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Expression of c-abl in Philadelphia-positive acute myelogenous leukemia
R Kurzrock, M Shtalrid, M Talpaz, WS Kloetzer and JU Gutterman
Department of Clinical Immunology, M.D. Anderson Hospital and Tumor
Institute at Houston, TX 77030.
The identical cytogenetic marker, t(9;22)(q34;q11) (Philadelphia [Ph]
translocation), is found in approximately 90%, 20%, and 2% of adult
patients with chronic myelogenous leukemia (CML), acute lymphoblastic
leukemia (ALL), and acute myelogenous leukemia (AML), respectively. In CML,
the molecular events resulting from the Ph translocation include a break
within the bcr locus on chromosome 22, transfer of the c-abl protooncogene
from chromosome 9 to 22, and formation of an aberrant 210- kD bcr-abl
fusion protein (p210bcr-abl). Recently, the absence of bcr rearrangement
and expression of a distinct aberrant 190-kd abl protein (p190c-abl) has
been described in Ph-positive ALL, with the suggestion that the two abl
variants may be pathogenetically associated with myeloid v lymphoid
leukemogenesis. Here we report that the genomic configuration and
translation product of Ph-positive AML can be similar to that of
Ph-positive ALL: the break at 22q11 may occur outside the 5.8 kb bcr region
and result in expression of a 190-kD abl protein lacking these bcr
sequences. Phosphokinase enzymatic activity, a fundamental property of
p210bcr-abl, was also associated with AML- derived p190c-abl. Our current
observations indicate that p190c-abl can be found in cells of lymphoid or
myeloid lineage and is therefore unlikely to play a specific role in the
development of lymphoid leukemias. Formation of p190c-abl instead of
p210bcr-abl appears to be a characteristic of the acute rather than the
chronic Ph-positive leukemic state.
Volume 70,
Issue 5,
pp. 1584-1588,
11/01/1987
Copyright © 1987 by The American Society of Hematology
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