We know for a few years that the microenvironment, the non-immune microenvironment, actually participates in the pathogenesis of the myeloma. We know that the stromal cells are producing a number of cytokines and growth factors that contribute to the growth of the myeloma cells, but we don’t really know the details on how this system is working. We are accumulating more information, but as I said, the difficulties are actually being able to interrogate the right cells and to do the functional assays to demonstrate that these cytokines, that these other cell-to-cell interaction mechanisms may actually be participating in how they induce the progression and actually how they induce resistance to therapy...
We know for a few years that the microenvironment, the non-immune microenvironment, actually participates in the pathogenesis of the myeloma. We know that the stromal cells are producing a number of cytokines and growth factors that contribute to the growth of the myeloma cells, but we don’t really know the details on how this system is working. We are accumulating more information, but as I said, the difficulties are actually being able to interrogate the right cells and to do the functional assays to demonstrate that these cytokines, that these other cell-to-cell interaction mechanisms may actually be participating in how they induce the progression and actually how they induce resistance to therapy. We know, for instance, that when we treat myeloma cells, just plain myeloma cells, with chemotherapy, the cells respond very rapidly. However, when we establish more complex microenvironment culture systems including mesenchymal stromal cells and other types of cells, the response to the different therapies varies. So that means that those cells are interfering with the efficacy of the drugs and that’s something that happens in vivo. So we really need to understand that to be able to improve our therapies.
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