{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T10:48:14Z","timestamp":1784198894522,"version":"3.55.0"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T00:00:00Z","timestamp":1345593600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2012,10]]},"abstract":"Abstract<\/jats:title>Spindle\u2010shaped diffuse large B\u2010cell lymphoma (Sp\u2010DLBCL<\/jats:styled-content>) has been recognized as a rare morphologic variant of DLBCL<\/jats:styled-content>. However, the biological processes that contribute to the specific features of Sp\u2010DLBCL<\/jats:styled-content> remain poorly understood. In this study, a combined immunophenotypic and genetic analysis was performed in 10 Sp\u2010DLBCL<\/jats:styled-content>. First, we investigated several unique markers for anaplasia (CD<\/jats:styled-content>30, ALK<\/jats:styled-content>, CD<\/jats:styled-content>68, and EBER<\/jats:styled-content>\u2010ISH<\/jats:styled-content>), mesenchyma (SMA<\/jats:styled-content>, desmin, and vimentin), and B\u2010cell differentiation (CD<\/jats:styled-content>10, BCL<\/jats:styled-content>6<\/jats:italic>, and MUM<\/jats:styled-content>1). We also performed conventional cytogenetic and fluorescence in situ<\/jats:italic> hybridization studies to look for common chromosomal break points (BCL<\/jats:styled-content>2<\/jats:italic>, BCL<\/jats:styled-content>6<\/jats:italic>, and MYC<\/jats:styled-content><\/jats:italic>). We found that most Sp\u2010DLBCL<\/jats:styled-content>s were germinal center B cell\u2010like and that none had any other specific phenotypes or any karyotypic abnormalities. Instead, T cells, CD<\/jats:styled-content>68\u2010positive macrophages and SMA<\/jats:styled-content>\u2010positive myofibroblasts were significantly increased in Sp\u2010DLBCL<\/jats:styled-content> when compared with conventional GCB<\/jats:styled-content> origin DLBCL<\/jats:styled-content> cases (n<\/jats:italic>\u00a0=\u00a010) (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.012, P\u00a0<\/jats:italic><\u00a0<\/jats:italic>0.001, and P\u00a0<\/jats:italic><\u00a0<\/jats:italic>0.0001, respectively). To further characterize Sp\u2010DLBCL<\/jats:styled-content>, we next compared the expression of fibroblast growth factor 2 (FGF<\/jats:styled-content>2) and transforming growth factor\u2010\u03b21 (TGF<\/jats:styled-content>\u03b21) between the two types of DLBCL<\/jats:styled-content>. Finally, we confirmed that the number of FGF<\/jats:styled-content>2\u2010 and TGF<\/jats:styled-content>\u03b21\u2010positive stromal cells was markedly increased in Sp\u2010DLBCL<\/jats:styled-content> and that the difference between these and conventional GCB<\/jats:styled-content> origin DLBCL<\/jats:styled-content>s was significant (P\u00a0<\/jats:italic><\u00a0<\/jats:italic>0.0001 and P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0017, respectively). Thus, T\u2010cell\/myofibrohistio\u2010rich stromal alterations in Sp\u2010DLBCL<\/jats:styled-content>, especially those mediated by TGF<\/jats:styled-content>\u03b21 and FGF<\/jats:styled-content>2, may play a role in the transition of lymphoma cells into those with spindle\u2010shaped features.<\/jats:p>","DOI":"10.1111\/j.1600-0609.2012.01826.x","type":"journal-article","created":{"date-parts":[[2012,6,28]],"date-time":"2012-06-28T11:49:06Z","timestamp":1340884146000},"page":"302-310","source":"Crossref","is-referenced-by-count":15,"title":["A spindle cell variant of diffuse large B\u2010cell lymphoma is characterized by T\u2010cell\/myofibrohistio\u2010rich stromal alterations: analysis of 10 cases and a review of the literature"],"prefix":"10.1111","volume":"89","author":[{"given":"Yoshizo","family":"Kimura","sequence":"first","affiliation":[{"name":"Department of Pathology School of Medicine Kurume University Kurume Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumiko","family":"Arakawa","sequence":"additional","affiliation":[{"name":"Department of Pathology School of Medicine Kurume University Kurume Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junichi","family":"Kiyasu","sequence":"additional","affiliation":[{"name":"Department of Pathology School of Medicine Kurume University Kurume Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroaki","family":"Miyoshi","sequence":"additional","affiliation":[{"name":"Department of Pathology School of Medicine Kurume University Kurume Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maki","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Department of Pathology School of Medicine Kurume University Kurume 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