Yeah, I think it fits very well. I mean, basically what we have learned so far, to make it very simple, and of course also the subject of my talk, is that we have to convert cold tumors into hot tumors, or inflamed tumors, to put it more precisely, to have immunotherapy work. And the patients that do not have inflamed environments, they are not responding to immunotherapy...
Yeah, I think it fits very well. I mean, basically what we have learned so far, to make it very simple, and of course also the subject of my talk, is that we have to convert cold tumors into hot tumors, or inflamed tumors, to put it more precisely, to have immunotherapy work. And the patients that do not have inflamed environments, they are not responding to immunotherapy. And what we see is that we basically need to target these difficult tumors in many different ways. So you need to combine, you could say, as many pathways as possible in each patient to get success. So I visualize that you will have multiple combinations in the coming years, even though we have had, you can say there have been a lot of disappointments in the last couple of years with some of these trials, but you need to look at the biology and think about what makes sense. If you think about immunomodulatory vaccines and checkpoint inhibitors. In the immunomodulatory vaccine, you can basically both target the immune suppressive environment, but you can also start de novo T-cell activity within the environment. And you need T-cell inflammation to get checkpoint inhibitors to work. So that biologically makes sense to combine. So that is how you need to develop future immunotherapy.
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