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Article: High BCL6 expression predicts better prognosis, independent of BCL6 translocation status, translocation partner, or BCL6-deregulating mutations, in gastric lymphoma

TitleHigh BCL6 expression predicts better prognosis, independent of BCL6 translocation status, translocation partner, or BCL6-deregulating mutations, in gastric lymphoma
Authors
Issue Date2006
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2006, v. 108 n. 7, p. 2373-2383 How to Cite?
AbstractTo investigate the role of BCL6 in the pathogenesis of gastric lymphoma, we analyzed the BCL6 promoter region for BCL6 translocations, somatic hypermutations, and deregulating mutations in 43 gastric lymphomas, including 4 extranodal marginal-zone B-cell lymphomas of mucosa-associated lymphoid tissues (MALT lymphomas), 33 diffuse large B-cell lymphomas (DLBCLs), and 6 composite DLBCLs with residual MALT lymphoma (DLCLMLs). BCL6 promoter substitutions by immunoglobulin (Ig) and non-Ig translocation partners, resulting in its deregulation, were frequently involved in DLBCL (36.4%) and DLCLML (50%). Two novel BCL6 translocation partner genes, 28S rRNA and DMRT1, and a new BCL6 translocation breakpoint in intron 2 were also identified. Deregulating mutations were found only in DLBCL (24.2%), which correlated significantly with high BCL6 protein expression. Significantly, high BCL6 expression correlated strongly with longer overall survival (OS), independent of mechanism in gastric DLBCL and DLCLML. Gastric DLBCLs were further subclassified into germinal center B-cell-like (GCB) and non-GCB subgroups immunohistochemically. High BCL6 expression was detected in all GCB cases, irrespective of BCL6 genetic alterations. In the non-GCB subgroup, BCL6-deregulating mutations correlated significantly with high BCL6 expression level. No significant correlation was found between the BCL6 expression level and OS in the non-GCB subgroup, which had significantly poorer prognosis than the GCB subgroup. © 2006 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/148480
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, YWen_HK
dc.contributor.authorHu, XTen_HK
dc.contributor.authorLiang, ACen_HK
dc.contributor.authorAu, WYen_HK
dc.contributor.authorSo, CCen_HK
dc.contributor.authorWong, MLen_HK
dc.contributor.authorShen, Len_HK
dc.contributor.authorTao, Qen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorKwong, YLen_HK
dc.contributor.authorLiang, RHen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.date.accessioned2012-05-29T06:13:12Z-
dc.date.available2012-05-29T06:13:12Z-
dc.date.issued2006en_HK
dc.identifier.citationBlood, 2006, v. 108 n. 7, p. 2373-2383en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148480-
dc.description.abstractTo investigate the role of BCL6 in the pathogenesis of gastric lymphoma, we analyzed the BCL6 promoter region for BCL6 translocations, somatic hypermutations, and deregulating mutations in 43 gastric lymphomas, including 4 extranodal marginal-zone B-cell lymphomas of mucosa-associated lymphoid tissues (MALT lymphomas), 33 diffuse large B-cell lymphomas (DLBCLs), and 6 composite DLBCLs with residual MALT lymphoma (DLCLMLs). BCL6 promoter substitutions by immunoglobulin (Ig) and non-Ig translocation partners, resulting in its deregulation, were frequently involved in DLBCL (36.4%) and DLCLML (50%). Two novel BCL6 translocation partner genes, 28S rRNA and DMRT1, and a new BCL6 translocation breakpoint in intron 2 were also identified. Deregulating mutations were found only in DLBCL (24.2%), which correlated significantly with high BCL6 protein expression. Significantly, high BCL6 expression correlated strongly with longer overall survival (OS), independent of mechanism in gastric DLBCL and DLCLML. Gastric DLBCLs were further subclassified into germinal center B-cell-like (GCB) and non-GCB subgroups immunohistochemically. High BCL6 expression was detected in all GCB cases, irrespective of BCL6 genetic alterations. In the non-GCB subgroup, BCL6-deregulating mutations correlated significantly with high BCL6 expression level. No significant correlation was found between the BCL6 expression level and OS in the non-GCB subgroup, which had significantly poorer prognosis than the GCB subgroup. © 2006 by The American Society of Hematology.en_HK
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.subject.meshBase Sequenceen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshDna-Binding Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulins - Chemistryen_US
dc.subject.meshLymphoma - Geneticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMutationen_US
dc.subject.meshPrognosisen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProtein Transporten_US
dc.subject.meshSequence Homology, Nucleic Aciden_US
dc.subject.meshStomach Neoplasms - Geneticsen_US
dc.titleHigh BCL6 expression predicts better prognosis, independent of BCL6 translocation status, translocation partner, or BCL6-deregulating mutations, in gastric lymphomaen_HK
dc.typeArticleen_HK
dc.identifier.emailSo, CC:scc@pathology.hku.hken_HK
dc.identifier.emailChu, KM:chukm@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.emailLiang, RH:rliang@hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.authoritySo, CC=rp00391en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.identifier.authorityLiang, RH=rp00345en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1182/blood-2006-05-022517en_HK
dc.identifier.pmid16772602-
dc.identifier.scopuseid_2-s2.0-33749349935en_HK
dc.identifier.hkuros125542-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749349935&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume108en_HK
dc.identifier.issue7en_HK
dc.identifier.spage2373en_HK
dc.identifier.epage2383en_HK
dc.identifier.eissn1528-0020-
dc.identifier.isiWOS:000240848700040-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, YW=7601441119en_HK
dc.identifier.scopusauthoridHu, XT=14824949100en_HK
dc.identifier.scopusauthoridLiang, AC=14825292900en_HK
dc.identifier.scopusauthoridAu, WY=7202383089en_HK
dc.identifier.scopusauthoridSo, CC=7102919978en_HK
dc.identifier.scopusauthoridWong, ML=37021112700en_HK
dc.identifier.scopusauthoridShen, L=7401704659en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.scopusauthoridLiang, RH=26643224900en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK

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