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, Andrew P. Feinberg

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3144-3147
Number of pages4
JournalBlood
Volume91
Issue number9
StatePublished - May 1 1998

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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  • Cite this

    Randhawa, G. S., Cui, H., Barletta, J. A., Strichman-Almashanu, L. Z., Talpaz, M., Kantarjian, H., Deisseroth, A. B., Champlin, R. C., & Feinberg, A. P. (1998). Loss of imprinting in disease progression in chronic myelogenous leukemia. Blood, 91(9), 3144-3147.