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Selective loss of B‐cell phenotype in lymphocyte predominant Hodgkin lymphoma
Author(s) -
Tedoldi S,
Mottok A,
Ying J,
Paterson JC,
Cui Y,
Facchetti F,
van Krieken JHJM,
Ponzoni M,
Özkal S,
Masir N,
Natkunam Y,
Pileri SA,
Hansmann ML,
Mason DY,
Tao Q,
Marafioti T
Publication year - 2007
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2242
Subject(s) - germinal center , cd19 , biology , lymphoma , b cell , lymphocyte , phenotype , reed–sternberg cell , cancer research , gene , microbiology and biotechnology , cell , genetics , immunology , hodgkin lymphoma , antibody
The neoplastic Reed–Sternberg cells characteristic of classical Hodgkin's lymphoma (cHL) are of B‐cell origin but they almost always show striking loss of a range of B‐cell‐associated molecules. In contrast, the neoplastic cells found in lymphocyte predominant Hodgkin's lymphoma (LPHL) (L&H cells) are traditionally thought of as possessing the full repertoire of features associated with germinal centre B cells (eg BCL‐6 expression, ‘ongoing’ Ig gene mutation). In the present paper, we report an extensive phenotypic analysis of L&H cells which revealed down‐regulation of a number of markers associated with the B‐cell lineage (eg CD19, CD37) and with the germinal centre maturation stage (eg PAG, LCK). The promoter methylation status of three of these down‐regulated genes (CD10, CD19, and LCK) was further studied in microdissected L&H cells, and this revealed that their promoters were unmethylated. In contrast, these genes showed promoter methylation in cell lines derived from CHL. Further investigation of the mechanisms responsible for the deregulation of these molecules in L&H cells may provide new insights into the genetic abnormalities underlying LPHL. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.