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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2001-12-0244.
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Blood, 15 June 2002, Vol. 99, No. 12, pp. 4568-4577
NEOPLASIA
The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex
(9;12) translocations in human leukemia, induces distinct
myeloproliferative disease in mice
Ryan P. Million,
Jon Aster,
D. Gary Gilliland, and
Richard A. Van
Etten
From The Center for Blood Research and Department of
Genetics and Department of Pathology, Brigham and Women's Hospital;
Harvard Institutes of Medicine; and Howard Hughes Medical Institute,
Harvard Medical School, Boston, MA.
Several patients with clinical features of chronic myeloid leukemia
(CML) have fusion of the TEL (ETV6) gene on
12p13 with ABL on 9q34 and express a chimeric Tel-Abl
protein that contains the same portion of the Abl tyrosine kinase fused
to Tel, an Ets family transcription factor, rather than Bcr. In a
murine retroviral bone marrow transduction-transplantation model, a Tel
(exon 1-5)-Abl fusion protein induced 2 distinct illnesses: a CML-like
myeloproliferative disease very similar to that induced by Bcr-Abl but
with increased latency and a novel syndrome characterized by
small-bowel myeloid cell infiltration and necrosis, increased
circulating endotoxin and tumor necrosis factor  levels, and
fulminant hepatic and renal failure. Induction of both diseases
required the Tel pointed homology oligomerization domain and Abl
tyrosine kinase activity. Myeloid cells from mice with both diseases
expressed Tel-Abl protein. CML-like disease induced by Tel-Abl and
Bcr-Abl was polyclonal and originated from cells with multilineage
(myeloid, erythroid, and B- and T-lymphoid) repopulating ability and
the capacity to generate day-12 spleen colonies in secondary
transplantations. In contrast to findings with Bcr-Abl, however,
neither Tel-Abl-induced disease could be adoptively transferred to
irradiated secondary recipient syngeneic mice. These results show that
Tel-Abl has leukemogenic properties from distinct from those of Bcr-Abl
and may act in a different bone marrow progenitor.
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