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Cancer Discov. 2019 Aug;9(8):998-1000. doi: 10.1158/2159-8290.CD-19-0575.

Polyclonal Heterogeneity: The New Norm for Secondary Clinical Resistance to Targeted Monotherapy in Relapsed Leukemia?

Wei AH1,2, Roberts AW3,4,5.

Author information

1
The Alfred Hospital, Melbourne, Victoria, Australia.
2
Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
3
Royal Melbourne Hospital and Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia. roberts@wehi.edu.au.
4
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
5
Centre for Cancer Research, University of Melbourne and the Victorian Comprehensive Cancer Centre, Parkville, Victoria, Australia.

Abstract

In this issue, McMahon and colleagues demonstrate that secondary clinical resistance to the FLT3 inhibitor gilteritinib in relapsed acute myeloid leukemia is often polyclonal and commonly mediated by heterogeneous mutations that activate downstream RAS-MAPK pathways. These findings and recent data from others indicate that emergence of multiple clones, each with distinct mechanisms of resistance, is a common finding at secondary failure of single-agent-targeted therapies for relapsed leukemias.See related article by McMahon et al., p. 1050.

PMID:
31371322
DOI:
10.1158/2159-8290.CD-19-0575
[Indexed for MEDLINE]

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