![]() The distinction between germinal center B-cell (GCB) and non-GCB type, on the basis of gene expression profiling, was available for 108 de novo DLBCL samples as previously published. 1 All RS cases represented DLBCL transformed from a typical CLL. Diagnoses were made following the recommended criteria. RS and DLBCL samples were collected from nodal or extranodal biopsies. CLL-phase and CLL-U samples were collected from peripheral blood at diagnosis. The CLL phase preceding RS had not a generalized increase in genomic complexity compared with untransformed CLL, but it presented clear differences in the frequency of specific genetic lesions.Īll clinical specimens were derived from pathological sites and obtained in the course of routine diagnostic procedures, before the initiation of therapy. Although RS shared some of the lesions seen in de novo DLBCL, its genomic profile was clearly separate. A second major subgroup was characterized by the presence of trisomy 12 and comprised one third of the cases. Cell-cycle deregulation via inactivation of TP53 and of CDKN2A was a main mechanism in the histologic transformation from CLL phase, being present in approximately one half of the cases, and affected the outcome of the RS patients. RS demonstrated a genomic complexity intermediate between CLL and DLBCL. ![]() To better understand the pathogenesis of RS, we analyzed a series of cases including 59 RS, 28 CLL phase of RS, 315 CLL, and 127 de novo DLBCL. Although RS, usually represented by the histologic transformation to a diffuse large B-cell lymphoma (DLBCL), is associated with a very poor outcome, especially when clonally related to the preexisting CLL, the mechanisms leading to RS have not been clarified. Richter syndrome (RS) occurs in up to 15% of patients with chronic lymphocytic leukemia (CLL). ![]()
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