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iwAL 2025 | Key genomic and epigenetic drivers of clonal evolution in therapy-related myeloid neoplasms
Koichi Takahashi, MD, The University of Texas MD Anderson Cancer Center, Houston, TX, comments on the key genomic and epigenetic drivers of clonal evolution in therapy-related myeloid neoplasms. Dr Takahashi highlights the importance of P53 mutations, which have the highest leukemic potential, and suggests potential mechanisms for clonal evolution. This interview took place at the 7th International Workshop on Acute Leukemias (iwAL 2025), held in Washington, DC.
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Transcript
From genetically, we definitely learned that P53 mutated clonal hematopoiesis really has the highest leukemic potential. But the question is, from our study, is that one patient can have multiple different types of P53 mutated clones, and theoretically, each clone has almost equal potential to become leukemia, but only one becomes leukemia. And the question is, what determines that? And one finding that we found is that additional chromosomal abnormality, particularly if you lose the other allele of p53, that really determines the transformation...
From genetically, we definitely learned that P53 mutated clonal hematopoiesis really has the highest leukemic potential. But the question is, from our study, is that one patient can have multiple different types of P53 mutated clones, and theoretically, each clone has almost equal potential to become leukemia, but only one becomes leukemia. And the question is, what determines that? And one finding that we found is that additional chromosomal abnormality, particularly if you lose the other allele of p53, that really determines the transformation. But then what exactly determines that is another question. And I think there will be some epigenetic component that in our study we couldn’t really tease that out because we really focused on the genetic analysis. But I think the future question and future project will focus on epigenetic determinants of clonal selection.
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