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231223s2010 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2009.10.007
|2 doi
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|a eng
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| 100 |
1 |
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|a Castello, Giuseppe
|e verfasserin
|4 aut
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| 245 |
1 |
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|a HCV-related hepatocellular carcinoma
|b From chronic inflammation to cancer
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| 264 |
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1 |
|c 2010
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|a ƒa Online-Ressource
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|a Date Completed 18.03.2010
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|a Date Revised 17.02.2010
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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| 520 |
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|a 2009 Elsevier Inc. All rights reserved.
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|a Hepatitis C virus (HCV) infection is a worldwide health problem because of its incidence and pathogenicity. It might evolve into chronic disease, cirrhosis, and/or hepatocellular carcinoma (HCC) and the outcome is mainly determined by the host immune response. For viral clearance, combined innate and adaptive immune responses are required; resolution requires a vigorous, durable, polyclonal CD4(+) and CD8(+) T-cell response, with an increase in virus-specific CD8(+) T cells or cytotoxic T lymphocytes. Failure of efficient immune response can lead to chronic inflammation, tissue remodeling through cell growth, apoptosis and/or necrosis and induction of oxidative stress. Development of fibrosis and/or cirrhosis plus a microenvironment conducive to genomic instability mutations will promote neoplastic transformation. System governance derives from cellular (regulatory cells) and humoral (cytokines and chemokines) immune networks. Therefore, HCC pathogenesis may be a model to study the disease progression from chronic inflammation to cancer allowing design of new strategies targeting the immune response, thereby modifying disease outcome
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Review
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|a Scala, Stefania
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Palmieri, Giuseppe
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Curley, Steven A
|e verfasserin
|4 aut
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| 700 |
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|a Izzo, Francesco
|e verfasserin
|4 aut
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|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 134(2010), 3 vom: 01. März, Seite 237-50
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|g month:03
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