Omar Abdel-Wahab

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. pmc Mutations in epigenetic modifiers in myeloid malignancies and the prospect of novel epigenetic-targeted therapy
    Amir T Fathi
    Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA
    Adv Hematol 2012:469592. 2012
  2. doi request reprint The ASXL-BAP1 axis: new factors in myelopoiesis, cancer and epigenetics
    O Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Leukemia 27:10-5. 2013
  3. doi request reprint Clinical implications of novel mutations in epigenetic modifiers in AML
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA
    Hematol Oncol Clin North Am 25:1119-33. 2011
  4. ncbi request reprint Molecular genetics of acute myeloid leukemia: clinical implications and opportunities for integrating genomics into clinical practice
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Hematology 17:S39-42. 2012
  5. pmc Unraveling the genetic underpinnings of myeloproliferative neoplasms and understanding their effect on disease course and response to therapy: proceedings from the 6th International Post-ASH Symposium
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Am J Hematol 87:562-8. 2012
  6. doi request reprint Genetics of the myeloproliferative neoplasms
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Curr Opin Hematol 18:117-23. 2011
  7. pmc ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Cancer Cell 22:180-93. 2012
  8. pmc Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program, 2 Leukemia Service, 3 Gerstner Sloan Kettering Graduate School of Biomedical Sciences, and 4 Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065
    J Exp Med 210:2641-59. 2013
  9. pmc The potential for isocitrate dehydrogenase mutations to produce 2-hydroxyglutarate depends on allele specificity and subcellular compartmentalization
    Patrick S Ward
    Cancer Biology and Genetics Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    J Biol Chem 288:3804-15. 2013
  10. pmc Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy
    Priya Koppikar
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nature 489:155-9. 2012

Detail Information

Publications50

  1. pmc Mutations in epigenetic modifiers in myeloid malignancies and the prospect of novel epigenetic-targeted therapy
    Amir T Fathi
    Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA
    Adv Hematol 2012:469592. 2012
    ..We also discuss exciting developments in DNA methyltransferase inhibitor strategies and the prospect of novel histone lysine methyltransferase inhibitors...
  2. doi request reprint The ASXL-BAP1 axis: new factors in myelopoiesis, cancer and epigenetics
    O Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Leukemia 27:10-5. 2013
    ..Future studies investigating the mechanism of transformation by loss of BAP1 and ASXL1 may result in new therapeutic approaches to treat hematological malignancies...
  3. doi request reprint Clinical implications of novel mutations in epigenetic modifiers in AML
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA
    Hematol Oncol Clin North Am 25:1119-33. 2011
    ....
  4. ncbi request reprint Molecular genetics of acute myeloid leukemia: clinical implications and opportunities for integrating genomics into clinical practice
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Hematology 17:S39-42. 2012
    ..Further improvements in cost, throughput, and clinical validation of second-generation sequencing technologies may allow for clinical implementation of comprehensive genetic profiling in the clinical care of AML patients...
  5. pmc Unraveling the genetic underpinnings of myeloproliferative neoplasms and understanding their effect on disease course and response to therapy: proceedings from the 6th International Post-ASH Symposium
    Omar Abdel-Wahab
    Leukemia Service and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Am J Hematol 87:562-8. 2012
    ..Tariq Mughal. The current document is the first of two reports on this post-ASH event and summarizes the most recent preclinical and clinical advances in polycythemia vera, essential thrombocythemia,and primary myelofibrosis...
  6. doi request reprint Genetics of the myeloproliferative neoplasms
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Curr Opin Hematol 18:117-23. 2011
    ..The purpose of this review is to outline the most recent discoveries of the genetic alterations found in patients with MPNs...
  7. pmc ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Cancer Cell 22:180-93. 2012
    ..We demonstrate that ASXL1 associates with the PRC2, and that loss of ASXL1 in vivo collaborates with NRASG12D to promote myeloid leukemogenesis...
  8. pmc Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program, 2 Leukemia Service, 3 Gerstner Sloan Kettering Graduate School of Biomedical Sciences, and 4 Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065
    J Exp Med 210:2641-59. 2013
    ..These findings underscore the importance of Asxl1 in Polycomb group function, development, and hematopoiesis. ..
  9. pmc The potential for isocitrate dehydrogenase mutations to produce 2-hydroxyglutarate depends on allele specificity and subcellular compartmentalization
    Patrick S Ward
    Cancer Biology and Genetics Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    J Biol Chem 288:3804-15. 2013
    ..The consequences of 2HG elevation are dose-dependent, and the non-equivalent 2HG accumulation resulting from IDH1 and IDH2 mutations may underlie their differential prognosis and prevalence in various cancers...
  10. pmc Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy
    Priya Koppikar
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nature 489:155-9. 2012
    ..Consequently, therapies that result in JAK2 degradation retain efficacy in persistent cells and may provide additional benefit to patients with JAK2-dependent malignancies treated with JAK2 inhibitors...
  11. pmc Validation of a prognostic model and the impact of mutations in patients with lower-risk myelodysplastic syndromes
    Rafael Bejar
    Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Clin Oncol 30:3376-82. 2012
    ..The identification of patients with greater-than-predicted prognostic risk could influence the selection of therapy and improve the care of patients with lower-risk MDS...
  12. pmc CD25 expression status improves prognostic risk classification in AML independent of established biomarkers: ECOG phase 3 trial, E1900
    Mithat Gonen
    Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 120:2297-306. 2012
    ..We conclude that CD25(POS) status provides prognostic relevance in AML independent of known biomarkers and is correlated with stem cell gene-expression signatures associated with adverse outcome in AML...
  13. pmc Genetic analysis of patients with leukemic transformation of myeloproliferative neoplasms shows recurrent SRSF2 mutations that are associated with adverse outcome
    Su Jiang Zhang
    Human Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 119:4480-5. 2012
    ..10-7.00) and multivariate analysis (P<.05; HR, 2.11; 95% CI, 1.01-4.42). These data suggest that SRSF2 mutations contribute to the pathogenesis of LT and may guide novel therapeutic approaches for MPN patients who undergo LT...
  14. pmc IDH mutation impairs histone demethylation and results in a block to cell differentiation
    Chao Lu
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nature 483:474-8. 2012
    ..Together these data demonstrate that 2HG can inhibit histone demethylation and that inhibition of histone demethylation can be sufficient to block the differentiation of non-transformed cells...
  15. pmc Genetic analysis of transforming events that convert chronic myeloproliferative neoplasms to leukemias
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Cancer Res 70:447-52. 2010
    ..Given the presence of sAML that have no preexisting JAK2/TET2/ASXL1/IDH1 mutations, our work indicates the existence of other mutations yet to be identified that are necessary for leukemic transformation...
  16. ncbi request reprint Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation
    Maria E Figueroa
    Weill Cornell Medical College, New York, NY 10065, USA
    Cancer Cell 18:553-67. 2010
    ..Finally, either expression of mutant IDH1/2 or Tet2 depletion impaired hematopoietic differentiation and increased stem/progenitor cell marker expression, suggesting a shared proleukemogenic effect...
  17. pmc Clinical and pathologic impact of select chromatin-modulating tumor suppressors in clear cell renal cell carcinoma
    A Ari Hakimi
    Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Eur Urol 63:848-54. 2013
    ..PBRM1, SETD2, and BAP1 are located in close proximity to VHL within a commonly lost (approximately 90%) 3p locus. To date, the clinical and pathologic significance of mutations in these novel candidate tumor suppressors is unknown...
  18. doi request reprint Interpreting new molecular genetics in myelodysplastic syndromes
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Hematology Am Soc Hematol Educ Program 2012:56-64. 2012
    ..Finally, mutations in mRNA splicing genes have also been described recently in MDS, underscoring the molecular complexity that underlies the development of this heterogeneous disease...
  19. pmc Progression of RAS-mutant leukemia during RAF inhibitor treatment
    Margaret K Callahan
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    N Engl J Med 367:2316-21. 2012
    ..Exposure to vemurafenib induced hyperactivation of ERK signaling and proliferation of the leukemic cell population, an effect that was reversed on drug withdrawal...
  20. doi request reprint JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation
    Fan Liu
    Molecular Pharmacology and Chemistry Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cancer Cell 19:283-94. 2011
    ..These results indicate that phosphorylation of PRMT5 contributes to the mutant JAK2-induced myeloproliferative phenotype...
  21. pmc HSP90 is a therapeutic target in JAK2-dependent myeloproliferative neoplasms in mice and humans
    Sachie Marubayashi
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    J Clin Invest 120:3578-93. 2010
    ..Importantly, PU-H71 treatment also reduced the mutant allele burden in mice. These data establish what we believe to be a novel therapeutic rationale for HSP90 inhibition in the treatment of JAK2-dependent MPN...
  22. pmc Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis
    Raajit Rampal
    Human Oncology and Pathogenesis Program, and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY Weill Cornell Medical College, New York, NY
    Blood 123:e123-33. 2014
    ....
  23. pmc Role of TET2 and ASXL1 mutations in the pathogenesis of myeloproliferative neoplasms
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Hematol Oncol Clin North Am 26:1053-64. 2012
    ....
  24. doi request reprint Translocation t(11;17) in de novo myelodysplastic syndrome not associated with acute myeloid or acute promyelocytic leukemia
    Muhamed Baljevic
    Department of Medicine, New York Presbyterian Hospital Weill Cornell Medical Center, New York, NY 10065, USA
    Acta Haematol 129:48-54. 2013
    ....
  25. ncbi request reprint The role of mutations in epigenetic regulators in myeloid malignancies
    Alan H Shih
    Human Oncology and Pathogenesis Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College, New York, New York, USA
    Nat Rev Cancer 12:599-612. 2012
    ....
  26. pmc Metabolism and the leukemic stem cell
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    J Exp Med 207:677-80. 2010
    ..These studies potentially converge on the concept that modulation of reactive oxygen species (ROS) abundance may influence the pathogenesis and treatment of acute myeloid leukemia (AML)...
  27. pmc Regulation of c-Myc ubiquitination controls chronic myelogenous leukemia initiation and progression
    Linsey Reavie
    Howard Hughes Medical Institute and Department of Pathology, New York University School of Medicine, New York, NY 10016, USA
    Cancer Cell 23:362-75. 2013
    ..These studies identify a ubiquitin ligase:substrate pair regulating LIC activity, suggesting that targeting of the Fbw7:c-Myc axis is an attractive therapy target in refractory CML...
  28. pmc A mathematical framework to determine the temporal sequence of somatic genetic events in cancer
    Camille Stephan Otto Attolini
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 107:17604-9. 2010
    ..RESIC represents the first evolutionary mathematical approach to identify the temporal sequence of mutations driving tumorigenesis and may be useful to guide the validation of candidate genes emerging from cancer genome surveys...
  29. pmc TET family proteins and their role in stem cell differentiation and transformation
    Luisa Cimmino
    Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA
    Cell Stem Cell 9:193-204. 2011
    ....
  30. pmc Clinical effect of point mutations in myelodysplastic syndromes
    Rafael Bejar
    Department of Medicine, Harvard Medical School and Brigham and Women s Hospital, Boston, MA 02115, USA
    N Engl J Med 364:2496-506. 2011
    ..Somatic mutations may influence the clinical phenotype but are not included in current prognostic scoring systems...
  31. pmc Efficacy of the JAK2 inhibitor INCB16562 in a murine model of MPLW515L-induced thrombocytosis and myelofibrosis
    Priya Koppikar
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Blood 115:2919-27. 2010
    ..However, we did not observe a decrease in the size of the malignant clone in the bone marrow of treated mice at the end of therapy, which suggests that JAK2 inhibitor therapy, by itself, was not curative in this MPN model...
  32. ncbi request reprint Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies
    Omar Abdel-Wahab
    1Human Oncology and Pathogenesis Program, 2Leukemia Service, 3Gastrointestinal Oncology Service, 4Melanoma and Immunotherapeutics Service, Department of Medicine, 5Molecular Diagnostics Service, Department of Pathology, 6Department of Radiology, 7Center for Molecular Oncology, 8Ludwig Center for Cancer Immunotherapy, and 9Molecular Pharmacology and Chemistry Program, Memorial Sloan Kettering Cancer Center and 10Weill Cornell Medical College, New York, New York
    Cancer Discov 4:538-45. 2014
    ..These data support testing of intermittent ERK pathway inhibition in the therapy for both RAS-mutant leukemia and BRAF-mutant melanoma. ..
  33. pmc The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate
    Patrick S Ward
    Abramson Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    Cancer Cell 17:225-34. 2010
    ....
  34. pmc Notch pathway activation targets AML-initiating cell homeostasis and differentiation
    Camille Lobry
    Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA
    J Exp Med 210:301-19. 2013
    ..These data demonstrate a novel tumor suppressor role for Notch signaling in AML and elucidate the potential therapeutic use of Notch receptor agonists in the treatment of this devastating leukemia...
  35. doi request reprint Epigenetic alterations in hematopoietic malignancies
    Young Rock Chung
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Int J Hematol 96:413-27. 2012
    ..The conclusions drawn from these data are valuable in understanding biological mechanisms and potential therapeutic targets...
  36. doi request reprint Disordered epigenetic regulation in the pathophysiology of myeloproliferative neoplasms
    Su Jiang Zhang
    Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, 408 East 69th Street, New York, NY 10065, USA
    Curr Hematol Malig Rep 7:34-42. 2012
    ..Moreover, the JAK2 mutation itself recently has been shown to directly affect histone post-translational modifications. This article reviews the clinical and functional implications of epigenetic alterations in the pathogenesis of MPNs...
  37. ncbi request reprint Hematopoietic stem cell origin of BRAFV600E mutations in hairy cell leukemia
    Stephen S Chung
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Sci Transl Med 6:238ra71. 2014
    ..These findings link the pathogenesis of HCL to somatic mutations that arise in HSPCs and further suggest that chronic lymphoid malignancies may be initiated by aberrant HSCs. ..
  38. pmc EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation
    Wendy Beguelin
    Division of Hematology Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA
    Cancer Cell 23:677-92. 2013
    ..GC B cell (GCB)-type diffuse large B cell lymphomas (DLBCLs) are mostly addicted to EZH2 but not the more differentiated activated B cell (ABC)-type DLBCLs, thus clarifying the therapeutic scope of EZH2 targeting...
  39. pmc Macrophages support pathological erythropoiesis in polycythemia vera and β-thalassemia
    Pedro Ramos
    Department of Pediatrics, Division of Hematology Oncology, Weill Cornell Medical College, New York, New York, USA
    Nat Med 19:437-45. 2013
    ..The contribution of macrophages to stress and pathological erythropoiesis, which we have termed stress erythropoiesis macrophage-supporting activity, may have therapeutic implications...
  40. ncbi request reprint Proposed criteria for response assessment in patients treated in clinical trials for myeloproliferative neoplasms in blast phase (MPN-BP): formal recommendations from the post-myeloproliferative neoplasm acute myeloid leukemia consortium
    John Mascarenhas
    Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY, USA
    Leuk Res 36:1500-4. 2012
    ..We plan to validate these proposed response criteria within multi-centered clinical trials...
  41. pmc Depletion of L3MBTL1 promotes the erythroid differentiation of human hematopoietic progenitor cells: possible role in 20q- polycythemia vera
    Fabiana Perna
    Molecular Pharmacology and Chemistry Program, Sloan Kettering Institute, New York, NY, USA
    Blood 116:2812-21. 2010
    ..Our data suggest that haploinsufficiency of L3MBTL1 contributes to some (20q-) myeloproliferative neoplasms, especially polycythemia vera, by promoting erythroid differentiation...
  42. pmc Janus kinase-2 inhibition induces durable tolerance to alloantigen by human dendritic cell-stimulated T cells yet preserves immunity to recall antigen
    Brian C Betts
    Laboratory of Cellular Immunobiology, Immunology Program, Sloan Kettering Institute for Cancer Research, New York, NY 10065, USA
    Blood 118:5330-9. 2011
    ....
  43. pmc Sequential azacitidine plus lenalidomide combination for elderly patients with untreated acute myeloid leukemia
    Daniel A Pollyea
    Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
    Haematologica 98:591-6. 2013
    ..In conclusion, a sequential combination of azacitidine plus lenalidomide has clinical activity in older patients with acute myeloid leukemia, and further studies of this combination are underway...
  44. ncbi request reprint Molecular alterations underlying eosinophilic and mast cell malignancies
    Hossein Sadrzadeh
    Center for Leukemia and the Bone Marrow Transplant Unit, Division of Hematology Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
    Discov Med 12:481-93. 2011
    ..Clinical trials are also investigating other novel small molecules that may have efficacy against targets currently resistant to imatinib and other TKIs...
  45. pmc Mutations in epigenetic modifiers in the pathogenesis and therapy of acute myeloid leukemia
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program, and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 121:3563-72. 2013
    ..Our understanding of the effects of these mutations on hematopoiesis and potential for therapeutic targeting of specific AML subsets is also reviewed here...
  46. pmc Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies
    Omar Abdel-Wahab
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Blood 114:144-7. 2009
    ..029). These data indicate that TET2 mutations are observed in different myeloid malignancies and may be important in AML prognosis...
  47. pmc Prognostic relevance of integrated genetic profiling in acute myeloid leukemia
    Jay P Patel
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10065, USA
    N Engl J Med 366:1079-89. 2012
    ..The prognostic value of recently identified somatic mutations has not been systematically evaluated in a phase 3 trial of treatment for AML...
  48. pmc D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice
    Esra A Akbay
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Genes Dev 28:479-90. 2014
    ..Together, these findings indicate that inhibitors of mutant IDH2 may be beneficial in the treatment of D2HGA and suggest that 2HG produced by IDH mutant tumors has the potential to provoke a paraneoplastic condition. ..
  49. pmc Recent advances in the treatment of acute myeloid leukemia
    Omar Abdel-Wahab
    Human Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center New York, NY 10065 USA
    F1000 Med Rep 2:55. 2010
    ..Lastly, we review a recent assessment of the role of allogeneic hematopoietic stem cell transplantation in AML in first complete remission...
  50. ncbi request reprint Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis
    Adi Diab
    Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Leuk Res 37:32-6. 2013
    ..These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival...