Genomes and Genes
Summary: Disorders in which one or more stimuli cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential.
Publications304 found, 100 shown here
- Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cellsAnn Mullally
Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 17:584-96. 2010..These findings provide insights into the consequences of JAK2 activation on HSC differentiation and function and have the potential to inform therapeutic approaches to JAK2V617F-positive MPN...
- Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disordersE Joanna Baxter
Department of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK
Lancet 365:1054-61. 2005Human myeloproliferative disorders form a range of clonal haematological malignant diseases, the main members of which are polycythaemia vera, essential thrombocythaemia, and idiopathic myelofibrosis...
- Mutation in TET2 in myeloid cancersFrancois Delhommeau
INSERM U790, Institut Gustave Roussy, Villejuif, France
N Engl J Med 360:2289-301. 2009The myelodysplastic syndromes and myeloproliferative disorders are associated with deregulated production of myeloid cells. The mechanisms underlying these disorders are not well defined.
- New mutations and pathogenesis of myeloproliferative neoplasmsWilliam Vainchenker
INSERM, UMR1009, Institut Gustave Roussy, Villejuif, France
Blood 118:1723-35. 2011..Their precise roles in hematopoiesis and in the pathogenesis of MPN, as well as their prognostic impact and potential as a therapeutic target, are currently under investigation...
- Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasmsAlfonso Quintas-Cardama
Department of Leukemia, University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
Blood 115:3109-17. 2010..Preliminary clinical results support these preclinical data and establish INCB018424 as a promising oral agent for the treatment of MPNs...
- MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasiaYana Pikman
Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
PLoS Med 3:e270. 2006....
- Janus kinases in immune cell signalingKamran Ghoreschi
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunol Rev 228:273-87. 2009..transformation, the most common being gain-of-function mutations of Jak2 in polycythemia vera and other myeloproliferative disorders. Our existing knowledge on Jak signaling pathways and fundamental work on their biochemical structure ..
- Role of JAK2 in the pathogenesis and therapy of myeloproliferative disordersRoss L Levine
Brigham and Women s Hospital, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02155, USA
Nat Rev Cancer 7:673-83. 2007The myeloproliferative disorders polycythaemia vera (PV), essential thombocythaemia (ET), and primary myelofibrosis (PMF) are clonal disorders of multipotent haematopoietic progenitors...
- Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1A Tefferi
Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 24:1128-38. 2010..However, it is not clear as to whether and how these abnormalities contribute to disease initiation, clonal evolution or blastic transformation...
- Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapyPriya 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...
- Inactivation of polycomb repressive complex 2 components in myeloproliferative and myelodysplastic/myeloproliferative neoplasmsJoannah Score
Faculty of Medicine, University of Southampton, Southampton, United Kingdom
Blood 119:1208-13. 2012..All 3 SUZ12 mutations tested and the EED mutation reduced PRC2 histone methyltransferase activity in vitro, demonstrating that PRC2 function may be compromised in myeloid disorders by mutation of distinct genes...
- Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic miceRalph Tiedt
Department of Research, Experimental Hematology, University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland
Blood 111:3931-40. 2008An acquired somatic mutation in the JAK2 gene (JAK2-V617F) is present in the majority of patients with myeloproliferative disorders (MPDs)...
- Janus kinase inhibitors for the treatment of myeloproliferative neoplasias and beyondAlfonso Quintas-Cardama
Department of Leukemia, Box 428, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA
Nat Rev Drug Discov 10:127-40. 2011..Preliminary results indicate that these agents hold great promise for the treatment of JAK-driven disorders...
- Genome integrity of myeloproliferative neoplasms in chronic phase and during disease progressionThorsten Klampfl
Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria
Blood 118:167-76. 2011..Our data provide insight into the genetic complexity of MPNs and implicate new genes involved in disease progression...
- CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasmsJeffrey W Tyner
Knight Cancer Institute, Oregon Health and Science University, Portland, OR 97239, USA
Blood 115:5232-40. 2010....
- Myeloproliferative neoplasm induced by constitutive expression of JAK2V617F in knock-in miceCaroline Marty
Inserm U1009, Institut Gustave Roussy, PR1, 114 rue Edouard Vaillant, 94805 Villejuif, France
Blood 116:783-7. 2010..In conclusion, constitutive heterozygous expression of JAK2(V617F) in mice is not embryo-lethal but results in severe PV-like disease with secondary myelofibrosis and not in ET-like disease as expected from patient study...
- FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant modelLouise M Kelly
Division of Hematology Oncology, Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
Blood 99:310-8. 2002..This model system should be useful to assess the contribution of additional cooperating mutations and to evaluate specific FLT3 inhibitors in vivo...
- mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasmsCostanza Bogani
Department of Medical and Surgical Care, Section of Hematology, University of Florence, Florence, Italy
PLoS ONE 8:e54826. 2013..The aim of the study was to characterize the effects in vitro of mTOR inhibitors, used alone and in combination with JAK2 inhibitors, against MPN cells...
- Constitutively active AKT depletes hematopoietic stem cells and induces leukemia in miceMichael G Kharas
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Blood 115:1406-15. 2010..This study demonstrates that enhanced AKT activation is an important mechanism of transformation in AML and that HSCs are highly sensitive to excess AKT/mTOR signaling...
- Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disordersAmy V Jones
Wessex Regional Genetics Laboratory, Salisbury District Hospital, Salisbury SP2 8BJ, United Kingdom
Blood 106:2162-8. 2005The analysis of rare chromosomal translocations in myeloproliferative disorders has highlighted the importance of aberrant tyrosine kinase signaling in the pathogenesis of these diseases...
- Classification and diagnosis of myeloproliferative neoplasms: the 2008 World Health Organization criteria and point-of-care diagnostic algorithmsA Tefferi
Division of Hematology, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 22:14-22. 2008..diseases (CMPDs) as a subdivision of myeloid neoplasms that includes the four classic myeloproliferative disorders (MPDs)-chronic myelogenous leukemia, polycythemia vera (PV), essential thrombocythemia (ET) and primary ..
- JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosisCatherine Lacout
Institut National de la Sante et de la Recherche Medicale INSERM U790, Universite Paris XI, Institut Gustave Roussy IGR, Villejuif, France
Blood 108:1652-60. 2006A JAK2(V617F) mutation is frequently found in several BCR/ABL-negative myeloproliferative disorders. To address the contribution of this mutant to the pathogenesis of these different myeloproliferative disorders, we used an adoptive ..
- Transgenic expression of JAK2V617F causes myeloproliferative disorders in miceShu Xing
Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, USA
Blood 111:5109-17. 2008The JAK2(V617F) mutation was found in most patients with myeloproliferative disorders (MPDs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis...
- The myeloproliferative disordersPeter J Campbell
Department of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom
N Engl J Med 355:2452-66. 2006
- Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signalingEdwin Chen
Cambridge Institute for Medical Research and Department of Haematology, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK
Cancer Cell 18:524-35. 2010..Our results illustrate the power of clonal analysis, indicate that the consequences of JAK2V617F reflect a balance between STAT5 and STAT1 activation and are relevant for other neoplasms associated with signaling pathway mutations...
- Dual PI3K/AKT/mTOR inhibitor BEZ235 synergistically enhances the activity of JAK2 inhibitor against cultured and primary human myeloproliferative neoplasm cellsWarren Fiskus
The University of Kansas Cancer Center, Kansas City, KS, USA
Mol Cancer Ther 12:577-88. 2013..These findings create a compelling rationale to determine the in vivo activity of dual PI3K/mTOR inhibitors in combination with JAK inhibitors against myelofibrosis HPCs...
- Genetics of the myeloproliferative neoplasmsOmar 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...
- A sensitive detection method for MPLW515L or MPLW515K mutation in chronic myeloproliferative disorders with locked nucleic acid-modified probes and real-time polymerase chain reactionAlessandro Pancrazzi
UF di Ematologia, University of Florence, Viale Morgagni 85, 50134 Florence, Italy
J Mol Diagn 10:435-41. 2008..been described in patients with primary myelofibrosis or essential thrombocythemia, which are chronic myeloproliferative disorders. We have developed a real-time polymerase chain reaction assay for the detection and quantification of ..
- Heat shock protein 90 inhibitor is synergistic with JAK2 inhibitor and overcomes resistance to JAK2-TKI in human myeloproliferative neoplasm cellsWarren Fiskus
The University of Kansas Cancer Center, Kansas City, USA
Clin Cancer Res 17:7347-58. 2011..1.7 and UKE-1) or primary human CD34(+) myeloproliferative neoplasm (MPN) cells...
- Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutationToshiyuki Araki
Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, NRB1038, 330 Brookline Ave, Boston, Massachusetts 02215, USA
Nat Med 10:849-57. 2004....
- Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformationPeter J Campbell
Department of Haematology, University of Cambridge, Cambridge, United Kingdom
Blood 108:3548-55. 2006The identification of an acquired mutation of JAK2 in patients with myeloproliferative disorders has raised questions about the relationship between mutation-positive and mutation-negative subtypes, timing of the JAK2 mutation, and ..
- TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutationsA Pardanani
Division of Hematology, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 21:1658-68. 2007JAK2V617F and MPLW515L/K represent recently identified mutations in myeloproliferative disorders (MPD) that cause dysregulated JAK-STAT signaling, which is implicated in MPD pathogenesis...
- JunB deficiency leads to a myeloproliferative disorder arising from hematopoietic stem cellsEmmanuelle Passegue
Institute of Cancer and Stem Cell Biology and Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
Cell 119:431-43. 2004..These results demonstrate a stem cell-specific role for JunB in normal and leukemic hematopoiesis and provide experimental evidence that leukemic stem cells (LSC) can reside at the LT-HSC stage of development in a mouse model of MPD...
- MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patientsAnimesh D Pardanani
Division of Hematology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
Blood 108:3472-6. 2006..Furthermore, MPL mutations may occur concurrently with the JAK2V617F mutation, suggesting that these alleles may have functional complementation in myeloproliferative disease...
- Jak2: normal function and role in hematopoietic disordersJames N Ihle
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Curr Opin Genet Dev 17:8-14. 2007..Recent studies have implicated de-regulation of Jak2 kinase activity by chromosomal translocations in hematopoietic tumors and mutations within the pseudokinase domain in a spectrum of myeloproliferative diseases...
- Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in miceScott C Kogan
Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, 94143, USA
Blood 100:238-45. 2002..This classification will be of particular value to investigators seeking to develop, use, and communicate about mouse models of human hematopoietic neoplasms...
- JAK2 stimulates homologous recombination and genetic instability: potential implication in the heterogeneity of myeloproliferative disordersIsabelle Plo
INSERM, Unités Mixtes de Recherche 790, Villejuif, France
Blood 112:1402-12. 2008The JAK2(V617F) mutation is frequently observed in classical myeloproliferative disorders, and disease progression is associated with a biallelic acquisition of the mutation occurring by mitotic recombination...
- Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disordersElizabeth O Hexner
Division of Hematology and Oncology, University of Pennsylvania, Philadelphia, USA
Blood 111:5663-71. 2008Recent studies have demonstrated that patients with myeloproliferative disorders (MPDs) frequently have acquired activating mutations in the JAK2 tyrosine kinase...
- JAK2 inhibitor therapy in myeloproliferative disorders: rationale, preclinical studies and ongoing clinical trialsA Pardanani
Division of Hematology and Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 22:23-30. 2008..inhibitors that selectively target JAK2 kinase as an approach to pathogenesis-directed therapy of myeloproliferative disorders (MPD)...
- HSP90 is a therapeutic target in JAK2-dependent myeloproliferative neoplasms in mice and humansSachie 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...
- Clonal analysis of TET2 and JAK2 mutations suggests that TET2 can be a late event in the progression of myeloproliferative neoplasmsFranz X Schaub
Department of Biomedicine, Experimental Hematology, University Hospital Basel, Hebelstr 20, 4031 Basel, Switzerland
Blood 115:2003-7. 2010..The lack of a strict temporal order of occurrence makes it unlikely that mutations in TET2 represent a predisposing event for acquiring mutations in JAK2...
- Leukemogenic Ptpn11 causes fatal myeloproliferative disorder via cell-autonomous effects on multiple stages of hematopoiesisGordon Chan
Department of Stem Cell and Developmental Biology, Ontario Cancer Institute, Toronto, ON, Canada
Blood 113:4414-24. 2009..Our studies provide a mouse model for Ptpn11-evoked MPD and show that this disease results from cell-autonomous and distinct lineage-specific effects of mutant Ptpn11 on multiple stages of hematopoiesis...
- JAK2 V617F tyrosine kinase mutation in cell lines derived from myeloproliferative disordersH Quentmeier
DSMZ German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany
Leukemia 20:471-6. 2006..in the JH2 pseudokinase domain of the Janus kinase 2 gene (JAK2 V617F) has been described in chronic myeloproliferative disorders (MPD)...
- JAK2 the future: therapeutic strategies for JAK-dependent malignanciesLindsay M Lafave
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA
Trends Pharmacol Sci 33:574-82. 2012..These innovative therapies may translate to treatment of other diseases that are dependent on JAK signaling, including B-precursor acute lymphoblastic leukemia (B-ALL)...
- Mouse models of myeloproliferative neoplasms: JAK of all gradesJuan Li
Cambridge Institute for Medical Research and Department of Haematology, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK
Dis Model Mech 4:311-7. 2011..This Commentary briefly summarises the first two types of mouse models and then focuses on the more recently generated knock-in models...
- Targeting JAK2 in the therapy of myeloproliferative neoplasmsMamatha M Reddy
Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02215, USA
Expert Opin Ther Targets 16:313-24. 2012..MPNs are frequently associated with activating mutations in JAK2; small-molecule drugs targeting this molecule have entered clinical trials...
- Establishing optimal quantitative-polymerase chain reaction assays for routine diagnosis and tracking of minimal residual disease in JAK2-V617F-associated myeloproliferative neoplasms: a joint European LeukemiaNet/MPN&MPNr-EuroNet (COST action BM0902)J V Jovanovic
King s College London School of Medicine, Cancer Genetics Lab, Department of Medical and Molecular Genetics, London, UK
Leukemia 27:2032-9. 2013..This study has established a robust, reliable assay for sensitive JAK2-V617F detection, suitable for assessing response in clinical trials, predicting outcome and guiding management of patients undergoing allogeneic transplant...
- Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disordersT Bochtler
Clinical Cooperation Unit Molecular Hematology Oncology, German Cancer Research Center, DKFZ and Department of Internal Medicine V, University of Heidelberg, Heidelberg, Germany
Leukemia 26:728-35. 2012..kinase activation by reciprocal chromosomal translocation is a common pathogenetic mechanism in chronic myeloproliferative disorders. Since centrosomal proteins have been recurrently identified as translocation partners of tyrosine ..
- Disruption of the ASXL1 gene is frequent in primary, post-essential thrombocytosis and post-polycythemia vera myelofibrosis, but not essential thrombocytosis or polycythemia vera: analysis of molecular genetics and clinical phenotypesBrady L Stein
Medicine, Northwestern University Feinberg School of Medicine, USA
Haematologica 96:1462-9. 2011....
- Myeloid-specific expression of Api6/AIM/Sp alpha induces systemic inflammation and adenocarcinoma in the lungPeng Qu
Center for Immunobiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
J Immunol 182:1648-59. 2009..These studies suggest that dysregulation of myeloid cell populations by extracellular Api6 signaling leads to abnormal myelopoiesis and lung cancer...
- Adverse effects and benefits of two years of anagrelide treatment for thrombocythemia in chronic myeloproliferative disordersGunnar Birgegard
Dept Int Medicine, University Hospital, Uppsala, Sweden
Haematologica 89:520-7. 2004..This prospective study investigated clinical toxicity and efficacy of anagrelide during two years of treatment...
- Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198-fibroblast growth factor receptor-1 chimeric tyrosine kinaseMingqiang Ren
Medical College of Georgia Cancer Center, Augusta, GA 30912, USA
Blood 114:1576-84. 2009..Thus, we have defined an important event in the process of ZNF198-FGFR1-induced T-cell leukemia...
- Molecular aspects of myeloproliferative neoplasmsFrancois Delhommeau
INSERM, U1009, Institut Gustave Roussy, Universite Paris Sud, 39 rue Camille Desmoulins, 94805 Villejuif, France
Int J Hematol 91:165-73. 2010..Moreover, polymorphisms in the JAK2 gene have been recently described as associated with MPN. Additional studies of large cohorts are required to dissect the genetic events in MPNs and the mechanisms of these oncogenic cooperations...
- Sex differences in the JAK2 V617F allele burden in chronic myeloproliferative disordersBrady L Stein
Division of Hematology, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, USA
Haematologica 95:1090-7. 2010..Since variability in the JAK2(V617F) allele burden is partly responsible for the distinct phenotypes seen in the myeloproliferative disorders, the objective of this study was to identify modifiers of the allele burden.
- Tumor suppression by phospholipase C-beta3 via SHP-1-mediated dephosphorylation of Stat5Wenbin Xiao
Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA
Cancer Cell 16:161-71. 2009..The same mechanism for malignant transformation seems to be operative in other human lymphoid and myeloid malignancies. Thus, PLC-beta3 is likely a tumor suppressor...
- A pilot study of the Histone-Deacetylase inhibitor Givinostat in patients with JAK2V617F positive chronic myeloproliferative neoplasmsAlessandro Rambaldi
Haematology, Ospedali Riuniti di Bergamo, Largo Barozzi, Bergamo, Italy
Br J Haematol 150:446-55. 2010..Reverse transcription polymerase chain reaction identified a trend to reduction of the JAK2V617F allele burden. Givinostat was well tolerated and could induce haematological response in most PV and some MF patients...
- The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasmsJames W Vardiman
University of Chicago Medical Center, 5841 South Maryland Avenue, MC0008, Chicago, IL 60637, United States
Chem Biol Interact 184:16-20. 2010....
- Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITDJennifer L Rocnik
Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Blood 108:1339-45. 2006....
- JAK2(V617F): Prevalence in a large Chinese hospital populationXuesong Xu
Edmond H Fischer Signal Transduction Laboratory, College of Life Sciences, Jilin University, Changchun, 130023, China
Blood 109:339-42. 2007Recently, the JAK2(V617F) mutation was found in patients with myeloproliferative disorders (MPDs), including most with polycythemia vera (PV)...
- The burden of fatigue and quality of life in myeloproliferative disorders (MPDs): an international Internet-based survey of 1179 MPD patientsRuben A Mesa
Department of Hematology, Mayo Clinic, Rochester, Minnesota 55905, USA
Cancer 109:68-76. 2007Few objective data exist on the burden of fatigue and other constitutional symptoms in patients with myeloproliferative disorders (MPD).
- Induction of myeloproliferative disorder and myelofibrosis by thrombopoietin receptor W515 mutants is mediated by cytosolic tyrosine 112 of the receptorChristian Pecquet
Ludwig Institute for Cancer Research, Brussels, Belgium
Blood 115:1037-48. 2010..We propose that TpoR cytosolic phosphorylated Y112 and flanking sequences could become targets for pharmacologic inhibition in MPNs...
- Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2J Schwaller
Division of Hematology and Oncology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cell 6:693-704. 2000..These data define a critical role for Stat5a/b and mOSM in the pathogenesis of TEL/JAK2 disease...
- A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cellsDan Xu
Department of Medicine, Division of Hematology Oncology, Center for Stem Cell and Regenerative Medicine, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA
Blood 116:3611-21. 2010..Collectively, our data suggest that oncogenic Ptpn11 induces MPD by aberrant activation of HSCs. This study also identifies Gab2 as an important mediator for the pathogenic effects of Ptpn11 mutations...
- Deletions of the transcription factor Ikaros in myeloproliferative neoplasmsR Jager
Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria
Leukemia 24:1290-8. 2010..Thus, IKZF1 loss is an important step in the leukemic transformation of a subpopulation of MPN patients...
- IDH1 and IDH2 mutation analysis in chronic- and blast-phase myeloproliferative neoplasmsA Pardanani
Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 24:1146-51. 2010..This study shows a relatively high incidence of IDH mutations in blast-phase MPN, regardless of JAK2 mutational status, and the occurrence of similar mutations in chronic-phase PMF...
- Targeting myeloproliferative neoplasms with JAK inhibitorsAnimesh Pardanani
Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
Curr Opin Hematol 18:105-10. 2011..Here, we review the current experience with JAK inhibitors used for the treatment of myelofibrosis and polycythemia vera/essential thrombocythemia...
- LNK mutation studies in blast-phase myeloproliferative neoplasms, and in chronic-phase disease with TET2, IDH, JAK2 or MPL mutationsA Pardanani
Department of Medicine, Division of Hematology, Mayo Clinic, Rochester, MN 55905, USA
Leukemia 24:1713-8. 2010....
- The myeloproliferative disorder-associated JAK2 V617F mutant escapes negative regulation by suppressor of cytokine signaling 3Michelle B Hookham
Infection and Immunity Group, Centre for Cancer Research and Cell Biology, Queen s University, 97 Lisburn Road, Belfast, Northern Ireland, UK
Blood 109:4924-9. 2007..detected in up to 90% of patients with polycythemia and in a sizeable proportion of patients with other myeloproliferative disorders such as essential thrombocythemia and idiopathic myelofibrosis...
- Inhibition of the Bcl-xL deamidation pathway in myeloproliferative disordersRui Zhao
Laboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, United Kingdom
N Engl J Med 359:2778-89. 2008The myeloproliferative disorders are clonal disorders with frequent somatic gain-of-function alterations affecting tyrosine kinases. In these diseases, there is an increase in DNA damage and a risk of progression to acute leukemia...
- Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorderRyan M O'Connell
Department of Biology, California Institute of Technology, Pasadena, CA 91125, USA
J Exp Med 205:585-94. 2008....
- Concordance of assays designed for the quantification of JAK2V617F: a multicenter studyEric Lippert
Laboratoire d Hematologie, Centre Hospitalier Universitaire, Institut de Biologie, Bordeaux, France
Haematologica 94:38-45. 2009..Many different techniques have been designed for the quantification of JAK2V617F allelic burden, sometimes producing discrepant results...
- Characterization of murine JAK2V617F-positive myeloproliferative diseaseThomas G P Bumm
Center for Hematologic Malignancies, Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
Cancer Res 66:11156-65. 2006..patients with essential thrombocythemia and idiopathic myelofibrosis, and less frequently in atypical myeloproliferative disorders (MPD)...
- Myeloproliferative disordersRoss L Levine
Human Oncology and Pathogenesis Program, Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Blood 112:2190-8. 2008..vera (PV), essential thombocytosis (ET), and primary myelofibrosis (PMF) as pathogenetically related myeloproliferative disorders (MPD)...
- Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocationsSergei Roumiantsev
Children s Hospital, 330 Longwood Avenue, Boston, MA 02115, USA
Cancer Cell 5:287-98. 2004..These results implicate different signaling pathways originating from both kinase and fusion partner in the pathogenesis of CML and EMS...
- Essential thrombocythemia, polycythemia vera, and myelofibrosis: current management and the prospect of targeted therapyAyalew Tefferi
Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, Minnesota55905, USA
Am J Hematol 83:491-7. 2008..Herein, I will first outline my views regarding current management in ET, PV, and PMF and then discuss emerging data on preclinical and clinical activity of anti-JAK2 small molecule drugs. Am. J. Hematol., 2008. (c) 2008 Wiley-Liss, Inc...
- Genetic and epigenetic complexity in myeloproliferative neoplasmsNicholas C P Cross
Faculty of Medicine, University of Southampton, and Wessex Regional Genetics Laboratory, Salisbury, United Kingdom
Hematology Am Soc Hematol Educ Program 2011:208-14. 2011..This review summarizes the established facts relating to the genetics of MPNs, but highlights recent findings and areas of controversy...
- 8p11 myeloproliferative syndrome: a reviewCourtney C Jackson
Department of Hematopathology, The University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
Hum Pathol 41:461-76. 2010..The most common partner is ZNF198 on chromosome 13q12. In the current World Health Organization classification, the 8p11 myeloproliferative syndrome is designated as "myeloid and lymphoid neoplasms with FGFR1 abnormalities."..
- Design and evaluation of a real-time PCR assay for quantification of JAK2 V617F and wild-type JAK2 transcript levels in the clinical laboratoryJason D Merker
Department of Pathology, Stanford University Medical Center, 300 Pasteur Dr, L235, Stanford, CA 94305 5324, USA
J Mol Diagn 12:58-64. 2010....
- Methylation of miR-34a, miR-34b/c, miR-124-1 and miR-203 in Ph-negative myeloproliferative neoplasmsChor Sang Chim
Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong
J Transl Med 9:197. 2011..MicroRNA (miR) miR-34a, -34b/c, -124-1 and -203 are tumor suppressor miRs implicated in carcinogenesis...
- The t(6;8)(q27;p11) translocation in a stem cell myeloproliferative disorder fuses a novel gene, FOP, to fibroblast growth factor receptor 1C Popovici
Laboratoire d Oncologie Moleculaire, U 119 INSERM, Institut de Cancérologie et d Immunologie de Marseille, France
Blood 93:1381-9. 1999..It may promote hematopoietic stem cell proliferation and leukemogenesis through a constitutive phosphorylation and activation of the downstream pathway of FGFR1...
- Effects of the JAK2 mutation on the hematopoietic stem and progenitor compartment in human myeloproliferative neoplasmsShubha Anand
Department of Haematology, University of Cambridge, Cambridge Institute for Medical Research, Cambridge, UK
Blood 118:177-81. 2011..Our findings have potential clinical relevance, as they predict that JAK2 inhibitors may control myeloproliferation, but may have limited efficacy in eradicating the leukemic stem cells that sustain the human MPN...
- Molecular diagnosis of the myeloproliferative neoplasms: UK guidelines for the detection of JAK2 V617F and other relevant mutationsAnthony J Bench
Molecular Malignancy Laboratory and Haemato Oncology Diagnostic Service, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, UK
Br J Haematol 160:25-34. 2013..Molecular results should be considered in the context of clinical findings and other haematological or laboratory results...
- AKT is a therapeutic target in myeloproliferative neoplasmsI Khan
Division of Hematology, Northwestern University, Chicago, IL, USA
Leukemia 27:1882-90. 2013..Together, these findings establish AKT as a rational therapeutic target in the MPNs. ..
- Genetic and epigenetic alterations of myeloproliferative disordersJelena D Milosevic
CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT25 3, 1090 Vienna, Austria
Int J Hematol 97:183-97. 2013..This review provides an overview of point mutations and cytogenetic lesions associated with MPN and addresses the role of these somatic lesions in MPN disease progression...
- The G allele of the JAK2 rs10974944 SNP, part of JAK2 46/1 haplotype, is strongly associated with JAK2 V617F-positive myeloproliferative neoplasmsAdrian P Trifa
Department of Medical Genetics, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania
Ann Hematol 89:979-83. 2010..Moreover, JAK2 46/1 seems to be associated with mutant allele burden >50% in JAK2 V617F-positive myeloproliferative neoplasms patients...
- A fourth case of BCR-FGFR1 positive CML-like disease with t(8;22) translocation showing an extensive deletion on the derivative chromosome 8pMassimo Pini
Hematol J 3:315-6. 2002
- Translocation (12;22) (p13;q11) in myeloproliferative disorders results in fusion of the ETS-like TEL gene on 12p13 to the MN1 gene on 22q11A Buijs
Department of Genetics, St Jude Children s Research Hospital, Memphis, Tennessee 38101 0318, USA
Oncogene 10:1511-9. 1995....
- Fusion of the BCR and the fibroblast growth factor receptor-1 (FGFR1) genes as a result of t(8;22)(p11;q11) in a myeloproliferative disorder: the first fusion gene involving BCR but not ABLT Fioretos
Department of Clinical Genetics, Lund University Hospital, Sweden
Genes Chromosomes Cancer 32:302-10. 2001....
- Constitutive Notch pathway activation in murine ZMYM2-FGFR1-induced T-cell lymphomas associated with atypical myeloproliferative diseaseMingqiang Ren
Georgia Health Sciences University Cancer Center, Augusta, GA, USA
Blood 117:6837-47. 2011..These data demonstrate the importance of Notch signaling in the etiology of SCLL, and suggest that targeting this pathway could provide a novel strategy for molecular therapies to treat SCLL patients...
- Clinical indications and biological mechanisms of splenic irradiation in chronic leukaemias and myeloproliferative disordersM Weinmann
Department of Radiation Oncology, , Hoppe-Seylerstrasse 3, , Germany
Radiother Oncol 58:235-46. 2001..one study and six case reports about SI in hairy cell leukaemia (HCL) and nine studies about SI in myeloproliferative disorders has been analyzed...
- Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndromeHelena Agerstam
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Genes Chromosomes Cancer 46:635-43. 2007..No point mutations were found in the other RUNX1 allele. The most likely functional outcome of the rearrangement was haploinsufficiency of RUNX1, which thus may be one mechanism by which EMS transforms to AML...
- Mutations in ASXL1 are associated with poor prognosis across the spectrum of malignant myeloid diseasesVéronique Gelsi-Boyer
Centre de Recherche en Cancerologie de Marseille, Laboratoire d Oncologie Moleculaire, UMR1068 Inserm, Institut Paoli Calmettes, Marseille, France
J Hematol Oncol 5:12. 2012..They are generally associated with signs of aggressiveness and poor clinical outcome. Because of this, a systematic determination of ASXL1 mutational status in myeloid malignancies should help in prognosis assessment...
- Mutation analysis of ASXL1, CBL, DNMT3A, IDH1, IDH2, JAK2, MPL, NF1, SF3B1, SUZ12, and TET2 in myeloproliferative neoplasmsMandy Brecqueville
Laboratoire d Oncologie Moleculaire, Centre de Recherche en Cancerologie de Marseille, UMR1068 Inserm, Institut Paoli Calmettes, Marseille, France
Genes Chromosomes Cancer 51:743-55. 2012..We found a high incidence of ASXL1 mutation in MF patients (20%) and a low incidence in PV (7%) and ET (4%) patients. Mutations in the other genes were rare (CBL, DNMT3A, IDH2, MPL, SF3B1, SUZ12, NF1) or absent (IDH1)...
- Regulation of hematopoietic stem and progenitor cell mobilization by cholesterol efflux pathwaysMarit Westerterp
Department of Medicine, Division of Molecular Medicine, Columbia University, New York, NY 10032, USA
Cell Stem Cell 11:195-206. 2012..Our data identify a role of cholesterol efflux pathways in the control of HSPC mobilization. This may translate into therapeutic strategies for atherosclerosis and hematologic malignancies...
- AML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2Wei Wang
Department of Experimental Anaesthesiology, University Hospital Freiburg, Center for Clinical Research, Breisacher Strasse 66, Freiburg, Germany
Blood 116:254-66. 2010..Our data identify NF-E2 as a novel AML1 target gene and delineate a role for aberrant AML1 expression in mediating elevated NF-E2 expression in MPN patients...
- Validation of the revised 2008 WHO diagnostic criteria in 75 suspected cases of myeloproliferative neoplasmToshinori Kondo
Department of Laboratory Medicine, Kawasaki Medical School, Okayama, Japan
Leuk Lymphoma 49:1784-91. 2008..In contrast, IE presented a good prognosis unlike MPN. Hereafter, the 2008 WHO criteria with JAK2 gene analysis are useful for precise diagnosis of MPN and the patients with erythrocytosis...
- Chronic myeloproliferative disorder with t(8;22)(p11;q11) can mime clonal cytogenetic evolution of authentic chronic myelogeneous leukemiaSteven Richebourg
Genes Chromosomes Cancer 47:915-8. 2008
- Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignanciesHideki Makishima
Taussig Cancer Institute R40, 9500 Euclid Ave, Cleveland OH 44195, USA
J Clin Oncol 27:6109-16. 2009..We examined the role and frequency of Cbl gene family mutations in MPN and related conditions...
- BCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repairKimberly Cramer
Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
Cancer Res 68:6884-8. 2008b>Myeloproliferative disorders (MPD) are stem cell-derived clonal diseases arising as a consequence of acquired aberrations in c-ABL, Janus-activated kinase 2 (JAK2), and platelet-derived growth factor receptor (PDGFR) that generate ..
- Dual lympho-myeloproliferative disorder in a patient with t(8;22) with BCR-FGFR1 gene fusionAnne Murati
Department of Molecular Oncology, Marseille Cancer Institute, UMR599 INSERM and Paoli Calmettes Institute, Marseille, France
Int J Oncol 26:1485-92. 2005..Although the FGFR1-MPD is rare, its study provides interesting clues to the understanding of hematopoietic stem cell biology and oncogene activation...
- The allele burden of JAK2 mutations remains stable over several years in patients with myeloproliferative disordersAlexandre Theocharides
Experimental Hematology, Department of Biomedicine, University Hospital Basel, Basel, Switzerland
Haematologica 93:1890-3. 2008..of the JAK2-V617F or JAK2 exon 12 allele burden in DNA from purified granulocytes from 48 patients with myeloproliferative disorders. The percentage of change between the first and last sample in JAK2-V617F positive patients without ..
- MOLECULAR PATHWAYS IN MYELOPROLIFERATIVE DISEASEGeorge Daley; Fiscal Year: 2002..and to develop an experimental framework for identifying and studying genes responsible for related myeloproliferative disorders. The specific aims outlined below will address how Bcr/Abl induces bone marrow proliferation by ..
- Analysis of the leukemic stem cell niche in chronic myeloid leukemiaDANIELA SANDRA KRAUSE; Fiscal Year: 2013..Van Etten, Chief of Hematology/Oncology at Tufts Medical Center and a leading expert in CML and other myeloproliferative disorders, and Dr. Charles Lin, Associate Professor at the Wellman Center for Photomedicine...
- Novel Strategies for Treatment of Myeloproliferative DisordersRoya Khosravi-Far; Fiscal Year: 2012..Thus, FOXO3a represents a potential therapeutic target for the treatment of myeloproliferative disorders. We base this hypothesis on the observations that 1) FOXO3a functions to regulate Bcr-Abl-induced ..
- Role of JAK2V617F in the Pathogenesis of Myeloproliferative Disorders.Golam Mohi; Fiscal Year: 2013b>Myeloproliferative disorders (MPDs) are clonal hematologic malignancies characterized by overproduction of one or more myeloid lineage cells...
- Training program in hematologic and oncologic diseasesYi Zheng; Fiscal Year: 2012..The areas of research include pediatric hematologic diseases such as leukemia, Fanconi anemia, myeloproliferative disorders, coagulation disorders, and sickle cell disease, immuno- deficiency disorders such as X-linked ..
- Role of MN1-TEL and MN1 in LeukemogenesisGerard C Grosveld; Fiscal Year: 2010The recurrent chromosome translocation t(12;22)(p12;q11) is associated with myeloproliferative disorders and acute myeloid leukemia (AML), and creates an MN1-TEL fusion gene in which the sequence encoding the N-terminal region of the ..
- Molecular genetic analysis of tyrosine kinases in myeloproliferative disordersRoss L Levine; Fiscal Year: 2010..The hypothesis is based on the observation that the majority of myeloproliferative disorders (MPDs) characterized thus far are caused by activating mutations n tyrosine kinases, including chronic ..
- Tyrosine Kinase JAK2 and Myeloproliferative DisordersZhizhuang Joe Zhao; Fiscal Year: 2010b>Myeloproliferative disorders (MPDs) are a group of conditions characterized by chronic increases in some or all of the blood cells...
- Modeling Multi-step Leukemogenesis Nf1 and Kras Mutant MiceJENNIFER LAUCHLE; Fiscal Year: 2009..MDSs) are usually associated with low blood cell counts and aberrant bone marrow morphology, while myeloproliferative disorders (MPDs) are characterized by over-proliferation of one or more lineages that retain the capacity to ..
- Role of Gab2 and Shp2 in Hematopoietic SignallingBenjamin G Neel; Fiscal Year: 2010..Abnormal PTKs cause myeloproliferative disorders (MPD) and/or leukemia;e.g., leukemia-associated translocations that encode fusion-PTKs (e.g...
- Clinical Hematology Research Career Development Program (K12) at HopkinsJames F Casella; Fiscal Year: 2013..strength within our institution: bone marrow failure and stem cell biology, sickle cel disease (SCD), myeloproliferative disorders, transfusion medicine, outcomes research and genetics...
- Clinical Hematology Research Career Development Program at Washington UniversityJ Evan Sadler; Fiscal Year: 2013..paroxysmal nocturnal hemoglobinuria, aplastic anemia, congenital anemias, myleodysplastic syndrome and myeloproliferative disorders, and cellular therapies using hematopoietic stem cells;(2) hemostatic and thrombotic disorders, ..
- Diagnostic Assay for ThrombocytosisDmitri V Gnatenko; Fiscal Year: 2010..ET represents a distinct subtype of myeloproliferative disorders, thrombocytosis, characterized by increased proliferation of megakaryocytes and resultant elevated ..
- Clinical Hematology Research Career Development AwardEllis J Neufeld; Fiscal Year: 2013..five years of NHLBI support, in diverse areas of hematology as defined for the program, to include myeloproliferative disorders and myelodysplastic syndrome, cell therapy (including gene therapy) and transfusion medicine, and ..
- Bypassing Oncogene Addiction: Mechanisms of off-target resistance in CMLGABRIEL ANTHONY REYES; Fiscal Year: 2013..Much like many of the other known myeloproliferative disorders, CML is associated with an activated tyrosine kinase...
- Multiplex Detection of Mutations in Leukemia PatientsEmmanuel Labourier; Fiscal Year: 2010..abnormalities in patients with acute myeloid leukemia (AML), chronic myelogenous leukemia (CML), and myeloproliferative disorders (MPDs). An estimated 44,000 new leukemia cases were predicted for 2008, with more than 21,000 deaths...
- 1st Annual Tandem ASPHO/PBMTC Educational Mtg: New Frontiers in Pediatric AlloSCTMitchell S Cairo; Fiscal Year: 2013..more rapid recovery of immunity;4) to identify strategies of utilizing AlloSCT in pediatric myeloproliferative disorders;5) to develop diagnostic and therapeutic approaches to hematological complications post pediatric ..
- Predictors of therapeutic responsiveness to lestaurtinib in myelofibrosisElizabeth O Hexner; Fiscal Year: 2012b>Myeloproliferative disorders (MPDs) characterized by prominent myelofibrosis have a poor prognosis with no effective therapies outside of allogeneic stem cell transplantation...
- MPD RESEARCH CONSORTIUMRonald Hoffman; Fiscal Year: 2013DESCRIPTION (provided by applicant): The Myeloproliferative Disorders Research Consortium (MPD-RC) focuses on the Philadelphia chromosome negative myeloproliferative neoplasms (MPN) including polycythemia vera (PV), essential ..
- A TRAINING PROGRAM IN MOLECULAR HEMATOLOGYRobert I Handin; Fiscal Year: 2010..In addition, some of the less frequent disorders like the leukemias and myeloproliferative disorders are models that have advanced our understanding of other forms of cancer...
- The Role of Oncogenic Ras in Leukemogenesis and Response to Targeted TherapiesQing Li; Fiscal Year: 2012..in myeloid malignancies including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and myeloproliferative disorders (MPD)...
- In Vivo Analysis of Oncogenic Kras in LeukemogenesisBENJAMIN BRAUN; Fiscal Year: 2009..common oncogenic lesions found in human cancer and are detected in approximately 30% of patients with myeloproliferative disorders (MPD), myelodysplastic syndrome, and acute myeloid leukemia...
- Modulation of aged hematopoietic stem cell nichesLaura M Calvi; Fiscal Year: 2013..system results in an increased risk of developing cytopenias, Myelodysplastic syndromes (MDS), myeloproliferative disorders and leukemias...
- Structure-function studies of single transmembrane helix receptorsSTEVEN OWEN SMITH; Fiscal Year: 2011..Mutations in the TM and JM domains of the Epo and Tpo receptors produce erythroleukemia and myeloproliferative disorders, respectively...
- IRF-8 as a Negative Regulator of CD11b+Gr-1+ Myeloid Cell Production and FunctionScott I Abrams; Fiscal Year: 2013..IRF-8 deficiency leads to myeloproliferative disorders. Collectively, these findings indicate that IRF-8 loss or down-regulation has profound pathologic ..
- CRLF2 signaling in B-cell acute lymphoblastic leukemiaDAVID MARC WEINSTOCK; Fiscal Year: 2013..The availability of therapeutic JAK inhibitors, which are now in clinical trials for the treatment of myeloproliferative disorders, has created an exciting opportunity to rapidly translate the discovery of CRLF2 into a directed ..
- Hematology &transfusion medicine research career development programCharles S Abrams; Fiscal Year: 2013..Program, which will be structured to cover: Hemostasis, Red Cell Disorders, Immune Hematology and Transfusion Medicine, Stem Cells, Bone Marrow Failure and Myeloproliferative Disorders to meet the intent of this K12 Competitive.
- MOLECULAR AND CELLULAR BIOLOGY OF THROMBOPOIETINKenneth Kaushansky; Fiscal Year: 2013..constitutive activity to Jak2 or c-Mpl, is known to underlie the development of congenital and acquired myeloproliferative disorders (MPDs), including polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (..
- Cardiofaciocutaneous Syndrome & Noonan Syndrome MeetingAmy Roberts; Fiscal Year: 2006..advances in protein tyrosine phosphorylase biology with regard to cardiovascular development and myeloproliferative disorders and for clinically oriented researchers, CFC International, and TNSSG to jointly plan for future ..
- ETS-1 AND ELF-1 AND MEGAKARYOPOIESISKevin Barton; Fiscal Year: 2001..with a megakaryocytic thrombocytopenia and myelodysplasia, as well as the thrombocytosis of the myeloproliferative disorders. Understanding the transcriptional regulation of the adhesion proteins in platelets has further ..
- COOPERATIVE STUDY OF POLYCYTHEMIA VERALouis Wasserman; Fiscal Year: 1980..the prospective, phase III randomized studies of polycythemia vera, to investigate the treatment of myeloproliferative disorders and to conduct efficacy trials of new agents in the treatment of polycythemia vera and the ..
- Cell Sorting and Molecular Analysis for Minimal Disease DetectionBarbara Zehentner; Fiscal Year: 2006..using gene rearrangement analysis for B-and T-cell leukemias and lymphomas; JAK2 point mutation for myeloproliferative disorders; FLT3 mutation analysis for AML; c-kit point mutation for mast cell disorders)...
- PLATELET REACTIVITY & DISORDERS OF PLATELET FUNCTIONHarvey Weiss; Fiscal Year: 1980..rat, (5) the biochemical basis of the impaired platelet function in DIC, immune-platelet injury, and myeloproliferative disorders, (6) the role of metal ions in secretion; whether there is some requirement for ADP in PGG2/TxA2 ..
- PURIFICATION OF PRIMITIVE HEMATOPOIETIC PROGENITOR CELLSRonald Hoffman; Fiscal Year: 1992..N.L.L.) and myeloproliferative disorders (M.P.D.)...
- MOLECULAR MECHANISMS CYTOKINE RECEPTOR SIGNALINGStephanie Watowich; Fiscal Year: 2000..Abnormal hematopoietic cell growth can lead to the development of disease, including myeloproliferative disorders, leukemia, or lymphoma...
- MOLECULAR EVENTS IN BLAST CRISIS OF CMLMartin Cline; Fiscal Year: 1993..for in related hematologic disorders including ph1 negative CML, Ph1 positive ALL and other evolving myeloproliferative disorders. The effects of altered p53 expression on the growth and diffentiation of hematopoietic cells will be ..
- Mechanisms of Immunomodulation by anti-RBC antibodiesJAMES ZIMRING; Fiscal Year: 2009..Some examples include: sickle cell anemia, alpha and beta thalassemia, aplastic anemia, renal failure, myeloproliferative disorders, bone marrow and solid organ transplantation, and other chronic anemias of various etiologies.
- Multiplex Detection of Mutations in Myeloproliferative Disorder and Leukemia PatiFei Ye; Fiscal Year: 2007..in patients with acute myeloid leukemia (AML), non-BCR/ABL chronic myelogenous leukemia (CML) and myeloproliferative disorders (MPDs)...
- Role of Src family kinases in hematopoietic proliferation and differentiationAndrew Schade; Fiscal Year: 2009..studies attempt to define the role of lipid raft-associated Src family kinase (SFK) activity in certain myeloproliferative disorders characterized by aberrant activation of cytokine receptor signaling...
- PUTATIVE MURINE COMPLEMENT RECEPTOR TYPE 2Joyce Fingeroth; Fiscal Year: 1992..Trisomy of the complement regulatory protein locus to which CR2 maps has been associated with several myeloproliferative disorders. A putative murine complement receptor which reacts with a rabbit antibody to the purified human ..
- Functional Studies of the Extracellular Domain of MplDANIEL SABATH; Fiscal Year: 2004..Constitutively activated receptors are associated with development of leukemias and myeloproliferative disorders. High levels of expression of Mpl are associated with a poor prognosis in leukemia and myelodysplasia, ..
- MEGAKARYOCYTIC REGULATION OF THE ALPHA-2 INTEGRIN GENEMARY ZUTTER; Fiscal Year: 2000..1 integrin expression, either due to congenital abnormalities or the development of myelodysplastic/myeloproliferative disorders, is associated with bleeding...
- MOLECULAR CONTRIBUTORS TO STEM CELL QUIESCENCERichard Steinman; Fiscal Year: 2003..and post-mitotic differentiated cells can result in a number of disease states including leukemias and myeloproliferative disorders. We hypothesize that cyclin-dependent kinase inhibitors (cdki's) such as p2l and p27 serve as ..
- HYDROXYUREA IN SICKLE CELL ANEMIASAMUEL CHARACHE; Fiscal Year: 1990..3. determine relatively short-term toxicity of HU at doses considerably less than those used to treat myeloproliferative disorders. 4. The RFA does not contemplate a controlled trial...
- PEDIATRIC ONCOLOGY GROUPPHILIP BREITFELD; Fiscal Year: 2002..stratification and chemotherapeutic management of patients with malignant lymphoproliferative and myeloproliferative disorders; 2) to develop protocols for specific brain tumor therapy which take advantage of our expanding ..
- MOLECULAR BASIS OF HEMATOPOIETIC GROWTH FACTOR SIGNALINGStephen Peiper; Fiscal Year: 1993..experiments should elucidate the proximal events that control the proliferation of normal hematopoietic progenitors and provide insight into the molecular basis for dysregulated proliferation as occurs in myeloproliferative disorders.
- LEUKEMIA THERAPY BASED ON ABNORMAL SIGNAL TRANSDUCTIONPeter Emanuel; Fiscal Year: 2003..of growth factor hypersensitivity is emerging as a potential common mechanism amongst many other myeloproliferative disorders and thus, JMML serves as an important model disease...
- Oncogene-Induced Evasion from ApoptosisRoya Khosravi Far; Fiscal Year: 2009..TRAIL, Bim and Hrk, in Bcr-Abl-induced evasion from apoptosis and their involvement in Bcr-Abl-induced myeloproliferative disorders (MPD) in vivo...
- CHRONIC MYELOCYTIC LEUKEMIA PATHOGENESIS & THERAPYRobert Taub; Fiscal Year: 1980..studies of neutrophil function in vitro, we will determine if cell surface receptors in CML and other myeloproliferative disorders may be impaired by excessive or ectopic sialoglycoproteins and if function can be restored by ..
- CHILDRENS CANCER GROUPKatherine Matthay; Fiscal Year: 2002..Our strong biology research laboratories in brain tumors, neuroblastoma and myeloproliferative disorders are conducting multiple biology studies in the Group and providing new information for future studies...
- Apoptosis in myelofibrosis with myeloid metaplasiaRuben Mesa; Fiscal Year: 2006..A defect in the normal process of apoptosis has been demonstrated in the related myeloproliferative disorders of chronic myeloid leukemia and polycythemia vera...
- High Throughput Screen for JAK2V617F Mutant Selective InhibitorsRoss Levine; Fiscal Year: 2008..The identical gain-of-function JAK2V617F allele is present in the majority of patients with the myeloproliferative disorders (MPD) polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF), and in ..
- Molecular Pathogenesis of Polycythemia VeraALISON MOLITERNO; Fiscal Year: 2008..End of Abstract) [unreadable] [unreadable]..
- VASCULAR CELL CATIONIC AMINO ACID TRANSPORT & METABOLISMANDREW SCHAFER; Fiscal Year: 2002..Elucidation of the molecular mechanisms that modulate the response to vascular injury will provide new rational targets for therapeutic intervention. ..
- BREAST CANCER/BONE MARROW STROMAL INTERACTIONSPranela Rameshwar; Fiscal Year: 2003..Since BC metastasis involves two major cell subsets, mesenchymal (stroma) and epithelial (BC), aim 4 will determine if regulation of PPT-I, NK-1 and NK-2 is tissue specific by studying their promoters in these cell subsets. ..
- Vaccine hurdle to anthrax and the emerging immune systemPranela Rameshwar; Fiscal Year: 2006..This study will also form the basis to develop in vivo model with human hematopoietic system to study anthrax infection and also to improve responses to anthrax vaccines. ..
- AML1 in Hematopoietic Cell DevelopmentROBERT LORSBACH; Fiscal Year: 2006..abstract_text> ..
- Revitalization of the Nation?s Physician-Scientist WorkforceANDREW SCHAFER; Fiscal Year: 2007..The conference is therefore only a starting point for implementing a long-term initiative for influencing and counteracting the decline in the physician-scientist workforce. [unreadable] [unreadable] [unreadable]..
- REGULATION OF PLATELET-ENDOTHELIAL INTERACTIONSANDREW SCHAFER; Fiscal Year: 2006....