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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 3088-3095
A New Fusion Gene TPM3-ALK in Anaplastic Large Cell
Lymphoma Created by a (1;2)(q25;p23) Translocation
Laurence Lamant,
Nicole Dastugue,
Karen Pulford,
Georges Delsol, and
Bernard Mariamé
From the Department of Pathology, Hematology Laboratory, and UPCM-ERS
1590 CNRS, CHU Purpan, Toulouse, France; and the LRF Immunodiagnostics
Unit, Department of Cellular Science, John Radcliffe Hospital,
Oxford, UK.
Anaplastic large cell lymphomas (ALCL) are frequently associated
with the t(2;5)(p23;q35). This translocation fuses the nucleophosmin (NPM) gene at 5q35, which encodes a nucleolar protein involved in shuttling ribonucleoproteins from the cytoplasm to the nucleus, to
the anaplastic lymphoma kinase (ALK) gene at 2p23, encoding a
tyrosine kinase receptor. In this report, we describe a typical case of
ALCL whose malignant cells exhibited a novel (1;2)(q25;p23) translocation. These cells expressed ALK protein, but, in contrast to
t(2;5)-positive ALCL (which show cytoplasmic, nuclear, and nucleolar
staining), labeling was restricted to the malignant cell cytoplasm.
Using a polymerase chain reaction (PCR)-based technique to walk on
chromosome 2 from the known ALK gene across the breakpoint, we
showed that the gene involved at 1q25 is TPM3, encoding a
nonmuscular tropomyosin. We subsequently identified, using reverse
transcription-PCR analysis of cases showing similar ALK
cytoplasm-restricted staining, fusion of the ALK and
TPM3 genes in 2 other cases of ALCL. The TPM3 gene has
been previously found in papillary thyroid carcinomas as a fusion
partner with the TRK kinase gene. We showed that TPM3 is
constitutively expressed in lymphoid cell lines, suggesting that, in
these t(1;2)-bearing ALCL cases, the TPM3 gene contributes an
active promoter for ALK expression. Activation of the
ALK catalytic domain probably results from homodimerization of the
hybrid protein TPM3-ALK, through the TPM3 protein-protein interaction
domain. The present cases of ALCL associated with a novel
t(1;2)(q25;p23) demonstrate that at least one fusion partner other than
NPM can activate the intracytoplasmic domain of the ALK kinase.
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