Localization of the NRAS:BCL-2 complex determines anti-apoptotic features associated with progressive disease in myelodysplastic syndromes.

[1]  M. Morgan,et al.  Selection for Evi1 activation in myelomonocytic leukemia induced by hyperactive signaling through wild-type NRas , 2013, Oncogene.

[2]  M. Konopleva,et al.  MEK inhibition enhances ABT-737-induced leukemia cell apoptosis via prevention of ERK-activated MCL-1 induction and modulation of MCL-1/BIM complex , 2012, Leukemia.

[3]  D. Green,et al.  A unified model of mammalian BCL-2 protein family interactions at the mitochondria. , 2011, Molecular cell.

[4]  M. Eberl,et al.  Suppression of apoptosis inhibitor c-FLIP selectively eliminates breast cancer stem cell activity in response to the anti-cancer agent, TRAIL , 2011, Breast Cancer Research.

[5]  B. Goh,et al.  The small GTPase Rac1 is a novel binding partner of Bcl-2 and stabilizes its antiapoptotic activity. , 2011, Blood.

[6]  J. Wright,et al.  A Phase 1 Trial Dose Escalation Study of Tipifarnib on a Week-On, Week-Off Schedule in Relapsed, Refractory or High-Risk Myeloid Leukemia , 2011, Leukemia.

[7]  C. Bloomfield,et al.  The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. , 2009, Blood.

[8]  M. Jädersten,et al.  Myelodysplastic syndromes: biology and treatment , 2009, Journal of internal medicine.

[9]  B. Smith,et al.  Phase II Trial of Tipifarnib as Maintenance Therapy in First Complete Remission in Adults with Acute Myelogenous Leukemia and Poor-Risk Features , 2008, Clinical Cancer Research.

[10]  I. Weissman,et al.  BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia. , 2007, Cancer research.

[11]  G. Mufti,et al.  Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia? , 2007, Cancer research.

[12]  G. Mufti,et al.  Histone Deacetylase Inhibitors (HDI) Cause DNA Damage in Leukemia Cells: A Mechanism for Leukemia-Specific HDI-Dependent Apoptosis? , 2006, Molecular Cancer Research.

[13]  A. Burnett,et al.  Ral Is both Necessary and Sufficient for the Inhibition of Myeloid Differentiation Mediated by Ras , 2006, Molecular and Cellular Biology.

[14]  C. Thompson,et al.  PKC regulates a farnesyl-electrostatic switch on K-Ras that promotes its association with Bcl-XL on mitochondria and induces apoptosis. , 2006, Molecular cell.

[15]  R. Hills,et al.  RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years. , 2005, Blood.

[16]  Ulrich Pohl,et al.  Reactive Oxygen Species: Players in the Platelet Game , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[17]  O. Sordet,et al.  Expression and activity of caspases 1 and 3 in myelodysplastic syndromes , 2000, Leukemia.

[18]  G. Mufti,et al.  The role of apoptosis, proliferation, and the Bcl-2-related proteins in the myelodysplastic syndromes and acute myeloid leukemia secondary to MDS. , 2000, Blood.

[19]  T. Jacks,et al.  Nf1 and Gmcsf interact in myeloid leukemogenesis. , 2000, Molecular cell.

[20]  Z. Estrov,et al.  The biology of chronic myeloid leukemia. , 1999, The New England journal of medicine.

[21]  P. Thall,et al.  The prognostic impact of BCL2 protein expression in acute myelogenous leukemia varies with cytogenetics. , 1999, Clinical cancer research : an official journal of the American Association for Cancer Research.

[22]  K. Calame,et al.  Signaling Pathways Activated by Oncogenic Forms of Abl Tyrosine Kinase* , 1999, The Journal of Biological Chemistry.

[23]  T. Naoe,et al.  Prognostic implication of FLT3 and N-RAS gene mutations in acute myeloid leukemia. , 1999, Blood.

[24]  M MacFarlane,et al.  Distinct Caspase Cascades Are Initiated in Receptor-mediated and Chemical-induced Apoptosis* , 1999, The Journal of Biological Chemistry.

[25]  I. Weissman,et al.  The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[26]  R. Darley,et al.  RAS and the myelodysplastic syndromes. , 1997, Pathologie-biologie.

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

[28]  D. Largaespada,et al.  Nf1 deficiency causes Ras-Dediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia , 1996, Nature Genetics.

[29]  I. Weissman,et al.  bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages , 1994, The Journal of experimental medicine.

[30]  I. Lemischka,et al.  Mitogenic signalling and substrate specificity of the Flk2/Flt3 receptor tyrosine kinase in fibroblasts and interleukin 3-dependent hematopoietic cells , 1993, Molecular and cellular biology.

[31]  J. Magaud,et al.  High expression of bcl-2 protein in acute myeloid leukemia cells is associated with poor response to chemotherapy. , 1993, Blood.

[32]  M. Barbacid,et al.  ras gene Amplification and malignant transformation , 1985, Molecular and cellular biology.

[33]  E. Scolnick,et al.  Growth of factor-dependent hemopoietic precursor cell lines , 1980, The Journal of experimental medicine.