## Abstract Classical Hodgkin lymphoma (HL) is characterized by the presence of Hodgkin and Reed‐Sternberg cells (H&RS) and a prominent lymphocytic infiltration. We previously reported Hodgkin‐like adult T‐cell leukemia/lymphoma (HL‐like ATLL) (new WHO classification). Various CXC and CC chemokines
Global correlation of genome and transcriptome changes in classical Hodgkin lymphoma
✍ Scribed by Joost Kluiver; Klaas Kok; Ines Pfeil; Debora de Jong; Tjasso Blokzijl; Geert Harms; Pieter van der Vlies; Arjan Diepstra; Çiğdem Atayar; Sibrand Poppema; Ralf Küppers; Anke van den Berg
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 490 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0278-0232
- DOI
- 10.1002/hon.804
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
To identify genes involved in the pathogenesis of classical Hodgkin lymphoma (cHL), we performed serial analysis of gene expression (SAGE) and array‐based comparative genomic hybridization (aCGH). Comparison of SAGE libraries of cHL cell lines L428 and L1236 with that of germinal centre B cells revealed consistent overexpression of only 14 genes. In contrast, 141 genes were downregulated in both cHL cell lines, including many B cell and HLA genes. aCGH revealed gain of 2p, 7p, 9p, 11q and Xq and loss of 4q and 11q. Eighteen percent of the differentially expressed genes mapped to regions with loss or gain and a good correlation was observed between underexpression and loss or overexpression and gain of DNA. Remarkably, gain of 2p and 9p did not correlate with increased expression of the proposed target genes c‐REL and JAK2. Downregulation of many genes within the HLA region also did not correlate with loss of DNA. FSCN1 and IRAK1 mapping at genomic loci (7p and Xq) that frequently showed gain were overexpressed in cHL cell lines and might be involved in the pathogenesis of cHL. Copyright © 2006 John Wiley & Sons, Ltd.
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## Abstract Survival of the malignant Hodgkin and Reed/Sternberg (HRS) cells in classical Hodgkin lymphoma (cHL) is dependent on constitutive activation of the nuclear factor κB (NF‐κB) transcription factor. The deubiquitinating enzyme CYLD is a negative regulator of NF‐κB and known to function as
## Abstract Hodgkin and Reed‐Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) show genotypic features of germinal centre‐derived B‐cells in most cases. Nevertheless, these cells typically lack expression of B‐cell antigens. Previous studies have suggested that plasma cell differentiation m
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