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Loss of Imprinting in Disease Progression in Chronic Myelogenous
Leukemia
Gurvaneet S. Randhawa,
Hengmi Cui,
Janet A. Barletta,
Liora Z. Strichman-Almashanu,
Moshe Talpaz,
Hagop Kantarjian,
Albert B. Deisseroth,
Richard C. Champlin, and
Andrew P. Feinberg
From the Departments of Medicine, Oncology, and Molecular Biology & Genetics, and the Graduate Program in Human Genetics, Johns Hopkins
University School of Medicine, Baltimore, MD; and the Department of
Hematology, MD Anderson Cancer Center, Houston, TX.
The pathophysiologic role of the Philadelphia chromosome
translocation in chronic myelogenous leukemia (CML) has been known for
nearly 20 years. However, the most significant morbidity and mortality
in CML are caused by progression to blast crisis, about which
comparatively little is known at the molecular level. Genomic imprinting is a chromosomal modification leading to
parental-origin-specific gene expression in somatic cells. Recently,
we and others have described loss of imprinting (LOI) of the
insulin-like growth factor-II gene (IGF2), leading to biallelic rather
than monoallelic expression in a wide variety of solid tumors. We have
now examined the imprinting status of IGF2 in samples from CML patients
in stable phase, accelerated phase, and blast crisis. Five of six stable-phase patients showed normal imprinting, but LOI was found in
all six cases of advanced disease (three accelerated phase, three blast
crisis), which was statistically highly significant (P < .01). Thus, LOI represents a novel type of genetic alteration in CML
that appears to be specifically associated with disease progression.
Blood, Vol. 91 No. 9 (May 1), 1998:
pp. 3144-3147
© 1998 by The American Society of Hematology.
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