TRANSCRIPTS OF THE NPM-ALK FUSION GENE IN ANAPLASTIC LARGE-CELL LYMPHOMA, HODGKINS-DISEASE, AND REACTIVE LYMPHOID LESIONS

Citation
Pg. Elmberger et al., TRANSCRIPTS OF THE NPM-ALK FUSION GENE IN ANAPLASTIC LARGE-CELL LYMPHOMA, HODGKINS-DISEASE, AND REACTIVE LYMPHOID LESIONS, Blood, 86(9), 1995, pp. 3517-3521
Citations number
25
Categorie Soggetti
Hematology
Journal title
BloodACNP
ISSN journal
00064971
Volume
86
Issue
9
Year of publication
1995
Pages
3517 - 3521
Database
ISI
SICI code
0006-4971(1995)86:9<3517:TOTNFG>2.0.ZU;2-3
Abstract
Anaplastic large cell lymphoma (ALCL) and Hodgkin's disease (HD) have some pathologic and immunohistochemical similarities, and a histogenet ic relationship between them has been suggested by some investigators. By cytogenetic study, the t(2;5)(p23;q35) translocation appears to be unique for ALCL. The breakpoints of the t(2;5)(p23;q35) have recently been cloned and are reported to involve a novel tyrosine kinase gene, anaplastic lymphoma kinase (alk), on chromosome 2 and the nucleophosm in gene (npm) on chromosome 5. Therefore, we studied the frequency of npm-alk translocation in ALCL using a reverse transcriptase-polymerase chain reaction (RT-PCR) assay. We also studied HD and a variety of re active lymphoid lesions since there is contradictory information in th e literature on the occurrence of the npm-alk rearrangement in HD. We detected npm-alk hybrid mRNA in 8 of 22 cases of ALCL (36%), but none of the 21 cases of HD or the 11 cases with reactive lesions contained amplifiable template. All positive ALCL had the T or indeterminate phe notype and occurred in young adults or children. There was very good c orrelation between a cytogenetically detectable t(2;5) and a positive signal by RT-PCR. Our results indicate a selective but relatively infr equent association between the t(2;5) and ALCL of T or indeterminate p henotype, not shared with HD or reactive hyperplasia. (C) 1995 by The American Society of Hematology.