Clonal evolution of AML on novel FMS-like tyrosine kinase-3 (FLT3) inhibitor therapy with evolving actionable targets

Pashtoon M. Kasi, Mark R. Litzow, Mrinal M. Patnaik, Shahrukh K. Hashmi, Naseema Gangat

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (Clinical Trial: NCT02014558; registered at: 〈. https://clinicaltrials.gov/ct2/show/NCT02014558〉).

Original languageEnglish (US)
Pages (from-to)7-10
Number of pages4
JournalLeukemia Research Reports
Volume5
DOIs
StatePublished - 2016

Keywords

  • ASP2215
  • Acute Leukemia
  • Clonal evolution
  • FMS-like tyrosine kinase-3 (FLT3) inhibitors
  • Philadelphia chromosome (BCR-ABL)
  • Ponatinib

ASJC Scopus subject areas

  • Hematology
  • Oncology

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