Oncology Exchange Discourse Apr 2006: Multiple Myeloma

MULTIPLE MYELOMA
A new era for an old disease

Nizar J. Bahlis, MD and Douglas A. Stewart, MD, FRCPC

MM cells are generated exclusively in the postgerminal centers, from B cells that have already undergone somatic hypermutation, antigen selection and immunoglobulin heavy chain (IgH) switch recombination (a type of DNA rearrangement). Errors — mutations or double-strand DNA breaks — in these specific DNA modifications result in the interposition of an oncogene near the immunoglobulin enhancer.

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Top-line summary

Multiple myeloma (MM) is the second most common hematologic malignancy, after non-Hodgkin’s lymphoma. It affects nearly 2000 Canadians per year with higher prevalence among men in their fifth to eighth decade. A clonal disorder of terminally differentiated B lymphocytes or plasma cells, it is characterized by a myriad of symptoms including bone pain and fractures, fatigue, neuropathy and recurrent infections. These symptoms result from the expansion (from a single progenitor cell) of plasma cells in the bone marrow leading to cytopenias, renal failure and loss of bone density due to osteoclast activation. The primary approach to treatment of multiple myeloma is systemic antineoplastic therapy. Conventional chemotherapy offers patients a median survival of approximately 3 years. Seminal advances over the last decade have led to better understanding of the biology and genetics of this disease, establishment of new prognostic indicators and, most importantly, introduction of new therapies that positively alter its natural history. Here, Oncology Exchange summarizes some of these developments, reviews recent therapeutic advances, including high-dose chemotherapy with stem cell rescue, and reports results with use of 2 novel classes of drugs, proteasome inhibitors and immunomodulatory drugs.

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