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Article: Reversing hepatocellular carcinoma progression by using networked biological therapies

TitleReversing hepatocellular carcinoma progression by using networked biological therapies
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2007, v. 13 n. 1, p. 11-17 How to Cite?
AbstractThe liver is distinguished from other tissues by (a) its detoxifying function, (b) its resistance to apoptosis, and (c) its regenerative response to damage. Hepatocellular carcinoma arises when chronic insults, such as hepatitis or iron overload, constitutively activate this regenerative program. Here, we propose that the proliferative response of the liver to damage underlies the resistance of hepatocellular carcinoma to cytotoxic therapy, and that hepatocellular carcinoma growth should therefore be more readily controlled by using a networked combination of noncytotoxic interventions to interrupt the damage-inducible regenerative pathway. To this end, hepatocellular carcinoma boasts a wealth of potential drug targets, including viral replication, the antiapoptotic immunosuppressant alpha-fetoprotein, hepatic iron overload, inflammatory signaling, extracellular proteases, and growth factors. By blocking these positive feedback loops in parallel, and so returning the host environment to a more normal state, epigenetic repression of tumor-suppressor gene function may be reversed and tumor dormancy restored. Noncytotoxic maneuvers that short circuit damage resistance loops may thus represent an indirect form of gene therapy meriting incorporation into hepatocellular carcinoma clinical trials.
Persistent Identifierhttp://hdl.handle.net/10722/76547
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314

 

DC FieldValueLanguage
dc.contributor.authorEpstein, Ren_HK
dc.contributor.authorLeung, TWTen_HK
dc.date.accessioned2010-09-06T07:22:24Z-
dc.date.available2010-09-06T07:22:24Z-
dc.date.issued2007en_HK
dc.identifier.citationClinical Cancer Research, 2007, v. 13 n. 1, p. 11-17en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76547-
dc.description.abstractThe liver is distinguished from other tissues by (a) its detoxifying function, (b) its resistance to apoptosis, and (c) its regenerative response to damage. Hepatocellular carcinoma arises when chronic insults, such as hepatitis or iron overload, constitutively activate this regenerative program. Here, we propose that the proliferative response of the liver to damage underlies the resistance of hepatocellular carcinoma to cytotoxic therapy, and that hepatocellular carcinoma growth should therefore be more readily controlled by using a networked combination of noncytotoxic interventions to interrupt the damage-inducible regenerative pathway. To this end, hepatocellular carcinoma boasts a wealth of potential drug targets, including viral replication, the antiapoptotic immunosuppressant alpha-fetoprotein, hepatic iron overload, inflammatory signaling, extracellular proteases, and growth factors. By blocking these positive feedback loops in parallel, and so returning the host environment to a more normal state, epigenetic repression of tumor-suppressor gene function may be reversed and tumor dormancy restored. Noncytotoxic maneuvers that short circuit damage resistance loops may thus represent an indirect form of gene therapy meriting incorporation into hepatocellular carcinoma clinical trials.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.titleReversing hepatocellular carcinoma progression by using networked biological therapiesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=13&issue=1&spage=11&epage=7&date=2007&atitle=Reversing+hepatocellular+carcinoma+progression+using+networked+biological+therapiesen_HK
dc.identifier.emailEpstein, R: repstein@hku.hken_HK
dc.identifier.authorityEpstein, R=rp00501en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid17200333-
dc.identifier.hkuros131225en_HK

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