SOCS3 inhibits TPO-stimulated, but not spontaneous, megakaryocytic growth in primary myelofibrosis-Reference-Cited by-同舟云学术

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SOCS3 inhibits TPO-stimulated, but not spontaneous, megakaryocytic growth in primary myelofibrosis

Published:2009-02-19 Issue:6 Volume:23 Page:1186-1190
ISSN:0887-6924
Container-title:Leukemia
language:en
Short-container-title:Leukemia

Author:

Chaligné R, ,Tonetti C,Besancenot R,Marty C,Kiladjian J-J,Socié G,Bordessoule D,Vainchenker W,Giraudier S

Publisher

Springer Science and Business Media LLC

Subject

Oncology,Cancer Research,Hematology

Link

http://www.nature.com/articles/leu200922.pdf

Reference12 articles.

1. Jost E, do ON, Dahl E, Maintz CE, Jousten P, Habets L et al. Epigenetic alterations complement mutation of JAK2 tyrosine kinase in patients with BCR/ABL-negative myeloproliferative disorders. Leukemia 2007; 21: 505–510.

2. Fujimoto M, Naka T . Regulation of cytokine signaling by SOCS family molecules. Trends Immunol 2003; 24: 659–666.

3. Capello D, Deambrogi C, Rossi D, Lischetti T, Piranda D, Cerri M et al. Epigenetic inactivation of suppressors of cytokine signalling in Philadelphia-negative chronic myeloproliferative disorders. Br J Haematol 2008; 141: 504–511.

4. Teofili L, Martini M, Cenci T, Guidi F, Torti L, Giona F et al. Epigenetic alteration of SOCS family members is a possible pathogenetic mechanism in JAK2 wild type myeloproliferative diseases. Int J Cancer 2008; 123: 1586–1592.

5. Komura E, Chagraoui H, Mansat de Mas V, Blanchet B, de Sepulveda P, Larbret F et al. Spontaneous STAT5 activation induces growth factor independence in idiopathic myelofibrosis: possible relationship with FKBP51 overexpression. Exp Hematol 2003; 31: 622–630.

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4. Mechanistic insights into activation and SOCS3-mediated inhibition of myeloproliferative neoplasm-associated JAK2 mutants from biochemical and structural analyses;Biochemical Journal;2014-02-14

5. Disordered Signaling in Myeloproliferative Neoplasms;Hematology/Oncology Clinics of North America;2012-10

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