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
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.