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Article: Clonal Epstein-Barr virus genome in T-cell-rich lymphomas of B or probable B lineage

TitleClonal Epstein-Barr virus genome in T-cell-rich lymphomas of B or probable B lineage
Authors
Issue Date1992
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 1992, v. 140 n. 4, p. 981-989 How to Cite?
AbstractSeventeen nodal lymphomas (originally diagnosed as T-cell lymphomas based on histological features and immunohistochemical staining results) were studied for the presence of Epstein-Barr virus (EBV) genome, and the results correlated with immunoglobulin and T-cell receptor gene rearrangement analyses performed on the same tissue samples. All four EBV positive cases had clonal rearrangement of the joining region of the immunoglobulin heavy chain (IgJ(H)) gene without clonal T-cell receptor beta-chain (TCRβ) gene rearrangement. Of these, two cases also showed clonally rearranged light chain gene, and they were reclassified as T-cell rich B-cell lymphomas (TRBL). The other two cases lacked clonal κ or λ light chain rearrangement and they were reclassified as T-cell rich lymphomas of probable B lineage, based on their isolated IgJ(H) clonal rearrangement. These B-cell lymphomas may be easily misdiagnosed as T-cell lymphomas owing to the presence of an abundant reactive T-cell infiltrate masking the tumor population. The florid T-cell reaction may represent an unusual host response towards a clonal proliferation of EBV bearing B cells.
Persistent Identifierhttp://hdl.handle.net/10722/147917
ISSN
2021 Impact Factor: 5.770
2020 SCImago Journal Rankings: 1.589
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShee Loong Lokeen_HK
dc.contributor.authorHo, Fen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorKin Hang Fuen_HK
dc.contributor.authorLeung, Ben_HK
dc.contributor.authorLiang, Ren_HK
dc.date.accessioned2012-05-29T06:09:53Z-
dc.date.available2012-05-29T06:09:53Z-
dc.date.issued1992en_HK
dc.identifier.citationAmerican Journal Of Pathology, 1992, v. 140 n. 4, p. 981-989en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147917-
dc.description.abstractSeventeen nodal lymphomas (originally diagnosed as T-cell lymphomas based on histological features and immunohistochemical staining results) were studied for the presence of Epstein-Barr virus (EBV) genome, and the results correlated with immunoglobulin and T-cell receptor gene rearrangement analyses performed on the same tissue samples. All four EBV positive cases had clonal rearrangement of the joining region of the immunoglobulin heavy chain (IgJ(H)) gene without clonal T-cell receptor beta-chain (TCRβ) gene rearrangement. Of these, two cases also showed clonally rearranged light chain gene, and they were reclassified as T-cell rich B-cell lymphomas (TRBL). The other two cases lacked clonal κ or λ light chain rearrangement and they were reclassified as T-cell rich lymphomas of probable B lineage, based on their isolated IgJ(H) clonal rearrangement. These B-cell lymphomas may be easily misdiagnosed as T-cell lymphomas owing to the presence of an abundant reactive T-cell infiltrate masking the tumor population. The florid T-cell reaction may represent an unusual host response towards a clonal proliferation of EBV bearing B cells.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.subject.meshBlotting, Southernen_US
dc.subject.meshGene Rearrangementen_US
dc.subject.meshGenome, Viralen_US
dc.subject.meshHerpesvirus 4, Human - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshLymphoma, B-Cell - Genetics - Pathologyen_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshT-Lymphocytes - Pathologyen_US
dc.titleClonal Epstein-Barr virus genome in T-cell-rich lymphomas of B or probable B lineageen_HK
dc.typeArticleen_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1314029-
dc.identifier.scopuseid_2-s2.0-0026591488en_HK
dc.identifier.volume140en_HK
dc.identifier.issue4en_HK
dc.identifier.spage981en_HK
dc.identifier.epage989en_HK
dc.identifier.isiWOS:A1992HM48100025-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShee Loong Loke=7409715182en_HK
dc.identifier.scopusauthoridHo, F=7103408147en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridKin Hang Fu=7409594343en_HK
dc.identifier.scopusauthoridLeung, B=7102271395en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.issnl0002-9440-

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