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Blood, 15 January 2002, Vol. 99, No. 2, pp. 713-715
BRIEF REPORT
 1-Acid glycoprotein expressed in the plasma of
chronic myeloid leukemia patients does not mediate significant in vitro
resistance to STI571
Heather G. Jørgensen,
Moira A. Elliott,
Elaine K. Allan,
Christine E. Carr,
Tessa L. Holyoake, and
Kevin D. Smith
From the Academic Transfusion Medicine Unit, Department
of Medicine, University of Glasgow, and the Department of
Pharmaceutical Sciences and the Department of Bioscience and
Biotechnology, University of Strathclyde, Glasgow, United Kingdom.
Despite the efficacy of STI571 (Glivec, Novartis, Basle,
Switzerland) in treating chronic myeloid leukemia (CML), drug
resistance has already been noted both in vitro and in vivo. As plasma
proteins, including alpha-1-acid glycoprotein (AGP), may reduce drug
efficacy through binding, AGP was investigated for its ability to
interact with STI571.
At all stages of CML, AGP plasma level was significantly
higher than in normal controls (P < .05). The
glycoprotein was purified from normal plasma and individual chronic
myeloid leukemia (CML) patients' plasma by low-pressure
chromatography. The influence of  1-acid glycoprotein
(AGP), in the presence of STI571, on the proliferation of Philadelphia
chromosome-positive (Ph+) cells was examined. Normal AGP,
even at supraphysiological concentrations, did not block the effect of
STI571 on K562-cell proliferation in vitro. Moreover, CML-derived AGP
failed to block the effect of STI571 on Ph+ cells in vitro.
Thus, these in vitro findings suggest that AGP will not abrogate the
antileukemic activity of STI571.
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