Epstein–Barr virus‐induced B‐cell proliferation of Hodgkin's and Reed–Sternberg cell pheno‐ and genotype may develop in peripheral T‐cell lymphomas

Abstract

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Pheno- and Genotypic Features of Epstein-Barr Virus Associated B-Cell Lymphoproliferations in Peripheral T-Cell Lymphomas

“…This phenotype under these circumstances-CD45, TF and EBNA-2 negativity beside CD30, LMP-1 positivity being the most importanthas not been described yet in the literature available for us, in fact CD45 expression data were not always available and the IgH-TFs have not been investigated at all in the referred papers. Our observations-together with previous result on the molecular characteristics of FRI-CDRIII region in the IgH gene of sorted LBCs in such a case-imply that EBV infected LBCs indistinguishable in morphology, pheno-and genotype from those of HRS cells in cHL may also arise in TLs [3]. These cases should not be called TL composite with cHL as the unique, reactive cellular background of cHL was missing.…”

“…In those cases, however, the large cells always expressed at least one Tcell markers and atypical T-phenotype being concordant to that of the background T-lymphoma cells, furthermore, they proved to be negative for EBV. If the large cells in a TL are consistently negative for several T-cells markers, but positive for EBV, an accompanying or secondary B-cell proliferation might be suspected, which have been described with phenotypic heterogeneity and some controversy regarding the genotypic features [2,3,6,10,11]. Quintanilla-Martinez et al (1999) analyzed three such cases and found for the scattered large cells either an activated Bcell (CD15−, CD30+, CD20+) or cHL-HRS cell (CD15+, CD30+, CD20+) phenotype, polyclonal / oligoclonal IgH-R in microdissected cells and no progression to disseminated cHL.…”

“…Three cases have already been published from other aspects by us [3]. Four-micrometerthick sections were stained for hematoxylin-eosin, methylated-Giemsa and periodic acid-Schiff.…”

“…The distinction between PTCL and cHL is further complicated by the rare variant of PTCL resembling cHL because of the presence of HRS type of cells, which are constantly Epstein-Barr virus (EBV) and CD30 positive. Single cell molecular analysis of these cells indicated B-cell genotype, but controversy regarding clonality at the immunoglobulin heavy chain gene rearrangement (IgH-R) [2,3]. PTCL morphology might be complicated by admixed EBV positive scattered immunoblastic type of cells or homogeneous sheets of EBV positive immature B-cells, making the differential diagnostics between PTCL and Tcell rich B-cell lymphoma (TCR-BCL) as well as PTCL composite with either cHL or diffuse large B-cell lymphoma (DLBCL) demanding [4][5][6].…”

Έκφραση των πρωτεϊνών bcl-2, bax, bcl-x, fas και fas-ligand στη νόσο Hodgkin

“…94,95 Σε σπάνιες περιπτώσεις από αυτά τα EBV(+) κύτταρα μπορεί να προκύψει ένα διάχυτο λέμφωμα από Β-μεγάλα κύτταρα ή ακόμη και λέμφωμα με μορφολογικά και ανοσοϊστοχημικά χαρακτηριστικά κλασσικού λεμφώματος Hodgkin. [96][97][98][99][100][101] Επίσης λεμφώματα και λεμφοϋπερπλαστικές νόσοι που αναπτύσσονται σε ανοσοκαταστολή (πρωτοπαθής ανοσοκαταστολή, ή μετά από μεταμόσχευση, ή θεραπεία από μεθοτρεξάτη,) μπορεί να προσομοιάζουν το λέμφωμα Hodgkin. Η WHO ταξινόμηση στις καταστάσεις αυτές περιλαμβλάνει λέμφωμα Hodgkin και Hodgkin-like λεμφώματα.…”