Please use this identifier to cite or link to this item: https://doi.org/10.1158/1078-0432.CCR-08-2979
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dc.titleExpression of EBV latent antigens, mammalian target of rapamycin, and tumor suppression genes in EBV-positive smooth muscle tumors: Clinical and therapeutic implications
dc.contributor.authorOng, K.W.
dc.contributor.authorTeo, M.
dc.contributor.authorLee, V.
dc.contributor.authorOng, D.
dc.contributor.authorLee, A.
dc.contributor.authorChieh, S.T.
dc.contributor.authorVathsala, A.
dc.contributor.authorToh, H.C.
dc.date.accessioned2016-11-09T07:14:00Z
dc.date.available2016-11-09T07:14:00Z
dc.date.issued2009-09-01
dc.identifier.citationOng, K.W., Teo, M., Lee, V., Ong, D., Lee, A., Chieh, S.T., Vathsala, A., Toh, H.C. (2009-09-01). Expression of EBV latent antigens, mammalian target of rapamycin, and tumor suppression genes in EBV-positive smooth muscle tumors: Clinical and therapeutic implications. Clinical Cancer Research 15 (17) : 5350-5358. ScholarBank@NUS Repository. https://doi.org/10.1158/1078-0432.CCR-08-2979
dc.identifier.issn10780432
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/129984
dc.description.abstractPurpose: EBV-positive smooth muscle tumor (EBV+SMT) is a rare disease with no established therapy. We describe the largest single institution analysis in renal transplant recipients. It aims to define its clinical features and determine the expression of EBV latent genes as well as key molecular pathways. Experimental Design: Patients with EBV+SMT were identified from the Singapore General Hospital Renal Transplant Registry database. These tumors were investigated for expression of EBV latent genes with Southern blots, EBV latent antigens, mammalian target of rapamycin (mTOR), Akt, p70 S6 kinase, and vascular endothelial growth factor using immunohistochemistry, as well as methylation status of cancer-related genes using methylation-specific PCR. Results: Eight were found to be EBV+SMT in 1,123 transplant patients. All displayed indolent clinical courses and were unresponsive to immunosuppression reduction. Complete tumor regression was seen in one patient following administration of sirolimus. These tumors display the full range of known EBV latent genes. Immunohistochemistry with total and phosphorylated mTOR and Akt were positive for all patients, and vascular endothelial growth factor was positive in 25% of patients, suggesting activation of the mTOR/Akt pathway. Methylation of RASSF1A was found in all tissue samples, whereas promoter hypermethylation of RARβ, GSTP1, DAPK, and p14 was observed in some samples. Conclusions: Our results suggest that these tumors display a EBV type III latency pattern. The mTOR pathway is also activated. EBV may play a role in silencing RASSF1A. EBV-specific immunotherapy, mTOR inhibitors, and demethylating agents are possible therapeutic options in this disease. © 2009 American Association for Cancer Research.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1158/1078-0432.CCR-08-2979
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentPATHOLOGY
dc.contributor.departmentMEDICINE
dc.contributor.departmentDUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE
dc.description.doi10.1158/1078-0432.CCR-08-2979
dc.description.sourcetitleClinical Cancer Research
dc.description.volume15
dc.description.issue17
dc.description.page5350-5358
dc.description.codenCCREF
dc.identifier.isiut000269565800009
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