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13 Cards in this Set
- Front
- Back
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What are the four eli criteria?
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1. geographic = infection, cancer
2. Higher incidence of viral markers in cases vs control references 3. Viral markers should precede cancer 4. Reduction infection rates = reduce cancer |
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What are the three virologic criteria?
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1. Should transform cells "in vitro"
2. Virus genome in tumor but not normal cells 3. Tumor induction in experimental animals |
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What are three oncogenic retroviruses?
Mechanism? |
ALV and RSV = transduction (has v-oncogene, 100%, rapid)
HTLV-1 = non transducing, long latency ( contains a v-oncogene unrelated to c-oncogene, low tumor formation, months or years). C |
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What is the intermediate phase of retroviruses?
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Nontransducing oncogenic viruses (no v-oncogene, but can activate c-oncogene via integration, high rate of tumor formation, weeks to months).
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True or false. V-oncogenes are always active (constitutive).
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TRUE
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What general mechanism do RNA and DNA viruses use?
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Transformation by activation of signaling pathways
--increase/dysregulation in kinase --or upregulation of gene expression |
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Describe HTLV-1
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Causes ATL, Tax oncogene that infects CD4+ cells --stimulates Ikk -->NFkB moves to nucleus, leads to immortalization of cell.
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Describe EBV
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Herpes DNA virus latent in B-cells
Burkitt's lymphoma, Hodgkin's lymphoma LMP-1 (plasma membrane signaling protein) --> always active -->NFkB moves to nucleus and immortalizes B cell |
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Describe KSHV (human herpes virus 8)
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Kaposi's sacroma, pleural effusion lymphoma
vGPCR (g-protein coupled receptor that induces growh and transformation) --> constitutively active due to AA substitution v-cyclin produces which makes v-cyclin/CdK6 immune to inhibitors |
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Describe SV40 (Simian virus 40)
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Small sT antigen binds protein phosphatase 2A, inactivates phosphatase, increases half-life of phosphorylation events, kinase cascades sustained longer --> uncontrolled stimulation of cell division
Large sT antigen binds and inactivates Rb protein and p53 |
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Describe human papilloma virus (HPV)
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High risk = 16, 18, 35 (high numbers?..)
E2 disrupted which normally control expression of E6 and E7 E6 = binds p53 E7 = binds Rb |
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How HepC and B causes cancer?
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HCC causes decades long chronic infection and inflammation
Constant clearance and replication leads to uncontrolled cell proliferation HBV = HbX (may play a role in dysregulation of cell division) |
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How does EBV cause Burkitt's lymphoma?
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Errors in replication of B cells, places c-myc under control of powerful immunoglobulin heavy chain promoter, results in OVEREXPRESSION OF C-MYC
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