DELETION OF EPSTEIN-BARR-VIRUS LATENT MEMBRANE-PROTEIN-1 GENE IN UNITED-STATES AND BRAZILIAN HODGKINS-DISEASE AND REACTIVE LYMPHOID-TISSUE - HIGH-FREQUENCY OF A 30-BP DELETION
K. Hayashi et al., DELETION OF EPSTEIN-BARR-VIRUS LATENT MEMBRANE-PROTEIN-1 GENE IN UNITED-STATES AND BRAZILIAN HODGKINS-DISEASE AND REACTIVE LYMPHOID-TISSUE - HIGH-FREQUENCY OF A 30-BP DELETION, Human pathology, 28(12), 1997, pp. 1408-1414
A 30-basepair (bp) deletion in the Epstein-Barr virus (EBV) latent mem
brane protein 1 (LMP1) gene has been reported in nasopharyngeal carcin
oma and EBV-associated malignant lymphomas. Prior studies have found t
he deletion in about 10% to 28% of cases of Hodgkin's disease (HD), pa
rticularly in cases with aggressive histology. We studied the prevalen
ce of 30-bp LMP1 gene deletion in EBV-positive HD in the United States
(US) (12 cases) and Brazil (26 cases) with comparison to reactive lym
phoid tissues (21 cases) and HD without EBV-positive Reed-Sternberg ce
lls (15 cases). We studied the status of the LMP1 gene by Southern blo
t hybridization of polymerase chain reaction (PCR) products obtained a
fter amplification with primers spanning the site of the deletion. We
also performed EBV typing, EBER1 in situ hybridization, and LMP1 prote
in immunohistochemistry. EBV was detected in 12/26 (46%) cases of HD f
rom the US and 26/27 (96%) cases of Brazilian HD. The 30-bp LMP1 gene
deletion was observed in 4/12 (33%) cases of EBV-positive HD from US,
and 12/26 (46%) cases of Brazilian EBV-positive HD, including 3 cases
of type B EBV, as compared with 12/21 (57%) reactive lymphoid tissues
and 9/15 (60%) cases of EBV-negative HD. US and Brazilian HD showed a
higher prevalence of the 30-bp LMP1 gene deletion, compared with studi
es of others. The unexpected finding of high incidence of 30-bp deleti
on in LMP1 gene in reactive lymphoid tissue and HD without EBV-positiv
e Reed-Sternberg cells suggests that this deletion may not be relevant
to HD pathogenesis in most cases. Copyright (C) 1997 by W.B. Saunders
Company.