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Sequencing immune-based therapies in B-cell malignancies
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Crosstalk between Multiple Myeloma (MM) cells and bone marrow (BM) cells is critical for disease maintenance and progression, and therefore understanding the mechanism of this crosstalk is likely to provide clues for future therapeutic targets. In a recent article published in Blood in April 2017 by Vikas Gupta and colleagues from the Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, USA, MM cells were shown to strongly depend on expression of Mcl-1, which in turn was driven by signals emanating from Interleukin-6 (IL-6) secreted from BM stromal cells. Targeting IL-6 removed Mcl-1 dependence and sensitized MM cells to inhibitors of Bcl-2 and Bcl-2/Bcl-xL.
In conclusion, soluble IL-6 secreted from stromal cells is a dominant factor regulating Bcl-2 family dependence. This study, therefore, provides a rationale for a treatment regimen in which IL-6 inhibitors (such as siltuxumab) and JAK and/or MEK inhibitors (such as trametinib) are given to enhance Bcl-2 dependence, and are also combined with a specific Bcl-2 inhibitor, such as venetoclax. It will be intriguing to see data from future trials to assess these combined regimens.
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