Polyclonal heterogeneity: The new norm for secondary clinical resistance to targeted monotherapy in relapsed leukemia?

Andrew H. Wei, Andrew W. Roberts

Research output: Contribution to journalArticleOtherpeer-review

4 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)998-1000
Number of pages3
JournalCancer Discovery
Volume9
Issue number8
DOIs
Publication statusPublished - 1 Aug 2019

Cite this