Manmeet S. Ahluwalia, MD, Department of Internal Medicine, Fairview Hospital, Cleveland Clinic Health System, Cleveland, OH, USA.
Hamed A. Daw, MD, The Cleveland Clinic Cancer Center, Cleveland, OH, USA.

Multiple myeloma (MM) is a neoplasm of plasma cells that is characterized by tumour cell tropism of the bone marrow and production of monoclonal immunoglobulins (Ig) detectable in serum and/or urine. It often manifests as one or more of lytic bone lesions, monoclonal protein in the blood or urine, disease in the bone marrow, renal failure, anemia, and hypercalcemia. Better understanding of the biology of myeloma has led to the development of agents, such as bortezomib, CC-5013, and thalidomide, that target the myeloma cell and the bone-marrow microenvironment. Ongoing trials promise to define the roles of new agents, mini-allogeneic transplantation, and maintenance therapy.
Key words: bone marrow, biology, transplant, chemotherapy, multiple myeloma.

Richard A. Wells, MD, DPhil, FRCP(C), Assistant Professor of Medicine, University of Toronto; Staff Physician, Leukaemia Group, Princess Margaret Hospital; Scientist, Ontario Cancer Institute, Toronto, ON.

In myelodysplastic syndrome (MDS), genetic mutations in bone marrow stem cells result in production of defective blood cells. These defective cells fail to meet the intrinsic "quality control" standards of the bone marrow and are not released into the circulation, leading to anemia, leukopenia or thrombocytopenia. In some, but not all, patients with MDS, there also is a greatly increased risk of development of acute myelogenous leukemia. Until very recently, therapeutic options in MDS were extremely limited. This article reviews recent advances in risk-based classification of MDS, and describes new therapies that promise to revolutionize our approach to patients with this disorder.
Key words: myelodysplastic syndrome, bone marrow, anemia, acute myelogenous leukemia.

Kimby N. Barton, MSc
Associate Editor,
Geriatrics & Aging.

If you have ever known anyone with any degree of heart trouble you may be aware of the options available for the treatment of heart disease. We have medications that treat hypertension, medications that lower lipids and medications to prevent clotting. We can use diet and exercise to keep our arteries clear and our heart muscle healthy. But can we repair a heart once cells have been lost? Coronary heart disease accounts for 50% of all cardiovascular deaths and nearly 40% of the incidence of heart failure. Heart attacks lead to the death of vital cardiac myocytes and impair cardiac performance. The cells that survive an MI are unable to reconstitute the tissue that is lost, and eventually the heart begins to deteriorate. The victims of heart attack and their caregivers are well aware of the slow progression from heart attack to heart failure, and the lack of available therapies to stop this progression.

What if there was a way to re-vitalize the damaged cell population or to replace the cells that are lost? Unfortunately, in order to form a functional cardiac unit, the replacement cells must be able to survive, mature, electromechanically couple with pre-existing heart cells and have a beneficial effect on the function of the damaged heart.

Injury to a target organ is sensed by distant stem cells; these cells migrate to the site of damage and then differentiate, promoting structural and functional repair.