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Conference Paper: The role of RAP1 in graft injury induced cisplatin resistance after liver transplantation

TitleThe role of RAP1 in graft injury induced cisplatin resistance after liver transplantation
Authors
KeywordsMedical sciences
Gastroenterology medical sciences
Surgery
Issue Date2014
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021
Citation
The 2014 Joint International Congress of ILTS, ELITA and LICAGE, London, UK., 4-7 June 2014. In Liver Transplantation, 2014, v. 20 suppl. S1, p. S257, abstract P-343 How to Cite?
AbstractBACKGROUND & AIM: Liver transplantation dramatically improved the survival rate of HCC patients. However, tumor recurrence remains a huge threat without any promising curative treatment. We aim to clarify the mechanism of graft injury regulating chemoresistance after liver transplantation. MATERIALS AND METHODS: A rat orthotopic liver transplantation model with liver cancer development was established with applying whole or small-for-size (50%) graft. The expressions of multidrug resistant genes and RAP1 were compared between small and whole graft groups. RAP1 expression was also validated in clinical samples. The role of RAP1 was further explored in vitro and vivo. RESULTS: The expression of RAP1 was constantly higher in liver and tumor in small-for-size group in rat liver transplantation model. (see diagrams) CONCLUSIONS: Overexpression of intragraft RAP1, which upregulated by acute phase liver graft injury, may induce late phase cisplatin resistance after liver transplantation.
DescriptionPoster Session 2: P-343
This journal suppl. entitled: The ILTS 20th Annual International Congress
Persistent Identifierhttp://hdl.handle.net/10722/204489
ISSN
2015 Impact Factor: 3.951
2015 SCImago Journal Rankings: 1.763

 

DC FieldValueLanguage
dc.contributor.authorGeng, W-
dc.contributor.authorLo, CM-
dc.contributor.authorQi, X-
dc.contributor.authorLi, C-
dc.contributor.authorNg, KTP-
dc.contributor.authorLiu, X-
dc.contributor.authorMa, YY-
dc.contributor.authorMan, K-
dc.date.accessioned2014-09-19T23:57:02Z-
dc.date.available2014-09-19T23:57:02Z-
dc.date.issued2014-
dc.identifier.citationThe 2014 Joint International Congress of ILTS, ELITA and LICAGE, London, UK., 4-7 June 2014. In Liver Transplantation, 2014, v. 20 suppl. S1, p. S257, abstract P-343-
dc.identifier.issn1527-6465-
dc.identifier.urihttp://hdl.handle.net/10722/204489-
dc.descriptionPoster Session 2: P-343-
dc.descriptionThis journal suppl. entitled: The ILTS 20th Annual International Congress-
dc.description.abstractBACKGROUND & AIM: Liver transplantation dramatically improved the survival rate of HCC patients. However, tumor recurrence remains a huge threat without any promising curative treatment. We aim to clarify the mechanism of graft injury regulating chemoresistance after liver transplantation. MATERIALS AND METHODS: A rat orthotopic liver transplantation model with liver cancer development was established with applying whole or small-for-size (50%) graft. The expressions of multidrug resistant genes and RAP1 were compared between small and whole graft groups. RAP1 expression was also validated in clinical samples. The role of RAP1 was further explored in vitro and vivo. RESULTS: The expression of RAP1 was constantly higher in liver and tumor in small-for-size group in rat liver transplantation model. (see diagrams) CONCLUSIONS: Overexpression of intragraft RAP1, which upregulated by acute phase liver graft injury, may induce late phase cisplatin resistance after liver transplantation.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021-
dc.relation.ispartofLiver Transplantation-
dc.rightsLiver Transplantation. Copyright © John Wiley & Sons, Inc.-
dc.subjectMedical sciences-
dc.subjectGastroenterology medical sciences-
dc.subjectSurgery-
dc.titleThe role of RAP1 in graft injury induced cisplatin resistance after liver transplantation-
dc.typeConference_Paper-
dc.identifier.emailGeng, W: weigeng@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailQi, X: qixiang515@connect.hku.hk-
dc.identifier.emailLi, C: doclicx@hku.hk-
dc.identifier.emailNg, KTP: ledodes@hku.hk-
dc.identifier.emailLiu, X: liuxb301@hku.hk-
dc.identifier.emailMa, YY: yyma@hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityNg, KTP=rp01720-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.doi10.1002/lt.23901-
dc.identifier.hkuros237555-
dc.identifier.volume20-
dc.identifier.issuesuppl. S1-
dc.identifier.spageS257, abstract P-343-
dc.identifier.epageS257, abstract P-343-
dc.publisher.placeUnited States-

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