File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Dickkopfs and Wnt/β-catenin signalling in liver cancer

TitleDickkopfs and Wnt/β-catenin signalling in liver cancer
Authors
KeywordsDickkopf
Hepatocellular carcinoma
Tumourigenesis
Wnt/β-catenin signalling
Issue Date2011
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/2218-4333/
Citation
World Journal of Clinical Oncology, 2011, v. 2 n. 8, p. 311-325 How to Cite?
AbstractLiver cancer is the fifth and seventh most common cause of cancer in men and women, respectively. Wnt/beta-catenin signalling has emerged as a critical player in both the development of normal liver as well as an oncogenic driver in hepatocellular carcinoma (HCC). Based on the current understanding, this article summarizes the possible mechanisms for the aberrant activation of this pathway with specific focus on HCC. Furthermore, we will discuss the role of dickkopfs (DKKs) in regulating Wnt/beta-catenin signalling, which is poorly understood and understudied. DKKs are a family of secreted proteins that comprise at least four members, namely DKK1-DKK4, which act as inhibitors of Wnt/beta-catenin signalling. Nevertheless, not all members antagonize Wnt/beta-catenin signalling. Their functional significance in hepatocarcinogenesis remains to be further characterized for which these studies should provide new insights into the regulatory role of DKKs in Wnt/beta-catenin signalling in hepatic carcinogenesis. Because of the important oncogenic roles, there are an increasing number of therapeutic molecules targeting beta-catenin and the Wnt/beta-catenin pathway for potential therapy of HCC.
Persistent Identifierhttp://hdl.handle.net/10722/142547
ISSN
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorFatima, Sen_US
dc.contributor.authorLee, NPYen_US
dc.contributor.authorLuk, JMCen_US
dc.date.accessioned2011-10-28T02:50:58Z-
dc.date.available2011-10-28T02:50:58Z-
dc.date.issued2011en_US
dc.identifier.citationWorld Journal of Clinical Oncology, 2011, v. 2 n. 8, p. 311-325en_US
dc.identifier.issn2218-4333-
dc.identifier.urihttp://hdl.handle.net/10722/142547-
dc.description.abstractLiver cancer is the fifth and seventh most common cause of cancer in men and women, respectively. Wnt/beta-catenin signalling has emerged as a critical player in both the development of normal liver as well as an oncogenic driver in hepatocellular carcinoma (HCC). Based on the current understanding, this article summarizes the possible mechanisms for the aberrant activation of this pathway with specific focus on HCC. Furthermore, we will discuss the role of dickkopfs (DKKs) in regulating Wnt/beta-catenin signalling, which is poorly understood and understudied. DKKs are a family of secreted proteins that comprise at least four members, namely DKK1-DKK4, which act as inhibitors of Wnt/beta-catenin signalling. Nevertheless, not all members antagonize Wnt/beta-catenin signalling. Their functional significance in hepatocarcinogenesis remains to be further characterized for which these studies should provide new insights into the regulatory role of DKKs in Wnt/beta-catenin signalling in hepatic carcinogenesis. Because of the important oncogenic roles, there are an increasing number of therapeutic molecules targeting beta-catenin and the Wnt/beta-catenin pathway for potential therapy of HCC.-
dc.languageengen_US
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/2218-4333/-
dc.relation.ispartofWorld Journal of Clinical Oncologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectDickkopf-
dc.subjectHepatocellular carcinoma-
dc.subjectTumourigenesis-
dc.subjectWnt/β-catenin signalling-
dc.titleDickkopfs and Wnt/β-catenin signalling in liver canceren_US
dc.typeArticleen_US
dc.identifier.emailFatima, S: sarwat@hkucc.hku.hken_US
dc.identifier.emailLee, NPY: nikkilee@hku.hken_US
dc.identifier.emailLuk, JMC: jmluk@hkucc.hku.hken_US
dc.identifier.authorityLee, NPY=rp00263en_US
dc.identifier.authorityLuk, JMC=rp00349en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.5306/wjco.v2.i8.311-
dc.identifier.pmid21876852-
dc.identifier.pmcidPMC3163259-
dc.identifier.hkuros196725en_US
dc.identifier.volume2en_US
dc.identifier.issue8en_US
dc.identifier.spage311en_US
dc.identifier.epage325en_US
dc.publisher.placeChina-
dc.identifier.citeulike9930523-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats