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ASH 2025 | Genetic and metabolic drivers of Richter’s transformation
Elisa Ten Hacken, PhD, Weill Cornell Medicine, New York, NY, briefly discusses the genetic and metabolic drivers of Richter’s transformation, their impact on the tumor microenvironment, and how immunocompetent mouse models are advancing understanding of immunotherapy response and resistance. This interview took place at the 67th ASH Annual Meeting and Exposition, held in Orlando, FL.
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Transcript
We do see a combination of events. Richter’s is such a dramatic change in CLL disease course. It is characterized by a change in morphology of the CLL cell itself, which depends on enhanced metabolism, so tumor intrinsic changes that depend on genetics. And in turn, these genetic events change the way the cell behaves with respect to the microenvironment, including the interaction with T cells and myeloid cells and facilitating immune evasion and facilitating disease transformation...
We do see a combination of events. Richter’s is such a dramatic change in CLL disease course. It is characterized by a change in morphology of the CLL cell itself, which depends on enhanced metabolism, so tumor intrinsic changes that depend on genetics. And in turn, these genetic events change the way the cell behaves with respect to the microenvironment, including the interaction with T cells and myeloid cells and facilitating immune evasion and facilitating disease transformation. And because we’re now having the ability to build immunocompetent mouse models, we can learn more about the tumor microenvironment, which is also a key part in how these Richter’s transformation cases respond to immunotherapy, which is widely used. We’ve heard a lot at the meeting about novel use of immune checkpoint blockade, bispecifics, CAR-T, but we still incompletely understand when and how they work and what are the mechanisms of response and resistance.
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