Tomorrow I will be presenting the results of this Phase 1/2 clinical trial using ipilimumab, nivolumab, and trabectedin for advanced leiomyosarcoma. And the results of the study. I believe it is a small study, but I believe it has the potential of being a game changer for patients with advanced leiomyosarcoma.
The rationale, so why immunotherapy for advanced leiomyosarcoma? Previously, there have been scattered reports of activity or anti-tumor activity of immunotherapy in patients with sarcoma, but not with leiosarcoma...
Tomorrow I will be presenting the results of this Phase 1/2 clinical trial using ipilimumab, nivolumab, and trabectedin for advanced leiomyosarcoma. And the results of the study. I believe it is a small study, but I believe it has the potential of being a game changer for patients with advanced leiomyosarcoma.
The rationale, so why immunotherapy for advanced leiomyosarcoma? Previously, there have been scattered reports of activity or anti-tumor activity of immunotherapy in patients with sarcoma, but not with leiosarcoma. And it’s not definitive. I believe we are the first to study the combination of chemotherapy and immunotherapy together for advanced leiomyosarcoma. The decision to do this is based on the fact that sarcoma cells are more immunogenic at the onset earlier in the course of the disease. And it undergoes a process called cancer immuno-editing during the time when you’re giving chemotherapy and radiation therapy.
So while they are quiet at the time, they undergo immuno-editing of themselves so that at the end they become anergic. Meaning to say they’re no longer immunogenic. And the reason that many of the studies don’t work is because they’re giving it at the very end when the cancer cells are non-immunogenic. Okay. So our hypothesis then is that if you gave it earlier at the onset, or earlier in the course of the disease, that this immunotherapy combined with chemotherapy, which is an immune modulator, will be most effective for patients with advanced leiomyosarcoma and the rationale for this, again, the mechanism of action is that ipilimumab blocks the CTLA-4 receptor present in T-cells and nivolumab blocks the PD-1 receptor present in T-cells. And when you block PD-1, you also will block, as an effect, the interaction between PD-1 and PD-L1 that is present in tumor cells. Now ipilimumab then does those things and the other part of it, so there’s nivolumab and ipilimumab, then there is T called trabectedin, which is not only a cytotoxic chemotherapy, but it also is an immune modulator and it will deplete. In addition to killing the cancer cells, it will deplete the growth promoting macrophages in the tumor micro environment. And the net effect of that, of course, is tumor eradication.
