1. 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.
- Author
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García, Rolando, Timmons, Charles, Luu, Hung, Miller, Valerie, Fuda, Franklin, Chen, Weina, and Koduru, Prasad
- Subjects
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HODGKIN'S disease , *B cells , *MANTLE cell lymphoma , *FLUORESCENCE in situ hybridization , *CELL cycle , *CHROMOSOME analysis - Abstract
• First case of a cHL with t(11;14) identified by chromosome and FISH analysis with sustained CCND1 expression. • Mantle cell lymphoma and cHL are closely related sharing a common post germinal precursor with t(11;14)+. • Early acquisition of genetic lesions, such as loss of 9q, suggests the potential to develop a cHL phenotype with deregulated cell cycle and signaling pathways. 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. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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