One of the prevailing hypotheses for disease progression in advanced platinum-resistant ovarian cancer has been the role of these myeloid-type cells in promoting metastases and basically making the tumor a more hostile place for T cell-based therapies to work. So what we did was we had two parallel studies, two parallel expansion studies, where we took two different approaches...
One of the prevailing hypotheses for disease progression in advanced platinum-resistant ovarian cancer has been the role of these myeloid-type cells in promoting metastases and basically making the tumor a more hostile place for T cell-based therapies to work. So what we did was we had two parallel studies, two parallel expansion studies, where we took two different approaches. In one approach, we tried to stimulate these myeloid cells to be more inflammatory, so perhaps we could recruit them to help fight the cancer. And in a separate parallel study, we re-tuned or we deleted the macrophages and these myeloid cells. Basically, take them out of the equation. The hypothesis there being that if you remove them, perhaps you would create a more favorable microenvironment. What we found was that in either case, whether you stimulated these myeloid cells and made them more pro-inflammatory, or you deleted them and took them off the chessboard completely, the results were fairly the same, which was stable disease. So we were able to stabilize the disease, but not really accomplish any meaningful shrinkage in either. Thankfully, both treatments were manageable in terms of the toxicities. And what this tells us is that our hypothesis for the roles of myeloid cells, at least in ovarian cancer, might need to be re-examined. We’ve seen them play more active roles in other disease types, but in ovarian cancer, at least in the platinum resistance setting, their roles in tumor initiation and tumor maintenance might actually be distinct entities, which will require further testing in either the platinum sensitive setting or even in the newly diagnosed setting.
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