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26 Cards in this Set
- Front
- Back
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1. Which of the following growth factor is encoded by SIS; (P293)
A. FGF B. PDGF C. TGF D. HGF E. EGF |
(1:B, SIS encodes the β-chain of PDGE)
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2. Which of the following is a tumor-suppressor mechanism of TGF-β; (P300)
A. Maintain cytoskeletal stability B. Inhibit p21 inhibitor C. Increase p27 D. Form ubiquitin ligases E. Stimulate apoptosis |
(2:B)
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3. Which of the following is the anti-angiogenetic factor derived from proteolytic cleavage of plasminogen; (P309)
A. Thrombospondin B. Endostatin C. Tumstatin D. Plasmstatin E. Angiostatin |
(3:E)
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4. In normal tissue, MAGE (melanoma antigen) expression is restricted to; (P329)
A. Bladder B. Breast C. Testis D. Prostate E. Skin |
(4:C)
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5. All of the following are included in the paraneoplastic syndromes EXCEPT; (P333,334)
A. Hypercalcemia due to skeletal metastases B. Hypoglycemia due to insulin or insulin-like substance C. Cushing syndrome due to ACTH or ACTH-like substance D. Polycythemia due to erythropoietin E. Carcinoid syndrome due to serotonin or bradykinin |
(5:A)
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6. All of the following statements are true EXCEPT; (P277,288)
A. Tumors are formed by the clonal expansion of a single precursor cell that has incurred the genetic damage. B. Protooncogenes are referred to as recessive oncogenes because both normal alleles must be lost or inactivated for transformation to occur. C. Carcinogenesis is a multistep process at both the phenotypic and the genetic levels. D. Mutator phenotype refers to a propensity to mutations and neoplastic transformation caused by a disability in the DNA repair genes. E. With progressive growth, the tumor cells generate heterogeneity and tumor mass becomes enriched for variant. |
(6:B)
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7. Which of the following enzyme keeps E2F silent during E2F/DP1/RB complex; (P289)
A. DNA polymerase B. Thymidine kinases C. Dihydrofolate reductase D. Cellular phosphatase E. Histone deacetylase |
(7:E)
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8. During tumor-associated angiogenesis, VEGF is mostly produced by; (P309)
A. Endothelial cell B. Fibroblast C. Macrophage D. Tumor cell E. Platelet |
(8:D)
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9. In colorectal carcinoma progression, which of the following gene loss or mutation is the first step; (P317)
A. p53 B. APC C. RAS D. TGF-β receptor gene E. SMAD2 |
(9:B)
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1. All followings regarding tumor development are correct EXCEPT:
A. Initiation is reversible genetic changes. B. At least a single round of DNA replication is necessary for fixation of the change by initiator. C. Promoters are not mutagenic. D. Promoters’ effects are reversible. E. Progression is the final stage of tumor development, including the conversion of benign tumor to an increasingly malignant tumor. |
(1:A p.266, Initiation is irreversible.)
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2. All followings regarding mechanisms of invasion and metastasis are correct EXCEPT:
A. During invasion and metastasis, carcinoma cells often express increased numbers of laminin receptor and fibronection receptor. B. During invasion proteases and antiproteases are produced and activated by the tumor cell themselves or non-neoplastic stroma cells. C. Proteases playing important role in tumor metastasis include type IV collagenase (matrix metalloproteinases) and urokinase (serine protease). D. Tumor cell migration is stimulated by autocrine growth factors (hepatocyte growth factor, also called “scatter factor”) and by cleavage products of ECM components (fragments of collagen). E. In vessels, tumor cells may be recognized and attached by host lymphocytes or may be surrounded by platelets, which inhibit tumor metastasis. |
(2:E p.270, Platelets may actually protect the tumor embolus and enhance tumor metastasis.)
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3. Order the steps of metastasis:
a. Secrete proteolytic enzymes, including type IV collagenase and plasminogen activator. b. Loss of cadherin or catenin function. c. Degradation of the basement membrane d. Attach to the basement membrane via laminin receptors e. Tumor cell migration A. a→b→c→d→e B. b→a→d→c→e C. b→d→a→c→e D. b→d→c→a→e E. d→b→a→c→e |
(3:C p.270)
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4. All followings regarding tumor stroma are correct EXCEPT:
A. Amyloid may be present in the stroma of rare tumor, both mesenchymal and epithelial. B. Tumor stroma may both enhance and limit tumor development and spred. C. PDGF released by tumor cells stimulated tumor-associated fibroblasts to increase the production of collagen. D. TGF-α of tumor origin can stimulate tumor-associated fibroblasts to differentiate into myofibroblasts. E. Tumor-associated fibroblasts may secrete a fetal type of ECM, and acquire non-genetic changes but not genetic changes. |
(4:E p.272, Tumor-associated fibroblasts may acquire heritable genetic and epigenetic changes.)
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5. Match the antigens and their definition/statements:
A. Tumor-specific antigens B. Tumor-associated antigens C. Tumor-specific shared antigens D. Tissue-specific antigens E. Differentiation antigens a. Antigens encoded by genes that have very limited expression in adult tissue but that are expressed by many types of tumor tissue b. Antigens shared by tumors and the normal tissues from which they arise c. Antigens derived from oncogenic viruses or altered cellular products encoded by mutated genes d. Antigens expressed only at specific stages of differentiation in the normal tissue e. Antigens restricted to tumor cells f. Antigen present on both tumor cells and normal cells g. MAGE family of proteins |
(5: A:c,e; B:f; C:a; D:b; E:d p.275)
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6. All followings regarding tumor immunity are correct EXCEPT:
A. All tumor antigens are presented to CD8+ T lymphocytes by MHC class I molecules. B. Immunosurveillance is the immune system which is capable of recognizing self-antigens on tumor cells as foreign and attacking antigen-bearing tumor cells. C. Tumor cells that express MHC class I molecules are specifically targeted by NK cells. D. The antitumor activity is stimulated by IFN-γ, which is produced by both T lymphocytes and NK cells. E. Antitumor antibodies may be bound by their constant regions to NK cells or macrophages, leaving the variable regions of the immunogloblins available for specific recognition of tumor antigens, which induces antibody-dependent cell-mediated cytotoxicity (ADCC). |
(6:C p.276, Tumor cells that express MHC class I molecules are preferentially spared by NK cells, whereas cells lacking MHC molecules are specifically targeted.)
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7. All followings regarding evasion of immune response of tumor cells are correct EXCEPT:
A. Some humoral responses to tumor antigens may promote tumor survival by protecting tumor antigens from recognition by cytotoxic T lymphocytes. B. Tumor antigens shared with normal tissue usually are not able to evoke an immune response. C. Many tumor cells produce TGF-β, which inhibits the proliferation and function of lymphocytes and macrophages. D. Tumor may produce Fas ligand, which binds to Fas receptor on nearby T lymphocytes and triggers apoptosis of tumor cells. E. Tumor cells release tumor antigens into the circulation that form immune complexes with antibodies, which may be immunosuppressive. |
(7:D p.278, FasL on tumor cells binding to Fas receptor on T cells triggers apoptosis of T cells.)
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8. All followings regarding genetic changes in cancer are correct EXCEPT:
A. The 5’ untranslated region of a gene generally contains its promoter and the 3’untrasnlated region often contains mRNA stabilization motifs. B. Aneuploidy is alterations in chromosome number. C. The internal tandem duplication (ITD) of the c-kit gene is present in canine mast cells. D. Cancer cells show global hypermethylation with hypermethylated CpG islands. E. Genetic imprinting is monoallelic expression controlled in part by DNA methylation. |
(8:D p.284, Cancer cells show global hypomethylation with hypermethylated CpG islands, whereas normal cells show global hypermethylation with hypomethylated CpG islands.)
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9. All followings regarding cancer etiology are correct EXCEPT:
A. Many of the familial cancer syndromes are due to mutations in recessive turmor suppressor genes, and the syndromes generally show a predominantly autosomal recessive pattern of inheritance. B. Unlike chemicals, all forms of radiation are complete carcinogenesis (i.e., able to initiate and, with continued exposure, to promote tumotigenesis). C. Papillomavirus genomes include the E6 and E7 genes that encode inhibitors of the p53 and pRb tumor suppressor proteins, respectively. D. Bovine papillomavirus uses a hit and run mechanism, transformation of tumor cells by transient virus residence. E. Marek’s disease and hepatitis viruses are examples of indirect mechanism – Marek’s virus suppressing the ability of the host to eliminate transformed cells; Hepatitis viruses stimulating cell proliferation. |
(9:A p.285, Familial cancer syndromes are predominantly autosomal dominant pattern of inheritance.)
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10. All followings regarding tumor suppressor genes are correct EXCEPT:
A. A bona fide tumor suppressor gene within the boundaries of the common lesions loss in many tumors. B. p53 is a DNA-binding protein, and which increases transcription of p53 target genes p21 in cell-cycle arrest and GADD45 in DNA repair. C. RB is a target for inactivation both in germline and somatic cells, and RB is hypophosphorylated in quiescent cells. D. When RB is active, the cell can proceed through the G1/S transition, involving other host genes, such as p16INK4a, cyclin D, and CDK4. E. Tumor suppressor genes generally need inactivation of both alleles for tumor growth; however, for certain genes inactivation of only one copy is sufficient for tumor growth (haploinsufficiency). |
(10:D p.292, When RB is hyperphosphorylated and inactive, the cell can proceed through the G1/S transition.
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11. All of followings regarding tumors are correct EXCEPT:
A. The anchoring of RAS to the cell membrane by the farnesyl moiety is essential for its action. B. RAS exchanges GDP for GTP, and RAS bound to GTP is the active form, which triggers the RAS-RAF-MAPK pathway. C. Squamous cell carcinomas that have undergone epithelial-to-mesenchymal transformation with have areas positive for cytokeratin or vimentin, and the transition areas may be positive for both. D. The presence of a clonal population means that it is a malignancy. E. MLH1 and MSH2, ATM, and BRCA1 and 2 are DNA repair genes. |
(11:D p.286, Canine ehrlichiosis can give rise to clonal lymphocyte populations.)
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1. Which is a receptor for LPS?
A) CD3 B) CD14 C) CD21 D) CD28 E) CD40 |
(1:B p.388)
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2. Which complement system is activated by LPS?
A) Classical pathway B) Alternative pathway C) Lectin pathway D) Classical and alternative pathways E) Classical and lectin pathways |
(2:D p.389)
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3. Which coagulation pathway(s) is/ are associated with developing diffuse microvascular thrombosis with endotoxemia?
A) Intrinsic coagulation pathway B) Extrinsic coagulation pathway C) Both intrinsic and extrinsic coagulation pathways |
(3:C p.389 Lead to enhanced expression of tissue thromboplastin (factor III, tissue factor) on the surfaces of monocytes and macrophages)
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4. All of the following are true about IL-1
A) Endotoxin is one of the most potent inducers B) Induction of fever C) Inhibit procoagulant (tissue factor) expression D) Enhance endothelial cell adhesiveness E) Interface with the fibrinolytic system |
(4:C p.390; IL-1 enhance procoagulant expression)
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5. Which mouse model results from a mutation in V(D)J rearrangement?
A) Beige mouse B) Nude mouse C) NOD mouse D) SCID mouse E) Xid mouse |
(5:D p.289)
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6. Which factor is absent in SCID Jack Russell Terriers?
A) Gene encoding IL-2 receptor B) Gene encoding IL-4 receptor C) Gene encoding IL-7 receptor D) Gene encoding IL-21 receptor E) DNA-PK activity |
(6:E Vet Pathol 41:95-100, 2004; γ-chain of IL-2 receptor defect in Cardigan Welsh Cogi and Basset Hound)
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