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Conference Paper: Imbalanced expression of α and β isoforms of PRDM1 contributes to the pathogenesis of nasal type NK/T-cell lymphoma

TitleImbalanced expression of α and β isoforms of PRDM1 contributes to the pathogenesis of nasal type NK/T-cell lymphoma
Authors
Issue Date2016
Publisher.
Citation
The 105th Annual Meeting of the Japanese Society of Pathology, Sendai, Miyagi, Japan, 12-14 May 2016. How to Cite?
AbstractOne of the main characteristics of nasal NK/T-cell lymphoma (NKTCL) is frequent deletions on chromosome 6q. PRDM1 is a tumour suppressor gene located in 6q21, and its protein exists as two isoforms (α and β), generated from the same locus via alternative transcription initiation sites. PRDM1α isoform was previously shown to have tumor suppressive effects in NKTCL. As PRDM1β lacks a positive regulatory (PR) domain but maintains normal DNA-binding activity, it was proposed as a negative regulator of PRDM1α, though its role in the pathogenesis of NKTCL has not been elucidated. Our study showed that upregulation of PRDM1β via tumor-specific promoter hypomethylation counteracted the tumor suppressive effects of PRDM1α. In addition, NKTCL patients (n=17) showing both PRDM1α promoter hyperemethylation and PRDM1β promoter hypomethylation had inferior overall survival (p=0.046) compared to patients with PRDM1α promoter hypermethylation alone, when treated with the SMILE regimen. In conclusion, the imbalanced expression of the α and β isoforms of PRDM1 contributes to the pathogenesis of NKTCL and influences prognosis of these patients.
DescriptionConference Theme: World’s local pathology meeting: back to the principle of pathology through the case analysis
Persistent Identifierhttp://hdl.handle.net/10722/235034

 

DC FieldValueLanguage
dc.contributor.authorAu Yeung, KHR-
dc.contributor.authorGuo, T-
dc.contributor.authorChen, WYW-
dc.contributor.authorWong, KY-
dc.contributor.authorWong, MLY-
dc.contributor.authorChan, YP-
dc.contributor.authorShimizu, N-
dc.contributor.authorLoong, F-
dc.contributor.authorTse, EWC-
dc.contributor.authorKwong, YL-
dc.contributor.authorSrivastava, G-
dc.date.accessioned2016-10-14T13:50:51Z-
dc.date.available2016-10-14T13:50:51Z-
dc.date.issued2016-
dc.identifier.citationThe 105th Annual Meeting of the Japanese Society of Pathology, Sendai, Miyagi, Japan, 12-14 May 2016.-
dc.identifier.urihttp://hdl.handle.net/10722/235034-
dc.descriptionConference Theme: World’s local pathology meeting: back to the principle of pathology through the case analysis-
dc.description.abstractOne of the main characteristics of nasal NK/T-cell lymphoma (NKTCL) is frequent deletions on chromosome 6q. PRDM1 is a tumour suppressor gene located in 6q21, and its protein exists as two isoforms (α and β), generated from the same locus via alternative transcription initiation sites. PRDM1α isoform was previously shown to have tumor suppressive effects in NKTCL. As PRDM1β lacks a positive regulatory (PR) domain but maintains normal DNA-binding activity, it was proposed as a negative regulator of PRDM1α, though its role in the pathogenesis of NKTCL has not been elucidated. Our study showed that upregulation of PRDM1β via tumor-specific promoter hypomethylation counteracted the tumor suppressive effects of PRDM1α. In addition, NKTCL patients (n=17) showing both PRDM1α promoter hyperemethylation and PRDM1β promoter hypomethylation had inferior overall survival (p=0.046) compared to patients with PRDM1α promoter hypermethylation alone, when treated with the SMILE regimen. In conclusion, the imbalanced expression of the α and β isoforms of PRDM1 contributes to the pathogenesis of NKTCL and influences prognosis of these patients.-
dc.languageeng-
dc.publisher.-
dc.relation.ispartof105th Annual Meeting of the Japanese Society of Pathology-
dc.relation.ispartof第105回日本病理学会総会-
dc.titleImbalanced expression of α and β isoforms of PRDM1 contributes to the pathogenesis of nasal type NK/T-cell lymphoma-
dc.typeConference_Paper-
dc.identifier.emailAu Yeung, KHR: rex.auyeung@hku.hk-
dc.identifier.emailChen, WYW: wywchen@hkucc.hku.hk-
dc.identifier.emailWong, KY: kywonga@hkucc.hku.hk-
dc.identifier.emailWong, MLY: mlywong@hkucc.hku.hk-
dc.identifier.emailChan, YP: bchanyp@hkucc.hku.hk-
dc.identifier.emailLoong, F: floong@hkucc.hku.hk-
dc.identifier.emailTse, EWC: ewctse@hku.hk-
dc.identifier.emailKwong, YL: ylkwong@hkucc.hku.hk-
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hk-
dc.identifier.authorityAu Yeung, KHR=rp01877-
dc.identifier.authorityTse, EWC=rp00471-
dc.identifier.authorityKwong, YL=rp00358-
dc.identifier.authoritySrivastava, G=rp00365-
dc.identifier.hkuros269252-
dc.identifier.volume.-
dc.identifier.spage.-
dc.identifier.epage.-
dc.publisher.place.-

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