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Blood, Vol. 94 No. 9 (November 1), 1999:
pp. 3265-3268
TRK-Fused Gene (TFG) Is a New Partner of ALK in
Anaplastic Large Cell Lymphoma Producing Two Structurally Different
TFG-ALK Translocations
Luis Hernández,
Magda Pinyol,
Silvia Hernández,
Silvia Beà,
Karen Pulford,
Andreas Rosenwald,
Laurence Lamant,
Brunangelo Falini,
German Ott,
David Y. Mason,
Georges Delsol, and
Elias Campo
From the Laboratory of Pathology, Hospital Clinic, Institut
d'Investigacions Biomediques August Pi i Sunyer, University of
Barcelona, Barcelona, Spain; LRF Immunodiagnostics Unit, Nuffield
Department of Clinical Biochemistry and Cellular Science, John
Radcliffe Hospital, Oxford, UK; Institute of Pathology, University of
Würzburg, Würzburg, Germany; Laboratory Department of
Pathology and UPCM-ERS 1590 CNRS, CHU Purpan, Toulouse, France;
Institute of Hematology, Perugia University, Perugia, Italy.
Anaplastic large cell lymphoma (ALCL) is associated with the
t(2;5)(p23;q35), which generates the NPM-ALK fusion gene
encoding an 80-kD protein. Several studies have
suggested that genes other than NPM may be fused to the
ALK gene. Here we have identified TRK-fused gene
(TFG) as a new ALK partner in 2 ALCL, 1 of which exhibited a t(2;3)(p23;q21). In these cases, TFG was involved in 2 different fusion genes, TFG-ALKS and
TFG-ALKL, coding respectively 85-kD and
97-kD chimeric proteins. The ALK breakpoint in these
translocations was the same as in the classic t(2;5) translocation.
These 2 proteins were both active in an in vitro tyrosine kinase assay
showing that the new cloned cDNA sequences are translated into chimeric
proteins with functional activity. These findings indicate that
TFG can provide an alternative to NPM as a fusion
partner responsible for activation of the ALK and the
pathogenesis of ALCL.
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