Indeed, it is up-regulated when the stem cells acquire a JAK mutation. We also know it’s higher as the disease progresses. So because it’s sort of a level of expression, the higher the level certainly would correlate with a poor phenotype. And so I think it is a very interesting question. We haven’t examined that rigorously, but we do know, for example, even in platelets, so platelet transcriptomes, we can see higher levels of HMGA in more advanced disease...
Indeed, it is up-regulated when the stem cells acquire a JAK mutation. We also know it’s higher as the disease progresses. So because it’s sort of a level of expression, the higher the level certainly would correlate with a poor phenotype. And so I think it is a very interesting question. We haven’t examined that rigorously, but we do know, for example, even in platelets, so platelet transcriptomes, we can see higher levels of HMGA in more advanced disease. And so I think it’s quite an interesting question because platelets and blood cells can easily be taken. All of our patients get their blood drawn frequently. And so we could look at levels. The thing we don’t know is whether or not the high level precedes the progression or if it’s concurrent with progression. But certainly when we see it in our patient samples using diverse approaches to look at gene expression, it correlates with poorer outcomes in advanced disease.
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