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Lack of the expression of EBNA-2 and LMP-1 in T-cell neoplasms possessing
Epstein-Barr virus
H Suzushima, N Asou, T Fujimoto, S Nishimura, T Okubo, H Yamasaki, M Osato, M Matsuoka, A Tsukamoto and K Takai
Second Department of Internal Medicine, Kumamoto University School of
Medicine, Japan.
We investigated 34 cases of T-cell neoplasm [15 cases of T-cell granular
lymphocytic leukemia (T-GLL), 10 cases of T-cell non-Hodgkin's lymphoma
(T-NHL), six cases of T-cell chronic lymphocytic leukemia (T- CLL), and
three cases of cutaneous T-cell lymphoma] to study their association with
Epstein-Barr virus (EBV). In 4 (three T-NHL and one T- GLL) of 34 cases,
EBV genome was detected in a single episomal form, while polyclonal EBV-DNA
was detected in one (T-NHL) of the remaining cases. All three cases of
T-NHL having monoclonal EBV episome showed histologically diffuse
large-cell lymphoma and developed leukemic conversion. Phenotypic analysis
showed that two of these four cases were CD4+, CD8-, and the remaining two
cases were CD4-, CD8+. The cells from all four cases were confirmed to be
in T-cell lineage by detecting the rearrangement of T-cell receptor (TCR)
beta or gamma chain gene. By reverse transcription-polymerase chain
reaction (RT-PCR), EBNA-1 was detected at low levels, and neither EBNA-2
nor LMP-1 were found in any of the three cases examined. Lack of the
expression of EBNA-2 and LMP-1 was also confirmed by immunocytochemical
staining. The cells of these four cases did not show rearrangement or
overexpression of c-myc and bcl-2 genes by Southern and Northern blots, and
the mutation of p53 gene was detected in only one patient. These results
suggest that other latent gene products of EBV or other cellular oncogenes
are involved in the development of Japanese T-cell neoplasm after EBV
infection.
Volume 85,
Issue 2,
pp. 480-486,
01/15/1995
Copyright © 1995 by The American Society of Hematology
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