A t(11;14)(q13;q32)/CCND1::IGH carrying progenitor germinal B-cell with subsequent cytogenetic aberrations contributes to the development of classic Hodgkin lymphoma

Classic Hodgkin lymphoma (cHL) is characterized by the presence of Hodgkin Reed-Sternberg (HRS) cells. Although HRS cells express PAX5, cHL frequently lacks other B-cell markers. There is now evidence that HRS cells are monoclonal and are derived from germinal center B-cells. In terms of genetic aberrations, cHL frequently exhibit activated NF-kB signaling pathway. In this study, we present a case of cHL har-boring a t(11;14) (q13;q32)/CCND1::IGH, identified by chromosome and fluorescence in situ hybridization analysis and with CCND1 expression in HRS cells. We also analyzed recurrent cytogenetic aberrations in t(11;14) positive mantle cell lymphoma (MCL) and those found in cHL from the literature to assess genetic overlap, clonal evolution, and to identify potential signaling pathways in cHL with CCND1::IGH. This analysis suggests the development of t(11;14) + cHL and MCL from a transformed precursor cell with t(11;14) through genetic evolution and consequent deregulated pathways, including the NF -KB and NOTCH1 signaling. Published by Elsevier Inc.

Automated summary

Classic Hodgkin lymphoma (cHL) is characterized by the presence of Hodgkin Reed-Sternberg (HRS) cells. This study identified a genetic aberration (t(11;14)/CCND1::IGH) in cHL and analyzed its potential signaling pathways. The findings suggest the development of cHL and mantle cell lymphoma (MCL) from a transformed precursor cell through genetic evolution and deregulated pathways.