The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib-Reference-Cited by-同舟云学术

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The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib

Published:2013-01-16 Issue:6 Volume:27 Page:1416-1418
ISSN:0887-6924
Container-title:Leukemia
language:en
Short-container-title:Leukemia

Author:

Albers C,Leischner H,Verbeek M,Yu C,Illert A L,Peschel C,von Bubnoff N,Duyster J

Publisher

Springer Science and Business Media LLC

Subject

Oncology,Cancer Research,Hematology

Link

http://www.nature.com/articles/leu201314.pdf

Reference8 articles.

1. Zarrinkar PP, Gunawardane RN, Cramer MD, Gardner MF, Brigham D, Belli B et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood 2009; 114: 2984–2992.

2. von Bubnoff N, Engh RA, Aberg E, Sanger J, Peschel C, Duyster J . FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro. Cancer Res 2009; 69: 3032–3041.

3. von Bubnoff N, Rummelt C, Menzel H, Sigl M, Peschel C, Duyster J . Identification of a secondary FLT3/A848P mutation in a patient with FLT3-ITD-positive blast phase CMML and response to sunitinib and sorafenib. Leukemia 2010; 24: 1523–1525.

4. Cools J, Mentens N, Furet P, Fabbro D, Clark JJ, Griffin JD et al. Prediction of resistance to small molecule FLT3 inhibitors: implications for molecularly targeted therapy of acute leukemia. Cancer Res 2004; 64: 6385–6389.

5. Heidel F, Solem FK, Breitenbuecher F, Lipka DB, Kasper S, Thiede MH et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. Blood 2006; 107: 293–300.

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