Response of high-risk MDS to azacitidine and lenalidomide is impacted by baseline and acquired mutations in a cluster of three inositide-specific genes

[1]  R. Sadeghi,et al.  Prognostic significance of SRSF2 mutations in myelodysplastic syndromes and chronic myelomonocytic leukemia: a meta-analysis , 2016, Hematology.

[2]  A. Gavin,et al.  Impact of spliceosome mutations on RNA splicing in myelodysplasia: dysregulated genes/pathways and clinical associations. , 2018, Blood.

[3]  M. Patnaik,et al.  Prognostic impact of ASXL1 mutations in patients with myelodysplastic syndromes and multilineage dysplasia with or without ring sideroblasts. , 2018, Leukemia research.

[4]  W. Shi,et al.  Germline-activating mutations in PIK3CD compromise B cell development and function , 2018, The Journal of experimental medicine.

[5]  K. Metzeler,et al.  Gene mutations and clonal architecture in myelodysplastic syndromes and changes upon progression to acute myeloid leukaemia and under treatment , 2018, British journal of haematology.

[6]  E. Hara,et al.  Modeling ASXL1 mutation revealed impaired hematopoiesis caused by derepression of p16Ink4a through aberrant PRC1-mediated histone modification , 2018, Leukemia.

[7]  Qian-yu Li,et al.  Long non-coding RNA FEZF1-AS1 promotes cell growth in multiple myeloma via miR-610/Akt3 axis. , 2018, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[8]  A. Tefferi,et al.  Mutations and prognosis in myelodysplastic syndromes: karyotype‐adjusted analysis of targeted sequencing in 300 consecutive cases and development of a genetic risk model , 2018, American journal of hematology.

[9]  D. Steensma Myelodysplastic syndromes current treatment algorithm 2018 , 2018, Blood Cancer Journal.

[10]  W. Hiddemann,et al.  Persistence of pre-leukemic clones during first remission and risk of relapse in acute myeloid leukemia , 2017, Leukemia.

[11]  J. McCubrey,et al.  Nuclear inositide signaling and cell cycle. , 2017, Advances in biological regulation.

[12]  G. Bejerano,et al.  Mutations of AKT3 are associated with a wide spectrum of developmental disorders including extreme megalencephaly , 2017, Brain : a journal of neurology.

[13]  J. McCubrey,et al.  Nuclear translocation of PKC‐ α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs) , 2017, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[14]  R. Armstrong,et al.  Splicing factor mutations in the myelodysplastic syndromes: target genes and therapeutic approaches. , 2017, Advances in biological regulation.

[15]  M. R. Ricciardi,et al.  Targeting the Akt, GSK-3, Bcl-2 axis in acute myeloid leukemia. , 2017, Advances in biological regulation.

[16]  J. McCubrey,et al.  Nuclear Inositide Signaling Via Phospholipase C , 2017, Journal of cellular biochemistry.

[17]  Susan R. Wilson,et al.  Integrative Genomics Identifies the Molecular Basis of Resistance to Azacitidine Therapy in Myelodysplastic Syndromes. , 2017, Cell reports.

[18]  L. Lou,et al.  Puquitinib, a novel orally available PI3Kδ inhibitor, exhibits potent antitumor efficacy against acute myeloid leukemia , 2017, Cancer science.

[19]  C. Bloomfield,et al.  Randomized Phase II Study of Azacitidine Alone or in Combination With Lenalidomide or With Vorinostat in Higher-Risk Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia: North American Intergroup Study SWOG S1117. , 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[20]  S. Miyano,et al.  Clonal evolution in myelodysplastic syndromes , 2017, Nature Communications.

[21]  B. Ebert,et al.  Clinical Implications of Genetic Mutations in Myelodysplastic Syndrome. , 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[22]  F. Alt,et al.  Phosphatidylinositol 3-Kinase (PI3K) δ blockade increases genomic instability in B cells , 2017, Nature.

[23]  Braden D. Siempelkamp,et al.  Conformational disruption of PI3Kδ regulation by immunodeficiency mutations in PIK3CD and PIK3R1 , 2017, Proceedings of the National Academy of Sciences.

[24]  A. Zeidan,et al.  Trends in Clinical Investigation for Myelodysplastic Syndromes. , 2016, Clinical lymphoma, myeloma & leukemia.

[25]  J. McCubrey,et al.  Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes , 2016, Expert opinion on therapeutic targets.

[26]  J. McCubrey,et al.  Selective Activation of Nuclear PI-PLCbeta1 During Normal and Therapy-Related Differentiation. , 2016, Current pharmaceutical design.

[27]  C. Finelli,et al.  Clinical Impact of Hypomethylating Agents in the Treatment of Myelodysplastic Syndromes. , 2016, Current pharmaceutical design.

[28]  Shaoyuan Wang,et al.  Prognostic significance of SRSF2 mutations in myelodysplastic syndromes and chronic myelomonocytic leukemia: a meta-analysis. , 2016 .

[29]  Christopher A. Miller,et al.  Dynamic Changes in the Clonal Structure of MDS and AML in Response to Epigenetic Therapy , 2016, Leukemia.

[30]  B. Ebert,et al.  The novel mechanism of lenalidomide activity. , 2015, Blood.

[31]  C. Finelli,et al.  An increased expression of PI‐PLCβ1 is associated with myeloid differentiation and a longer response to azacitidine in myelodysplastic syndromes , 2015, Journal of leukocyte biology.

[32]  U. Platzbecker,et al.  Influence of total genomic alteration and chromosomal fragmentation on response to a combination of azacitidine and lenalidomide in a cohort of patients with very high risk MDS. , 2015, Leukemia research.

[33]  M. Calasanz,et al.  Targeted resequencing analysis of 31 genes commonly mutated in myeloid disorders in serial samples from myelodysplastic syndrome patients showing disease progression , 2015, Leukemia.

[34]  P. Suh,et al.  Phosphoinositide-specific phospholipase C in health and disease , 2015, Journal of Lipid Research.

[35]  L. Cocco,et al.  Protein kinase C involvement in cell cycle modulation. , 2014, Biochemical Society transactions.

[36]  C. Finelli,et al.  Strategic Role of Nuclear Inositide Signalling in Myelodysplastic Syndromes Therapy. , 2014, Mini reviews in medicinal chemistry.

[37]  Yan Luo,et al.  Differential effects of Akt isoforms on somatic cell reprogramming , 2014, Journal of Cell Science.

[38]  C. Bincoletto,et al.  PLCγ2 and PKC Are Important to Myeloid Lineage Commitment Triggered by M‐SCF and G‐CSF , 2014, Journal of cellular biochemistry.

[39]  M. Gobbi,et al.  Prospective Phase II Study on 5-Days Azacitidine for Treatment of Symptomatic and/or Erythropoietin Unresponsive Patients with Low/INT-1–Risk Myelodysplastic Syndromes , 2013, Clinical Cancer Research.

[40]  J. Maciejewski,et al.  Phase 2 study of the lenalidomide and azacitidine combination in patients with higher-risk myelodysplastic syndromes. , 2012, Blood.

[41]  Luca Malcovati,et al.  Revised international prognostic scoring system for myelodysplastic syndromes. , 2012, Blood.

[42]  M. Konopleva,et al.  Molecular characterization of de novo Philadelphia chromosome-positive acute myeloid leukemia , 2012, Leukemia & lymphoma.

[43]  M. Gobbi,et al.  Epigenetic regulation of nuclear PI-PLCbeta1 signaling pathway in low-risk MDS patients during azacitidine treatment , 2012, Leukemia.

[44]  Helga Thorvaldsdóttir,et al.  Integrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration , 2012, Briefings Bioinform..

[45]  Eva Hellström-Lindberg,et al.  TP53 mutations in low-risk myelodysplastic syndromes with del(5q) predict disease progression. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[46]  S. Paolini,et al.  Synergistic induction of PI-PLCβ1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes , 2011, Leukemia.

[47]  L. Cocco,et al.  The physiology and pathology of inositide signaling in the nucleus , 2011, Journal of cellular physiology.

[48]  A. Martelli,et al.  Nuclear inositide signaling in myelodysplastic syndromes , 2010, Journal of cellular biochemistry.

[49]  M. Baccarani,et al.  Reduction of phosphoinositide-phospholipase C beta1 methylation predicts the responsiveness to azacitidine in high-risk MDS , 2009, Proceedings of the National Academy of Sciences.

[50]  A. Verma,et al.  Mechanism of action of lenalidomide in hematological malignancies , 2009, Journal of hematology & oncology.

[51]  M. Baccarani,et al.  Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

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

[53]  E. Solary,et al.  Essential role for the p110δ isoform in phosphoinositide 3-kinase activation and cell proliferation in acute myeloid leukemia , 2005 .

[54]  A. Martelli,et al.  Nuclear phospholipase C signaling through type 1 IGF receptor and its involvement in cell growth and differentiation. , 2005, Anticancer research.

[55]  B. Hemmings,et al.  Physiological functions of protein kinase B/Akt. , 2004, Biochemical Society transactions.

[56]  Steven Henikoff,et al.  SIFT: predicting amino acid changes that affect protein function , 2003, Nucleic Acids Res..

[57]  K. Okkenhaug,et al.  PI3K in lymphocyte development, differentiation and activation , 2003, Nature Reviews Immunology.

[58]  N. Harris,et al.  The World Health Organization (WHO) classification of the myeloid neoplasms. , 2002, Blood.

[59]  J. Boultwood,et al.  Splicing factor gene mutations in the myelodysplastic syndromes: impact on disease phenotype and therapeutic applications. , 2017, Advances in biological regulation.

[60]  D. Braden,et al.  Conformational disruption of PI3K.DELTA. regulation by immunodeficiency mutations in PIK3CD and PIK3R1 , 2017 .

[61]  C. Finelli,et al.  Nuclear PI-PLC β1 and Myelodysplastic syndromes: from bench to clinics. , 2012, Current topics in microbiology and immunology.

[62]  E. Solary,et al.  Essential role for the p110delta isoform in phosphoinositide 3-kinase activation and cell proliferation in acute myeloid leukemia. , 2005, Blood.

[63]  R. Russell,et al.  Amino Acid Properties and Consequences of Substitutions , 2003 .