Links for fulltext
     (May Require Subscription)
Supplementary

Article: The significance of proline-rich tyrosine kinase2 (Pyk2) on hepatocellular carcinoma progression and recurrence

TitleThe significance of proline-rich tyrosine kinase2 (Pyk2) on hepatocellular carcinoma progression and recurrence
Authors
KeywordsDisease-free survival
Hepatocellular carcinoma
Invasiveness
Proline-rich tyrosine kinase2 (Pyk2)
Recurrence
Issue Date2007
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 2007, v. 97 n. 1, p. 50-57 How to Cite?
AbstractUnderstanding the precise molecular mechanisms that trigger liver cancer cell migration and invasion could develop novel therapeutic strategies targeting cancer cell invasion to increase the sensitivity to current treatment modalities. In the current study, 49 patients with hepatocellular carcinoma (HCC) were included prospectively. Liver tumour and adjacent non-tumour tissues were detected for the expression of Proline-rich tyrosine kinase 2 (Pyk2), focal adhesion kinase (FAK), ezrin and fibronectin at protein and/or gene levels. Correlation between the expressions of Pyk2/FAK with the clinical pathological data was analysed. Protein expression of Pyk2 was also examined in a nude mice orthotopic liver tumour model with higher metastatic potential. There were 59% (29 out of 49) and 57% (28 out of 49) of HCC patients with higher levels of Pyk2 and FAK protein/gene expression, respectively. We observed a positive correlation between the protein and gene expression levels of Pyk2 and FAK (P=0.000, r=0.875). Overexpression of Pyk2 and FAK was significantly correlated with shorter disease-free survival. Patients with higher levels of Pyk2/FAK had larger tumour size and advanced Edmonson grading. In the animal studies, Pyk2 overexpression was found in infiltrative tumour cells and lung metastatic nodules. In conclusion, overexpression of Pyk2 and FAK was found in nearly 60% of HCC patients and was significantly correlated with poor prognosis. The significance of Pyk2 in HCC invasiveness was confirmed by animal studies. © 2007 Cancer Research UK.
Persistent Identifierhttp://hdl.handle.net/10722/88538
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSun, CKen_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorSun, BSen_HK
dc.contributor.authorHo, JWYen_HK
dc.contributor.authorLee, TKen_HK
dc.contributor.authorNg, Ien_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorLiu, CLen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T09:44:41Z-
dc.date.available2010-09-06T09:44:41Z-
dc.date.issued2007en_HK
dc.identifier.citationBritish Journal Of Cancer, 2007, v. 97 n. 1, p. 50-57en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88538-
dc.description.abstractUnderstanding the precise molecular mechanisms that trigger liver cancer cell migration and invasion could develop novel therapeutic strategies targeting cancer cell invasion to increase the sensitivity to current treatment modalities. In the current study, 49 patients with hepatocellular carcinoma (HCC) were included prospectively. Liver tumour and adjacent non-tumour tissues were detected for the expression of Proline-rich tyrosine kinase 2 (Pyk2), focal adhesion kinase (FAK), ezrin and fibronectin at protein and/or gene levels. Correlation between the expressions of Pyk2/FAK with the clinical pathological data was analysed. Protein expression of Pyk2 was also examined in a nude mice orthotopic liver tumour model with higher metastatic potential. There were 59% (29 out of 49) and 57% (28 out of 49) of HCC patients with higher levels of Pyk2 and FAK protein/gene expression, respectively. We observed a positive correlation between the protein and gene expression levels of Pyk2 and FAK (P=0.000, r=0.875). Overexpression of Pyk2 and FAK was significantly correlated with shorter disease-free survival. Patients with higher levels of Pyk2/FAK had larger tumour size and advanced Edmonson grading. In the animal studies, Pyk2 overexpression was found in infiltrative tumour cells and lung metastatic nodules. In conclusion, overexpression of Pyk2 and FAK was found in nearly 60% of HCC patients and was significantly correlated with poor prognosis. The significance of Pyk2 in HCC invasiveness was confirmed by animal studies. © 2007 Cancer Research UK.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectDisease-free survivalen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectInvasivenessen_HK
dc.subjectProline-rich tyrosine kinase2 (Pyk2)en_HK
dc.subjectRecurrenceen_HK
dc.subject.meshCarcinoma, Hepatocellular - enzymology - genetics-
dc.subject.meshCell Line, Tumor-
dc.subject.meshCell Proliferation-
dc.subject.meshFocal Adhesion Kinase 2 - metabolism-
dc.subject.meshLiver Neoplasms - enzymology - genetics-
dc.titleThe significance of proline-rich tyrosine kinase2 (Pyk2) on hepatocellular carcinoma progression and recurrenceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=97&issue=1&spage=50&epage=57&date=2007&atitle=The+significance+of+proline-rich+tyrosine+kinase2+(Pyk2)+on+hepatocellular+carcinoma+progression+and+recurrenceen_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailNg, I: iolng@hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityNg, I=rp00335en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/sj.bjc.6603827en_HK
dc.identifier.pmid17551499-
dc.identifier.pmcidPMC2359657-
dc.identifier.scopuseid_2-s2.0-34347359742en_HK
dc.identifier.hkuros129735en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34347359742&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue1en_HK
dc.identifier.spage50en_HK
dc.identifier.epage57en_HK
dc.identifier.isiWOS:000247597200008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridSun, BS=23101636500en_HK
dc.identifier.scopusauthoridHo, JWY=7402649982en_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridNg, I=7102753722en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridLiu, CL=36063391100en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.citeulike1366250-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats