{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T23:06:44Z","timestamp":1792710404969,"version":"4.5.0"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T00:00:00Z","timestamp":1665532800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/ http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:p>Intravascular large B-cell lymphoma (IVLBCL) is an uncommon lymphoma with an aggressive clinical course characterized by selective growth of tumor cells within the vessels. Its pathogenesis is still uncertain and there is little information on the underlying genomic alterations. In this study, we performed a clinicopathologic and next-generation sequencing analysis of 15 cases of IVLBCL using a custom panel for the detection of alterations in 68 recurrently mutated genes in B-cell lymphomagenesis. Six patients had evidence of hemophagocytic syndrome. Four patients presented concomitantly a solid malignancy. Tumor cells outside the vessels were observed in 7 cases, 2 with an overt diffuse large B-cell cell lymphoma. In 4 samples, tumor cells infiltrated lymphatic vessel in addition to blood capillaries. Programmed death-ligand 1 (PD-L1) was positive in tumor cells in 4 of 11 evaluable samples and in macrophages intermingled with tumor cells in 8. <jats:italic toggle=\"yes\">PD-L1<\/jats:italic> copy number gains were identified in a higher proportion of cases expressing PD-L1 than in negative tumors. The most frequently mutated gene was <jats:italic toggle=\"yes\">PIM1<\/jats:italic> (9\/15, 60%), followed by <jats:italic toggle=\"yes\">MYD88<\/jats:italic>\n                           <jats:sup>L265P<\/jats:sup> and <jats:italic toggle=\"yes\">CD79B<\/jats:italic> (8\/15, 53% each). In 6 cases, <jats:italic toggle=\"yes\">MYD88<\/jats:italic>\n                           <jats:sup>L265P<\/jats:sup> and <jats:italic toggle=\"yes\">CD79B<\/jats:italic> mutations were detected concomitantly. We also identified recurrent mutations in <jats:italic toggle=\"yes\">IRF4<\/jats:italic>, <jats:italic toggle=\"yes\">TMEM30A<\/jats:italic>, <jats:italic toggle=\"yes\">BTG2<\/jats:italic>, and <jats:italic toggle=\"yes\">ETV6<\/jats:italic> loci (4\/15, 27% each) and novel driver mutations in <jats:italic toggle=\"yes\">NOTCH2<\/jats:italic>, <jats:italic toggle=\"yes\">CCND3<\/jats:italic>, and <jats:italic toggle=\"yes\">GNA13<\/jats:italic>, and an <jats:italic toggle=\"yes\">IRF4<\/jats:italic> translocation in 1 case each. The mutational profile was similar in patients with and without evidence of hemophagocytic syndrome and in cases with or without dissemination of tumor cells outside the vessels. Our results confirm the relevance of mutations in B-cell receptor\/nuclear factor-\u03baB signaling and immune escape pathways in IVLBCL and identify novel driver alterations. The similar mutational profile in tumors with extravascular dissemination suggests that these cases may also be considered in the spectrum of IVLBCL.<\/jats:p>","DOI":"10.1097\/pas.0000000000001978","type":"journal-article","created":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T06:00:28Z","timestamp":1665554428000},"page":"202-211","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":32,"title":["Intravascular Large B-Cell Lymphoma Genomic Profile Is Characterized by Alterations in Genes Regulating NF-\u03baB and Immune Checkpoints"],"prefix":"10.1097","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1796-7248","authenticated-orcid":false,"given":"Blanca","family":"Gonzalez-Farre","sequence":"first","affiliation":[{"name":"Pathology Department, Hospital Cl\u00ednic de Barcelona, University of Barcelona"},{"name":"Institut d\u2019Investigacions Biom\u00e8diques August Pi i Sunyer 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Madrid"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leticia","family":"Quintanilla-Martinez","sequence":"additional","affiliation":[{"name":"Institute of Pathology and Neuropathology and Comprehensive Cancer Center T\u00fcbingen, University Hospital T\u00fcbingen, Eberhard-Karls-University, T\u00fcbingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Armando","family":"Lopez-Guillermo","sequence":"additional","affiliation":[{"name":"Institut d\u2019Investigacions Biom\u00e8diques August Pi i Sunyer (IDIBAPS)"},{"name":"Hematology Department, Hospital Clinic de Barcelona, University of Barcelona, Barcelona"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de C\u00e1ncer (CIBERONC), Madrid"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Itziar","family":"Salaverria","sequence":"additional","affiliation":[{"name":"Institut d\u2019Investigacions Biom\u00e8diques August Pi i Sunyer (IDIBAPS)"},{"name":"Centro de 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