1. ¹Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA
2. ²Department of Hematology and Oncology, ZymoGenetics Inc., Seattle, WA, USA

Correspondence: Dr SM Ansell, Division of Hematology and Internal Medicine, Mayo Clinic, 200 First St SW, Rochester, Minnesota 55905, USA. E-mail: ansell.stephen@mayo.edu

Received 2 April 2008; Revised 26 June 2008; Accepted 14 August 2008; Published online 2 October 2008.

Abstract

Multiple myeloma (MM) is a progressive disease that results from dysregulated proliferation of plasma cells. Although, causative factors such as genetic events and altered expression of anti-apoptotic factors have been described in a number of patients, the mechanistic details that drive myeloma development and continued growth of malignant cells remain largely undefined. Numerous growth factors, including interleukin (IL)-6, Insulin-like growth factor-1 and IL-10 have been shown to promote growth of MM cells suggesting a significant role for cytokines in this disease. Interferon (IFN)-1 is a new member of the Class II cytokine family that, similar to IFN-, has been shown to mediate viral immunity. In light of data supporting a role for cytokines in myeloma, we investigated the significance of IFN-1 on myeloma cell biology. Our studies show for the first time that myeloma cells bind to soluble IFN-1, and that IFN-1 induces myeloma cell growth and protects against dexamethasone-induced cell death. Our data also show that IFN-1 induces phosphorylation of STAT1, STAT3 and Erk. Taken together, our results suggest that IFN-1 may regulate myeloma cell biology and could prove to be therapeutically important.