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Lack of Interferon Consensus Sequence Binding Protein (ICSBP)
Transcripts in Human Myeloid Leukemias
Manuel Schmidt,
Stefan Nagel,
Jutta Proba,
Christian Thiede,
Markus Ritter,
Jeffrey F. Waring,
Frank Rosenbauer,
Dieter Huhn,
Burghardt Wittig,
Ivan Horak, and
Andreas Neubauer
From the Medizinische Klinik I, Universitätsklinik Carl Gustav
Carus, Dresden; Abteilung für Innere Medizin m.S.
Hämatologie, Virchow Klinikum der Humboldt Universität
Berlin, Berlin; Forschungsinstitut für Molekulare
Pharmakologie, Berlin; and Institut für Molekularbiologie,
Biochemie und Bioinformatik, Freie Universität Berlin, Berlin,
Germany.
Interferon consensus sequence binding protein (ICSBP) was
first identified as a transcription factor of the interferon (IFN) regulatory factor family (IRF) which regulates expression of
IFN-dependent genes by binding to DNA at specific sites, IFN-stimulated
responsive elements. Analysis of ICSBP-deficient mice showed
hematologic alterations similar to chronic myelogenous leukemia (CML)
in humans and suggested a novel role for ICSBP in regulating
proliferation and differentiation of hematopoietic progenitor cells.
Here we show that ICSBP-mRNA expression is impaired in human
myeloid leukemias: 27 of 34 CML patients (79%) and 21 of 32 patients
with acute myeloid leukemia (AML) (66%) showed very
low or absent transcript numbers of ICSBP. In contrast, only 2 of 33 normal volunteers (6%) showed low transcription of ICSBP
(P < .0001 both for CML and AML values). The lack of
expression was not associated with lack of lymphatic cells, which
normally have been shown to express ICSBP at the highest level.
More detailed analysis showed an absence of ICSBP-mRNA also in
sorted B cells derived from CML patients. To analyze whether ICSBP may be induced in leukemic cells, ex vivo
experiments using a known inducer of ICSBP, IFN- , were
performed. Ex vivo treatment of primary CML cells using IFN-
resulted in induction of ICSBP transcripts. Furthermore,
samples of CML patients during IFN- treatment were analyzed. In 11 of 12 CML patients ICSBP-mRNA was inducible upon in
vivo treatment with IFN-, but decreased with progression of CML.
Stable transfection of K-562 cell line with ICSBP led to no
difference in bcr-abl expression in vitro, although two
patients showed an inverse correlation between bcr-abl and ICSBP in vivo. These data suggest that lack of ICSBP
may have an important role also in human myeloid leukemogenesis.
Blood, Vol. 91 No. 1 (January 1), 1998:
pp. 22-29
© 1998 by The American Society of Hematology.
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