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Deciphering the mechanisms of resistance to these drugs requires the dissection of AML at a single-cell level.

Acute myeloid leukemia (AML) is a highly heterogeneous hematological malignancy characterized by the overproduction of abnormal myeloblasts. Gene mutation-targeted therapies are a treatment option for patients with relapsed/refractory AML. For patients with FLT3 mutated AML, the FLT3 inhibitors (FLT3i), gilteritinib and quizartinib, can improve patient outcomes.

However, the development of secondary resistance to these drugs remains a major challenge. The acquisition of new mutations and the emergence of new subclones during the course of therapy can drive relapse. Although conventional bulk DNA sequencing can be used to identify the mutations in an entire sample, it cannot identify the mutations present in individual clones. Rather, deciphering the mechanisms of resistance to these drugs requires the dissection of AML at a single-cell level.

In this webinar, the speaker will discuss studies that investigate the genotype-immunophenotype relationships of AML and uncover mechanisms of resistance to FLT-3 inhibitors (gilteritinib and quizartinib) and chemotherapy treatment. She will discuss the role of off-target (non-FLT3) mutations that activate downstream RAS–MAPK pathways as well as heterogeneity in FLT3 kinase domain (KD) mutations. Given the clinical relevance of these results, she will highlight the potential to use single-cell DNA sequencing to inform combination therapies and dynamic strategies for improved treatment of AML.

Join Dr. Catherine Smith, MD, Assistant Professor, Division of Hematology/Oncology, Department of Medicine, UCSF in a live webinar on Thursday, May 6, 2021 at 1pm EDT.

For more information, or to register for this event, visit Acute Myeloid Leukemia (AML): Utilizing Single-Cell Multi-Omics to Uncover its Evolution and Resistance Mechanisms.

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