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Articles related to 18504399 [Unique ID], provided by the PubMed system
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Ishihara K, Kaneko M, Kitamura H, et al. 
Mechanism for the decrease in the FIP1L1-PDGFRalpha protein level in EoL-1 cells by histone deacetylase inhibitors. [Journal Article, Research Support, Non-U.S. Gov't]
Int Arch Allergy Immunol 2008.:7-10.
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Kaneko M, Ishihara K, Takahashi A, et al. 
Mechanism for the Differentiation of EoL-1 Cells into Eosinophils by Histone Deacetylase Inhibitors. [JOURNAL ARTICLE]
Int Arch Allergy Immunol 2007.:28-32.
Abstract | Full Citation
Ishihara K, Takahashi A, Kaneko M, et al. 
Differentiation of eosinophilic leukemia EoL-1 cells into eosinophils induced by histone deacetylase inhibitors. [JOURNAL ARTICLE]
Life Sci 2007 Jan 11.
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Ishihara K, Kitamura H, Hiraizumi K, et al. 
Mechanisms for the proliferation of eosinophilic leukemia cells by FIP1L1-PDGFRalpha. [JOURNAL ARTICLE]
Biochem Biophys Res Commun 2007 Dec 14.
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Ishihara K, Hong J, Zee O, et al. 
Possible mechanism of action of the histone deacetylase inhibitors for the induction of differentiation of HL-60 clone 15 cells into eosinophils. [Journal Article]
Br J Pharmacol 2004 Jul; 142(6):1020-30.
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Cools J, Quentmeier H, Huntly BJ, et al. 
The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. [Journal Article]
Blood 2004 Apr 1; 103(7):2802-5.
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Lierman E, Folens C, Stover EH, et al. 
Sorafenib (BAY43-9006) is a potent inhibitor of FIP1L1-PDGFR{alpha} and the imatinib resistant FIP1L1-PDGFR{alpha} T674I mutant. [JOURNAL ARTICLE]
Blood 2006 Apr 27.
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Li B, Zhang GS, Dai CW, et al. 
[The activation of JAK/STAT signal pathway in hypereosinophilic syndrome and the patients therapeutic response to imatinib] [Journal Article]
Zhonghua Yi Xue Za Zhi 2005 Feb 23; 85(7):448-52.
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Crescenzi B, Chase A, Starza RL, et al. 
FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells. [JOURNAL ARTICLE]
Leukemia 2007 Jan 11.
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