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Adhesion of multiple myeloma cells to the bone marrow microenvironment: implications for future therapeutic strategies
Affiliation:1. Barwon South Western Regional Integrated Cancer Services, Barwon Health, Geelong, Victoria, Australia;2. Andrew Love Cancer Centre, Barwon Health, Geelong, Victoria, Australia;3. Pattern Recognition and Data Analytics, Deakin University, Geelong, Victoria, Australia;4. School of Medicine, Deakin University, Geelong, Victoria, Australia;1. Integrative Program for Biological and Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA;2. Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA;3. Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA;1. Department of Surgery, Stony Brook Medicine, Stony Brook, NY;2. Department of Medicine, Stony Brook Medicine, Stony Brook, NY;3. Department of Family, Population and Preventive Medicine, Stony Brook Medicine, Stony Brook, NY;1. Neon Therapeutics/BioNTech US, Cambridge, MA, USA;2. Dana Farber Cancer Institute, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA, USA;3. Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA;1. Department of Surgery, Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Washington University School of Medicine, Saint Louis, MO, USA;2. Department of Medicine, Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Washington University School of Medicine, Saint Louis, MO, USA;3. Department of Pathology and Immunology, Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Washington University School of Medicine, Saint Louis, MO, USA;4. Department of Radiation Oncology, Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Washington University School of Medicine, Saint Louis, MO, USA;5. Mallinckrodt Institute of Radiology, Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Washington University School of Medicine, Saint Louis, MO, USA
Abstract:Multiple myeloma is characterized by excess plasma cells within the bone marrow in association with monoclonal antibody protein in the serum and/or urine. Tumor cells localize within the marrow via an interaction of cell-surface adhesion molecules with their respective ligands on marrow stromal cells and extracellular matrix proteins. Stimulation of myeloma cells via these cell-surface molecules, either directly or via tumor cell adhesion to stromal cells, can induce autocrine or paracrine tumor cell growth mediated by interleukin 6. It might therefore be possible to develop innovative treatment strategies either to inhibit interleukin 6 production or to interrupt interleukin 6 signal transduction in multiple myeloma.
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