{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T19:13:30Z","timestamp":1781982810176,"version":"3.54.5"},"reference-count":64,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,5,6]],"date-time":"2008-05-06T00:00:00Z","timestamp":1210032000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hematological Oncology"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>B\u2010cell post\u2010transplant lymphoproliferative disorders (PTLD) are classified as early lesions, polymorphic lymphomas (P\u2010PTLD) and monomorphic lymphomas (M\u2010PTLD). These morphologic categories are thought to reflect a biologic continuum, although supporting genetic data are lacking. To gain better insights into PTLD pathogenesis, we characterized the phenotypes, immunoglobulin (Ig) gene alterations and non\u2010Ig gene (<jats:italic>BCL6<\/jats:italic>, <jats:italic>RhoH\/TTF<\/jats:italic>, <jats:italic>c\u2010MYC<\/jats:italic>, <jats:italic>PAX5<\/jats:italic>, <jats:italic>CIITA<\/jats:italic>, <jats:italic>BCL7A<\/jats:italic>, <jats:italic>PIM1<\/jats:italic>) mutations of 21 PTLD, including an IM\u2010like lesion, 8 P\u2010PTLD and 12 M\u2010PTLD. Gene expression profile analysis was also performed in 12 cases. All PTLD with clonal Ig rearrangements showed evidence of germinal centre (GC) transit based on the analysis of Ig and <jats:italic>BCL6<\/jats:italic> gene mutations, and 74% had a non\u2010GC phenotype (BCL6\u2009\u00b1\u2009MUM1+). Although surface Ig abnormalities were seen in 6\/19 (32%) PTLD, only three showed \u2018crippling\u2019 Ig mutations indicating other etiologies for loss of the B\u2010cell receptor. Aberrant somatic hypermutation (ASHM) was almost exclusively observed in M\u2010PTLD (8\/12 vs. 1\/8 P\u2010PTLD) and all three recurrent cases analysed showed additional mutations in genes targeted by ASHM. Gene expression analysis showed distinct clustering of PTLD compared to B\u2010cell non\u2010Hodgkin lymphomas (B\u2010NHL) without segregation of P\u2010PTLD from non\u2010GC M\u2010PTLD or EBV+ from EBV\u2212 PTLD. The gene expression pattern of PTLD appeared more related to that of memory and activated B\u2010cells. Together, our results suggest that PTLD represent a distinct type of B\u2010NHL deriving from an antigen experienced B\u2010cell, whose evolution is associated with accrual of genetic lesions. Copyright \u00a9 2008 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/hon.859","type":"journal-article","created":{"date-parts":[[2008,5,6]],"date-time":"2008-05-06T09:46:18Z","timestamp":1210067178000},"page":"199-211","source":"Crossref","is-referenced-by-count":86,"title":["Genetic and phenotypic analysis of B\u2010cell post\u2010transplant lymphoproliferative disorders provides insights into disease biology"],"prefix":"10.1002","volume":"26","author":[{"given":"Efsevia","family":"Vakiani","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katia","family":"Basso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulf","family":"Klein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahesh 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