So the MRD is very important. Right now obviously it doesn’t dictate how we do induction and consolidation. We like to see though, we like to see if our patients achieve MRD negativity. For example, for FLT3 now we have much more sensitive assays, NGS assays, and we can detect the FLT3 at a sensitivity level of 10 to the minus 5, 10 to the minus 6. So patients who achieve MRD negativity, we know that the risk of relapses in general is lower in these patients...
So the MRD is very important. Right now obviously it doesn’t dictate how we do induction and consolidation. We like to see though, we like to see if our patients achieve MRD negativity. For example, for FLT3 now we have much more sensitive assays, NGS assays, and we can detect the FLT3 at a sensitivity level of 10 to the minus 5, 10 to the minus 6. So patients who achieve MRD negativity, we know that the risk of relapses in general is lower in these patients. But for the FLT3 purposes, obviously with the FLT3 ITD mutated patients right now, the general consensus is that they proceed with allogeneic transplant as a consolidation treatment. So, and when they go to transplant, we do FLT3 MRD assay before transplant, after transplant. And particularly patients who have MRD positivity in the peritransplant era, before or after, we know that the FLT3 inhibitors benefit those patients. It increases the risk of relapse. I’m sorry, it decreases the risk of relapse in these patients. That’s why we like to use FLT3 inhibitors. However, patients who already achieve a deep MRD negativity, the benefit of FLT3 inhibitors are not clear at this point. So technically, if they are MRD negative, adding FLT3 inhibitor, I’m talking based on the data from the Morpho trial with gilteritinib, we know that the overall survival is overlapping in those patients. But right now, if they are MRD positive, yes, it dictates how we treat. We do put these patients on FLT3 inhibitors as a maintenance therapy after allogeneic transplant.
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