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Primary central nervous system malignant non–Hodgkin's lymphomas from HIV‐infected and non‐infected patients:expression of cellular surface proteins and Epstein‐Barr viral markers

Primary central nervous system malignant non–Hodgkin's lymphomas from HIV‐infected and... The increased incidence of primary central nervous system malignant non–Hodgkin's lymphomas (PCNSL) in HIV– and non–HIV–infected patients and the demonstration of Epstein–Barr virus (EBV) in these tumours may indicate relationships between PCNSL and EBV. Consequently expression of EBV–induced antigens and cellular markers were studied in 11 HIV–infected and seven non–infected patients by in situ hybridization (ISH) and immunocytochemistry in monoclonal B cell PCNSL. In HIV–infected patients EBV genome was present in 9/11 cases, LMP in 11/11 cases and EBNA2 in 10/11 cases. The expression of adhesion and activation molecules was low or absent. In HIV non–infected patients, EBV genome was present in 5/7 cases, with LMP in 4/7 cases. EBNA2 was never detected. All these lymphomas expressed LFAlbeta. Whatever the population, no lytic cycle EBV markers were detected. Compared with other types of EBV lymphomas, our results suggest a different EBV latency state in primary B cell lymphomas of the CNS from HIV–infected or non–infected patients. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuropathology & Applied Neurobiology Wiley

Primary central nervous system malignant non–Hodgkin's lymphomas from HIV‐infected and non‐infected patients:expression of cellular surface proteins and Epstein‐Barr viral markers

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References (46)

Publisher
Wiley
Copyright
Copyright © 1994 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0305-1846
eISSN
1365-2990
DOI
10.1111/j.1365-2990.1994.tb00966.x
Publisher site
See Article on Publisher Site

Abstract

The increased incidence of primary central nervous system malignant non–Hodgkin's lymphomas (PCNSL) in HIV– and non–HIV–infected patients and the demonstration of Epstein–Barr virus (EBV) in these tumours may indicate relationships between PCNSL and EBV. Consequently expression of EBV–induced antigens and cellular markers were studied in 11 HIV–infected and seven non–infected patients by in situ hybridization (ISH) and immunocytochemistry in monoclonal B cell PCNSL. In HIV–infected patients EBV genome was present in 9/11 cases, LMP in 11/11 cases and EBNA2 in 10/11 cases. The expression of adhesion and activation molecules was low or absent. In HIV non–infected patients, EBV genome was present in 5/7 cases, with LMP in 4/7 cases. EBNA2 was never detected. All these lymphomas expressed LFAlbeta. Whatever the population, no lytic cycle EBV markers were detected. Compared with other types of EBV lymphomas, our results suggest a different EBV latency state in primary B cell lymphomas of the CNS from HIV–infected or non–infected patients.

Journal

Neuropathology & Applied Neurobiology – Wiley

Published: Jun 1, 1994

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