001     120385
005     20240228135019.0
024 7 _ |a 10.3748/wjg.v20.i35.12367
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024 7 _ |a pmc:PMC4168070
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024 7 _ |a 1007-9327
|2 ISSN
024 7 _ |a 2219-2840
|2 ISSN
024 7 _ |a altmetric:2893221
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037 _ _ |a DKFZ-2017-00818
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Herzer, Kerstin
|b 0
245 _ _ |a Hepatitis C-associated liver carcinogenesis: role of PML nuclear bodies.
260 _ _ |a Beijing
|c 2014
|b WJG Press
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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|x Review Article
336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Successful escape from immune response characterises chronic hepatitis C virus (HCV) infection, which results in persistence of infection in about 80% of the patients. The deleterious consequences are cirrhosis and hepatocellular carcinoma. HCV accounts the most frequent cause for hepatocellular carcinoma (HCC) and liver transplantation (LT) in the western world. The underlying molecular mechanisms how HCV promotes tumor development are largely unknown. There is some in vitro and in vivo evidence that HCV interferes with the tumor suppressor PML and may thereby importantly contribute to the HCV-associated pathogenesis with respect to the development of HCC. The tumor suppressor protein 'promyelocytic leukemia' (PML) has been implicated in the regulation of important cellular processes like differentiation and apoptosis. In cancer biology, PML and its associated nuclear bodies (NBs) have initially attracted intense interest due to its role in the pathogenesis of acute promyelocytic leukemia (APL). More recently, loss of PML has been implicated in human cancers of various histologic origins. Moreover, number and intensity of PML-NBs increase in response to interferons (IFNs) and there is evidence that PML-NBs may represent preferential targets in viral infections. Thus, PML could not only play a role in the mechanisms of the antiviral action of IFNs but may also be involved in a direct oncogenic effect of the HCV on hepatocytes. This review aims to summarise current knowledge about HCV-related liver carcinogenesis and to discuss a potential role of the nuclear body protein PML for this this hard-to-treat cancer.
536 _ _ |a 311 - Signalling pathways, cell and tumor biology (POF3-311)
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588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Nuclear Proteins
|2 NLM Chemicals
650 _ 7 |a Promyelocytic Leukemia Protein
|2 NLM Chemicals
650 _ 7 |a Transcription Factors
|2 NLM Chemicals
650 _ 7 |a Tumor Suppressor Proteins
|2 NLM Chemicals
650 _ 7 |a PML protein, human
|0 143220-95-5
|2 NLM Chemicals
700 1 _ |a Gerken, Guido
|b 1
700 1 _ |a Hofmann, Thomas
|0 P:(DE-He78)99ae95278bd95e30462a4fb2d12026c6
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|e Last author
|u dkfz
773 _ _ |a 10.3748/wjg.v20.i35.12367
|g Vol. 20, no. 35, p. 12367 -
|0 PERI:(DE-600)2084831-6
|n 35
|p 12367 -
|t World journal of gastroenterology
|v 20
|y 2014
|x 1007-9327
909 C O |o oai:inrepo02.dkfz.de:120385
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910 1 _ |a Deutsches Krebsforschungszentrum
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914 1 _ |y 2014
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