Create your Personal Health Record and unlock support built around you
- Treatments and trials you qualify for
- Education for your stage of care
- Financial support for your medications
- Solutions to your side effects

What Drives Myeloma Relapse? Myeloma Stem Cells May be the Cause with Dr. William Matsui, MD, Johns Hopkins School of Medicine
Dr. William Matsui, MD Johns Hopkins School of Medicine Interview Date: May 6, 2016
Dr. William Matusi of the Johns Hopkins School of Medicine wants to understand why myeloma patients almost always relapse. His study led him to understand the difference between myeloma B-cells (stem cells) and more mature myeloma plasma cells. He noticed that the B-cells could generate more tumor cells while the mature plasma cells could not and also noticed that they were different in their sensitivity to chemo. Additionally, proteasome inhibitors target the proteins on the myeloma cells' surface, but these early B-cells don't make a lot of protein.To add more complexity, as a patient relapses, their M-spike number becomes less informative as to how their disease is or is not progressing. Because these B-cells can be counted in a patient's blood, Dr. Matsui is measuring levels with a special flow cytometry test. He shares his research of borrowing B-cell treatments like rituximab from lymphoma, but found that the CD20 target typically used for this type of blood cancer didn't work in myeloma. When he used a new CD19 target, however, he saw dramatic impact in multiple myeloma and he believes that the recent UPenn success further validates the idea that CD19 could be present on myeloma stem cells.
Thanks to our episode sponsor
Dr. William Matsui, MD Johns Hopkins School of Medicine Interview Date: May 6, 2016
Dr. William Matusi of the Johns Hopkins School of Medicine wants to understand why myeloma patients almost always relapse. His study led him to understand the difference between myeloma B-cells (stem cells) and more mature myeloma plasma cells. He noticed that the B-cells could generate more tumor cells while the mature plasma cells could not and also noticed that they were different in their sensitivity to chemo. Additionally, proteasome inhibitors target the proteins on the myeloma cells' surface, but these early B-cells don't make a lot of protein.To add more complexity, as a patient relapses, their M-spike number becomes less informative as to how their disease is or is not progressing. Because these B-cells can be counted in a patient's blood, Dr. Matsui is measuring levels with a special flow cytometry test. He shares his research of borrowing B-cell treatments like rituximab from lymphoma, but found that the CD20 target typically used for this type of blood cancer didn't work in myeloma. When he used a new CD19 target, however, he saw dramatic impact in multiple myeloma and he believes that the recent UPenn success further validates the idea that CD19 could be present on myeloma stem cells.
Thanks to our episode sponsor

William Matsui, MD

Jennifer Ahlstrom
