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Conference Paper: Regulation of epithelial mesenchymal transition (EMT) by Serum Amyloid A 1 (SAA1) is dependent on integrin in esophageal squamous cell carcinoma (ESCC)

TitleRegulation of epithelial mesenchymal transition (EMT) by Serum Amyloid A 1 (SAA1) is dependent on integrin in esophageal squamous cell carcinoma (ESCC)
Authors
Issue Date2014
PublisherMetastasis Research Society (MRS). The Abstracts Book's web site is located at http://www.umm.uni-heidelberg.de/inst/cbtm/mbio/mrs/download/MRS_2014_Abstractbook.pdf
Citation
The 15th International Biennial Congress of the Metastasis Research Society (MRS 2014), Heidelberg, Germany, 28 June-1 July 2014. In Abstracts Book, 2014, p. 182, abstract no. B5 How to Cite?
AbstractEsophageal Squamous Cell Carcinoma (ESCC) is the predominant type comprising more than 90% of esophageal cancer, which is a highly metastatic and fatal cancer, and is ranked the eighth in mortality rate in Hong Kong cancer patients (Hong Kong Cancer Registry, Hospital Authority, 2010). Using a functional complementation approach, SAA1 was identified as one of the tumor suppressor gene candidates. The SAA1 is an acute phase protein, which is highly expressed in response to inflammation by the liver. It is also present as a secretary protein in histologically normal human epithelial tissues. The expression of SAA1 was found to be down-regulated in ESCC. Interestingly, the gene expression of SAA1 and the mesenchymal marker N-cadherin was found to be inversely correlated in a panel of ESCC and the immortalized esophageal epithelial cell lines. Therefore, we want to determine whether SAA1 could regulate EMT in ESCC ...
DescriptionPoster abstract: no. B5
Persistent Identifierhttp://hdl.handle.net/10722/198641

 

DC FieldValueLanguage
dc.contributor.authorMan, OYen_US
dc.contributor.authorLung, MLen_US
dc.contributor.authorLung, HLen_US
dc.date.accessioned2014-07-07T08:26:49Z-
dc.date.available2014-07-07T08:26:49Z-
dc.date.issued2014en_US
dc.identifier.citationThe 15th International Biennial Congress of the Metastasis Research Society (MRS 2014), Heidelberg, Germany, 28 June-1 July 2014. In Abstracts Book, 2014, p. 182, abstract no. B5en_US
dc.identifier.urihttp://hdl.handle.net/10722/198641-
dc.descriptionPoster abstract: no. B5-
dc.description.abstractEsophageal Squamous Cell Carcinoma (ESCC) is the predominant type comprising more than 90% of esophageal cancer, which is a highly metastatic and fatal cancer, and is ranked the eighth in mortality rate in Hong Kong cancer patients (Hong Kong Cancer Registry, Hospital Authority, 2010). Using a functional complementation approach, SAA1 was identified as one of the tumor suppressor gene candidates. The SAA1 is an acute phase protein, which is highly expressed in response to inflammation by the liver. It is also present as a secretary protein in histologically normal human epithelial tissues. The expression of SAA1 was found to be down-regulated in ESCC. Interestingly, the gene expression of SAA1 and the mesenchymal marker N-cadherin was found to be inversely correlated in a panel of ESCC and the immortalized esophageal epithelial cell lines. Therefore, we want to determine whether SAA1 could regulate EMT in ESCC ...-
dc.languageengen_US
dc.publisherMetastasis Research Society (MRS). The Abstracts Book's web site is located at http://www.umm.uni-heidelberg.de/inst/cbtm/mbio/mrs/download/MRS_2014_Abstractbook.pdf-
dc.relation.ispartofInternational Biennial Congress of the Metastasis Research Society, MRS 2014en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleRegulation of epithelial mesenchymal transition (EMT) by Serum Amyloid A 1 (SAA1) is dependent on integrin in esophageal squamous cell carcinoma (ESCC)en_US
dc.typeConference_Paperen_US
dc.identifier.emailLung, ML: mlilung@hku.hken_US
dc.identifier.emailLung, HL: hllung2@hku.hken_US
dc.identifier.authorityLung, ML=rp00300en_US
dc.identifier.authorityLung, HL=rp00299en_US
dc.description.naturepostprint-
dc.identifier.hkuros229930en_US
dc.identifier.spage182-
dc.identifier.epage182-
dc.publisher.placeGermany-

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