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iwAL 2026 | Exploring CARM1 as a leukemia-specific stem cell vulnerability whilst retaining normal hematopoiesis
Stephen Nimer, MD, Sylvester Comprehensive Cancer Center, University of Miami Health System, Miami, FL, discusses the potential of targeting leukemia stem cell vulnerabilities that are sufficiently leukemia-specific to provide a therapeutic window, highlighting his lab’s work on CARM1, which has shown that deleting CARM1 can eliminate leukemia without impacting normal stem cells. Dr Nimer notes that this approach, along with CAR T-cell therapies, may offer a way to target leukemic cells while sparing normal hematopoiesis. This interview took place at the 8th International Workshop on Acute Leukemias (iwAL 2026), held in Boston, MA.
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Transcript
It’s a perfect opportunity to talk about some work from my lab, which I will be talking about on Saturday, that relates to CARM1, which is a protein arginine methyltransferase. We created a knockout mouse, and the hematopoiesis of the knockout mouse is pretty normal. So normal stem cell self-renewal does not require CARM1. If we try to initiate leukemia with AML1-ETO, with MLL-AF9, we cannot initiate leukemia in these otherwise normal stem cells that lack CARM1...
It’s a perfect opportunity to talk about some work from my lab, which I will be talking about on Saturday, that relates to CARM1, which is a protein arginine methyltransferase. We created a knockout mouse, and the hematopoiesis of the knockout mouse is pretty normal. So normal stem cell self-renewal does not require CARM1. If we try to initiate leukemia with AML1-ETO, with MLL-AF9, we cannot initiate leukemia in these otherwise normal stem cells that lack CARM1. And if we establish the leukemia and then we delete CARM1, the leukemia disappears. So there are some other targets like CARM1, but that work seems to identify exactly the goal. We can eliminate the leukemia. We don’t impact the normal stem cells. And I think that’s the goal. We’ve heard today also about CAR T-cell approaches that may be able to target the leukemic cell and leave normal hematopoiesis. So that’s the holy grail.
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