Treatment of higher risk myelodysplastic syndrome patients unresponsive to hypomethylating agents with ON 01910.Na.

[1]  G. Garcia-Manero.  Treatment of higher-risk myelodysplastic syndrome. , 2011, Seminars in oncology.

[2]  B. Esterni,et al.  Outcome of high-risk myelodysplastic syndrome after azacitidine treatment failure. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  C. Bloomfield,et al.  NCCN Clinical Practice Guidelines in Oncology: myelodysplastic syndromes. , 2011, Journal of the National Comprehensive Cancer Network : JNCCN.

[4]  F. Zunino,et al.  Modulation of cell sensitivity to antitumor agents by targeting survival pathways. , 2010, Biochemical pharmacology.

[5]  Nancy R. Zhang,et al.  Nanoscale approaches to define biologic signatures and measure proteomic response to targeted therapies in hematologic and solid tumors , 2010 .

[6]  J. Issa,et al.  Outcome of patients with myelodysplastic syndrome after failure of decitabine therapy , 2010, Cancer.

[7]  Patrick Mayeux,et al.  Role of the PI3K/AKT and mTOR signaling pathways in acute myeloid leukemia , 2010, Haematologica.

[8]  H. Mure,et al.  Akt2 and Akt3 play a pivotal role in malignant gliomas. , 2010, Neuro-oncology.

[9]  Nancy R. Zhang,et al.  Abstract B178: Nanoscale quantification of phosphorylated and unphosphorylated ERK and MEK isoforms differentiates tumor and nontumor clinical specimens , 2009 .

[10]  Robert Tibshirani,et al.  Relationship of differential gene expression profiles in CD34+ myelodysplastic syndrome marrow cells to disease subtype and progression. , 2009, Blood.

[11]  Christian Bailly,et al.  Polo-like kinase 1 is overexpressed in acute myeloid leukemia and its inhibition preferentially targets the proliferation of leukemic cells. , 2009, Blood.

[12]  P. Schöffski.  Polo-like kinase (PLK) inhibitors in preclinical and early clinical development in oncology. , 2009, The oncologist.

[13]  K. Otsuka,et al.  The PI3K/Akt pathway as a target in the treatment of hematologic malignancies. , 2009, Anti-cancer agents in medicinal chemistry.

[14]  S. Cosenza,et al.  Preclinical pharmacokinetics and in vitro activity of ON 01910.Na, a novel anti-cancer agent , 2009, Cancer Chemotherapy and Pharmacology.

[15]  Yasodha Natkunam,et al.  Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimens , 2009, Nature Medicine.

[16]  E. Reddy,et al.  Styryl sulfonyl compounds inhibit translation of cyclin D1 in mantle cell lymphoma cells , 2009, Oncogene.

[17]  Valeria Santini,et al.  Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study. , 2009, The Lancet. Oncology.

[18]  A. Jimeno,et al.  Evaluation of the novel mitotic modulator ON 01910.Na in pancreatic cancer and preclinical development of an ex vivo predictive assay , 2009, Oncogene.

[19]  A. Jimeno,et al.  Phase I study of ON 01910.Na, a novel modulator of the Polo-like kinase 1 pathway, in adult patients with solid tumors. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[20]  N. Young,et al.  Suppression of Cyclin D 1 (CD1) by on 01910.Na Is Associated with Decreased Survival or Trisomy 8 Myelodysplastic Bone Marrow: A Potential Targetted Therapy for Trisomy 8 MDS. , 2008 .

[21]  N. Young,et al.  Suppression of Cyclin D1 by on 01910.Na Is Associated with Decreased Survival of Trisomy 8 Myelodyplastic Bone Marrow Progenitors: A Potential Targetted Therapy. , 2007 .

[22]  G. Martinelli,et al.  The Akt/mammalian target of rapamycin signal transduction pathway is activated in high-risk myelodysplastic syndromes and influences cell survival and proliferation. , 2007, Cancer research.

[23]  N. Young,et al.  CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) express early apoptotic markers but avoid programmed cell death by up-regulation of antiapoptotic proteins. , 2006, Blood.

[24]  J. Issa,et al.  Update of the decitabine experience in higher risk myelodysplastic syndrome and analysis of prognostic factors associated with outcome , 2007, Cancer.

[25]  Xiahui Bi,et al.  Isoelectric focusing technology quantifies protein signaling in 25 cells , 2006, Proceedings of the National Academy of Sciences.

[26]  B. Cheson,et al.  Clinical application and proposal for modification of the International Working Group (IWG) response criteria in myelodysplasia. , 2006, Blood.

[27]  A M Martelli,et al.  Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia , 2006, Leukemia.

[28]  Kiranmai Gumireddy,et al.  ON01910, a non-ATP-competitive small molecule inhibitor of Plk1, is a potent anticancer agent. , 2005, Cancer cell.

[29]  K. Strebhardt,et al.  Polo-like kinases and oncogenesis , 2005, Oncogene.

[30]  A. Khwaja,et al.  PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kB, MAPkinase and p53 pathways , 2005, Leukemia.

[31]  Xiaoqi Liu,et al.  Polo-like kinase (Plk)1 depletion induces apoptosis in cancer cells , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[32]  R. Medema,et al.  Polo-like kinase-1 is a target of the DNA damage checkpoint , 2000, Nature Cell Biology.

[33]  T Hamblin,et al.  International scoring system for evaluating prognosis in myelodysplastic syndromes. , 1997, Blood.