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Nuclear factor B as a target for new drug development in myeloid malignancies

From the Division of Hematology and Internal Medicine, Department of Clinical and Biological Sciences, University of Turin (DC, FM, GS); Institute of Haematology and Medical Oncology "L. and A. Seragnoli" University of Bologna (GM, MB)

Correspondence: Daniela Cilloni, M.D, PhD, Dept. of Clinical and Biological Sciences of the University of Turin, San Luigi Hospital, Gonzole 10, 10043 Orbassano, Turin, Italy. E-mail: daniela.cilloni{at}unito.it

ABSTRACT

The transcription nuclear factor B (NF-B) can intervene in oncogenesis through to its capacity to regulate the expression of a large number of genes that regulate apoptosis, cell proliferation and differentiation as well as inflammation, angiogenesis and tumor migration. Impaired NF-B activity has been demonstrated not only in solid cancers but also in various types of hematologic malignancies including acute myeloid leukemia, chronic myelogenous leukemia and in a subset of myelodysplastic syndromes. The underlying mechanisms, illustrated in the text and although quite diverse in different diseases, provide the rationale for new therapeutic strategies combining different NF-B or proteasome inhibitors. It has, therefore, been proposed that inhibition of NF-B could be an adjuvant therapy for cancer and many phase I/II clinical studies are ongoing with different inhibitors. This review highlights the in vitro and in vivo results of NF-B inhibition in myeloid malignancies.

Key words: NF-B, proteasome inhibitors, acute myeloid leukemia, chronic myelogenous leukemia.