Of course, linked to what I have just said, it’s very, very important to know more about the biology of leukemia relapse because it’s, as I said, we can have different type of relapse. Some can be genetic, some others, even more, I may say, are not genetic. So, it’s very important to know by using, by using specific technologies, the nature of relapse. And luckily, we have now several possibility to treat patients with this type of relapse, which is epigenetic...
Of course, linked to what I have just said, it’s very, very important to know more about the biology of leukemia relapse because it’s, as I said, we can have different type of relapse. Some can be genetic, some others, even more, I may say, are not genetic. So, it’s very important to know by using, by using specific technologies, the nature of relapse. And luckily, we have now several possibility to treat patients with this type of relapse, which is epigenetic.
As I said, we can use, we have already in use in clinical trials, hypomethylating agents for those patients that show the other motivation of the promoter of CPTA. We can use several compounds targeting PRC2 complex. PRC2 is a repressor complex that close the chromatin at the level of the target genes. So, if you target this complex or the subunit of this complex, you can recover the phenotype and then rendering the leukemia cells, again, susceptible to the action of the T-cells.
It’s not just that. We have sever several compounds, epigenetic compounds with small molecules that are actually in use. So azacitidine, again, [inaudible] hypomethylating agents and several other compounds that can act or to epigenetics in order to treat these patients. Of course, we need more research about this in order to uncover the other mechanism. As I said, that’s another mechanism, which is the up-regulation of PD-1 or PD-L1 on the leukemic cells. So, it’s very important to uncover the genetic basis of this in order to find the way of closing the chromatin in this, in these specific cases, in order to rescue the leukemia, the graft-versus-leukemia effect.
