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Neutrophilic-chronic myeloid leukemia: a distinct disease with a specific
molecular marker (BCR/ABL with C3/A2 junction) [see comments]
F Pane, F Frigeri, M Sindona, L Luciano, F Ferrara, R Cimino, G Meloni, G Saglio, F Salvatore and B Rotoli
CEINGE-Biotecnologie Avanzate, Dipartimento di Biochimica e Biotecnologie
Mediche, Universita di Napoli Federico II, Italy.
Neutrophilic-chronic myeloid leukemia (CML-N) is a rare myeloproliferative
disorder that runs a much more benign course than chronic myeloid leukemia,
and for which no specific underlying molecular lesion has been described so
far. We have analyzed the genomic DNA by Southern blotting and the BCR/ABL
hybrid gene transcripts by reverse transcriptase-polymerase chain reaction
in three patients with clinical findings of CML-N, who did have a t(9;22)
chromosomal translocation. In all patients we have found a rare type of
BCR/ABL rearrangement, with a breakpoint between exons c3 and c4 of the BCR
gene (corresponding to BCR exons 19 and 20). This was confirmed by
hybridization with an oligonucleotide probe spanning the c3/a2 region. This
type of junction causes almost the entire BCR gene to fuse with ABL. The
junction is in frame and it gives rise to a fusion protein of predicted 230
kD. Our data now provide a molecular diagnostic marker for CML-N, and they
are consistent with the notion that the inclusion or exclusion of BCR exons
in the fusion protein affects dramatically its capacity to derange myeloid
proliferation and differentiation, leading to the appearance of different
disease phenotypes.
Volume 88,
Issue 7,
pp. 2410-2414,
10/01/1996
Copyright © 1996 by The American Society of Hematology
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