Identification of molecular variants of p210bcr-abl in chronic myelogenous
leukemia
R Kurzrock, WS Kloetzer, M Talpaz, M Blick, R Walters, RB Arlinghaus and JU Gutterman
The aberrant abl protein product of a chronic myelogenous leukemia (CML)
blast crisis cell line (K562) and of five Philadelphia chromosome- positive
CML patients in blast crisis were analyzed by an immune complex kinase
assay using two antipeptide sera generated against the hydrophilic domain
of v-abl and a region within the third exon of the breakpoint cluster
region (bcr) respectively. Both the anti-abl and anti-bcr sera detected a
210 kd band in extracts derived from K562 cells and from two CML patients
with myeloid blast crisis. p210 was detected by the anti-abl but not the
anti-bcr sera in three CML patients with myeloid (one patient) and lymphoid
(two patients) blast crisis, indicating the absence of bcr exon 3 in this
protein. Southern blot analysis on DNA derived from one of the patients in
the latter group was consistent with the break on chromosome 22 occurring
5' to bcr exon 3. Our observations demonstrate that the Philadelphia
translocation results in the generation of a chimeric bcr-abl protein with
at least two molecular variants, both of which are enzymatically active as
protein kinases.
Volume 70,
Issue 1,
pp. 233-236,
07/01/1987
Copyright © 1987 by The American Society of Hematology
