” hypothesis
General pathology 2008-2009
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B. Loss of heterozygosity
C. Loss of a single normal allele
D. A&B
E. B&C
A. 1,2,3,4,5
B. 2,3,5,1,4
C. 2,5,1,3,4
D. 2,5,1,4,3
E. 5,4,3,2,1
Q50. Which of the following is false regarding the p53 gene and its protein?
1. Increased WNT
2. Decreased WNT
3. Increased APC
4. Decreased APC
5. Increased E-cadherin
A. 1,3
B. 1,4
C. 2,3
D. 2,4
E. 2,4,5
A. Endostatin
B. Tumstatin
C. Vasostatin
D. Angiostatin
E. Thromobospondin-1
General pathology 2008-2009
Compiled by Bhupinder Bawa
Q53. p53 can inhibit angiogenesis by all of the following methods except?
A. Increased synthesis of thrombospondin-1
B. Decreased synthesis of VEGF
C. Decreased synthesis of HIF-1
D. Decreased synthesis of bFGF
E. None of the above.
A. ATM
B. RAD15
C. BRCA-1
D. BRCA-2
E. CHEK-2
A. VEGF
B. bFGF (basic fibroblast growth factor)
C. PDGF
D. a and b
E. All of the above
Q58. Which of the following does NOT play a role in metastasis of an epithelial
tumor?
A. Secretion of proteases
B. Mobilization of VEGF
C. Downregulation of integrins
D. Down-regulation of E-cadherin expression
E. Upregulation of laminin and fibronectin receptors
General pathology 2008-2009
Compiled by Bhupinder Bawa
Q59. Gene translocations can activate protooncogenes in which of the following
ways?
A. Inactivation of p53
B. Overexpression of protooncogenes by removal from their regulatory elements
C. Recombination and formation of hybrid genes that encode growth-promoting proteins
D. B and C
E. All of the above
Q66. Which of the following would not promote vascular invasion and metastasis?
A. Over-expression of CD44
B. Down-regulation of E-cadherin
C. Inhibition of type IV collagenase secretion
D. Up-regulation of laminin-binding receptors
E. Increased expression of chemokine receptors
A. 1,2
B. 1,3
C. 1,4
D. 1,5
E. 2,3
Q79. Which of the following tumor antigens are not used for host immune response
A. Antigens produced by oncogenic viruses
B. Aberrantly expressed cellular proteins
C. Cell-specific differentiation antigens
D. Altered cell surface glycoproteins
E. Products of mutated genes
Q82. Which of the following would NOT stimulate a CD8+ T-cell immune response?
A. Presentation of an overexpressed self-protein
B. Presentation of a radiation-induced mutated self-protein
C. Presentation of a protein encoded by a mutated oncogene
D. Presentation of oncogenic virus-particles by an infected cell
E. Presentation of antigens from a phagocytosed tumor cell by an antigen-presenting cell
Q86. Which of the following is not a criterion used for staging tumors?
A. Number of mitoses
B. Size of primary lesion
C. Presence of metastisis
D. Extent of spread to lymph nodes
E. All are criteria
Q87. The principal mechanism of tumor immunity is killing of tumor cell by?
A. Antibodies
B. CD8+ CTLs
C. Macrophages
D. B-lymphocytes
E. Natural killer cell
Q88. Tumor cells can escape immune system by all of the following mechanisms
except?
Q89. Which of the following is the most important molecule implicated in causing
hypercalcemia of malignancy?
A. IL-1
General pathology 2008-2009
Compiled by Bhupinder Bawa
B. TNF-α
C. TGF- α
D. PTHRP
E. Dihydroxyvitamin D
Q91. In the absence of ozone shield, which UV wavelength can lead to increased
incidence of cutaneous cancers?
A. UVA
B. UVB
C. UVC
D. Both UVA and UVB
E. Both UVB and UVC
Answers:
1) B (Robbins pp 273-274)
2) D (Robbins pp 276) as tumor grows more cells leave proliferative pool due to lack of
nutrients, by differentiating or by reversion to G0 phase
3) D (Robbins pp 272)
4) E (Robbins pp 275)
5) E (Robbins pp 273)
6) E (Robbins pp 274) Generally, the better the differentiation of the transformed cell,
the more completely it retains functional capabilities and morphology
7) D (Robbins pp 275) Mitotic figures are more abundant than usual with cellular
dysplasia, but they almost invariably conform to normal patterns. Abnormal mitotic
figures are an important feature of malignancy.
8) A (Robbins 273/274)
9) C (Robbins p. 276)
10) C (Robbins p. 278)
11) A (Robbins p. 286)
12) E (Robbins p. 288)
13) D p287 Table 7-6 Robbins. (a) associated with various tumors, (b) Adenomatous
polyposis, (c) Breast cancer and ovarian tumors, (e) Melanoma.
14) C (Robbins p. 276)– total cell-cycle time for many tumors is equal to or longer than
their non-neoplastic counterparts.
15) A (Robbins p. 279, 280)
16) A (Robbins 279)
17) E (Robbins 289)
18) D (Robbins 288)
19) D (Robbins 288)
20) E (Robbins 288) Recessive oncogene = both normal alleles must be damaged for
transformation to occur (refers to tumor suppressor genes).
21) E (Robbins pp 288-291)
22) A (Robbins pp 288)
23) C (Robbins pp 292)
24) A (p 291 fig 7-29 Robbins) CDK 2 is bound to Cyclin E at the G1/S checkpoint and
bound to Cyclin A at the G2/M checkpoint.
25) A (p291 Fig 7-30 Robbins)
26) D ( p291-292 Robbins)
27) A – (Robbins pp 289) The cyclins are induced in a cell following signaling by growth
factors and by induction of transcription by transcription factor E2F. CDKs are
constitutively expressed.
General pathology 2008-2009
Compiled by Bhupinder Bawa
28) D (Robbins pp 290)
29) B (Robbins pp 290-291)
30) E (Robbins pp 292)
31) D (Robbins pp 289)
32) B (Robbins pp 289)
33) E (Robbins pp 291)p14ARF is a cell cycle inhibitor. It normally inhibits MDM2,
which is an inhibitor of p53. So normally, by blocking the inhibitor, you get
increased p53 which increases p21, which is an inhibitor of the cyclin D/CDK4
complex, thus inhibiting the cell cycle. Clear so far? So, if you decrease p14ARF,
you lose inhibition of MDM2. If MDM2 increases, this will inhibit p53. So
decreased p53 will decrease p21 which will release the inhibition of cyclin D/CDK4
complex which will activate EF2 and allow progression into the cell cycle.
34) B (Robbins pp 289)
35) A (Robbins pp 289) (G1/S transition is the point of no return)
36) A (Robbins pp 296)
37) A (Robbins pp 298)
38) E (Robbins pp 302)
39) D (Robbins pp 304) Increased expression of β-catenin can have increased
transcription of cyclin D, c-MYC increased cell proliferation, however there will
not be increased free APC as whatever APC is there will try to bind to β-catenin
40) C (Robbins pp 300)
41) D (Robbins pp 302)
42) E – both alleles need to be lost/mutated before malignant transformation occurs
(p. 302)
43) E (Robbins p. 297) RAS is a signal-transducing oncogene
44) B (Robbins p. 297) GTP hydrolysis converts GTP-bound active RAS to the GDP-
bound inactive form
45) E (Robbins 294) (BCL-2 is an apoptotic gene)
46) A (p53 is a tumor suppressor gene)
47) C (Robbins 300)
48) D (Robbins 299)
49) C (Robbins 304)
50) C (Robbins p. 302)
51) B (Robbins p. 304)
52) C (Robbins pp 309)
53) D (Robbins pp 309)
54) A (Robbins pp 307) ATM protein senses double-strand breaks a type of damage
caused by ionizing radiation and free radicals. BRCA-1, BRCA-2 are involved in
DNA repair by homologous recombination. CHEK-2 is a protein kinase activated by
DNA damage and phosphorylates BRCA-1 and RAD15. RAD15 is an enzyme
involved in DNA recombination repair (Fig 7-39)
55) E (Robbins pp 318)
56) C (Robbins pp 317)
57) D (p. 309)
58) C (p. 311-312) Upregulation of integrins usually occurs to allow cells to adhere to
endothelium at distant sites
General pathology 2008-2009
Compiled by Bhupinder Bawa
59) D (Robbins p. 317)
60) E (p. 318)
61) E (p. 320)
62) E (p. 320-321). Carcinogen-induced damage usually does not result in initiation as
DNA repair genes can repair the damage prior to it becoming fixed/permanent.
63) E (Robbins p. 306) BRCA-1 and BRCA-2 participate in DNA repair
64) A (Robbins p. 308)
65) E (Robbins p. 309) Angiogenic switch is when some tumor cells change to an
angiogenic phenotype
66) C (Robbins p. 312)Degradation of basement membrane by type IV collagenases is
important for tumor migration
67) D (Robbins pp 314)
68) D (Robbins pp 318) - BRCA-1 is a caretaker gene (affect genomic stability)
69) D (Robbins pp 323)
70) B (Robbins pp 3093) (potential)
71) A (Robbins pp 309)
72) E (Robbins pp 311)
73) D (Robbins pp 313) (organ tropism is independent of blood drainage)
74) D (Robbins 315)
75) E (Robbins 317)
76) C (Robbins 321)
77) C (Robbins 322)
78) D (Robbins 323)
79) C (Robbins 329, 330 – Cell specific differentiation antigens are normal self-antigens,
therefore, no immune response is expected)
80) D (Robbins 331 – Loss of MHC molecules is a tumor evasion mechanism)
81) A (Robbins 333)
82) E (p.329-330). This would be presented by MHCII and therefore illicit a CD4+
response.
83) D
84) C (Robbins p. 330)
85) D (Robbins p. 333)
86) A (Robbins p. 335) - Number of mitoses is involved in grading a tumor
87) B (Robbins pp 330)
88) C (Robbins pp 331) There is lack of costimulation; another mechanism is antigen
masking.
89) D ( Robbins pp 334) the others are also implicate but the most important is PTHrp
90) C (Robbins pp 320) Promoters does not directly affect the DNA
91) E ( Robbins pp 323) UVB is usually carcinogenic, as UVC is shielded by ozone
92) E (Robbins pp 318)
93) C (Robbins pp 317)
94)
A) Pleomorphism
B) Loss of polarity
C) Tumor giant cells
D) Normal differentiation
E) Abnormal nuclear morphology
Which of the followings are main factors determined rate of tumor growth?
a. 1,2,3
b. 1,3,4
c. 1,3,5
d. 1,4,5
e. 3,4,5
A) 1, 2
B) 1, 3
C) 2, 3
D) 2, 4
E) 3, 5
The following are true regarding the normal cell cycle except:
A) Cyclin D/CDK4 complex phosphorylates RB
B) Exit from mitosis requires inactivation of cyclin B-CDK1
C) Phosphorylation of RB activates the transcriptional activity of E2F
D) Cyclin B-CDK1 is the main mediator that propels cell beyond prophase
E) The G2/M transition is intiated by E2F-mediated transcription of Cyclin D
a. p14ARF
b. p16INK4
c. p21
d. p27
e. p57
The following product of oncogenes causes over expression of growth factor genes
due to role as signal transducer:
A) RB
B) RAS
C) SIS
D) NF-1
E) APC
The following product of oncogenes works with another protein (MAX) as a potent
transcriptional activator of target genes associated with cell proliferation:
A) SIS
B) RAS
C) MYC
D) BRCA-1
E) Cyclin-D
The following tumor suppressor genes and gene products are key regulators of the
cell cycle except:
A) Cyclin D
B) P16INK4a
C) APC/β-catenin
D) CDK4
E) RB
The following are true regarding the components of chemical carcinogenesis except:
A) Promoters induce tumors in initiated cells
B) Initiators alone can’t cause tumor formation
C) Promoters can be tumorigenic by themselves
D) Direct-acting intitators are highly reactive electrophiles
E) Initiators cause permanent DNA damage that is irreversible and has memory
Matching
1. scirrhous
2. dysplasia
3. epithelial
4. choristoma
5. hamartoma
The size of a cell population can be increased by which of the following mechanisms?
A. 1,2,3
B. 1,2,4
C. 1,2,3,4
D. 1,2,3,5
E. 1,2,3,4,5
Matching
1. p21
2. CDK4
3. p14ARF
4. cyclin B-CDK1
General pathology 2008-2009
Compiled by Bhupinder Bawa
5. histone dacetylase
1. degradation of β-catenin
2. decreased cell cycle activity
3. increased transcription of c-MYC
4. increased transcription of CYCLIN D1
5. complex formation between β-catenin and TCF
A. 1,2,3
B. 1,3,5
C. 1,4,5
D. 2,3,5
E. 3,4,5
1. increase in INK4a
2. decrease in MDM2
3. increased transcription of BID
4. increased transcription of BAX
5. increased transcription of BCL-2
A. 1
B. 1,2
C. 1,2,3
D. 1,2,3,4
E. 1,2,3,4,5
1. SV40
2. Polyoma virus
3. Maedi-Visna virus
4. feline leukemia virus
5. feline immunodeficiency virus
A. 1,2,3
B. 1,4,5
C. 2,3,4
D. 2,3,5
E. 3,4,5
A. 1,2,3
B. 1,2,3,4
C. 1,2,3,5
D. 2,3,4,5
E. 1,2,3,4,5