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Lack of the t(2;5) or other mutations resulting in expression of anaplastic
lymphoma kinase catalytic domain in CD30+ primary cutaneous
lymphoproliferative disorders and Hodgkin's disease
GS Wood, DL Hardman, R Boni, R Dummer, YH Kim, BR Smoller, M Takeshita, M Kikuchi and G Burg
Department of Dermatology, Case Western Reserve University, Cleveland, OH,
USA.
The t(2;5) (p23;q35) chromosomal translocation has been found in a high
proportion of lymph node-based CD30+ large cell lymphomas of T-cell
lineage. This translocation is believed to result in the expression of a
fusion protein containing the catalytic domain of anaplastic lymphoma
kinase (ALK) under the control of the promoter for nucleophosmin, a
nucleolar phosphoprotein. Expression of ALK activity, which does not
normally occur in lymphocytes, is postulated to be involved in the
pathogenesis of lymphomas bearing the t(2;5) translocation. Several primary
cutaneous lymphoproliferative disorders and Hodgkin's disease are also
known to contain CD30+ large lymphoid cells. To determine the role of the
t(2;5) translocation in these diseases, we developed a DNA- based
polymerase chain reaction (PCR)/Southern blot assay to detect this
translocation at the genomic level in lymphomatoid papulosis (14 cases),
primary cutaneous CD30+ large cell lymphoma of T-lineage (10 cases) and
Hodgkin's disease (13 cases). Two cases of pityriasis lichenoides were also
studied. The t(2;5) translocation was not present in any of these
specimens. To determine if some other somatic mutation might have resulted
in inappropriate expression of ALK catalytic domain, we devised an
RNA-based reverse transcriptase-PCR assay to detect transcripts encoded by
this ALK region. None were found in the six additional cases of
lymphomatoid papulosis that were studied. In aggregate, these results
strongly suggest that inappropriate expression of ALK is not involved in
the pathogenesis of these CD30+ lymphoproliferative disorders, and that
lymph node-based CD30+ large cell lymphoma is a disease that is
biologically distinct from skin- based CD30+ lymphoproliferative disorders
and Hodgkin's disease. Using methods developed for this report, we also
cloned and sequenced the t(2;5) genomic junctional sequences present in the
SUP-M2 and SU-DHL-1 cell lines. These intron sequences will be useful for
mapping t(2;5) breakpoint clusters.
Volume 88,
Issue 5,
pp. 1765-1770,
09/01/1996
Copyright © 1996 by The American Society of Hematology
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