Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155-Reference-Cited by-同舟云学术

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Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155

Published:2012-01-16 Issue:37 Volume:31 Page:4085-4094
ISSN:0950-9232
Container-title:Oncogene
language:en
Short-container-title:Oncogene

Author:

Lee D W,Futami M,Carroll M,Feng Y,Wang Z,Fernandez M,Whichard Z,Chen Y,Kornblau S,Shpall E J,Bueso-Ramos C E,Corey S J

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Molecular Biology

Link

http://www.nature.com/articles/onc2011579.pdf

Reference45 articles.

1. Aul C, Germing U, Gattermann N, Minning H . (1998). Increasing incidence of myelodysplastic syndromes: real or fictitious? Leuk Res 22: 93–100.

2. Cantley LC, Neel BG . (1999). New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway. Proc Natl Acad Sci USA 96: 4240–4245.

3. Corey SJ, Minden MD, Barber DL, Kantarjian H, Wang JC, Schimmer AD . (2007). Myelodysplastic syndromes: the complexity of stem-cell diseases. Nat Rev Cancer 7: 118–129.

4. Costinean S, Sandhu SK, Pedersen IM, Tili E, Trotta R, Perrotti D et al. (2009). Src homology 2 domain-containing inositol-5-phosphatase and CCAAT enhancer-binding protein beta are targeted by miR-155 in B cells of Emicro-MiR-155 transgenic mice. Blood 114: 1374–1382.

5. Dahia PL, Aguiar RC, Alberta J, Kum JB, Caron S, Sill H et al. (1999). PTEN is inversely correlated with the cell survival factor Akt/PKB and is inactivated via multiple mechanisms in haematological malignancies. Hum Mol Genet 8: 185–193.

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