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Multiple Myeloma Cancer Stem Cells

Carol Ann Huff, William Matsui

From the Sidney Kimmel Comprehensive Cancer Center and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD

Corresponding author: William Matsui, MD, Department of Oncology, Johns Hopkins University School of Medicine, CRB245, 1650 Orleans St, Baltimore, MD 21231; e-mail: matsuwi{at}jhmi.edu

Multiple myeloma is characterized by the clonal expansion of neoplastic plasma cells within the bone marrow, elevated serum immunoglobulin, and osteolytic bone disease. The disease is highly responsive to a wide variety of anticancer treatments including conventional cytotoxic chemotherapy, corticosteroids, radiation therapy, and a growing number of agents with novel mechanisms of action. However, few if any patients are cured with these modalities and relapse remains a critical issue. A better understanding of clonogenic multiple myleoma cells is essential to ultimately improving long-term outcomes, but the nature of the cells responsible for myeloma regrowth and disease relapse is unclear. We review evidence that functional heterogeneity exists in multiple myeloma and discuss potential strategies and clinical implications of the stem-cell model of cancer in this disease.

Supported by Grants No. CA107040, CA93657, CA1539632 from the National Institutes of Health, The International Myeloma Foundation, The Sidney Kimmel Foundation for Cancer Research, and by the American Society of Clinical Oncology.

Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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