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Endothelial hyperplasia and endothelial galectin‐3 expression are prognostic factors in primary central nervous system lymphomas
Author(s) -
D’Haene Nicky,
Catteau Xavier,
Maris Calliope,
Martin Benoit,
Salmon Isabelle,
Decaestecker Christine
Publication year - 2008
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06929.x
Subject(s) - medicine , angiogenesis , pathology , hyperplasia , galectin 3 , primary central nervous system lymphoma , immunohistochemistry , lymphoma
Summary Recently, considerable attention has been focused on the identification of clinically relevant prognostic markers for primary central nervous system lymphomas (PCNSL). The present study investigated whether three morphological features, i.e. necrosis, reactive perivascular T‐cell infiltrate and endothelial hyperplasia, and galectin‐1 and galectin‐3 immunohistochemical expression have prognostic roles in a series of 58 PCNSL samples from 44 immunocompetent and 14 immunocompromised patients. The presence of endothelial hyperplasia (identified in 21% of the assessable cases) was identified as a bad prognostic factor for immunocompetent PCNSL patients, whereas the other morphological features were not associated with any prognostic value. Lymphomatous cells of eight PCNSL cases expressed galectin‐3 without any prognostic value, and lymphomatous cells did not express galectin‐1. In contrast, endothelial expression of galectin‐3 was identified (by means of uni‐ and multi‐variate analyses) as a bad prognostic factor for immunocompetent PCNSL patients. In addition, a combination of endothelial hyperplasia and/or endothelial galectin‐3 expression was shown to be an independent prognostic factor for immunocompetent PCNSL patients treated with methotrexate‐based chemotherapy. In summary, this study suggests that endothelial‐related markers can identify risk groups of PCNSL patients and indicates that galectin‐3 could be involved in PCNSL angiogenesis.