Yeah, I’m sure that we will see even more biomarkers. At this time point, it’s actually very few which are in clinical practice. For melanoma, it’s only PD-L1. But in a broader perspective, it’s PD-L1 and tumor mutational burden. But we do have a lot of indicators of whether a patient will respond or not. And I believe that these kind of signatures, for example, interferon gamma signatures, which are a level of expression of inflammation in the tumor lesion will be important...
Yeah, I’m sure that we will see even more biomarkers. At this time point, it’s actually very few which are in clinical practice. For melanoma, it’s only PD-L1. But in a broader perspective, it’s PD-L1 and tumor mutational burden. But we do have a lot of indicators of whether a patient will respond or not. And I believe that these kind of signatures, for example, interferon gamma signatures, which are a level of expression of inflammation in the tumor lesion will be important. But also, I would say that we could also look into more of the genomic profile of the cells and of the tumor microenvironment. And here we had a presentation at a late-breaking abstract by Mario Presti, who also looked into these kind of refractory mechanisms also for TIL therapy, which looked like what we have already seen for checkpoint inhibitors, that you have a downregulation of all these immune-supporting pathways during this refractory development.
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