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

Cancer Genet. 2022 Nov;268-269:97-102. doi: 10.1016/j.cancergen.2022.09.009. Epub 2022 Oct 13.

Abstract

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 harboring 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-κB and NOTCH1 signaling.

Keywords: Classic Hodgkin lymphoma; Mantle cell lymphoma; Shared pathways.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Chromosome Aberrations
  • Cyclin D1 / genetics
  • Hodgkin Disease* / genetics
  • Humans
  • In Situ Hybridization, Fluorescence
  • Lymphoma, Mantle-Cell* / genetics
  • Lymphoma, Mantle-Cell* / pathology
  • Translocation, Genetic / genetics

Substances

  • CCND1 protein, human
  • Cyclin D1