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ALK gene products in anaplastic large cell lymphomas and Hodgkin's disease
H Herbst, J Anagnostopoulos, B Heinze, H Durkop, M Hummel and H Stein
Konsultations-und Referenzzentrum fur Lymphknoten-und Hamatopathologie am
Institut fur Pathologie, Klinikum Benjamin Franklin, Freie Universitat
Berlin, Germany.
The translocation t(2;5)(p23;q35), discovered in CD30+ anaplastic large
cell (ALC) lymphomas, creates a potentially oncogenic fusion gene, part of
which is contributed by a novel tyrosine kinase, ALK. Absence of ALK
expression from normal hematolymphoid cells provides a basis for the
morphologic assessment of t(2;5). The distribution of the t(2;5) in ALC
lymphomas and Hodgkin's disease (HD), as assayed by nonmorphologic methods,
is controversial. We used in situ hybridization and/or immunohistology to
show ALK gene products in 85 ALC lymphomas, 82 HD cases, 40 other
lymphoproliferations, as well as in 6 HD- and 4 ALC lymphoma-derived cell
lines. ALK gene products were restricted to t(2;5)-positive ALC lymphoma
cell lines and tumor cells of 16 primary non-B cell, common-type ALC
lymphomas. These were mainly from young patients with initial lymphonodal
disease. ALK expression was not detectable in any other specimen, including
all cases of HD and HD-like type ALC lymphoma as well as secondary ALC
lymphomas. Full congruence was noted for labeling results obtained with
both methods. In agreement with cytogenetic analyses, but at variance with
recently published studies, ALK gene expression distinguishes a subset of
ALC lymphomas from other CD30+ lymphomas, including HD. The results do not
support concepts attributing a significant role to the t(2;5) in the
development of HD.
Volume 86,
Issue 5,
pp. 1694-1700,
09/01/1995
Copyright © 1995 by The American Society of Hematology
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