By Jennifer Ahlstrom | Posted - May 3rd, 2016

 

 

 

 

Our Next Show: Killing Myeloma Stem Cells to Prevent Myeloma Progression Using a Monoclonal Antibody with Dr. William Matsui, Friday, May 6 @ 1 pm EST

Friday, May 6, 10 am PST, 11 am MST, Noon CST, 1 pm ESTCall In by Phone to Listen Live: (347) 637-2631 or Listen Live Via ComputerMyeloma stem cells are believed to cause the growth of multiple myeloma and can continue to mature into myeloma plasma cells, even while on treatment. Dr. Matsui tested a new monoclonal antibody with lenalidomide and dex. When len/dex were used alone, he saw myeloma stem cells increase by 2.5 times, but when the new monoclonal antibody was added, it decreased the myeloma stem cells by half. Learn more about this up and coming new immunotherapy in clinical trials that could potentially kill myeloma cells at their source. 

Dr. William Matsui is Professor of Oncology at the Sidney Kimmel Comprehensive Cancer Center. He is a Member of the Department of Oncology and Member of the Graduate Program in Pathobiology and Cellular and Molecular Medicine. He is on the editorial and review boards of Haematologica, Immunology and Immunogenetic Insights, is a SPORE recipient award researcher for lymphoma, has won multiple teaching awards in the Johns Hopkins departments of Medicine and Oncology and has received the Kimmel Foundation Scholar, Sidney Kimmel Foundation for Cancer Research award as well as the LLS Scholar in Clinical Research award. Presently and for the past six years he has served on the National Cancer Institute Investigational Drug Steering Committee (IDSC) and is Co-Chair for the Cancer Stem Cell Taskforce.

Thanks to our episode sponsor, Takeda Oncology.

multiple myeloma
 
Jennifer Ahlstrom
About the Author

Jennifer Ahlstrom - Jenny A - Myeloma survivor, patient advocate, wife, mom of 6. Believer that patients can help accelerate a cure by weighing in and participating in clinical trials. Founder of Myeloma Crowd, Myeloma Crowd Radio, HealthTree and the CrowdCare Foundation.

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