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Single Cell Sequencing of Polyclonal Resistance to FLT3 Inhibitors in AML

Catherine Smith, MD
Monday, April 23, 2018
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Chapters

  • Introduction
    • FLT3: The Most Frequently Mutated Gene in AML
      • FLT3 Mutations in AML
        • FLT3 KD Mutations are the Most Frequently Described Resistance Mechanism in Patients
          • On-Target and Off-Target Resistance: Mutually Exclusive?
            • ASP2215 (GILTERITINIB): A Type I AXL/FLT3 Inhibitor
              • ASP2215 Achieves >40%CRC in R/R FLT3 Mutant AML
                • Study Design
                  • Acquired Somatic Mutations
                    • Resistance Mechanisms to FLT3 Inhibitors: Role of Clonal Heterogeneity
                      • Resistance Mechanisms to FLT3 Inhibitors: Clonal Heterogeneity
                        • NRAS Mutations Confer Resistance to GILTERITINIB
                          • Tapestri Analysis UCSF 4169
                            • Tapestri Analysis PENN 4885
                              • Tapestri Analysis PENN 5475
                                • Longitudinal Analysis Reveals Preexisting Resistant Clones
                                  • Single-Cell Analysis Can Uniquely Inform Therapy
                                    • Summary: Clinical Resistance to FLT3 Inhibitors
                                      • Acknowledgements
                                        • Audience Questions

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