Chronic myeloid leukemia may be associated with several bcr-abl transcripts
including the acute lymphoid leukemia-type 7 kb transcript [see comments]
L Selleri, M von Lindern, A Hermans, D Meijer, G Torelli and G Grosveld
Department of Cell Biology and Genetics, Erasmus University, Rotterdam, The
Netherlands.
In the majority of Philadelphia (Ph)-positive chronic myeloid leukemia
(CML) patients, the c-abl gene is fused to the bcr gene, resulting in the
transcription of an 8.5 kb chimeric bcr-abl mRNA, which is translated into
a p210bcr-abl fusion protein. In about 50% of the Ph- positive acute
lymphoid leukemias (ALL), the bcr-abl gene fusion is identical to CML,
while in 50% an alternative fusion between these two genes occurs, in which
the central bcr-sequences are absent. This results in transcription of a 7
kb bcr-abl mRNA, encoding a P190bcr-abl fusion protein. Cloning and
sequencing of the chimeric part of bcr-abl cDNAs from two Ph-positive CML
patients in chronic phase showed that in one patient, as in the Ph-positive
ALL, all central bcr sequences are absent, while in the other patient, part
of the bcr central sequences are deleted. Therefore, we speculate that the
presence of the 7 kb chimeric ALL type mRNA in one of the patients is not
sufficient to drive an acute rather than a chronic leukemic process in this
case. The deletions of the central bcr-sequences described here define the
minimal sequence requirement of the bcr-abl fusion gene in CML patients so
far.
Volume 75,
Issue 5,
pp. 1146-1153,
03/01/1990
Copyright © 1990 by The American Society of Hematology
