Please use this identifier to cite or link to this item: https://doi.org/10.1158/1078-0432.CCR-08-2979
DC FieldValue
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, Kong Wee
dc.contributor.authorTeo, Marissa
dc.contributor.authorLee, Victor
dc.contributor.authorOng, Danny
dc.contributor.authorLee, Ann
dc.contributor.authorTan, Chieh Suai
dc.contributor.authorVathsala, A
dc.contributor.authorToh, Han Chong
dc.date.accessioned2022-07-29T07:03:26Z
dc.date.available2022-07-29T07:03:26Z
dc.date.issued2009-09-01
dc.identifier.citationOng, Kong Wee, Teo, Marissa, Lee, Victor, Ong, Danny, Lee, Ann, Tan, Chieh Suai, Vathsala, A, Toh, Han Chong (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.issn1078-0432
dc.identifier.issn1557-3265
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/229441
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.language.isoen
dc.publisherAMER ASSOC CANCER RESEARCH
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectOncology
dc.subjectEPSTEIN-BARR-VIRUS
dc.subjectOF-THE-LITERATURE
dc.subjectNASOPHARYNGEAL CARCINOMA
dc.subjectPROMOTER HYPERMETHYLATION
dc.subjectEPITHELIAL-CELLS
dc.subjectLYMPHOPROLIFERATIVE DISEASE
dc.subjectMYOGENIC TUMORS
dc.subjectBINDING PARTNER
dc.subjectMULTIPLE GENES
dc.subjectMTOR PATHWAY
dc.typeArticle
dc.date.updated2022-07-23T13:05:09Z
dc.contributor.departmentMEDICINE
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.placeUnited States
dc.published.statePublished
Appears in Collections:Staff Publications
Elements

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Expression of EBV Latent Antigens, mTOR_ClinicalCancerResearch2009.pdf644.46 kBAdobe PDF

CLOSED

None

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.