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Thursday, April 07, 2016 11:35:13 PM
Will that be the same in the current P3 trial? Maybe.
A little later in his presentation, he notes that "if they had progressive tumors at the time that we were beginning vaccination, OR if they had expression of some genes that are known to be immune inhibitors, such as TGF beta, or IL-10, that these patients didn’t mount responses. They didn’t induce T-cell infiltration after the vaccination." I do wonder if these patients represent the more rapid progression population of patients, because note that he states these patients were already progressing as they were beginning their vaccination.
But in this same presentation, he makes it clear that the mesenchymal patients, who often have the worst prognosis, have the longest survival. They theorize that this is because these patients are more immunogenic, whereas the Proneural and Classical, are not. The mesenchymal patients had more endogenous T-cells - even before their therapy started. And after therapy, that had a significantly higher T-cell count.
In fact, they all have a significantly higher T-cell count after DCVax. However, the macrophages and myeloid cells in these less immunogenic subtypes (Proneural and Classical), were actually expressing PDL-1.. which in turn blinded to the T-cells and turned OFF their functional activity.
So their thinking is that if they induce a T-cell response, AND block a negative regulatory molecule with an antibody, they can then get a significant rejection of the tumor for these other subtypes as well.
Don't I just sound like I know exactly what I'm talking about here? That's because I transcribed that entire section, lol, and now have a more clear understanding of their line of thinking. :)
Here it is from minute 8:24 up to where he talks about the partnering with BMS and Merck. I stopped there for now, although the remaining portion is also important. It's time for a drink though. :)
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