File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Up-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesis

TitleUp-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesis
Authors
KeywordsFas
FasL
Oral
Premalignant lesions
Squamous cell carcinoma
Issue Date1999
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/oraloncology
Citation
Oral Oncology, 1999, v. 35 n. 6, p. 548-553 How to Cite?
AbstractAn important molecule involved in delivering the death signal that initiates apoptosis is called Fas, or Apo-1, which sits on the cell surface. When another molecule called the Fas ligand (FasL) binds to it, Fas triggers a series of events inside the cell that leads to apoptosis. In order to investigate the mechanism of immune escape and the expression of Fas and FasL in oral premalignant lesions (OPLs) and oral squamous cell carcinomas (OSCCs), a total of 64 samples were evaluated by an immunohistochemical method using a labelled streptavidin-biotin assay. These samples comprised nine hyperkeratotic and 24 oral premalignant lesions (nine of mild, moderate, and six of severe dysplastic lesions), and 24 OSCCs, together with seven healthy controls. The results demonstrated that the majority of invasive OSCCs showed down-regulation of Fas expression but up-regulation of FasL expression. These phenomena were also detected in OPLs. The results indicate that the expression of Fas and FasL is involved in oral carcinogenesis and this may be a mechanism by which the cancer cells evade the host immune assault. Perhaps, in future, Fas/FasL system may be used as a prognostic biomarker in predicting the behavior of oral premalignant lesions.
Persistent Identifierhttp://hdl.handle.net/10722/66443
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.257
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Qen_HK
dc.contributor.authorSamaranayake, LPen_HK
dc.contributor.authorZhen, Xen_HK
dc.contributor.authorLuo, Gen_HK
dc.contributor.authorNie, Men_HK
dc.contributor.authorLi, Ben_HK
dc.date.accessioned2010-09-06T05:46:24Z-
dc.date.available2010-09-06T05:46:24Z-
dc.date.issued1999en_HK
dc.identifier.citationOral Oncology, 1999, v. 35 n. 6, p. 548-553en_HK
dc.identifier.issn1368-8375en_HK
dc.identifier.urihttp://hdl.handle.net/10722/66443-
dc.description.abstractAn important molecule involved in delivering the death signal that initiates apoptosis is called Fas, or Apo-1, which sits on the cell surface. When another molecule called the Fas ligand (FasL) binds to it, Fas triggers a series of events inside the cell that leads to apoptosis. In order to investigate the mechanism of immune escape and the expression of Fas and FasL in oral premalignant lesions (OPLs) and oral squamous cell carcinomas (OSCCs), a total of 64 samples were evaluated by an immunohistochemical method using a labelled streptavidin-biotin assay. These samples comprised nine hyperkeratotic and 24 oral premalignant lesions (nine of mild, moderate, and six of severe dysplastic lesions), and 24 OSCCs, together with seven healthy controls. The results demonstrated that the majority of invasive OSCCs showed down-regulation of Fas expression but up-regulation of FasL expression. These phenomena were also detected in OPLs. The results indicate that the expression of Fas and FasL is involved in oral carcinogenesis and this may be a mechanism by which the cancer cells evade the host immune assault. Perhaps, in future, Fas/FasL system may be used as a prognostic biomarker in predicting the behavior of oral premalignant lesions.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/oraloncologyen_HK
dc.relation.ispartofOral Oncologyen_HK
dc.subjectFas-
dc.subjectFasL-
dc.subjectOral-
dc.subjectPremalignant lesions-
dc.subjectSquamous cell carcinoma-
dc.subject.meshAntigens, CD95 - metabolismen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCarcinoma, Squamous Cell - metabolismen_HK
dc.subject.meshChinaen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshFas Ligand Proteinen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMembrane Glycoproteins - metabolismen_HK
dc.subject.meshMouth Neoplasms - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleUp-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1368-8375&volume=35&spage=548&epage=553&date=1999&atitle=Up-regulation+of+Fas+ligand+and+down-regulation+of+Fas+expression+in+oral+carcinogenesisen_HK
dc.identifier.emailSamaranayake, LP:lakshman@hku.hken_HK
dc.identifier.authoritySamaranayake, LP=rp00023en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S1368-8375(99)00029-9en_HK
dc.identifier.pmid10705088-
dc.identifier.scopuseid_2-s2.0-0032705132en_HK
dc.identifier.hkuros47500en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032705132&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue6en_HK
dc.identifier.spage548en_HK
dc.identifier.epage553en_HK
dc.identifier.isiWOS:000083287100003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChen, Q=16244214800en_HK
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_HK
dc.identifier.scopusauthoridZhen, X=7004818243en_HK
dc.identifier.scopusauthoridLuo, G=55112399500en_HK
dc.identifier.scopusauthoridNie, M=11540273000en_HK
dc.identifier.scopusauthoridLi, B=16202895000en_HK
dc.identifier.issnl1368-8375-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats