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ASH 2025 | Phenotypic heterogeneity and remodeling drive resistance to venetoclax treatment in AML
Koichi Takahashi, MD, The University of Texas MD Anderson Cancer Center, Houston, TX, discusses the findings of a study analyzing longitudinally collected bone marrow samples from a clinical trial (NCT03404193) of decitabine and venetoclax in patients with acute myeloid leukemia (AML). Dr Takahashi highlights that the study identified gene expression signatures that may predict treatment response and revealed that venetoclax resistance is driven by changes in the phenotypic or differentiation states of leukemia cells. This interview took place at the 67th ASH Annual Meeting and Exposition, held in Orlando, FL.
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Transcript
There was a clinical trial at MD Anderson several years ago using 10 days decitabine and venetoclax for acute myeloid leukemia patients. This trial was originally done by Dr. Marina Konopleva and also Dr. Courtney DiNardo. And in our lab, we stored these longitudinally collected bone marrow samples from this trial, and we essentially performed a multi-single-cell omics analysis, as well as bulk RNA sequencing...
There was a clinical trial at MD Anderson several years ago using 10 days decitabine and venetoclax for acute myeloid leukemia patients. This trial was originally done by Dr. Marina Konopleva and also Dr. Courtney DiNardo. And in our lab, we stored these longitudinally collected bone marrow samples from this trial, and we essentially performed a multi-single-cell omics analysis, as well as bulk RNA sequencing. There were a few highlights from the analysis of this that we first identified gene expression signatures that may be able to predict the treatment response against the decitabine and venetoclax treatment. And secondly, through this single-cell multi-omics study, we revealed that the venetoclax resistance is not only through acquisition of new genetic mutations or emergence of the new clone, but actually these leukemia cells change their phenotypic states or differentiation states and that itself may cause the resistance against the venetoclax treatment. This has been known from other previous works like monocytic cells may be resistant to venetoclax but in our work we also highlight that other cell states like erythroid cell states or the dendritic cell states may also contribute to the resistance. So those are the new findings from these studies.
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