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CD44 expression in human gliomas

Background and Objectives Glioma invasiveness involves the attachment of tumor cells to the brain extracellular matrix, rich in hyaluronic acid (HA). CD44, the principal receptor for HA is found as a standard molecule (CD44s) or as variants (CD44v). We undertook a retrospective study to evaluate the...

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Bibliographic Details
Published in:Journal of surgical oncology 2002-01, Vol.79 (1), p.30-36
Main Authors: Ranuncolo, Stella Maris, Ladeda, Virginia, Specterman, Sergio, Varela, Mirta, Lastiri, José, Morandi, Ana, Matos, Elena, De Kier Joffe, Elisa Bal, Puricelli, Lydia, Pallotta, María Guadalupe
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Language:English
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Summary:Background and Objectives Glioma invasiveness involves the attachment of tumor cells to the brain extracellular matrix, rich in hyaluronic acid (HA). CD44, the principal receptor for HA is found as a standard molecule (CD44s) or as variants (CD44v). We undertook a retrospective study to evaluate the expression pattern of CD44s, the isoforms CD44v3, v4/5 and v6 and to correlate their expression with clinical‐anatomopathological parameters and survival rate. Methods The expression of these molecules was evaluated immunohistochemically in 84 gliomas. Results No expression of CD44v was detected in any tumors. CD44s staining of tumor cells was found in 70 of 84 (83.3%) of the gliomas. In 23 of 39 (59.0%) of the GBM more than the 70% of the cells were stained, while only 2 of 21 (9.5%) of LGA showed high expression. The association between CD44 and histological grade remained when the prognostic variables were considered in a multivariate analysis. Higher expression of CD44 was associated with worse overall survival rate; however, the Cox analysis indicated that survival was not associated with CD44. Conclusions Our results suggest that overexpression of CD44s could be relevant in determining the highly invasive behaviour of gliomas, though it does not behave as an independent prognostic factor for survival. J. Surg. Oncol. 2002;79:30–36. © 2002 Wiley‐Liss, Inc.
ISSN:0022-4790
1096-9098
DOI:10.1002/jso.10045