{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T13:35:33Z","timestamp":1791466533729,"version":"4.3.4"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,11,8]],"date-time":"2023-11-08T00:00:00Z","timestamp":1699401600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["acsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2024,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Marginal zone lymphomas (MZLs) comprise a diverse group of indolent lymphoproliferative disorders; however, some patients develop histologic transformation (HT) with rapid progression to aggressive lymphoma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Forty\u2010three MZLs with HT (HT\u2010MZLs), 535 MZLs, and 174 de novo diffuse large B\u2010cell lymphomas (DLBCLs) without rearrangements of <jats:italic>MYC<\/jats:italic>, <jats:italic>BCL2<\/jats:italic>, and <jats:italic>BCL6<\/jats:italic> were collected. Among these, 22 HT\u2010MZLs, 39 MZLs, and 174 DLBCLs were subjected to 148\u2010gene targeted exome sequencing. The clinicopathologic features of patients who had HT\u2010MZL and their genetic alterations were compared with those of patients who had MZLs and DLBCLs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>All 43 HT\u2010MZLs corresponded to DLBCLs. No HT\u2010MZLs harbored <jats:italic>BCL2<\/jats:italic> and <jats:italic>MYC<\/jats:italic> and\/or <jats:italic>BCL6<\/jats:italic> rearrangements. Bone marrow involvement and higher levels of lactate dehydrogenase were significantly more common in HT\u2010MZLs than in MZLs. Furthermore, upregulated BCL6, MUM1, C\u2010MYC, and Ki\u201067 expression was observed more frequently in HT\u2010MZLs than in MZLs. <jats:italic>TBL1XR1<\/jats:italic> was the most frequently altered gene (63.6%) in HT\u2010MZLs, followed by <jats:italic>CCND3<\/jats:italic> (31.8%), <jats:italic>CARD11<\/jats:italic>, <jats:italic>ID3<\/jats:italic>, and <jats:italic>TP53<\/jats:italic> (22.7%). A trend toward worse progression\u2010free survival in patients with <jats:italic>TBL1XR1<\/jats:italic> mutations was observed. Compared with MZLs and non\u2013germinal center B\u2010cell (GCB) type DLBCLs, significantly higher frequencies of <jats:italic>TBL1XR1<\/jats:italic> and <jats:italic>ID3<\/jats:italic> mutations were identified in HT\u2010MZLs. <jats:italic>PIM1<\/jats:italic> mutations frequently occurred in DLBCLs and were significantly associated with <jats:italic>TBL1XR1<\/jats:italic> mutations but were mutated less in HT\u2010MZLs that had <jats:italic>TBL1XR1<\/jats:italic> mutations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The current findings reveal the clinicopathologic and genetic features of HT\u2010MZLs, suggesting that these tumors might constitute a group distinct from MZL and de novo non\u2013GCB type DLBCL. <jats:italic>TBL1XR1<\/jats:italic> mutations may be considered a predictor of HT in 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