General pathology 2008-2009 Compiled by Bhupinder Bawa Q1.

All of the following are the markers of anaplasia except? A. B. C. D. E. Cellular and nuclear pleomorphism Nucleus to cytoplasm ratio of 1:4 Presence of tumor giant cells Bizarre mitotic figures Loss of polarity

Q2. All of the following are true regarding rate of growth of a neoplasm except? A. Fast growing tumors have high cell turnover B. Most cells in cancers remain in G0 or G1 phase C. Growth rate is inversely correlated to differentiation D. With tumor growth more cells enter proliferative pool E. Latent period before a tumor is clinical detectable is more than 90 days 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. B. C. D. E. Carcinoma Carcinsarcoma Carcinoma in situ Carcinoma in vivo Squamous cell carcinoma

Q5. What is malignant neoplasia of skeletal muscle called? A. B. C. D. E. Leiomyoma Rhabdomyoma Musculosarcoma Leiomyosarcoma Rhabdomyosarcoma

Q6. Which is not a typical characteristic of poorly differentiated neoplastic cells? A. Increased mitosis

General pathology 2008-2009 Compiled by Bhupinder Bawa B. C. D. E. Hyperchromatic nuclei Loss of normal polarity Cellular and nuclear pleomorphism Increased production of normal secretory product

Q7. Which feature can typically be used to distinguish neoplastic from dysplastic cells? A. B. C. D. E. Disorderly architecture Hyperchromatic nuclei Cellular pleomorphism Abnormal mitotic figures Nuclear:cytoplasmic ratios

Q8. Which of the following is not a characteristic of anaplasia A. B. C. D. E. Mitoses Loss of polarity Pleomorphism Tumor giant cells Abnormal nuclear morphology

Q9. By the time a tumor is clinically detectable, most cells are in which stage of the cell cycle? A. B. C. D. E. S M G0 G1 G2

Q10. Next to the development of distant metastasis, what is the most reliable feature that differentiates a malignant from a benign neoplasm? A. B. C. D. E. Mitotic rate Rate of growth Tissue invasiveness Size of primary tumor Cellular differentiation

A. B. C. D.

Q11. Which of the following cellular or tissue changes would least likely lead to malignant transformation? Atrophy Dysplasia Metaplasia Hyperplasia

General pathology 2008-2009 Compiled by Bhupinder Bawa E. Regeneration Q12. Which of the following regulatory genes can be involved with malignant cellular transformation when mutated? Protooncogenes DNA repair genes Tumor suppressor genes Genes regulating apoptosis All of the above Q13. Mutations in all of the following genes can lead to inherited cancer syndromes EXCEPT? A. B. C. D. E. p53 APC BRCA1 p14ARF p161NK4A Q14. The most important factors that determine the rate of tumor growth are: 1. Rate of cell loss 2. The cell of origin 3. Increased cell cycle time 4. Doubling time of tumor cells 5. Fraction of tumor cells in the replicative pool A. B. C. D. E. 1, 2 1, 3, 4 1, 4, 5 3, 4, 5 4, 5 Q15. A mammary carcinoma is most likely to metastasize via: A. B. C. D. E. Lymphatic spread Seeding into a body cavity Hematogenous dissemination Implantation into surrounding tissues following biopsy All of the above are equally likely Q16. Which of the following is not a pathway of metastasis A. Local expansion B. Lymphatic spread

A. B. C. D. E.

General pathology 2008-2009 Compiled by Bhupinder Bawa C. Hematogenous spread D. Seeding of body cavities E. None of the above Q17. Which of the following is not a change in cell physiology to determine malignant phenotype A. B. C. D. E. Evasion of apoptosis Defects in DNA repair Sustained angiogenesis Limitless replicative potential Insufficency in self-growth signals

Q18. Which of the following is not a target of genetic damage in tumor formation A. B. C. D. E. Genes that regulate apoptosis Genes involved with DNA repair Growth-promoting protooncogenes Genes involved with cytoskeletal formation Growth-inhibiting tumor suppression genes

Q19. Which of the following serves as a marker for clonality in B-cell lymphoma? A. B. C. D. E. Uniform cytoplasmic staining for CD21 Uniform cytoplasmic staining for CD79a A high mitotic rate in a uniform population of lymphocytes Demonstration of immunoglobulin receptor gene rearrangement Demonstration of a monomorphic population of medium lymphocytes Q20. Which of the following is/are considered to be recessive oncogenes? A. B. C. D. E. RB p53 p16INK4A a and b a, b and c Q21. Which of the following can phosphorylate RB? A. B. C. D. E. Cyclin D/cdk4 Cyclin D/cdk6 Cyclin E/cdk2 A only 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. B. C. D. E. p53 activation p53 degradation inhibiting cyclin D/cdk4 complex inhibiting cyclin E/cdk 2 complex all of the above

Q23. A defect in DNA before replication is detected and repaired at which of the following checkpoints? A. B. C. D. E. S phase M phase G1/S transition G2/M transition All of the above phases

Q24. Which of the following is needed to progress through both the G1/S and G2/M checkpoints? A. B. C. D. E. CDK 2 CDK 1 Cyclin D Cyclin E Cyclin A Q25. Hypophosphorylated RB is complexed to which of the following? A. B. C. D. E. E2F/DP1/Histone deacetylase Histone deacetylase/E2F DP1/ Histone deacetylase E2F/DP1 E2F Q26. Cell cycle inhibitor p161NK4 functions by which of the following mechanisms? A. B. C. D. E. Binds to RB inhibits MDM2 Inhibits Cyclin E/CDK2 Binds to Cyclin D/ CDK4 inactivates Cyclin B/ CDK 1 Q27. Which of the following are constitutively expressed in a cell? 1. CDK2 2. CDK4

General pathology 2008-2009 Compiled by Bhupinder Bawa 3. Cyclin A 4. Cyclin D 5. Cyclin E A. B. C. D. E. 1, 2 1, 2, 3 2, 4 3, 4, 5 4, 5 Q28. The cyclin-CDK complex required to drive the cell through the G1/S restriction point is: Cyclin A-CDK2 Cyclin B-CDK1 Cyclin D-CDK4 Cyclin E-CDK2 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. B. C. D. E. 1, 3, 2, 4, 5 3, 1, 4, 5, 2 3, 2, 1, 5, 4 3, 2, 1, 4, 5 3, 5, 4, 1, 2 Q30. Following DNA damage, the role of p53 is to: A. B. C. D. E. A. B. C. D. E. Activate histone deacetylase Block cyclin-CDK complexes via activation of p21 Trigger apoptosis by activation of pro-apoptotic genes a and b b and c Q31. Which of the following cyclins is first detectable in G1 of the cell cycle? Cyclin A Cyclin B Cyclin C Cyclin D Cyclin E

A. B. C. D. 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)? DP1 EF2 CDK-4 CDK-2 p16INK4 Q33. Which of the following would not likely result from a mutation leading to a decreased production of p14ARF? Decreased levels of p21 Decreased levels of p53 Increased levels of MDM2 Increased activation of EF2 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. B. C. D. E. 1,2,3,4,5 1,5,2,3,4 1,2,5,3,4 1,2,3,5,4 5,4,3,2,1

A. B. C. D. E.

A. B. C. D. E.

Q35. The main barrier to cell-cycle progression is A. B. C. D. E. Phosphorylation of RB The G1/S phase transition Formation of Cyclin D/cdk 4 Inactivation of Cip/Kip family Inhibition of INK4/ARF family

Q36. Uncontrolled RAS activity is prevented by? A. B. C. D. E. GAP GTP RAF-1 MAP kinases 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. B. C. D. E. MYC MYB FOS JUN Cyclin D Q38. p53 helps in DNA repair by transcription of ? A. B. C. D. E. p21 BAX BCL-2 MDM2 GAAD45

Q39. A genetic defect leading to overexpression of β-catenin and considering no WNT signaling can have all of the following except? A. B. C. D. E. Increased expression of c-MYC and cyclin D Increased adhesiveness of mutant cells Increased degradation of β-catenin Increased intracellular free APC Increased proliferation of cells.

Q40. Inhibition of cellular proliferation by TGF- is mediated by upregulation of which CDK inhibitor? A. B. C. D. E. p53 p21 p27 cip/kip P16INK4a

Q41. If DNA damage is repaired successfully cell cycle progression continues by? A. B. C. D. E. Activation of CDK inhibitor protein p21 Proteolysis of p53 by ubiquitin proteosome pathway Activation of MDM2 by p53 which degrade p21 Self degradation of p53 by activation of MDM2 All of the following

Q42. Which of the following statements about p53 protein is FALSE? A. It is a DNA-binding protein confined to the nucleus

General pathology 2008-2009 Compiled by Bhupinder Bawa B. C. D. E. MDM2 normally inhibits its activity by causing increased p53 degradation Increased p53 leads to cell-cycle arrest Increased p53 can induce BAX, leading to apoptosis Mutation of one p53 allele causes a 100% increase in risk for malignant cell transformation Q43. Which of the following is not a transcription factor oncogene? FOS JUN MYB MYC RAS Q44. Which of the following mutations would most likely lead to uncontrolled RAS activity? A. B. C. D. E. ATPase GTPase ADP kinase GTP kinase all of the above
Q45. Which of the following is not a recognized protooncogene A. B. C. D. E. SIS RAS MYC ECFR BCL-2

A. B. C. D. E.

Q46. Which of the following is not a characteristic of oncogene mutations A. B. C. D. E. Homozygous loss of p53 Abnormal expression of cyclins Self-production of growth factors Constitutive dimerization of growth factor receptors Mutant proteins binding to GTP-ase activating proteins

Q47. Which of the following is not a tumor suppressor gene
A. B. C. D. E. RB p53 RAS INK4a APC/β-catenin

Q48. Which of the following describes oncogenesis via the RB gene A. “two-hit” hypothesis

General pathology 2008-2009 Compiled by Bhupinder Bawa
B. C. D. E. Loss of heterozygosity Loss of a single normal allele A&B B&C

Q49. What is the order of oncogenesis in the APC/ β-catenin pathway 1. 2. 3. 4. 5. A. B. C. D. E. β-catenin binds with TCF Germ line mutation of APC gene Increased transcription of Cyclin D Uncontrolled proliferation of cell line Increase in cellular levels of β-catenin 1,2,3,4,5 2,3,5,1,4 2,5,1,3,4 2,5,1,4,3 5,4,3,2,1

Q50. Which of the following is false regarding the p53 gene and its protein? A. B. C. D. E. The p53 protein is localized in the cell nucleus The p53 induced cell-cycle arrest occurs in late G1 phase p53 induces activation of BAX after successful repair of DNA Most mutations are acquired in somatic cells, not in the germ line Li-Fraumeni syndrome results from inheriting one mutant p53 allele Q51. Which of the following changes result in increased cellular β-catenin? 1. Increased WNT 2. Decreased WNT 3. Increased APC 4. Decreased APC 5. Increased E-cadherin A. B. C. D. E. 1,3 1,4 2,3 2,4 2,4,5 Q52. All of the following can act as anti-angiogenesis factor except? A. B. C. D. E. Endostatin Tumstatin Vasostatin Angiostatin 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. Q54. A double strand break in DNA is sensed by? A. B. C. D. E. ATM RAD15 BRCA-1 BRCA-2 CHEK-2

Q55. Which of the following are caretaker genes? A. B. C. D. E. Genes involving RB pathway Genes involving p532 Mismatch repair genes DNA repair genes C and D both

Q56. Which of the following is an early event in development of colorectal cancers? A. B. C. D. E. Loss of p53 gene Mutation of RAS gene Loss or mutation of APC Loss of TGF- receptor I gene Loss of tumor suppressor gene

Q57. The most important angiogenic factor/s in tumors is/are? A. B. C. D. E. VEGF bFGF (basic fibroblast growth factor) PDGF a and b All of the above Q58. Which of the following does NOT play a role in metastasis of an epithelial tumor? Secretion of proteases Mobilization of VEGF Downregulation of integrins Down-regulation of E-cadherin expression Upregulation of laminin and fibronectin receptors

A. B. C. D. E.

General pathology 2008-2009 Compiled by Bhupinder Bawa Q59. Gene translocations can activate protooncogenes in which of the following ways? A. B. C. D. E. A. B. C. D. E. A. B. C. D. Inactivation of p53 Overexpression of protooncogenes by removal from their regulatory elements Recombination and formation of hybrid genes that encode growth-promoting proteins B and C All of the above Q60. Caretaker genes are genes that: Directly control tumor growth Prevent tumor formation when both alleles are normal Promote tumor growth by causing genetic translocations Require only mutation of one allele to cause tumor growth Affect genomic stability but do not directly control tumor growth Q61. Which of the following sequences will result in tumor formation? Application of an initiator only Repeated application of a promoter at weekly intervals Application of promoter followed by application of an initiator Application of initiator followed by monthly applications of a promoter E. Application of an initiator followed by repeated application of a promoter at twice-weekly intervals Q62. Which of the following statements about initiation of chemical carcinogenesis is incorrect? Most carcinogens are electrophiles Most carcinogens require metabolic activation DNA is the primary target of carcinogenic compounds Most carcinogens are metabolized by the cytochrome P-450 pathway E. Carcinogen-induced DNA damage usually results in initiation of carcinogenesis Q63. Which of the following is not involved with pro-apoptosis or pro-apoptotic pathways? p53 MYC BAX BCL-2 BRCA-1 Q64. Which is true regarding telomeres and telomerase? Decreased telomere size will activate p53 Telomerase is present in most somatic cells Telomere shortening is activated by telomerase Decreased telomerase activity is common in human cancers

A. B. C. D.

A. B. C. D. E. A. B. C. D.

General pathology 2008-2009 Compiled by Bhupinder Bawa E. A. B. C. D. E. Both b and d Q65. Which is false regarding angiogenesis? p53 can inhibit angiogenesis by inducing thrombospondin-1 Vascular networks formed by tumor cells are unstable and leaky The two most important angiogenic factors are VEGF and bFGF Angiogenesis is required for tumors larger than 1-2 mm in diameter Angiogenic switch is the shift from producing angiogenic factors to producing angiogenic inhibitors Q66. Which of the following would not promote vascular invasion and metastasis? Over-expression of CD44 Down-regulation of E-cadherin Inhibition of type IV collagenase secretion Up-regulation of laminin-binding receptors Increased expression of chemokine receptors Q67. What is the most common chromosomal abnormality involved in activating protooncogenes? Deletions Insertions Inversions Translocations Amplifications Q68. Which of the following is not a “gatekeeper” gene? RB APC NF-1 BRCA-1 Both a and b Q69. The carcinogenicity of UVB light is attributable to which mechanism? Immunostimulation Activation of CYCLIN D gene Formation of reactive electrophiles Formation of pyrimidine dimers in DNA Blocking of p53 and RB cell suppression pathways Q70. Replicative potential of neoplastic cells is dependent on A. Angiogenesis B. Telomerase activity C. Promotion of growth factors D. Formation of homozygous oncogenes E. All of the above

A. B. C. D. E.

A. B. C. D. E. A. B. C. D. E. A. B. C. D. E.

General pathology 2008-2009 Compiled by Bhupinder Bawa Q71. Which are the two most important tumor-associated angiogenic factors 1. bFGF 2. VEGF 3. PDGF 4. TGF-β 5. Angiopoietin 1 A. B. C. D. E. 1,2 1,3 1,4 1,5 2,3

Q72. Invasion of the ECM by neoplastic cells requires A. Detachment of neoplastic cells from each other B. Attachment to matrix components C. Degradation of the ECM D. Migration into the ECM E. All of the above Q73. Organ tropism of metastasis is due to A. Endothelial ligand expression B. Blood and lymphatic supply C. Specific chemokines D. A & C E. B & C Q74. An example of an epigenetic change is A. Genetic translocation B. Fusion of two genes into an oncogene C. Reduplication and amplification of an oncogene D. Hypermethylation of a promoter sequence without DNA change E. None of the above Q75. Transformation of non-immortalized cells in vitro requires A. Transformation of a single oncogene B. Loss of a single tumor suppressor gene C. Transformation of two or more oncogenes D. Loss of two or more tumor suppressor genes E. C & D Q76. Which of the following is a direct-acting carcinogen A. Azo dye B. Aflatoxin B1 C. Alkylating agent D. Polychlorinated biphenyl E. Polycyclic aromatic hydrocarbon

General pathology 2008-2009 Compiled by Bhupinder Bawa Q77. Promoters contribute to tumorigenesis by (Robbins 322) A. Inhibiting apoptosis B. Directly damage DNA C. Initiate cell proliferation D. Inhibit activation of caretaker genes E. Change protooncogenes into oncogenes Q78. The carcinogenicity of UVB light is attributed to (Robbins 323) A. Formation of pyrimidine dimers in RNA B. Formation of pyrimidine dimers in DNA C. Overwhelmed capacity of the NER pathway D. B & C E. All of the above 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 Q80. Which of the following is not a tumor evasion mechanism A. Antigen masking B. Fas ligand expression C. Immunosuppression D. Replication of MHC molecules E. Selective outgrowth of antigen-negative variants Q81. Which of the following is not a paraneoplastic syndrome A. sHypercalcemia from skeletal metastases B. Hypercalcemia from PTHRP production C. Hypertrophic osteoarthropathy D. Cushing’s syndrome E. Dermatomyositis A. B. C. D. E. Q82. Which of the following would NOT stimulate a CD8+ T-cell immune response? Presentation of an overexpressed self-protein Presentation of a radiation-induced mutated self-protein Presentation of a protein encoded by a mutated oncogene Presentation of oncogenic virus-particles by an infected cell Presentation of antigens from a phagocytosed tumor cell by an antigen-presenting cell Q83. Which of the following disorders is NOT expected as a paraneoplastic syndrome? Hypoglycemia

A.

General pathology 2008-2009 Compiled by Bhupinder Bawa B. C. D. E. A. B. C. D. E. A. B. C. D. E. A. B. C. D. E. Hypercalcemia Myasthenia gravis Hypoadrenocorticism Hypertrophic osteopathy Q84. What is the principle mechanism responsible for tumor immunity? Innate immunity Macrophage activation CD8+ killing of tumor cells Natural killer cell-mediated tumor lysis Production of complement-fixing antibody Q85. Which of the following is not involved with cancer cachexia? Increased TNF Reduced food intake Increased basal metabolic rate Nutritional demands of the tumor Alterations in protein and fat metabolism Q86. Which of the following is not a criterion used for staging tumors? Number of mitoses Size of primary lesion Presence of metastisis Extent of spread to lymph nodes All are criteria Q87. The principal mechanism of tumor immunity is killing of tumor cell by? A. B. C. D. E. Antibodies CD8+ CTLs Macrophages B-lymphocytes Natural killer cell

Q88. Tumor cells can escape immune system by all of the following mechanisms except? A. B. C. D. E. Selective outgrowth of antigen-negative variants Loss or reduced expression of MHC molecules Expression of costimulatory molecules Apoptosis of cytotoxic T-cells Immunusuppression

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. C. D. E. TNF-α TGF- α PTHRP Dihydroxyvitamin D

Q90. Which of the following is NOT true regarding chemical carcinogenesis? A. Initiator causes permanent, irreversible DNA damage B. Initiator alone is not sufficient for tumor formation C. Application of promoter can affect DNA directly D. Promoters can induce tumors in initiated cells E. Promoters are non-tumorigenic by themselves 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 Q92. Which of the following are caretaker genes? A. Genes involving RB pathway B. Genes involving p532 C. Mismatch repair genes D. DNA repair genes E. C and D both Q93. Which of the following is an early event in development of colorectal cancers? A. Loss of p53 gene B. Mutation of RAS gene C. Loss or mutation of APC D. Loss of TGF- receptor I gene E. Loss of tumor suppressor gene

General pathology 2008-2009 Compiled by Bhupinder Bawa

1) 2) 3) 4) 5) 6) 7) 8) 9) 10) 11) 12) 13) 14) 15) 16) 17) 18) 19) 20) 21) 22) 23) 24) 25) 26) 27)

Answers: B (Robbins pp 273-274) 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 D (Robbins pp 272) E (Robbins pp 275) E (Robbins pp 273) E (Robbins pp 274) Generally, the better the differentiation of the transformed cell, the more completely it retains functional capabilities and morphology 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. A (Robbins 273/274) C (Robbins p. 276) C (Robbins p. 278) A (Robbins p. 286) E (Robbins p. 288) D p287 Table 7-6 Robbins. (a) associated with various tumors, (b) Adenomatous polyposis, (c) Breast cancer and ovarian tumors, (e) Melanoma. C (Robbins p. 276)– total cell-cycle time for many tumors is equal to or longer than their non-neoplastic counterparts. A (Robbins p. 279, 280) A (Robbins 279) E (Robbins 289) D (Robbins 288) D (Robbins 288) E (Robbins 288) Recessive oncogene = both normal alleles must be damaged for transformation to occur (refers to tumor suppressor genes). E (Robbins pp 288-291) A (Robbins pp 288) C (Robbins pp 292) 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. A (p291 Fig 7-30 Robbins) D ( p291-292 Robbins) 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) 29) 30) 31) 32) 33) D (Robbins pp 290) B (Robbins pp 290-291) E (Robbins pp 292) D (Robbins pp 289) B (Robbins pp 289) 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. B (Robbins pp 289) A (Robbins pp 289) (G1/S transition is the point of no return) A (Robbins pp 296) A (Robbins pp 298) E (Robbins pp 302) 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 C (Robbins pp 300) D (Robbins pp 302) 42) E – both alleles need to be lost/mutated before malignant transformation occurs (p. 302) E (Robbins p. 297) RAS is a signal-transducing oncogene B (Robbins p. 297) GTP hydrolysis converts GTP-bound active RAS to the GDPbound inactive form E (Robbins 294) (BCL-2 is an apoptotic gene) A (p53 is a tumor suppressor gene) C (Robbins 300) D (Robbins 299) C (Robbins 304) C (Robbins p. 302) B (Robbins p. 304) C (Robbins pp 309) D (Robbins pp 309) 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) E (Robbins pp 318) C (Robbins pp 317) D (p. 309) C (p. 311-312) Upregulation of integrins usually occurs to allow cells to adhere to endothelium at distant sites

34) 35) 36) 37) 38) 39) 40) 41) 43) 44) 45) 46) 47) 48) 49) 50) 51) 52) 53) 54)

55) 56) 57) 58)

General pathology 2008-2009 Compiled by Bhupinder Bawa 59) D (Robbins p. 317) 60) E (p. 318) E (p. 320) 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. E (Robbins p. 306) BRCA-1 and BRCA-2 participate in DNA repair A (Robbins p. 308) E (Robbins p. 309) Angiogenic switch is when some tumor cells change to an angiogenic phenotype C (Robbins p. 312)Degradation of basement membrane by type IV collagenases is important for tumor migration D (Robbins pp 314) D (Robbins pp 318) - BRCA-1 is a caretaker gene (affect genomic stability) D (Robbins pp 323) B (Robbins pp 3093) (potential) A (Robbins pp 309) E (Robbins pp 311) D (Robbins pp 313) (organ tropism is independent of blood drainage) D (Robbins 315) E (Robbins 317) C (Robbins 321) C (Robbins 322) D (Robbins 323) C (Robbins 329, 330 – Cell specific differentiation antigens are normal self-antigens, therefore, no immune response is expected) D (Robbins 331 – Loss of MHC molecules is a tumor evasion mechanism) A (Robbins 333) E (p.329-330). This would be presented by MHCII and therefore illicit a CD4+ response. D C (Robbins p. 330) D (Robbins p. 333) A (Robbins p. 335) - Number of mitoses is involved in grading a tumor B (Robbins pp 330) C (Robbins pp 331) There is lack of costimulation; another mechanism is antigen masking. D ( Robbins pp 334) the others are also implicate but the most important is PTHrp C (Robbins pp 320) Promoters does not directly affect the DNA E ( Robbins pp 323) UVB is usually carcinogenic, as UVC is shielded by ozone E (Robbins pp 318) C (Robbins pp 317)

61) 62) 63) 64) 65) 66) 67) 68) 69) 70) 71) 72) 73) 74) 75) 76) 77) 78) 79) 80) 81) 82) 83) 84) 85) 86) 87) 88) 89) 90) 91) 92) 93) 94)

General Pathology May 31, 2005

John Ragsdale

General pathology 2008-2009 Compiled by Bhupinder Bawa

Which of the following is not a morphologic change characteristic of anaplastic cells? A) B) C) D) E) Pleomorphism Loss of polarity Tumor giant cells Normal differentiation Abnormal nuclear morphology D Page: 273-275

ANSWER:

The following morphologic changes are characteristics of anaplasia except: A) Large nuclei with coarsely clumped chromatin B) 1:4 nucleus-to-cytoplasm ratio C) Pleomorphic cells and nuclei D) Large numbers of bizarre mitosis E) Loss of polarity of cells Answer: B pages 273-274

Which of the followings are main factors determined rate of tumor growth? 1. 2. 3. 4. 5. a. b. c. d. e. Tumor cell doubling time The concentration of proteinases produced by tumor cells The fraction of tumor cells that are in the replicative pool The concentration of growth factors produced by tumor cells The rate at which cells are shed and lost in the growing lesions 1,2,3 1,3,4 1,3,5 1,4,5 3,4,5 c ref. page 276

Answer

Which of the following is true regarding dissemination of carcinomas? a. Direct transplantation through surgical instruments is impossible b. Direct seeding is the most common pathway for the initial dissemination c. Lymphatic spread is the most common pathway for the initial dissemination d. Hematogenous spread is the most common pathway for the initial dissemination

General pathology 2008-2009 Compiled by Bhupinder Bawa e. Regional lymph node enlargement means dissemination of the primary carcinoma Answer c ref. page 279

The following are true regarding cancer metastasis except: 1) Rarely occurs with benign neoplasms 2) Neoplasms may seed to joint space 3) Lymphatic spread is most common pathway for dissemination of Sarcomas 4) Lymphatic spread is most common pathway for dissemination of Carcinomas 5) Hematogenous spread is most common pathway for dissemination of Carcinomas A) 1, 2 B) 1, 3 C) 2, 3 D) 2, 4 E) 3, 5 Answer: D pages 279-280

The rate of growth of a tumor is determined by the following except: A) Fraction of tumor cells in replicative pool B) Shortened length of time for cell cycle C) Doubling time of tumor cells D) Rate at which cells are shed E) Rate of cellular apoptosis The following cellular changes determine a malignant phenotype except: A) Have unrestricted proliferative capacity associated with maintenance of telomere length B) May not respond to direct inhibitors of cyclin-dependent kinases C) Capacity to proliferate without external stimuli D) Frequently have up regulation of p53 E) May fail to repair DNA damage Answer: D page 289

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 Answer: E E2F transcribes cyclin A and E pages 290-291

General pathology 2008-2009 Compiled by Bhupinder Bawa Answer: B page 276

Which of the following cell-cycle inhibitor does p53 induce? a. b. c. d. e. p14ARF p16INK4 p21 p27 p57 c ref. page292

Answer

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 Answer: B page 294

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 Answer: G page 298

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 Answer: C page 300

The following prevent RB activation through the CyclinD/CDK4 pathway except: A) P53

General pathology 2008-2009 Compiled by Bhupinder Bawa B) TGF-β C) CDK inhibitors D) INK 4a inhibitors E) Oncogenic viruses Answer: E page 302

The following antigens on tumors are recognized by CD8+ cytotoxic T lymphcytes except: A) Oncofetal antigens B) Glycocalyx molecules C) Products of mutated oncogenes D) Overexpressed cellular proteins E) Antigens produced by oncogenic viruses Answer : B, it masks cell surface antigens pages 329-331

Protooncogenes can be activated in the following ways except: A) Chromosomal translocations that remove the gene from its regulatory elements B) Chromosomal translocation that causes formation of hybrid genes that encode growth promoting chimeric protein C) Reduplication and amplification of the genes DNA sequence D) Hypermethylation of promoter sequences for the gene E) None of the above Answer: D , pages 314-315

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 Answer: Matching A. disorganized but mature mesenchymal or epithelial tissues found in their normal anatomic location B. normal mature tissue located at an ectopic site C page 319

General pathology 2008-2009 Compiled by Bhupinder Bawa C. all three embryonic cell layers- endoderm, mesoderm, and ectoderm- can give rise to this type of tumor D. term for tumors which stimulate formation of abundant collagen in surrounding connective tissue E. abnormal pattern of tissue growth 1. 2. 3. 4. 5. 256 The size of a cell population can be increased by which of the following mechanisms? 1. 2. 3. 4. 5. A. B. C. D. E. shortening of the cell cycle increased rate of stem cell input increased rates of differentiation conversion of quiescent cells into proliferating cells increased rate of release of cytochrome C from mitochondria 1,2,3 1,2,4 1,2,3,4 1,2,3,5 1,2,3,4,5 Answer: C Matching A. B. C. D. E. 1. 2. 3. 4. exit from mitosis requires deactivation of this complexes with cyclin D to phosphorylate RB increases p53 levels by inhibiting MDM2 activity causes compaction of chromatin and inhibition of transcription induced by p53 to block cell cycle by binding to cyclin-CDK complexes p21 CDK4 p14ARF cyclin B-CDK1 pg 261-262, PBVD scirrhous dysplasia epithelial choristoma hamartoma Answer: A5, B4, C3, D1, E2 PBVD pg 253-

General pathology 2008-2009 Compiled by Bhupinder Bawa 5. histone dacetylase Answer: A4, B2, C3, D5, E1 Robbins pg 289-292

In the absence of APC protein which of the following occur? 1. 2. 3. 4. 5. A. B. C. D. E. degradation of β-catenin decreased cell cycle activity increased transcription of c-MYC increased transcription of CYCLIN D1 complex formation between β-catenin and TCF 1,2,3 1,3,5 1,4,5 2,3,5 3,4,5 Answer: E pg 304, robbins

Which of the following would result in increased apoptosis? 1. 2. 3. 4. 5. A. B. C. D. E. robbins All of the following are true concerning gatekeeper genes except: A. B. C. D. E. are defective in most tumors can directly control tumor growth includes INK4 proteins, cyclin D, and RB includes p53, MDM2, and mismatch repair genes have increased risk of mutation with loss of caretaker genes increase in INK4a decrease in MDM2 increased transcription of BID increased transcription of BAX increased transcription of BCL-2 1 1,2 1,2,3 1,2,3,4 1,2,3,4,5 Answer: D pg 291, 306

General pathology 2008-2009 Compiled by Bhupinder Bawa

Answer: D Which of the following are retroviruses? 1. 2. 3. 4. 5. A. B. C. D. E. SV40 Polyoma virus Maedi-Visna virus feline leukemia virus feline immunodeficiency virus 1,2,3 1,4,5 2,3,4 2,3,5 3,4,5 Answer: E

pg 318, robbins

pg 288, Table 6-5, PBVD

Which of the following are true concerning antitumor effector mechanisms? 1. the principal mechanism of tumor immunity is killing by CD8+ CTLs 2. cell-mediated immunity is believed to be the most effective antitumor defense 3. release of IFN-γ by NK cells activates MHC antigen independent tumor cell death via macrophages 4. reduced MHC expression by tumor cells may lead to increased killing by cytotoxic T lymphocytes 5. granzymes released by CTLs initiate caspase-dependent and caspaseindependent apoptosis of tumor cells A. B. C. D. E. 1,2,3 1,2,3,4 1,2,3,5 2,3,4,5 1,2,3,4,5 pg 330-331, PBVD pg 275-276

Answer: C

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