By now you might have heard about the light snowfall that covered the Atlanta area this past week where the American Society of Hematology 2017 meeting was held.
Unfortunately, these wintry weather conditions prevented the Support Group Leaders from attending a day’s worth of oral presentations. It was a humbling reminder that when traveling one must be willing to adapt to the prevailing conditions. I try and apply this same mindset to my journey with multiple myeloma. It is now a way of life and adjustments must be made in my daily life going forward.
Despite the delays, the meetings yielded a great deal of information about the new treatments therapies for myeloma. One such therapy that was covered was chimeric antigen receptor T-cell (CAR-T) therapy. The basis of this treatment is using one’s own white cells which are removed from the blood by leukapheresis. This process is similar to harvesting stem cells that have been used for stem cell transplants. These T- cells are then taken to a lab where they are activated and genetically modified using a virus to encode a chimeric antigen receptor. Modified cells target a specific protein on the myeloma cell and these T-cells then attach and destroy the myeloma cell. Prior to infusion of the cells, they are multiplied in the lab the collected and re-infused into the patient who has been pretreated to accept these engineered cells. Redesigned T-cells can multiply and survive circulating in the body for a period of time.
The most common and most serious side effects with this treatment are cytokine release syndrome (CRS) and neurotoxicity. CRS is an overwhelming immune response that causes multiple organs in the body to fail but with careful observations these toxicities can be controlled and reversed. This aggressive therapy has been successfully performed in children and adults with relapsed/refractory lymphomas.
Trials for CAR-T therapy are now being carried out in patients with refractory/relapsed multiple myeloma studies from china have paired two sets of CAR-T cells against two targeted proteins on myeloma cells.
Another topic of interest to me is the method for measuring residual or recurrent disease during or after treatment. Minimal Residual Disease (MRD) in various treatment regimens has been reported in oral presentations. The test for MRD measures myeloma cells present in blood or bone marrow and can be a useful predictor of prognosis as well as success of therapy. This test is remarkable in its ability to detect a single malignant plasma cell among a million other normal cells. This is an important measurement because it may signal disease before biochemical or CRAB abnormalities occur in recurrent myeloma. In the future, the level of MRD will determine the efficacy of treatment with drug and non-drug therapies.
Also of interest are the encouraging results of treatment of smoldering multiple myeloma (SMM) with monoclonal antibodies. This early treatment differs from the idea of waiting for multiple myeloma to develop and suggests that the earlier treatment strategies result in improved prognosis. This idea may be proven by the ongoing study (iStopMM) in Iceland, which is funded by the IMF. The study will screen 140,000 adults over the age of forty for early signs of multiple myeloma.
Finally, I will share a quote from Dr. Joseph Mikhael, in which he states, “Myeloma is multiple in every way.” This suggests that there are may different treatment options for this complex disease. We are undoubtedly on the frontier of personalized regimens for treating this complex disease to achieve better outcomes.