Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia-Reference-Cited by-同舟云学术

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Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia

Published:2014-05-12 Issue:1 Volume:29 Page:76-85
ISSN:0887-6924
Container-title:Leukemia
language:en
Short-container-title:Leukemia

Author:

Schafranek L,Nievergall E,Powell J A,Hiwase D K,Leclercq T,Hughes T P,White D L

Publisher

Springer Science and Business Media LLC

Subject

Oncology,Cancer Research,Hematology

Link

http://www.nature.com/articles/leu2014156.pdf

Reference40 articles.

1. Deininger MWN, Goldman JM, Melo JV . The molecular biology of chronic myeloid leukemia. Blood 2000; 96: 3343–3356.

2. Ilaria RL Jr, Van Etten RA . P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members. J Biol Chem 1996; 271: 31704–31710.

3. Soliera AR, Mariani SA, Audia A, Lidonnici MR, Addya S, Ferrari-Amorotti G et al. Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1. Leukemia 2012; 26: 1555–1563.

4. Kok CH, Watkins DB, Leclercq T, D'Andrea RJ, Hughes TP, White DL . Low GFI1 expression in white blood cells of CP-CML patients at diagnosis is strongly associated with subsequent blastic transformation. Leukemia 2014; 27: 1427–1430.

5. Traer E, MacKenzie R, Snead J, Agarwal A, Eiring AM, O'Hare T et al. Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors. Leukemia 2011; 26: 1140–1143.

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