Best Practice & Research Clinical Haematology
Volume 21, Issue 1 , Pages 13-20, March 2008

Can FLT3 inhibitors overcome resistance in AML?

  • Winnie F. Tam, PhD
    • ,
  • D. Gary Gilliland, PhD, MD

      Affiliations

    • Corresponding Author InformationDepartment of Medicine, Brigham and Women's Hospital, 1 Blackfan Circle, Room 5.0210, Boston, MA 02115, USA. Tel.: +1 (617) 355 9092; Fax: +1 (617) 355 9093.

Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Dana-Farber Cancer Institute, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA, USA

The identification of FLT3 mutations across a range of the cytogenetic subgroups of AML has opened up the possibility of a targeted therapeutic approach with broad applicability. Four agents are currently in clinical trials, at least 3 of which have both sufficient activity against AML and sufficiently acceptable toxicity profiles to support continued efforts to refine their inclusion into therapeutic regimens for AML. Better understanding of the genetics of inherent and acquired resistance is needed to guide development of second-generation agents. Optimizing the integration of FLT3 inhibitor therapy with chemotherapy has the potential both to decrease toxicity and improve response.

Key words: FLT3 inhibitors, resistance, staurosporine, midostaurin, PKC412, tandutinib, MLN 518, lestaurtinib, CEP701, SU11248, AML

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PII: S1521-6926(07)00093-X

doi:10.1016/j.beha.2007.11.003

Best Practice & Research Clinical Haematology
Volume 21, Issue 1 , Pages 13-20, March 2008

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