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Items 1 to 69 of about 69
1. Orazi A, O'Malley DP, Jiang J, Vance GH, Thomas J, Czader M, Fang W, An C, Banks PM: Acute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemia. Mod Pathol; 2005 May;18(5):603-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemia.
  • The WHO criteria for diagnosing acute panmyelosis with myelofibrosis are somewhat distinct from those for acute megakaryoblastic leukemia.
  • However, clinical and hematopathologic findings partially overlap.
  • To determine the potential importance of bone marrow biopsy supplemented by immunohistochemistry in distinguishing between these two conditions, we studied 17 bone marrow biopsies of well-characterized cases of acute panmyelosis with myelofibrosis (six cases) and acute megakaryoblastic leukemia (11 cases).
  • Acute panmyelosis with myelofibrosis is characterized by a multilineage myeloid proliferation with a less numerous population of blasts than acute megakaryoblastic leukemia (P<0.01).
  • In the former condition, blasts are always positive with CD34, while in acute megakaryoblastic leukemia they express CD34 in 60% of the cases.
  • The blasts in acute panmyelosis with myelofibrosis only rarely express megakaryocytic antigens.
  • By contrast, acute megakaryoblastic leukemia has a significantly higher proportion of blasts expressing megakaryocytic antigens (P<0.01 with CD42b).
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Megakaryoblastic, Acute / pathology. Primary Myelofibrosis / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / analysis. Child. Child, Preschool. Chromosome Aberrations. Diagnosis, Differential. Female. Flow Cytometry. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 15578075.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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2. Vassilopoulos G, Palassopoulou M, Zisaki K, Befani M, Bouronikou E, Giannakoulas N, Stathopoulou E, Matsouka P: Successful control of acute myelofibrosis with lenalidomide. Case Rep Med; 2010;2010:421239

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  • [Title] Successful control of acute myelofibrosis with lenalidomide.
  • Acute panmyelosis with myelofibrosis (APMF) is a rare, fatal hematological neoplasm that is characterized by the acute onset of cytopenias and fibrosis in the bone marrow in the absence of splenomegaly or fibrosis-related morphological changes in the RBCs.
  • We present the case of a 59-year-old female who presented with a two-month history of anemia, leucopenia and a normal platelet count.
  • At 4 months after diagnosis, the patient was started on Lenalidomide, 10 mg/day for a 21-d-course along with growth factor support.
  • To our knowledge, this is the first case for a medication that could reverse the fatal outcome of APMF.

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  • [Cites] Blood. 2007 Aug 1;110(3):986-93 [17473062.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3495-503 [12393681.001]
  • [Cites] Br Med J. 1963 Aug 24;2(5355):472-7 [14043710.001]
  • [Cites] N Engl J Med. 2005 Feb 10;352(6):549-57 [15703420.001]
  • [Cites] Mod Pathol. 2005 May;18(5):603-14 [15578075.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1158-64 [16609064.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):513-21 [15173958.001]
  • (PMID = 21274282.001).
  • [ISSN] 1687-9635
  • [Journal-full-title] Case reports in medicine
  • [ISO-abbreviation] Case Rep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3026984
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3. Takahashi N, Lee Y, Tsai DY, Ishii K, Kamio S: [Improvement of detection of early CT signs in hyperacute stroke using a novel noise reduction filter]. Nihon Hoshasen Gijutsu Gakkai Zasshi; 2008 Jul 20;64(7):881-2
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  • PURPOSE: In the diagnosis of hyperacute stroke, an early CT sign such as the loss of gray-white matter interface may be difficult to detect within the first hours of the onset of symptoms because of the presence of quantum noise on CT images.
  • METHODS AND MATERIALS: Our method provides an adaptive partial median filter (APMF), which can reduce local noise without blurring of anatomical structure using variable filter shape and size according to the pixel value distribution of object around a center pixel.
  • The APMF can enhance the loss of gray-white matter interface due to hyperacute stroke.
  • The CT images of 26 patients with acute (<5 hours) middle cerebral artery territory infarction were proved with follow-up CT.
  • The APMF was applied to all the CT images.
  • Four radiologists, without and with applying the APMF, indicated their confidence level regarding the presence (or absence) of the early CT signs on each CT images.
  • RESULTS: A 78% noise reduction with the APMF was obtained from simulation.
  • The average area under the ROC curve (Az) was improved from 0.868 to 0.924 for all radiologists by applying the APMF to the original images.
  • The difference in Az values with and without the APMF was statistically significant with a P value of .002 for all radiologists.
  • CONCLUSION: Our proposed APMF can improve the visibility of gray-white matter interface.
  • As a result, the APMF can help radiologists detect the early CT signs at emergency CT scan.
  • [MeSH-minor] Acute Disease. Chicago. Congresses as Topic. Humans. ROC Curve. Radiology. Societies, Medical

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  • (PMID = 18719308.001).
  • [ISSN] 0369-4305
  • [Journal-full-title] Nihon Hōshasen Gijutsu Gakkai zasshi
  • [ISO-abbreviation] Nihon Hoshasen Gijutsu Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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4. Orazi A, Czader MB: Myelodysplastic syndromes. Am J Clin Pathol; 2009 Aug;132(2):290-305
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  • Submitted cases highlighted important issues and difficulties in relation to the diagnosis and classification of MDS.
  • Much of the discussion focused on the correlation, or lack of it, between morphologic examination and other diagnostic techniques, cytogenetics in particular.
  • The cases included examples of isolated del(5q) chromosomal abnormality, including the "classical" 5q- syndrome and other myeloid neoplasms.
  • Particularly challenging is the correct identification of fibrotic subtypes of MDSs and their separation from subsets of acute myeloid leukemia with myelofibrosis such as acute panmyelosis with myelofibrosis.
  • At least for the foreseeable future, the diagnosis of MDS requires integration of morphologic, immunophenotypic, and genetic features in the light of patient history and clinical manifestations.

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  • (PMID = 19605823.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 79
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5. Tamaki K, Otaka M, Sakamoto N, Matsumoto K, Yamashina S, Watanabe S: Acute variceal bleeding in a patient with idiopathic myelofibrosis successfully treated with endoscopic variceal band ligation and chemotherapy: a case report. J Med Case Rep; 2010;4:25

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  • [Title] Acute variceal bleeding in a patient with idiopathic myelofibrosis successfully treated with endoscopic variceal band ligation and chemotherapy: a case report.
  • INTRODUCTION: Idiopathic myelofibrosis is a chronic myeloproliferative disorder characterized by leukoerythroblastosis, massive splenomegaly, and increases in the reticular and collagen fibers in the bone marrow.
  • Portal hypertension is observed in some patients with idiopathic myelofibrosis.
  • Gastrointestinal hemorrhages, which are due mostly to the rupture of the esophageal varices, have been sporadically reported to be an infrequent complication of idiopathic myelofibrosis.
  • CASE PRESENTATION: We report a case of a Japanese 63-year-old woman with myelofibrosis and variceal hemorrhage, with a background of concomitant portal and pulmonary hypertension.
  • CONCLUSION: This is the first known report on the successful application of endoscopic variceal ligation and chemotherapy as the therapeutic procedure for an esophageal variceal hemorrhage in a patient with myelofibrosis.

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  • [Cites] Intern Med. 2007;46(4):187-90 [17301514.001]
  • [Cites] Ann Intern Med. 1962 Sep;57:419-40 [14478106.001]
  • [Cites] Am J Gastroenterol. 1965 Dec;44(6):536-44 [5891822.001]
  • [Cites] Am J Clin Pathol. 1989 Mar;91(3):302-5 [2923095.001]
  • [Cites] Medicine (Baltimore). 1971 Sep;50(5):357-420 [4940717.001]
  • [Cites] J Gastroenterol. 1996 Apr;31(2):260-2 [8680548.001]
  • (PMID = 20181038.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2830976
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6. Takahashi N, Lee Y, Tsai DY, Ishii K, Kinoshita T, Tamura H, Kimura M: Improvement of detection of hypoattenuation in acute ischemic stroke in unenhanced computed tomography using an adaptive smoothing filter. Acta Radiol; 2008 Sep;49(7):816-26
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  • [Title] Improvement of detection of hypoattenuation in acute ischemic stroke in unenhanced computed tomography using an adaptive smoothing filter.
  • PURPOSE: To evaluate the effect of a previously proposed adaptive smoothing filter for improving detection of parenchymal hypoattenuation of acute ischemic stroke on unenhanced CT images.
  • The adaptive partial median filter (APMF) designed for improving detectability of hypoattenuation areas on unenhanced CT images was applied.
  • Seven radiologists, including four certified radiologists and three radiology residents, indicated their confidence level regarding the presence (or absence) of hypoattenuation on CT images, first without and then with the APMF processed images.
  • Their performances without and with the APMF processed images were evaluated by receiver operating characteristic (ROC) analysis.
  • RESULTS: The mean areas under the ROC curves (AUC) for all observers increased from 0.875 to 0.929 (P = 0.002) when the radiologists observed with the APMF processed images.
  • The mean sensitivity in the detection of hypoattenuation significantly improved, from 69% (126 of 182 observations) to 89% (151 of 182 observations), when employing the APMF (P = 0.012).
  • The specificity, however, was unaffected by the APMF (P = 0.41).
  • CONCLUSION: The APMF has the potential to improve the detection of parenchymal hypoattenuation of acute ischemic stroke on unenhanced CT images.


7. Tolmachev AV, Monroe ME, Purvine SO, Moore RJ, Jaitly N, Adkins JN, Anderson GA, Smith RD: Characterization of strategies for obtaining confident identifications in bottom-up proteomics measurements using hybrid FTMS instruments. Anal Chem; 2008 Nov 15;80(22):8514-25
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  • An alternative strategy considered here, termed accurate precursor mass filter (APMF), employs linear ion trap (low resolution) MS/MS identifications generated by an appropriate search engine, such as SEQUEST, refined with high resolution precursor ion data obtained from FTMS mass spectra.
  • The APMF results can be additionally filtered using the LC elution time information from the AMT tag database, which constitutes a precursor mass and time filter (PMTF), the third approach implemented in this study.
  • Both the APMF and the PMTF approaches are evaluated for coverage and confidence of peptide identifications and contrasted with the AMT tag strategy.
  • Comparison of the AMT, APMF and PMTF approaches indicates that the AMT tag approach is preferential for studies desiring a highest achievable number of identified peptides.
  • In contrast, the APMF approach does not require an AMT tag database and provides a moderate level of peptide coverage combined with acceptable confidence values of approximately 99%.
  • Since AMT tag databases that exclude incorrect identifications are desirable, this study points to the value of a multipass APMF approach to generate AMT tag databases, which are then validated using the PMTF approach.

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  • [Cites] Anal Chem. 2008 Mar 15;80(6):2018-25 [18275164.001]
  • [Cites] J Proteome Res. 2008 Mar;7(3):960-8 [18205298.001]
  • [Cites] Bioinformatics. 2008 Apr 1;24(7):1021-3 [18304935.001]
  • [Cites] Anal Chem. 2008 Nov 15;80(22):8514-25 [18855412.001]
  • [Cites] J Am Soc Mass Spectrom. 2000 Apr;11(4):320-32 [10757168.001]
  • [Cites] Proteomics. 2002 May;2(5):513-23 [11987125.001]
  • [Cites] Anal Chem. 2002 Oct 15;74(20):5383-92 [12403597.001]
  • [Cites] Nature. 2003 Mar 13;422(6928):198-207 [12634793.001]
  • [Cites] Anal Chem. 2003 Mar 1;75(5):1039-48 [12641221.001]
  • [Cites] J Proteome Res. 2002 Jan-Feb;1(1):21-6 [12643522.001]
  • [Cites] Anal Chem. 2003 Sep 1;75(17):4646-58 [14632076.001]
  • [Cites] J Proteome Res. 2004 May-Jun;3(3):621-6 [15253445.001]
  • [Cites] J Proteome Res. 2004 Jul-Aug;3(4):760-9 [15359729.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 14;101(37):13417-22 [15347803.001]
  • [Cites] Biotechniques. 2004 Oct;37(4):621-4, 626-33, 636 passim [15517975.001]
  • [Cites] OMICS. 2004 Fall;8(3):239-54 [15669716.001]
  • [Cites] Proteomics. 2005 Aug;5(12):3120-30 [16038018.001]
  • [Cites] Nat Methods. 2005 Sep;2(9):667-75 [16118637.001]
  • [Cites] Anal Chem. 2005 Nov 15;77(22):7246-54 [16285672.001]
  • [Cites] Anal Chem. 2005 Dec 1;77(23):7763-73 [16316187.001]
  • [Cites] Mass Spectrom Rev. 2006 May-Jun;25(3):450-82 [16429408.001]
  • [Cites] Mol Cell Proteomics. 2006 Apr;5(4):714-25 [16401633.001]
  • [Cites] J Microbiol Methods. 2006 Aug;66(2):223-33 [16417935.001]
  • [Cites] Genome Biol. 2006;7(5):R40 [16709260.001]
  • [Cites] Mol Cell Proteomics. 2006 Jul;5(7):1326-37 [16635985.001]
  • [Cites] Mol Cell Proteomics. 2006 Oct;5(10):1927-41 [16857664.001]
  • [Cites] J Microbiol Methods. 2006 Dec;67(3):473-86 [16919344.001]
  • [Cites] Anal Chem. 2006 Nov 1;78(21):7397-409 [17073405.001]
  • [Cites] Anal Chem. 2006 Dec 15;78(24):8374-85 [17165830.001]
  • [Cites] Nat Methods. 2007 Mar;4(3):207-14 [17327847.001]
  • [Cites] Genome Res. 2007 Mar;17(3):328-36 [17255552.001]
  • [Cites] Mol Cell Proteomics. 2007 Mar;6(3):377-81 [17164402.001]
  • [Cites] Bioinformatics. 2007 Aug 1;23(15):2021-3 [17545182.001]
  • [Cites] Proteomics. 2007 Oct;7(19):3470-80 [17726677.001]
  • [Cites] Anal Chem. 2008 Feb 1;80(3):693-706 [18163597.001]
  • [Cites] Anal Chem. 2008 Feb 15;80(4):961-71 [18189369.001]
  • [Cites] Anal Chem. 2008 Mar 15;80(6):1871-82 [18271604.001]
  • (PMID = 18855412.001).
  • [ISSN] 1520-6882
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P41 RR018522; United States / NCRR NIH HHS / RR / RR 018522; United States / NCRR NIH HHS / RR / P41 RR018522-06; United States / NIGMS NIH HHS / GM / R01 GM063883; United States / NIAID NIH HHS / AI / Y1-AI-4894-01; United States / NCRR NIH HHS / RR / RR018522-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; EC 3.4.21.4 / Trypsin
  • [Other-IDs] NLM/ NIHMS112764; NLM/ PMC2692492
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8. Orazi A: Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases. Pathobiology; 2007;74(2):97-114
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  • [Title] Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases.
  • In spite of the impressive advances in the area of molecular pathology, bone marrow morphology remains the diagnosis cornerstone to identify the various subtypes of myeloid neoplasms.
  • Immunohistochemistry of bone marrow biopsy with markers reactive in paraffin-embedded tissues represents a powerful diagnostic tool; its results can be easily correlated with those obtained by other techniques such as flow cytometry and genetic analysis, and above all, the clinical findings.
  • Particular emphasis is being given to the correct identification of cases of myeloid neoplasms associated with myelofibrosis and for which the bone marrow biopsy represents the only available diagnostic mean.
  • Such cases include two subtypes of acute myeloid leukemia which typically cause diagnostic difficulties: acute megakaryoblastic leukemia and acute panmyelosis with myelofibrosis (acute myelosclerosis).
  • Acute myeloid leukemia with multilineage dysplasia, therapy-related myelodysplastic syndrome/therapy-related acute myeloid leukemia and de novo myelodysplastic syndromes (MDS) will also be discussed.
  • In MDS, in particular, bone marrow biopsy may help in confirming a suspected diagnosis by excluding reactive conditions in which dyshematopoietic changes may also be observed.
  • In both of these variants, the presence of reticulin fibrosis or fatty changes in the bone marrow can make accurate disease characterization very difficult or impossible using bone marrow aspirates.
  • Finally, the important group of the myelodysplastic/myeloproliferative disorders can only be accurately categorized by a careful multiparametric approach in which the bone marrow biopsy exerts a pivotal role.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid / diagnosis. Myelodysplastic Syndromes / diagnosis. Myeloproliferative Disorders / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD34 / analysis. Antineoplastic Agents / adverse effects. Biopsy / methods. Diagnosis, Differential. Humans. Immunohistochemistry. Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / pathology. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / pathology. Prognosis. Reticulin / analysis


9. Boruchov AM: Thrombocytopenia in myelodysplastic syndromes and myelofibrosis. Semin Hematol; 2009 Jan;46(1 Suppl 2):S37-43
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  • [Title] Thrombocytopenia in myelodysplastic syndromes and myelofibrosis.
  • Myelodysplastic syndromes (MDS) are a group of hematopoietic stem cell disorders characterized by ineffective hematopoeisis and an increased risk of transforming to acute myelogenous leukemia (AML).
  • Determining the molecular basis of the disease has been hampered by its heterogeneity.
  • Treating the underlying disorder with a variety of differentiation and immunosuppressive agents alleviates the problem in a small percentage of patients but more often complicates the issue.
  • Primary myelofibrosis (MF) is a chronic myeloproliferative disorder associated with hepatosplenomegaly and refractory cytopenias.
  • However, there are currently no standard therapies to treat the thrombocytopenia that is often found in patients with this disease.
  • [MeSH-major] Myelodysplastic Syndromes / complications. Primary Myelofibrosis / complications. Thrombocytopenia / blood. Thrombocytopenia / etiology. Thrombocytopenia / therapy
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / therapy


10. Naoe T: Developing target therapy against oncogenic tyrosine kinase in myeloid maliganacies. Curr Pharm Biotechnol; 2006 Oct;7(5):331-7
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  • Fusion genes involving ABL, ARG, PDGFRs, JAK2, SYK, TRKC, and FGFRs, and gain-of-function mutations of FLT3, KIT and JAK2 have been detected at various rates in myeloproliferative disease and acute myeloid leukemia.
  • Since the fusion or mutation of tyrosine kinase is a primary and central event in chronic myeloproliferative diseases, targeting the kinase activity has been thought to be an ideal intervention to treat these diseases.
  • The clinical success of imatinib for chronic myeloid leukemia has made this idea a reality, and has accelerated the development of new tyrosine kinase inhibitors (TKIs).
  • Challenging studies with TKIs have also been reported for acute myeloid leukemia.

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  • (PMID = 17076649.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 111
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11. Mascarenhas J, Navada S, Malone A, Rodriguez A, Najfeld V, Hoffman R: Therapeutic options for patients with myelofibrosis in blast phase. Leuk Res; 2010 Sep;34(9):1246-9
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  • [Title] Therapeutic options for patients with myelofibrosis in blast phase.
  • Myelofibrosis (MF) is a clonal stem cell disorder with the potential to transform to acute leukemia, referred to as myelofibrosis in blast phase (MF-BP).
  • The outcome of patients with MF-BP is grave with a median survival of only 2.7 months.
  • MF-BP is largely refractory to conventional chemotherapy and intensive induction therapy fails to have a significant impact with a median survival of 3.9 months.
  • [MeSH-major] Primary Myelofibrosis / therapy

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  • [Copyright] Published by Elsevier Ltd.
  • (PMID = 20627294.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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12. Jurisic V, Terzic T, Pavlovic S, Colovic N, Colovic M: Elevated TNF-alpha and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis. Pathol Res Pract; 2008;204(2):129-32
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  • [Title] Elevated TNF-alpha and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis.
  • Myelofibrosis is a clonal myeloproliferative disorder characterized by splenomegaly, abnormal deposition of collagen in the bone marrow, extramedullary hematopoiesis, dacriocytosis, and leukoerythroblastic blood smear.
  • Osteosclerosis is the most frequently observed bone change in myelofibrosis.
  • Based on this, we present an atypical case of leukemic transformation in myelofibrosis associated with diffuse osteolytic lesions and extremely elevated TNF-alpha and lactate dehydrogenase (LDH).
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. L-Lactate Dehydrogenase / blood. Leukemia, Myeloid, Acute / blood. Osteolysis / blood. Parathyroid Hormone / blood. Primary Myelofibrosis / complications. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17976926.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Parathyroid Hormone; 0 / Tumor Necrosis Factor-alpha; EC 1.1.1.27 / L-Lactate Dehydrogenase
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13. Brink DS: Transient leukemia (transient myeloproliferative disorder, transient abnormal myelopoiesis) of Down syndrome. Adv Anat Pathol; 2006 Sep;13(5):256-62
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  • [Title] Transient leukemia (transient myeloproliferative disorder, transient abnormal myelopoiesis) of Down syndrome.
  • Transient leukemia of Down syndrome (DS-TL), also known as transient myeloproliferative disorder of Down syndrome (DS) and transient abnormal myelopoiesis of DS, occurs in approximately 10% of DS neonates and in phenotypically normal neonates with trisomy 21 mosaicism.
  • DS-TL neonates have a approximately 15% risk of developing potentially fatal liver disease and show <10% incidence of hydrops fetalis.
  • Additional manifestations of DS-TL include cutaneous involvement, hyperviscosity, myelofibrosis, cardiopulmonary failure, splenomegaly, and spleen necrosis.
  • Despite its typical transient nature, 20% to 30% of DS-TL patients develop overt (nontransient) acute leukemia, usually within 3 years and typically of the M7 phenotype (acute megakaryoblastic leukemia).
  • The pathogenesis of DS-TL (and of subsequent acute leukemia) involves mutation of GATA1 (on chromosome X), which normally encodes a transcription factor integral to normal development of erythroid, megakaryocytic, and basophilic/mast cell lines.
  • [MeSH-major] Down Syndrome / complications. Myeloproliferative Disorders / complications. Myeloproliferative Disorders / physiopathology

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  • (PMID = 16998319.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 81
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14. Liu ML, Kallakury B, Kessler C, Hartmann DP, Azumi N, Ozdemirli M: Chronic idiopathic myelofibrosis terminating in extramedullary anaplastic plasmacytoma. Leuk Lymphoma; 2006 Feb;47(2):315-22
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  • [Title] Chronic idiopathic myelofibrosis terminating in extramedullary anaplastic plasmacytoma.
  • Chronic idiopathic myelofibrosis (CIMF) is a chronic myeloproliferative disorder (CMPD) with progressive fibrosis and extramedullary hematopoiesis.
  • Similar to other CMPDs, the stem cell in CIMF has the potential to differentiate into myeloid or lymphoid lineages, and thus CIMF can culminate in acute leukemia of myeloid or, rarely, lymphoid lineage.
  • [MeSH-major] Hematopoiesis, Extramedullary. Plasmacytoma / pathology. Primary Myelofibrosis / pathology
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Lymph Nodes / pathology. Male. Middle Aged. Spleen / pathology

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  • (PMID = 16321864.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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15. Rain JD: [Polycythemia vera]. Rev Prat; 2005 Oct 15;55(15):1659-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera (PV) is a chronic myeloproliferative disorder due to a haematopoietic stem cell's clonal proliferation.
  • This acquired disorder is often associated with thrombocytosis, leukocytosis and splenomegaly.
  • Generally, diagnosis remains easy, based on basic clinical and biological abnormalities.
  • Sometimes, positive diagnosis required more sophisticated tests as assay of endogenous erythroid colony, erythropoietin blood level and bone marrow biopsy.
  • Usually natural history of disease remains long with a good quality of life.
  • In some cases complications occur: mainly thrombosis and late myeloid metaplasia with myelofibrosis and acute leukemia.
  • Therapeutic approachs remain complex and difficult to optimize based up on age and disease severity.
  • [MeSH-major] Polycythemia Vera / diagnosis. Polycythemia Vera / drug therapy
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Diagnosis, Differential. Erythroid Cells. Erythropoietin / blood. Humans. Leukemia / chemically induced. Leukemia / prevention & control. Quality of Life. Severity of Illness Index

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  • (PMID = 16334202.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin
  • [Number-of-references] 16
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16. Amemiya S, Akahane M, Takita J, Igarashi T, Ohtomo K: Imaging findings of upper abdominal involvement by acute megakaryoblastic leukaemia. Pediatr Radiol; 2008 Apr;38(4):457-61
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  • [Title] Imaging findings of upper abdominal involvement by acute megakaryoblastic leukaemia.
  • Acute megakaryoblastic leukaemia (AMKL), a relatively rare type of acute myeloid leukaemia, is characterized by frequent involvement of the liver, spleen and lymph nodes in addition to myelofibrosis in children.
  • Diagnosis is difficult both clinically and pathologically, and the hepatic or lymph node involvement is not uncommonly misinterpreted as solid tumour.
  • With the association of splenic lesion and lymphadenopathy, the imaging findings were considered indicative of a haematological disorder.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / diagnosis. Liver Neoplasms / diagnosis
  • [MeSH-minor] Contrast Media. Diagnosis, Differential. Fatal Outcome. Humans. Infant. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed. Ultrasonography

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  • [Cites] Leukemia. 2000 Jan;14(1):216-8 [10637500.001]
  • [Cites] Radiographics. 1994 Nov;14 (6):1291-307 [7855342.001]
  • [Cites] AJR Am J Roentgenol. 1999 Oct;173(4):1063-4 [10511179.001]
  • [Cites] Histopathology. 1995 Apr;26(4):311-21 [7607619.001]
  • [Cites] Am J Clin Pathol. 1992 Aug;98(2):214-21 [1510033.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1495-6 [15920489.001]
  • (PMID = 18172635.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
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17. Hélias C, Struski S, Gervais C, Leymarie V, Mauvieux L, Herbrecht R, Lessard M: Polycythemia vera transforming to acute myeloid leukemia and complex abnormalities including 9p homogeneously staining region with amplification of MLLT3, JMJD2C, JAK2, and SMARCA2. Cancer Genet Cytogenet; 2008 Jan 1;180(1):51-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polycythemia vera transforming to acute myeloid leukemia and complex abnormalities including 9p homogeneously staining region with amplification of MLLT3, JMJD2C, JAK2, and SMARCA2.
  • Polycythemia vera (PV) is a clonal stem cell disorder characterized by an excessive erythrocyte production.
  • At diagnosis, a normal karyotype is found in < or =80% of cases, but an abnormal karyotype frequently develops with evolution.
  • Trisomy 9 and gains on 9p are some of the most frequent cytogenetic abnormalities, together with trisomy 8 and del(20q) in both PV and idiopathic myelofibrosis.
  • We report the case of a 54-year-old man whose disease was classified as an acute myeloid transformation of PV.
  • [MeSH-major] Gene Amplification. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Polycythemia Vera / complications. Transcription Factors / genetics

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  • (PMID = 18068534.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KDM4C protein, human; 0 / MLLT3 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / SMARCA2 protein, human; 0 / Transcription Factors; EC 1.14.11.- / Jumonji Domain-Containing Histone Demethylases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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18. Gangat N, Tefferi A: Pharmacotherapy of essential thrombocythemia. Expert Opin Pharmacother; 2008 Jul;9(10):1679-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The natural history of essential thrombocythemia is characterized by an increased incidence of thrombotic and hemorrhagic events and, in the long-term, a tendency for disease transformation to myelofibrosis or acute leukemia.
  • OBJECTIVE: The aim of this study was to outline the current evidence and the authors' opinion regarding the clinical management of patients with essential thrombocythemia.
  • RESULTS/CONCLUSIONS: Cytoreductive agents can reduce the rate of thrombotic events, but do not affect the overall survival or rate of disease transformation.
  • The management of intermediate-risk patients needs to be individualized: however, low-dose aspirin can be used after excluding acquired von Willebrand's disease.
  • [MeSH-minor] Age Factors. Antineoplastic Agents / therapeutic use. Aspirin / therapeutic use. Disease Progression. Humans. Hydroxyurea / therapeutic use. Interferon-alpha / therapeutic use. Janus Kinase 2 / antagonists & inhibitors. Risk Factors

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  • (PMID = 18570601.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Platelet Aggregation Inhibitors; EC 2.7.10.2 / Janus Kinase 2; R16CO5Y76E / Aspirin; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 51
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19. Barbui T, Finazzi G: Therapy for polycythemia vera and essential thrombocythemia is driven by the cardiovascular risk. Semin Thromb Hemost; 2007 Jun;33(4):321-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The clinical course of polycythemia vera (PV) and essential thrombocythemia (ET) is characterized by an increased incidence of thrombotic and hemorrhagic complications and an inherent tendency to progress into myelofibrosis or acute myeloid leukemia.
  • [MeSH-minor] Disease Management. Humans. Risk Assessment

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  • (PMID = 17525889.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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20. Petrides PE: [Primary thrombocythemia: diagnosis and therapy]. Med Klin (Munich); 2006 Aug 15;101(8):624-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary thrombocythemia: diagnosis and therapy].
  • BACKGROUND: Primary thrombocythemia is a rare acquired chronic disorder of the bone marrow which can occur at any age.
  • Diagnosis is based upon elevated platelet counts, morphologically and functionally altered platelets and characteristic bone marrow alterations as well as the exclusion of related myeloproliferative disorders which can also be accompanied by increased platelet counts.
  • Possible disease complications are thromboembolic and hemorrhagic events as well as a transformation into myelofibrosis or acute leukemia.
  • Inhibition of platelet aggregation with aspirin for the prevention of thromboembolic complications is first-line therapy; cytoreductive therapy with drugs such as hydroxyurea or interferon-alpha or thromboreductive therapy with the platelet-reducing agent anagrelide is required when thromboembolic complications are already present at diagnosis (secondary prevention) or when platelet counts are steadily increasing or various additional risk factors are present (primary prevention).
  • In up to 50% of the patients the recently discovered V617F mutation in the JAK2 gene can be identified which is supposed to be involved in the pathogenesis of this disease.
  • CLINICAL STUDIES: Because of the rarity of primary thrombocythemia thus far only two prospectively randomized studies have been carried out to compare cyto- and thromboreductive therapies.
  • CONCLUSION: Due to the existence of randomized clinical studies expert opinion will, in the future, be increasingly replaced by evidence-based therapy guidelines.
  • The improved knowledge of the molecular basis of the disease because of the discovery of the V617F mutation in the JAK2 gene has improved the molecular diagnosis and opened new avenues to molecular-targeted therapies.
  • [MeSH-minor] Adult. Aged. Aspirin / administration & dosage. Aspirin / therapeutic use. Child. Diagnosis, Differential. Drug Therapy, Combination. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / therapeutic use. Female. Follow-Up Studies. Humans. Hydroxyurea / administration & dosage. Hydroxyurea / therapeutic use. Immunologic Factors / administration & dosage. Immunologic Factors / therapeutic use. Interferon-alpha / administration & dosage. Interferon-alpha / therapeutic use. Male. Mutation. Platelet Aggregation Inhibitors / administration & dosage. Platelet Aggregation Inhibitors / therapeutic use. Platelet Count. Pregnancy. Pregnancy Complications, Hematologic. Primary Prevention. Prospective Studies. Quinazolines / administration & dosage. Quinazolines / therapeutic use. Randomized Controlled Trials as Topic. Risk Assessment. Risk Factors. Time Factors

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  • (PMID = 16896569.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide; R16CO5Y76E / Aspirin; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 45
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21. Finazzi G, Harrison C: Essential thrombocythemia. Semin Hematol; 2005 Oct;42(4):230-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Significant progress in our understanding of the molecular pathogenesis of essential thrombocythemia (ET) and the other Philadelphia (Ph) chromosome-negative myeloproliferative disorders (MPDs) has recently been achieved.
  • Unfortunately, the diagnosis of ET still relies on a set of exclusion criteria developed years ago, as recent advances have yet to be evaluated for this purpose.
  • The clinical course of ET is characterized by an increased incidence of thrombotic and hemorrhagic complications and an inherent tendency to progress into myelofibrosis or acute myeloid leukemia (AML).
  • [MeSH-major] Pregnancy Complications, Hematologic / diagnosis. Pregnancy Complications, Hematologic / drug therapy. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / drug therapy

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  • (PMID = 16210036.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 80
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22. Mesa RA, Quintás-Cardama A, Verstovsek S: Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia. Curr Hematol Malig Rep; 2007 Feb;2(1):25-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia.
  • Myelofibrosis with myeloid metaplasia (MMM) is currently classified as a classic (ie, BCR-ABL-negative) myeloproliferative disorder characterized by anemia, multiorgan extramedullary hematopoiesis, constitutional symptoms, and premature death from either leukemic transformation or other disease complications.
  • Current pharmacologic therapy has been beneficial mainly in terms of palliating disease-associated cytopenias, constitutional symptoms, splenomegaly, and other organ damage from excess myeloproliferation.
  • [MeSH-major] Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Aged. Alkylating Agents / therapeutic use. Anemia / drug therapy. Anemia / etiology. Antimetabolites, Antineoplastic / therapeutic use. Blood Coagulation Disorders / drug therapy. Blood Coagulation Disorders / etiology. Disease Progression. Drug Delivery Systems. Drugs, Investigational / therapeutic use. Erythropoietin / therapeutic use. Hematopoiesis, Extramedullary / drug effects. Humans. Immunologic Factors / therapeutic use. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / drug therapy. Middle Aged. Mutation, Missense. Palliative Care. Point Mutation. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Signal Transduction / drug effects. Thrombocytopenia / drug therapy. Thrombocytopenia / etiology

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  • (PMID = 20425385.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antimetabolites, Antineoplastic; 0 / Drugs, Investigational; 0 / Immunologic Factors; 0 / Protein Kinase Inhibitors; 11096-26-7 / Erythropoietin; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 76
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23. Brière JB: Essential thrombocythemia. Orphanet J Rare Dis; 2007;2:3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Essential thrombocythemia (ET) is an acquired myeloproliferative disorder (MPD) characterized by a sustained elevation of platelet number with a tendency for thrombosis and hemorrhage.
  • The median age at diagnosis is 65 to 70 years, but the disease may occur at any age.
  • The clinical picture is dominated by a predisposition to vascular occlusive events (involving the cerebrovascular, coronary and peripheral circulation) and hemorrhages.
  • Acute leukemia or myelodysplasia represent only rare and frequently later-onset events.
  • The molecular pathogenesis of ET, which leads to the overproduction of mature blood cells, is similar to that found in other clonal MPDs such as chronic myeloid leukemia, polycythemia vera and myelofibrosis with myeloid metaplasia of the spleen.
  • Polycythemia vera, myelofibrosis with myeloid metaplasia of the spleen and ET are generally associated under the common denomination of Philadelphia (Ph)-negative MPDs.
  • [MeSH-major] Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / therapy
  • [MeSH-minor] Adult. Age Distribution. Aged. Diagnosis, Differential. Disease Progression. Female. Hematologic Agents / therapeutic use. Humans. Incidence. Janus Kinase 2 / genetics. Male. Middle Aged. Mutation. Practice Guidelines as Topic. Pregnancy. Pregnancy Complications, Hematologic / diagnosis. Pregnancy Complications, Hematologic / therapy. Prevalence. Prognosis. Risk Assessment / methods. Sex Distribution. Sweden / epidemiology. Thrombocytosis / diagnosis

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  • [Cites] Br J Haematol. 1996 Jun;93(4):962-5 [8703834.001]
  • [Cites] Clin Lab Haematol. 1995 Sep;17(3):217-20 [8719893.001]
  • [Cites] Am J Hematol. 1996 Sep;53(1):6-10 [8813089.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:15-29 [8951769.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:31-40 [8951770.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):577-83 [10997967.001]
  • [Cites] Haematologica. 2000 Nov;85(11):1126-34 [11064463.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4261-6 [11110700.001]
  • [Cites] Mayo Clin Proc. 2001 Jan;76(1):22-8 [11155408.001]
  • [Cites] Br J Haematol. 2000 Dec;111(3):943-53 [11122159.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:149-60 [8951786.001]
  • [Cites] Blood. 1997 Jan 1;89(1):128-34 [8978285.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):29-39 [9025160.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):51-4 [9025162.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):179-84 [9136963.001]
  • [Cites] Br J Haematol. 1997 May;97(2):453-6 [9163613.001]
  • [Cites] Semin Thromb Hemost. 1997;23(4):371-7 [9263354.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3370-7 [9345019.001]
  • [Cites] Blood. 1997 Nov 15;90(10):4031-8 [9354672.001]
  • [Cites] Am J Hematol. 1997 Nov;56(3):168-72 [9371529.001]
  • [Cites] Blood. 1998 Jan 15;91(2):616-22 [9427717.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1091-6 [9694695.001]
  • [Cites] Br J Haematol. 1998 Dec;103(3):772-7 [9858229.001]
  • [Cites] Blood. 1999 Jan 15;93(2):417-24 [9885203.001]
  • [Cites] Leukemia. 1999 Feb;13(2):150-4 [10025886.001]
  • [Cites] Br J Haematol. 1999 Mar;104(4):929 [10192463.001]
  • [Cites] Ann Hematol. 1999 May;78(5):219-22 [10391102.001]
  • [Cites] Ann Hematol. 1999 Sep;78(9):389-92 [10525825.001]
  • [Cites] Am J Med. 2004 Nov 15;117(10):755-61 [15541325.001]
  • [Cites] Am J Obstet Gynecol. 2004 Dec;191(6):2016-20 [15592285.001]
  • [Cites] Br J Haematol. 2005 Feb;128(3):275-90 [15667529.001]
  • [Cites] Br J Haematol. 2005 Mar;128(5):583-92 [15725078.001]
  • [Cites] Leuk Res. 2005 May;29(5):481-91 [15755500.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] Br J Haematol. 2005 May;129(3):293-306 [15842653.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Br J Haematol. 2005 May;129(4):553-60 [15877740.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4187-90 [15817681.001]
  • [Cites] N Engl J Med. 2005 Jul 7;353(1):33-45 [16000354.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:57-63 [8951773.001]
  • [Cites] Blood. 2006 Sep 15;108(6):2037-40 [16709929.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3548-55 [16873677.001]
  • [Cites] Leukemia. 2007 Feb;21(2):277-80 [17251900.001]
  • [Cites] Br J Haematol. 2002 Apr;117(1):47-53 [11918532.001]
  • [Cites] Thromb Haemost. 2002 May;87(5):802-7 [12038780.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1596-601 [12176877.001]
  • [Cites] Br J Haematol. 2002 Sep;118(3):786-90 [12181046.001]
  • [Cites] Am J Hematol. 2002 Sep;71(1):1-6 [12221665.001]
  • [Cites] Leukemia. 2002 Oct;16(10):2078-83 [12357360.001]
  • [Cites] Ann Hematol. 2003 Mar;82(3):148-52 [12634946.001]
  • [Cites] Best Pract Res Clin Haematol. 2003 Jun;16(2):227-42 [12763489.001]
  • [Cites] Clin Appl Thromb Hemost. 1999 Apr;5(2):131-5 [10725994.001]
  • [Cites] Clin Appl Thromb Hemost. 1999 Oct;5(4):247-51 [10726022.001]
  • [Cites] Haematologica. 2000 May;85(5):492-5 [10800165.001]
  • [Cites] Eur J Haematol. 2000 Aug;65(2):132-9 [10966175.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):153-65 [16029444.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1847-9 [16079890.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):208-13 [16197451.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2862-4 [15985544.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:201-8 [16304381.001]
  • [Cites] Lancet. 2005 Dec 3;366(9501):1945-53 [16325696.001]
  • [Cites] Br J Haematol. 2006 Jan;132(2):244-5 [16398659.001]
  • [Cites] Haematologica. 2006 Feb;91(2):169-75 [16461300.001]
  • [Cites] Blood. 2006 May 1;107(9):3676-82 [16373657.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):171-3 [16673273.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):174-207 [16673274.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):219-30 [16673276.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):231-45 [16673277.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):246-50 [16673278.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):251-9 [16673279.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4214-22 [16484586.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1181-3 [16598303.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2397-405 [16639737.001]
  • [Cites] Blood. 2006 Jul 1;108(1):346-52 [16537803.001]
  • [Cites] Semin Thromb Hemost. 2006 Jun;32(4 Pt 2):381-98 [16810614.001]
  • [Cites] Ann Hematol. 1999 Oct;78(10):437-44 [10550553.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Ann Hematol. 1999 Dec;78(12):539-43 [10647877.001]
  • [Cites] Ann Hematol. 2000 Jan;79(1):40-2 [10663620.001]
  • [Cites] Cancer. 2003 Jul 1;98(1):100-9 [12833462.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1869-71 [12730106.001]
  • [Cites] Am J Hematol. 2003 Sep;74(1):26-31 [12949887.001]
  • [Cites] Haematologica. 2003 Oct;88(10):1130-8 [14555309.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:200-24 [14633783.001]
  • [Cites] N Engl J Med. 2004 Jan 8;350(2):114-24 [14711910.001]
  • [Cites] Haematologica. 2004 Feb;89(2):215-32 [15003898.001]
  • [Cites] Hematol J. 2004;5(2):161-7 [15048067.001]
  • [Cites] Ann Hematol. 2004 Jun;83(6):364-70 [15034760.001]
  • [Cites] Pathol Biol (Paris). 2004 Jun;52(5):267-74 [15217712.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):504-12 [15164229.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):495-7 [15175894.001]
  • [Cites] J Clin Oncol. 1990 Mar;8(3):556-62 [2307991.001]
  • [Cites] Cancer. 1991 May 15;67(10):2658-63 [2015567.001]
  • [Cites] Br J Haematol. 1993 Feb;83(2):198-203 [8457467.001]
  • [Cites] Acta Haematol. 1994;91(2):84-8 [8023650.001]
  • [Cites] Ann Hematol. 2001 Feb;80(2):74-8 [11261328.001]
  • [Cites] Exp Hematol. 2001 Jun;29(6):670-6 [11378261.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):855-61 [11886392.001]
  • [Cites] Haematologica. 1993 Nov-Dec;78(6 Suppl 2):18-21 [8039753.001]
  • [Cites] N Engl J Med. 1995 Apr 27;332(17):1132-6 [7700286.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):748-56 [7772511.001]
  • (PMID = 17210076.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hematologic Agents; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 108
  • [Other-IDs] NLM/ PMC1781427
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24. Condat B, Valla D: Nonmalignant portal vein thrombosis in adults. Nat Clin Pract Gastroenterol Hepatol; 2006 Sep;3(9):505-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT.
  • Acute PVT usually presents as abdominal pain.
  • Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy.
  • Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease.
  • Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively.
  • A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT.
  • Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.
  • [MeSH-minor] Adult. Clinical Trials as Topic. Humans. Hypertension, Portal / diagnosis. Hypertension, Portal / drug therapy. Hypertension, Portal / etiology. Risk Factors. Tomography, X-Ray Computed. Ultrasonography, Doppler, Color


25. Pardanani A, Hood J, Lasho T, Levine RL, Martin MB, Noronha G, Finke C, Mak CC, Mesa R, Zhu H, Soll R, Gilliland DG, Tefferi A: TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations. Leukemia; 2007 Aug;21(8):1658-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations.
  • JAK2V617F and MPLW515L/K represent recently identified mutations in myeloproliferative disorders (MPD) that cause dysregulated JAK-STAT signaling, which is implicated in MPD pathogenesis.
  • In a human JAK2V617F-expressing acute myeloid leukemia cell line, TG101209-induced cell cycle arrest and apoptosis, and inhibited phosphorylation of JAK2V617F, STAT5 and STAT3.
  • [MeSH-major] Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Janus Kinase 2 / antagonists & inhibitors. Mutation / genetics. Myeloproliferative Disorders / drug therapy. Pyrimidines / pharmacology. Receptors, Thrombopoietin / antagonists & inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Colony-Forming Units Assay. Humans. Janus Kinase 3 / antagonists & inhibitors. Janus Kinase 3 / genetics. Janus Kinase 3 / metabolism. Mice. Mice, SCID. Phosphorylation / drug effects. Polycythemia Vera / drug therapy. Polycythemia Vera / genetics. Polycythemia Vera / metabolism. Primary Myelofibrosis / drug therapy. Primary Myelofibrosis / genetics. Primary Myelofibrosis / metabolism. STAT Transcription Factors / metabolism. Stem Cells / drug effects. Thrombopoietin / metabolism. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 17541402.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Pyrimidines; 0 / Receptors, Thrombopoietin; 0 / STAT Transcription Factors; 0 / Sulfonamides; 0 / TG101209; 143641-95-6 / MPL protein, human; 9014-42-0 / Thrombopoietin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3
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26. Oki Y, Kantarjian HM, Zhou X, Cortes J, Faderl S, Verstovsek S, O'Brien S, Koller C, Beran M, Bekele BN, Pierce S, Thomas D, Ravandi F, Wierda WG, Giles F, Ferrajoli A, Jabbour E, Keating MJ, Bueso-Ramos CE, Estey E, Garcia-Manero G: Adult acute megakaryocytic leukemia: an analysis of 37 patients treated at M.D. Anderson Cancer Center. Blood; 2006 Feb 1;107(3):880-4
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  • [Title] Adult acute megakaryocytic leukemia: an analysis of 37 patients treated at M.D. Anderson Cancer Center.
  • To characterize acute megakaryocytic leukemia (FAB M7 AML), we identified 37 patients with M7 AML treated at M.D.
  • The median age of the M7 AML group was 56 years (range, 21-78 years); 22 patients (59%) had an antecedent hematologic disorder or myelodysplastic syndrome or both, and 7 patients (19%) had previously received chemotherapy for other malignancies.
  • Median disease-free survivals were 23 versus 52 weeks, respectively (P < .001).
  • These results confirm the poor prognosis of M7 AML and indicate that other biologic characteristics beyond cytogenetic abnormalities likely play a role in this disease.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human. Leukemia, Megakaryoblastic, Acute / mortality. Leukemia, Megakaryoblastic, Acute / pathology
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Neoplasms. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / pathology. Neoplasms, Second Primary / therapy. Primary Myelofibrosis / mortality. Primary Myelofibrosis / pathology. Primary Myelofibrosis / therapy. Retrospective Studies

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  • (PMID = 16123215.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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27. Vannucchi AM, Guglielmelli P: Advances in understanding and management of polycythemia vera. Curr Opin Oncol; 2010 Nov;22(6):636-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE OF REVIEW: Polycythemia vera is a relatively common myeloproliferative neoplasm (MPN) molecularly defined by the presence of mutations in the janus kinase (JAK2) gene.
  • Yet, many aspects of pathogenesis remain to be ascertained and no effective treatment for curing the disease or preventing major cardiovascular events and progression to myelofibrosis or acute leukemia exists.
  • Clinical trials with JAK2 inhibitors, either specific or not, have been initiated and first results are available.

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  • (PMID = 20805747.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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28. Oyekunle A, Koehl U, Schieder H, Ayuk F, Renges H, Fehse N, Zabelina T, Fehse B, Klingebiel T, Sputtek A, Zander A, Kröger N: CD34(+)-selected stem cell boost for delayed or insufficient engraftment after allogeneic stem cell transplantation. Cytotherapy; 2006;8(4):375-80
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  • We present the results for eight patients (median age 46 years) transplanted initially for myelofibrosis, acute leukemia, myeloma and NHL.
  • No patient had developed acute or chronic GvHD.
  • [MeSH-minor] Adolescent. Adult. Female. Graft vs Host Disease. Humans. Male. Middle Aged. Transplantation, Homologous

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  • (PMID = 16923613.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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29. Larghero J, Gervais N, Cassinat B, Rain JD, Schlageter MH, Padua RA, Chomienne C, Rousselot P: Farnesyltransferase inhibitor tipifarnib (R115777) preferentially inhibits in vitro autonomous erythropoiesis of polycythemia vera patient cells. Blood; 2005 May 1;105(9):3743-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera (PV) is an acquired myeloproliferative disorder with primary expansion of the red cell mass leading to an increased risk of thrombosis and less frequently to myelofibrosis and secondary acute leukemia.
  • Because long-term exposure to cytotoxic chemotherapy may increase the risk of acute transformation, new therapeutic options are needed.
  • Thus tipifarnib may specifically target PV stem cells and may be of clinical interest in the treatment of patients with PV.

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  • (PMID = 15632209.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinolones; 11096-26-7 / Erythropoietin; 192185-72-1 / tipifarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
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30. Kreft A, Springer E, Lipka DB, Kirkpatrick CJ: Wild-type JAK2 secondary acute erythroleukemia developing after JAK2-V617F-mutated primary myelofibrosis. Acta Haematol; 2009;122(1):36-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wild-type JAK2 secondary acute erythroleukemia developing after JAK2-V617F-mutated primary myelofibrosis.
  • A 54-year-old female patient developed acute erythroleukemia after an 8-year course of primary myelofibrosis.
  • A bone marrow trephine biopsy disclosed 2 morphologically distinct areas of chronic primary myelofibrosis and acute erythroleukemia.
  • Although the activating JAK2-V617F mutation was not maintained in blasts of acute erythroleukemia, it was detectable in the chronic phase of primary myelofibrosis, indicating that this mutation did not play a role in the leukemic transformation of erythroid cells.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Erythroblastic, Acute / genetics. Primary Myelofibrosis / complications. Primary Myelofibrosis / genetics

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  • [Copyright] 2009 S. Karger AG, Basel
  • (PMID = 19713696.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
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31. Mesa RA: Navigating the evolving paradigms in the diagnosis and treatment of myeloproliferative disorders. Hematology Am Soc Hematol Educ Program; 2007;:355-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Navigating the evolving paradigms in the diagnosis and treatment of myeloproliferative disorders.
  • The diagnosis and management of the BCR-ABL-negative myeloproliferative disorders (MPDs) of polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) are at an explosive crossroads of scientific investigation and evolving paradigms since the discovery of the tyrosine kinase-activating JAK2V617F mutation in 2005.
  • No current medical therapy has altered the natural trend of the MPDs to lead to overt severe myelofibrosis or acute leukemia.
  • Specific inhibition of JAK2 itself appears promising by in vitro investigations, and clinical trials with multiple agents are planned to commence enrollment in 2007.

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  • (PMID = 18024651.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 47
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32. Tefferi A: Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era. Hematology Am Soc Hematol Educ Program; 2006;:240-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era.
  • JAK2V617F, a somatic gain-of-function mutation involving the JAK2 tyrosine kinase gene, occurs in nearly all patients with polycythemia vera (PV) but also in a variable proportion of patients with other myeloid disorders; mutational frequency is estimated at approximately 50% in both essential thrombocythemia (ET) and myelofibrosis (MF), up to 20% in certain subcategories of atypical myeloproliferative disorder (atypical MPD), less than 3% in de novo myelodysplastic syndrome (MDS) or acute myeloid leukemia, and 0% in chronic myeloid leukemia (CML).
  • Current information on disease-specific prognostic relevance of JAK2V617F is inconclusive and confounded by inter-study differences in the performance of mutation screening assays.

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  • (PMID = 17124067.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 41
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33. Kar B, Nandhini B, Revathi R: Ring chromosome 8 and trisomy 8 in a patient with acute myeloid leukemia. Indian J Hematol Blood Transfus; 2009 Mar;25(1):30-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ring chromosome 8 and trisomy 8 in a patient with acute myeloid leukemia.
  • We describe a child with Acute Myeloid Leukemia (AML M7) with trisomy 8 and ring chromosome 8.
  • This 15-month-old girl had presented with a history of fever, weight loss of 1 kg, gum bleeds and pallor.
  • Clinical examinations revealed no nodes or organomegaly.
  • She developed acute myelofibrosis soon after the second cycle of chemotherapy with swinging fever and rapidly enlarging spleen.
  • She passed away on day 11 post transplantation of veno-occlusive disease of liver and multiorgan failure.

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  • [Cites] Hematol Pathol. 1992;6(3):161-7 [1429344.001]
  • [Cites] Cancer Genet Cytogenet. 1992 May;60(1):53-9 [1591707.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Nov;57(1):79-85 [1756488.001]
  • [Cites] Am J Hematol. 1997 Dec;56(4):224-9 [9395183.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1883-90 [8946926.001]
  • [Cites] Cancer Genet Cytogenet. 1994 Dec;78(2):181-8 [7828151.001]
  • [Cites] Eur J Haematol. 1988 Oct;41(4):341-6 [3197821.001]
  • (PMID = 23100969.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453485
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Ring chromosome 8 / Trisomy 8
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34. Awasthi A, Das R, Varma N, Ahluwalia J, Gupta A, Marwaha RK, Garewal G: Hematological disorders in Down syndrome: ten-year experience at a Tertiary Care Centre in North India. Pediatr Hematol Oncol; 2005 Sep;22(6):507-12
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  • These comprised 4 cases of transient myeloproliferative disorder (TMD), 3 cases of TMD/acute leukemia, 4 cases of acute leukemia (AL), 2 of dual deficiency anemia, and 1 case each of myelofibrosis and idiopathic thrombocytopenia.
  • TMD can be differentiated from acute leukemia only on follow-up.
  • [MeSH-major] Down Syndrome. Hematologic Diseases / diagnosis

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  • (PMID = 16169817.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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35. Saint-Martin C, Leroy G, Delhommeau F, Panelatti G, Dupont S, James C, Plo I, Bordessoule D, Chomienne C, Delannoy A, Devidas A, Gardembas-Pain M, Isnard F, Plumelle Y, Bernard O, Vainchenker W, Najman A, Bellanné-Chantelot C, French Group of Familial Myeloproliferative Disorders: Analysis of the ten-eleven translocation 2 (TET2) gene in familial myeloproliferative neoplasms. Blood; 2009 Aug 20;114(8):1628-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the ten-eleven translocation 2 (TET2) gene in familial myeloproliferative neoplasms.
  • The JAK2(V617F) mutation does not elucidate the phenotypic variability observed in myeloproliferative neoplasm (MPN) families.
  • In a patient with 2 TET2 mutations, the analysis of 5 blood samples at different phases of her disease showed the sequential occurrence of JAK2(V617F) and TET2 mutations concomitantly to the disease evolution.
  • TET2 mutations were mainly observed (10 of 12) in patients with primary myelofibrosis or patients with polycythemia vera or essential thrombocythemia who secondarily evolved toward myelofibrosis or acute myeloid leukemia.
  • [MeSH-major] Bone Marrow Neoplasms / genetics. DNA-Binding Proteins / genetics. Myeloproliferative Disorders / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adult. Aged. Cells, Cultured. DNA Mutational Analysis. Family. Female. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Pedigree. Phenotype


36. Levine RL, Heaney M: New advances in the pathogenesis and therapy of essential thrombocythemia. Hematology Am Soc Hematol Educ Program; 2008;:76-82
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  • Essential thrombocythemia (ET) is a hematopoietic disorder that manifests clinically as thrombocytosis, and patients with ET are at increased risk for developing thrombosis, myelofibrosis, and transformation to acute myeloid leukemia.
  • Although ET was recognized as a distinct clinical syndrome more than 6 decades ago and was classified as a myeloproliferative neoplasm (MPN) by William Dameshek in 1951, the molecular pathogenesis of ET remained unknown until 2005, when activating mutations in the JAK2 tyrosine kinase (JAK2V617F) were identified in a significant proportion of patients with ET, polycythemia vera (PV) and primary myelofibrosis (PMF).

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  • (PMID = 19074062.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Receptors, Thrombopoietin; EC 1.1.1.49 / Glucosephosphate Dehydrogenase; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 67
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37. Marchioli R, Finazzi G, Landolfi R, Kutti J, Gisslinger H, Patrono C, Marilus R, Villegas A, Tognoni G, Barbui T: Vascular and neoplastic risk in a large cohort of patients with polycythemia vera. J Clin Oncol; 2005 Apr 1;23(10):2224-32
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  • PURPOSE: The clinical course of polycythemia vera is often complicated by thrombosis as well as by the possible transition to myeloid metaplasia with myelofibrosis or acute myeloid leukemia.
  • PATIENTS AND METHODS: Overall, 1,638 patients from 12 countries were enrolled onto a large, prospective multicenter project aimed at describing the clinical history of polycythemia vera for the following outcomes: survival, the cumulative rate of cardiovascular death and thrombosis, the cumulative rate of leukemia, myelodysplasia, and myelofibrosis.
  • The mean duration of the disease at entry and the duration of the follow-up were 4.9 and 2.7 years, respectively.
  • Antiplatelet therapy, but not cytoreductive treatment, was significantly associated with a lower risk of cardiovascular events.
  • We found a consistent association between age and risk of leukemia, and between duration of the disease with risk of myelofibrosis.
  • The persistently high mortality rate from hematologic malignancies characterizes the unmet therapeutic need of polycythemic patients and suggests a priority for future studies in this disease.

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  • (PMID = 15710945.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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38. Hoffman R, Prchal JT, Samuelson S, Ciurea SO, Rondelli D: Philadelphia chromosome-negative myeloproliferative disorders: biology and treatment. Biol Blood Marrow Transplant; 2007 Jan;13(1 Suppl 1):64-72
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  • [Title] Philadelphia chromosome-negative myeloproliferative disorders: biology and treatment.
  • The Philadelphia chromosome (Ph)-negative myeloproliferative disorders (MPDs) include essential thrombocythemia (ET), idiopathic myelofibrosis (IMF), and polycythemia vera (PV).
  • Both mutations activate JAK-STAT signaling pathways and likely play a role in disease progression.
  • Both ET and PV are associated with prolonged clinical courses associated with frequent thrombotic and hemorrhagic events, and progression to myelofibrosis and acute leukemia.
  • Intermediate/high-risk IMF or myelofibrosis after ET or PV is associated with a sufficiently poor prognosis to justify the use of allogeneic stem cell transplantation, which is capable of curing such patients.
  • [MeSH-major] Janus Kinase 2 / genetics. Myeloproliferative Disorders / genetics. Myeloproliferative Disorders / therapy

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  • (PMID = 17222772.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108671-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 68
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39. Kawagoe H, Grosveld GC: Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9. Blood; 2005 Dec 15;106(13):4269-77
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  • [Title] Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9.
  • Coexpression of MN1-TEL and IL-3, but not SCF, rapidly caused a fatal myeloproliferative disease rather than acute myeloid leukemia (AML).
  • Thus, the leukemogenic effect of MN1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome.

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  • [Cites] J Leukoc Biol. 1999 Feb;65(2):217-31 [10088605.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Oncogene. 2000 Feb 3;19(5):608-16 [10698505.001]
  • [Cites] Mol Cell Biol. 2000 May;20(9):3274-85 [10757811.001]
  • [Cites] Int J Hematol. 2000 Jun;71(4):301-8 [10905048.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(24):9281-93 [11094079.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Feb;23(2):122-5 [11216704.001]
  • [Cites] Exp Hematol. 2001 Jul;29(7):856-63 [11438208.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Int Immunol. 2002 Jul;14(7):813-22 [12096041.001]
  • [Cites] Oncogene. 2003 Feb 6;22(5):699-709 [12569362.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5428-37 [14500378.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):1256-69 [14729970.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2522-9 [14630789.001]
  • [Cites] Biotechnol Bioeng. 2004 Apr 20;86(2):174-87 [15052637.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6091-100 [15342392.001]
  • [Cites] Genes Dev. 2004 Oct 1;18(19):2336-41 [15371326.001]
  • [Cites] EMBO J. 1989 Jan;8(1):133-6 [2653809.001]
  • [Cites] Blood. 1991 Dec 1;78(11):3012-20 [1954386.001]
  • [Cites] Hematol Oncol Clin North Am. 1992 Jun;6(3):571-86 [1613007.001]
  • [Cites] EMBO J. 1993 Oct;12(10):3835-46 [8104786.001]
  • [Cites] Leuk Lymphoma. 1993 Oct;11(3-4):197-205 [8260894.001]
  • [Cites] Cell. 1994 Apr 22;77(2):307-16 [8168137.001]
  • [Cites] Oncogene. 1995 Apr 20;10(8):1511-9 [7731705.001]
  • [Cites] Oncogene. 1995 Apr 20;10(8):1521-8 [7731706.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):516-26 [7734349.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1427-9 [7660125.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):159-67 [8563754.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4804-8 [8639852.001]
  • [Cites] J Immunol Methods. 1996 Oct 16;197(1-2):139-50 [8890901.001]
  • [Cites] Int J Biochem Cell Biol. 1997 Dec;29(12):1371-87 [9570133.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Genes Dev. 1998 Aug 15;12(16):2475-87 [9716401.001]
  • [Cites] Leukemia. 1999 Jan;13(1):6-13 [10049061.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4278-86 [16081688.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12804-9 [10536003.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1761-72 [10477702.001]
  • (PMID = 16105979.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA217G; United States / NCI NIH HHS / CA / CA72999-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / Mn1 protein, mouse; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; 0 / homeobox protein HOXA9
  • [Other-IDs] NLM/ PMC1895240
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40. Agerstam H, Järås M, Andersson A, Johnels P, Hansen N, Lassen C, Rissler M, Gisselsson D, Olofsson T, Richter J, Fan X, Ehinger M, Fioretos T: Modeling the human 8p11-myeloproliferative syndrome in immunodeficient mice. Blood; 2010 Sep 23;116(12):2103-11
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  • [Title] Modeling the human 8p11-myeloproliferative syndrome in immunodeficient mice.
  • The 8p11 myeloproliferative syndrome (EMS), also referred to as stem cell leukemia/lymphoma, is a chronic myeloproliferative disorder that rapidly progresses into acute leukemia.
  • This study suggests that FGFR1 fusion oncogenes, by themselves, are capable of initiating an EMS-like disorder, and provides the first humanized model of a myeloproliferative disorder transforming into acute leukemia in mice.
  • The established in vivo EMS model should provide a valuable tool for future studies of this disorder.
  • [MeSH-major] Chromosomes, Human, Pair 8. Disease Models, Animal. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Animals. DNA-Binding Proteins / genetics. Humans. Mice. Mice, SCID. Mice, Transgenic. Oncogene Proteins, Fusion. Primary Myelofibrosis. Proto-Oncogene Proteins c-bcr / genetics. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Transcription Factors / genetics

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  • (PMID = 20554971.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / ZMYM2 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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41. Chim CS, Kwong YL, Lie AK, Ma SK, Chan CC, Wong LG, Kho BC, Lee HK, Sim JP, Chan CH, Chan JC, Yeung YM, Law M, Liang R: Long-term outcome of 231 patients with essential thrombocythemia: prognostic factors for thrombosis, bleeding, myelofibrosis, and leukemia. Arch Intern Med; 2005 Dec 12-26;165(22):2651-8
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  • [Title] Long-term outcome of 231 patients with essential thrombocythemia: prognostic factors for thrombosis, bleeding, myelofibrosis, and leukemia.
  • BACKGROUND: Essential thrombocythemia (ET) is a clonal myeloproliferative disease associated with thrombohemorrhagic complications and myeloid transformation to diseases such as myelofibrosis and acute myeloid leukemia.
  • Thrombosis rates at and after diagnosis of ET were comparable to those of white patients, but bleeding rates at and after diagnosis were much lower.
  • There were no deaths among patients 60 years or younger during a maximum follow-up of 15 years, and splenomegaly at diagnosis of ET appeared to protect against thrombosis.
  • The probability of myelofibrosis transformation was 9.7% at 10 years.
  • Prior myelofibrosis (P = .008) and the use of melphalan treatment (P = .002) were risk factors for acute myeloid leukemia evolution.
  • CONCLUSIONS: Essential thrombocythemia is a benign disease of older persons.
  • Chinese patients have a low risk of bleeding, and prior myelofibrosis is a major risk factor for evolution to acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Primary Myelofibrosis / epidemiology. Thrombocythemia, Essential / mortality. Thrombosis / epidemiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Asian Continental Ancestry Group. Cell Transformation, Neoplastic. Female. Follow-Up Studies. Hong Kong / epidemiology. Humans. Hydroxyurea / therapeutic use. Male. Melphalan / therapeutic use. Middle Aged. Multivariate Analysis. Myeloablative Agonists / therapeutic use. Prognosis. Risk Factors. Sex Factors. Splenomegaly. Survival Analysis. beta-Thalassemia / epidemiology

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  • (PMID = 16344424.001).
  • [ISSN] 0003-9926
  • [Journal-full-title] Archives of internal medicine
  • [ISO-abbreviation] Arch. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; Q41OR9510P / Melphalan; X6Q56QN5QC / Hydroxyurea
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42. Linardi Cda C, Pracchia LF, Buccheri V: Diagnosis and treatment of polycythemia vera: Brazilian experience from a single institution. Sao Paulo Med J; 2008 Jan 2;126(1):52-7
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  • [Title] Diagnosis and treatment of polycythemia vera: Brazilian experience from a single institution.
  • CONTEXT AND OBJECTIVE: Polycythemia vera (PV) is a chronic myeloproliferative disorder characterized by predominant proliferation of erythroid precursors.
  • The aim of this study was to describe clinical and demographic characteristics of PV patients at diagnosis and analyze their long-term outcomes.
  • Clinical and demographic characteristics, thrombotic events, transformation to acute leukemia, myelofibrosis and survival were evaluated.
  • Thirty-six (54.5%) were females, with a median age at diagnosis of 61 years.
  • At diagnosis, the median hemoglobin concentration was 18.8 mg/dl and the median platelet count was 593,000/mm(3).
  • The overall incidence of leukemia and myelofibrosis was 0.42% per patient-year and 1.06% per patient-year, respectively.
  • [MeSH-major] Polycythemia Vera / diagnosis. Polycythemia Vera / therapy

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  • (PMID = 18425288.001).
  • [ISSN] 1516-3180
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Hemoglobins
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43. Zhang S, Qiu H, Fischer BS, Li W, Duan L, Sun X, Xu W, Li J: JAK2 V617F patients with essential thrombocythemia present with clinical features of polycythemia vera. Leuk Lymphoma; 2008 Apr;49(4):696-9
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  • [Title] JAK2 V617F patients with essential thrombocythemia present with clinical features of polycythemia vera.
  • Moreover, JAK2 V617F patients with essential thrombocythemia (ET) have been found to have some clinical features similar to PV.
  • A total of 99 Chinese myeloproliferative disorder patients and 120 additional patients with acute myeloid leukemia, acute lymphoblastic leukemia and myelodysplastic syndromes were studied.
  • The V617F mutation was detected in genomic DNA of peripheral blood samples of 16 of 23 PV patients (69.6%), 21 of 45 ET patients (46.7%) and 3 of 8 patients with idiopathic myelofibrosis (37.5%).
  • There were striking differences in clinical features such as hemoglobin, hematocrit and neutrophils percentages between V617F positive and negative patients with ET.
  • [MeSH-minor] Adult. Aged. Asian Continental Ancestry Group. Female. Genetic Testing. Hematocrit. Hemoglobins / analysis. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Middle Aged. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Neutrophils / cytology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18398736.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; EC 2.7.10.2 / Janus Kinase 2
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44. Geron I, Abrahamsson AE, Barroga CF, Kavalerchik E, Gotlib J, Hood JD, Durocher J, Mak CC, Noronha G, Soll RM, Tefferi A, Kaushansky K, Jamieson CH: Selective inhibition of JAK2-driven erythroid differentiation of polycythemia vera progenitors. Cancer Cell; 2008 Apr;13(4):321-30
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  • Polycythemia Vera (PV) is a myeloproliferative disorder (MPD) that is commonly characterized by mutant JAK2 (JAK2V617F) signaling, erythrocyte overproduction, and a propensity for thrombosis, progression to myelofibrosis, or acute leukemia.
  • Thus, TG101348 may be an effective inhibitor of JAK2V617F+ MPDs in clinical trials.


45. Kiladjian JJ, Rain JD, Bernard JF, Briere J, Chomienne C, Fenaux P: Long-term incidence of hematological evolution in three French prospective studies of hydroxyurea and pipobroman in polycythemia vera and essential thrombocythemia. Semin Thromb Hemost; 2006 Jun;32(4 Pt 2):417-21
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  • Despite recent discoveries made in myeloproliferative disorders other than chronic myelogenous leukemia, which it is hoped will result in earlier diagnosis, and better evaluation and management of patients, hematological evolution to myelofibrosis, acute leukemia, and myelodysplastic syndromes (AL/MDS) remain major causes of long-term mortality in polycythemia vera (PV) and essential thrombocythemia (ET) patients.
  • We report updated results of three French prospective trials of hydroxyurea and pipobroman in PV and ET patients with a median follow-up longer than 10 years.
  • Although hydroxyurea currently remains the first choice in the treatment of high-risk PV and ET patients, the use of nonleukemogenic drugs, such as interferon alpha (IFN-alpha) or anagrelide, should be assessed more widely in randomized trials using accurate diagnostic criteria and taking into account the presence of the JAK2 mutation, given that they may have an impact on disease evolution.

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  • (PMID = 16810617.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Interferon-alpha; 0 / Proto-Oncogene Proteins; 6Q99RDT97R / Pipobroman; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 42
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46. Weiss DJ: A retrospective study of the incidence and the classification of bone marrow disorders in the dog at a veterinary teaching hospital (1996-2004). J Vet Intern Med; 2006 Jul-Aug;20(4):955-61
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  • BACKGROUND: An 8-year retrospective study was conducted to evaluate the prevalence and the classification of canine bone marrow disorders in a clinical pathology service at a university referral hospital.
  • HYPOTHESIS: A better understanding of the spectrum and the prevalence of canine bone marrow disorders can be achieved with a multiyear retrospective study.
  • RESULTS: Bone marrow specimens were first categorized based on the presence or the absence of a primary bone marrow disorder.
  • Frequently observed pathologic disorders included nonregenerative immune-mediated anemia, pure red cell aplasia, bone marrow necrosis, myelofibrosis, and hemophagocytic syndrome.
  • One hundred twenty-six cases of neoplasia were divided into acute leukemia (n = 46), chronic leukemia (n = 7), stage 5 malignant lymphoma (n = 28), multiple myeloma (n = 25), malignant histiocytosis (n = 11), metastatic mast-cell tumor (n = 3), sarcoma (n = 5), and carcinoma (n = 1).
  • CONCLUSIONS AND CLINICAL IMPORTANCE: This study provides a general indication of the spectrum and the prevalence of canine bone marrow disorders at a referral center in North America.

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  • (PMID = 16955822.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Nelson ME, Steensma DP: JAK2 V617F in myeloid disorders: what do we know now, and where are we headed? Leuk Lymphoma; 2006 Feb;47(2):177-94
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  • Until very recently, the only TK mutations widely observed in myeloid neoplasia were the BCR/ABL1 fusions characteristic of chronic myeloid leukemia and some acute leukemias, and FLT3 activating mutations in a minority of acute myeloid leukemias.
  • Several rare TK mutations are found in various atypical myeloproliferative disorders, but big pieces of the pathobiological puzzle were glaringly missing.
  • Most affected patients suffer from the classic BCR/ABL1-negative myeloproliferative disorders (MPD), especially polycythemia vera (74% of n = 506), but a subset of people with essential thrombocythemia (36% of n = 339) or myelofibrosis with myeloid metaplasia (44% of n = 127) bear the identical mutation, as do a few individuals with myelodysplastic syndromes or an atypical myeloid disorder (7% of n = 556).
  • This long-sought common mutation in BCR/ABL1-negative MPD raises many provocative biological and clinical questions, and demands re-evaluation of prevailing diagnostic algorithms for erythrocytosis and thrombocytosis.
  • [MeSH-major] Myeloproliferative Disorders / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics

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  • [ErratumIn] Leuk Lymphoma. 2006 May;47(5):957
  • (PMID = 16321848.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA 90628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 143
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48. Fruchtman SM, Petitt RM, Gilbert HS, Fiddler G, Lyne A, Anagrelide Study Group: Anagrelide: analysis of long-term efficacy, safety and leukemogenic potential in myeloproliferative disorders. Leuk Res; 2005 May;29(5):481-91
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  • [Title] Anagrelide: analysis of long-term efficacy, safety and leukemogenic potential in myeloproliferative disorders.
  • Appropriate treatment for nonreactive thrombocytosis resulting from a myeloproliferative disorder (MPD) is surrounded by controversy.
  • Although few doubt the association of thrombocytosis with increased risk for life-threatening events such as thrombosis or hemorrhage, or the association between clonal myeloproliferation and the progression to acute leukemia or myelofibrosis, controversy exists regarding the timing and nature of appropriate therapeutic intervention.
  • An ideal cytoreductive treatment for long-term use should minimize thrombosis and avoid long-term complications, especially acute leukemia (AL).
  • Acute leukemia/myelodysplasia developed in 2.1% of ET patients (47/2251) with a maximum follow-up of 7.1 years.
  • Of the PV patients, 2.8% developed acute leukemia/myelodysplastic syndrome (13/462), with a maximum follow-up of 7.0 years.
  • With maximum follow-up over 7 years, anagrelide achieved platelet control in over 75% of MPD patients and did not increase the conversion to acute leukemia during the treatment duration analyzed.
  • [MeSH-major] Myeloproliferative Disorders / drug therapy. Platelet Aggregation Inhibitors / therapeutic use. Quinazolines / therapeutic use

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  • (PMID = 15755500.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide
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49. Di Nisio M, Barbui T, Di Gennaro L, Borrelli G, Finazzi G, Landolfi R, Leone G, Marfisi R, Porreca E, Ruggeri M, Rutjes AW, Tognoni G, Vannucchi AM, Marchioli R, European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Investigators: The haematocrit and platelet target in polycythemia vera. Br J Haematol; 2007 Jan;136(2):249-59
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  • Polycythemia vera (PV) is a chronic myeloproliferative disorder whose major morbidity and mortality are thrombohaemorragic events and progression to acute leukaemia or myelofibrosis.
  • High platelet count was associated with a lower progression rate to acute leukaemia/myelofibrosis, whereas it had no significant relationship with thrombotic events or mortality.
  • [MeSH-minor] Aged. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Disease Progression. Female. Follow-Up Studies. Hematocrit. Hemorrhage / etiology. Humans. Leukemia / blood. Male. Middle Aged. Platelet Count. Primary Myelofibrosis / blood. Prognosis. Proportional Hazards Models. Prospective Studies. Thrombosis / etiology


50. Rabin KR, Whitlock JA: Malignancy in children with trisomy 21. Oncologist; 2009 Feb;14(2):164-73
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  • Patients with Down syndrome (DS) display a unique spectrum of malignancies, with a 10- to 20-fold higher risk of acute leukemias, and a markedly lower incidence of solid tumors.
  • This review discusses the current understanding of the basis for this distinctive pattern of cancer incidence and the clinical and biologic features of the malignant disorders most frequent in DS individuals: transient myeloproliferative disease, acute megakaryoblastic leukemia, and acute lymphoblastic leukemia.

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  • [Cites] Cancer. 2007 Nov 1;110(9):2067-74 [17849462.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5442-7 [18048827.001]
  • [Cites] Mutat Res. 2008 Jan 1;637(1-2):118-23 [17765270.001]
  • [Cites] Nature. 2008 Jan 3;451(7174):73-5 [18172498.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):414-20 [18202418.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1575-83 [17971484.001]
  • [Cites] Pediatr Clin North Am. 2008 Feb;55(1):53-70, x [18242315.001]
  • [Cites] Blood. 2008 Mar 15;111(6):2991-8 [18182574.001]
  • [Cites] Paediatr Perinat Epidemiol. 2008 May;22(3):288-95 [18426524.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):515-21 [18521927.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2480-9 [14656875.001]
  • [Cites] Br J Haematol. 2004 Jun;125(6):729-42 [15180862.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1617-23 [15343346.001]
  • [Cites] Lancet. 1972 Jun 24;1(7765):1359-61 [4113564.001]
  • [Cites] Am J Dis Child. 1981 Mar;135(3):251-5 [6452055.001]
  • [Cites] Lancet. 1986 Oct 18;2(8512):914 [2876340.001]
  • [Cites] Eur J Pediatr. 1987 Jul;146(4):416-22 [2958283.001]
  • [Cites] J Pediatr. 1987 Oct;111(4):606-12 [2958611.001]
  • [Cites] Am J Med Genet Suppl. 1990;7:204-12 [2149949.001]
  • [Cites] Am J Med Genet Suppl. 1990;7:231-3 [2149953.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1484-92 [18805579.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4220-6 [18755984.001]
  • [Cites] Pediatr Blood Cancer. 2009 Jan;52(1):123-5 [18615507.001]
  • [Cites] Leuk Res. 2009 Feb;33(2):336-9 [18718659.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • [Cites] Leukemia. 2000 May;14(5):786-91 [10803507.001]
  • [Cites] Leukemia. 2000 May;14(5):943-4 [10803530.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):512-24 [10997960.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] Arch Dis Child. 2001 Oct;85(4):321-5 [11567943.001]
  • [Cites] Blood. 2002 Jan 1;99(1):245-51 [11756178.001]
  • [Cites] Eur J Hum Genet. 2001 Nov;9(11):811-4 [11781696.001]
  • [Cites] Lancet. 2002 Mar 23;359(9311):1019-25 [11937181.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] Leukemia. 2003 Feb;17(2):277-82 [12592323.001]
  • [Cites] Lancet. 2003 Apr 12;361(9365):1281-9 [12699967.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4298-300 [12560215.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1905-7 [12970794.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2960-8 [12816863.001]
  • [Cites] Blood. 2004 Jan 1;103(1):252-7 [12958073.001]
  • [Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):728-35 [14744791.001]
  • [Cites] Am J Med Genet Suppl. 1990;7:267-71 [2149960.001]
  • [Cites] Blood. 1992 Nov 1;80(9):2210-4 [1384797.001]
  • [Cites] J Clin Oncol. 1993 Jul;11(7):1361-7 [8315434.001]
  • [Cites] Leuk Res. 1994 Mar;18(3):163-71 [8139285.001]
  • [Cites] N Engl J Med. 1996 May 30;334(22):1428-34 [8618581.001]
  • [Cites] Br J Haematol. 1996 Jul;94(1):82-8 [8757513.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1544-52 [9193351.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] Leukemia. 1998 May;12(5):645-51 [9593260.001]
  • [Cites] Clin Cancer Res. 1998 Sep;4(9):2169-77 [9748136.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1393-400 [10438727.001]
  • [Cites] Arch Dis Child. 1999 Jul;81(1):32-7 [10373130.001]
  • [Cites] Am J Clin Nutr. 1999 Oct;70(4):495-501 [10500018.001]
  • [Cites] AMA J Dis Child. 1957 Sep;94(3):289-93 [13457660.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1866-72 [15520821.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):21-8 [15368546.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):33-9 [15390307.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):13-20 [15534881.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):797-804 [15755283.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):613-9 [15895080.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):405-10 [15952191.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1355-60 [15920490.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1353-6 [15916804.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2090-100 [16304571.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4043-9 [16109782.001]
  • [Cites] Blood. 2006 Jan 1;107(1):87-97 [16144799.001]
  • [Cites] Int J Cancer. 2006 Apr 1;118(7):1769-72 [16231334.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1570-81 [16249385.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Ann Hematol. 2006 May;85(5):275-80 [16518605.001]
  • [Cites] Br J Haematol. 2006 Jun;133(6):646-8 [16704441.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4606-13 [16469874.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):807-12 [16783379.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] Am J Epidemiol. 2006 Aug 1;164(3):212-21 [16760223.001]
  • [Cites] Pediatrics. 2006 Nov;118(5):e1499-508 [17030598.001]
  • [Cites] Br J Haematol. 2006 Dec;135(5):595-602 [17054672.001]
  • [Cites] Epidemiology. 2007 Jan;18(1):158-61 [17099322.001]
  • [Cites] Leukemia. 2007 Mar;21(3):574-6 [17252020.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jun 15;48(7):651-62 [17183582.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1584-7 [17443226.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1077-9 [17644747.001]
  • [Cites] Pediatr Blood Cancer. 2007 Dec;49(7 Suppl):1066-9 [17943965.001]
  • (PMID = 19176633.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / 1 U10 CA098543-01; United States / NCI NIH HHS / CA / K12 CA090433-06; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 91
  • [Other-IDs] NLM/ NIHMS113124; NLM/ PMC2761094
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51. Varma S, Sharma A, Malhotra P, Kumari S, Jain S, Varma N: Thrombotic complications of polycythemia vera. Hematology; 2008 Dec;13(6):319-23
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  • BACKGROUND: Polycythemia vera (PV) is an uncommon clonal disorder of stem cells.
  • The literature regarding the thrombotic complications of this disorder in the developing countries is scarce.
  • Their clinical characteristics, laboratory parameters, clinical complications such as thrombosis and myelofibrosis, treatment modalities, malignancies and deaths, if any were noted.
  • The median age at the time of diagnosis was 56.5 years.
  • CONCLUSIONS: PV is an uncommon disorder when compared with other hematological disorders in northern India.
  • Twenty patients received hydroxyurea with a median follow-up of 57 months, none developed acute leukemia.

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  • (PMID = 19055858.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; X6Q56QN5QC / Hydroxyurea
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52. Jones AV, Kreil S, Zoi K, Waghorn K, Curtis C, Zhang L, Score J, Seear R, Chase AJ, Grand FH, White H, Zoi C, Loukopoulos D, Terpos E, Vervessou EC, Schultheis B, Emig M, Ernst T, Lengfelder E, Hehlmann R, Hochhaus A, Oscier D, Silver RT, Reiter A, Cross NC: Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders. Blood; 2005 Sep 15;106(6):2162-8
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  • [Title] Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders.
  • The analysis of rare chromosomal translocations in myeloproliferative disorders has highlighted the importance of aberrant tyrosine kinase signaling in the pathogenesis of these diseases.
  • Of the 480 myeloproliferative disorder (MPD) samples, the proportion of positive cases per disease subtype was 30 (20%) of 152 for atypical or unclassified MPD, 2 of 134 (2%) for idiopathic hypereosinophilic syndrome, 58 of 72 (81%) for polycythemia vera, 24 of 59 (41%) essential thrombocythemia (ET), and 15 of 35 (43%) for idiopathic myelofibrosis.
  • V617F was not identified in patients with systemic mastocytosis (n = 28), chronic or acute myeloid leukemia (n = 35), secondary erythrocytosis (n = 4), or healthy controls (n = 160).
  • [MeSH-major] Mutation, Missense. Myeloproliferative Disorders / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Case-Control Studies. Chronic Disease. Female. Homozygote. Humans. Janus Kinase 2. Male. Microsatellite Repeats. Molecular Epidemiology. Prevalence. Signal Transduction / genetics

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  • [CommentIn] Acta Haematol. 2016;136(2):123-8 [27410038.001]
  • (PMID = 15920007.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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53. McMullin MF: A review of the therapeutic agents used in the management of polycythaemia vera. Hematol Oncol; 2007 Jun;25(2):58-65
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  • The acquired clonal disorder Polycythaemia Vera leads to increased erythropoiesis, myelopoiesis and megakaryopoeisis.
  • These anomalies result in an increased incidence of thromboembolic events, transformation to acute leukaemia and myelofibrosis.

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  • [Copyright] Copyright 2007 John Wiley & Sons, Ltd.
  • (PMID = 17352450.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 6Q99RDT97R / Pipobroman; 9008-11-1 / Interferons; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 72
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54. Barbui T, Finazzi G: Evidence-based management of polycythemia vera. Best Pract Res Clin Haematol; 2006;19(3):483-93
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  • The clinical course of polycythemia vera is marked by significant thrombotic complications and a variable risk of the disease turning either into myeloid metaplasia with myelofibrosis or into acute myeloid leukemia.
  • However, there is concern that certain myelosuppressive drugs accelerate the disease progression to acute leukemia.
  • This chapter provides updated estimates of the risk of thrombosis and disease progression and evaluates the various randomized and observational studies in polycythemia vera, according to an evidence-based approach.

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  • (PMID = 16781485.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Platelet Aggregation Inhibitors; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 27
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55. Tefferi A, Spivak JL: Polycythemia vera: scientific advances and current practice. Semin Hematol; 2005 Oct;42(4):206-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera (PV) is a clonal disorder of unknown etiology involving a multipotent hematopoietic progenitor cell that is characterized by the accumulation of phenotypically normal red blood cells, white blood cells, and platelets in the absence of a definable cause; extramedullary hematopoiesis, marrow fibrosis, and, in a few patients, transformation to acute leukemia can also occur.
  • First described in 1892, the cause of the disease remains unknown and no potentially curative therapy other than bone marrow transplantation is currently available.
  • It is commonly held that PV is a rare disorder, when in fact with a minimum incidence of 2.6 per 100,000 it is more common than chronic myelogenous leukemia (CML) and is particularly prevalent in persons of Ashkenazi Jewish ancestry.
  • However, the incidence of PV is not as high as that of erythrocytosis from other causes collectively, which poses a problem in differential diagnosis when PV presents as isolated erythrocytosis.
  • In current clinical practice, two different clinical approaches have been used to diagnose PV.
  • However, it is very clear that some patients with classical PV lack the JAK2 V617F mutation, while some patients with other chronic myeloproliferative disorders such as idiopathic myelofibrosis (IMF) and essential thrombocytosis (ET) also express the JAK2 V617F mutation.
  • Therefore, by necessity, any discussion of PV must take into consideration these companion myeloproliferative disorders, and since erythrocytosis is the single clinical feature that sets PV apart from IMF and ET, it is clear that the presence of the JAK2 V617F mutation cannot by itself establish a diagnosis of PV.

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  • (PMID = 16210034.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 191
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56. Seddighi AS, Seddighi A: Extramedullary hematopoiesis presenting as a compressive cord and cerebral lesion in a patient without a significant hematologic disorder: a case report. J Med Case Rep; 2010;4:319

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary hematopoiesis presenting as a compressive cord and cerebral lesion in a patient without a significant hematologic disorder: a case report.
  • Often these cases occur in patients with an underlying hematological disorder such as acute myelogenic leukemia, myelofibrosis, or other myelodysplastic syndromes.

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  • (PMID = 20939863.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2972301
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57. Jones CM, Dickinson TM, Salvado A: Phase II open label trial of imatinib in polycythemia rubra vera. Int J Hematol; 2008 Dec;88(5):489-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia rubra vera is a chronic myeloproliferative disorder characterized by panmyelosis with the resultant potential for thrombosis, myelofibrosis, and acute leukemia.
  • Patients meeting the Polycythemia Vera Study group criteria for the diagnosis of polycythemia vera, either naïve or intolerant to prior treatment were allowed to enroll.

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  • (PMID = 19009241.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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58. Finazzi G, Barbui T: Expertise-based management in essential thrombocythemia and polycythemia vera. Cancer J; 2007 Nov-Dec;13(6):372-6
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  • The clinical courses of polycythemia vera (PV) and essential thrombocythemia (ET) are characterized by an increased incidence of thrombotic and hemorrhagic complications and an inherent tendency to progress into myelofibrosis or acute myeloid leukemia.
  • Interferon-alpha (IFN-alpha) or anagrelide could be considered in selected young patients or as second-line therapy in those intolerant of hydroxyurea or with refractory disease.

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  • (PMID = 18032974.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; R16CO5Y76E / Aspirin
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59. Gangat N, Wolanskyj AP, Tefferi A: Abdominal vein thrombosis in essential thrombocythemia: prevalence, clinical correlates, and prognostic implications. Eur J Haematol; 2006 Oct;77(4):327-33
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  • [Title] Abdominal vein thrombosis in essential thrombocythemia: prevalence, clinical correlates, and prognostic implications.
  • Among 460 consecutive patients with essential thrombocythemia (ET) seen at our institution, 19 cases (4%) of abdominal vein thrombosis (AVT) were documented either at (n = 9) or after (n = 10) diagnosis.
  • Accordingly, clinical comparisons were performed among three groups of female patients: those with AVT (group A; n = 17), a control group without AVT but closely matched to group A in terms of age and year of diagnosis (group B; n = 34), and all female patients without AVT (group C; n = 288).
  • Unexpectedly, however, compared with group B, group A displayed both a higher conversion rate into myelofibrosis/acute leukemia (P = 0.0008) and a shorter median survival (116 vs. 156 months; P = 0.0012).
  • We conclude that AVT in ET is a marker of aggressive disease biology.

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  • (PMID = 16856928.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
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60. Nussenzveig RH, Cortes J, Sever M, Quintás-Cardama A, Ault P, Manshouri T, Bueso-Ramos C, Prchal JT, Kantarjian H, Verstovsek S: Imatinib mesylate therapy for polycythemia vera: final result of a phase II study initiated in 2001. Int J Hematol; 2009 Jul;90(1):58-63
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  • Polycythemia vera (PV) is a chronic myeloproliferative neoplasm (MPN) characterized by excessive production of red blood cells.
  • Patients with PV are at a risk of thrombosis, bleeding, and transformation to myelofibrosis or acute myeloid leukemia.
  • We conducted an open-label phase II clinical trial of imatinib at the standard dose of 400 mg daily in 24 patients with PV.
  • Our data indicate that imatinib has minimal clinical activity in PV.

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  • (PMID = 19484334.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Other-IDs] NLM/ NIHMS672549; NLM/ PMC4378576
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61. Zona G, Spena G, Sbaffi PF, Spaziante R: A meningioma with islets of extramedullary myeloid metaplasia: case report. Neurosurgery; 2007 Aug;61(2):E418-9; discussion E419
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  • OBJECTIVE: Idiopathic myelofibrosis is a clonal stem cell disorder that leads to ineffective erythropoiesis accompanied by reactive myelofibrosis (bone marrow fibrosis).
  • Extramedullary hematopoiesis within central nervous system primary tumors have already been reported but, to our knowledge, never before in a patient with evidence of idiopathic myelofibrosis.
  • CLINICAL PRESENTATION: A patient experiencing generalized idiopathic myelofibrosis developed a hemorrhagic intracranial meningioma containing islets of extramedullary myeloid metaplasia.
  • After surgery, the patient recovered completely and was discharged with a normal neurological status.
  • CONCLUSION: The reasons for this uncommon association are uncertain, but we hypothesize that myeloid islets may be involved in the origin of the tumor as well as in its acute hemorrhagic onset.
  • Moreover, we suggest that in the presence of proven idiopathic myelofibrosis intracranial myeloid metaplasia should be ruled out by appropriate neuroimaging and considered as a potential diagnosis in the presence of brain lesions.
  • [MeSH-major] Brain Neoplasms / pathology. Hematopoiesis, Extramedullary. Meningeal Neoplasms / pathology. Meningioma / pathology. Primary Myelofibrosis / pathology

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  • (PMID = 17762725.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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62. Shaikh MA, Byrd RP Jr, Roy TM: Pulmonary nocardiosis: an unusual cause of a solitary pulmonary nodule. J Ky Med Assoc; 2006 May;104(5):184-9
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  • This infection may be transient and subclinical or may result in an acute or chronic bronchopulmonary process.
  • Although an unusual cause of pulmonary infection in immunocompentent individuals, human nocardiosis is now documented more often in patients whose cell-mediated immunity is compromised by immunosuppression from comorbid disease or as a result of modern medical intervention.
  • The diagnosis is often elusive unless a high index of suspicion is maintained.
  • We present a patient with localized pulmonary nocardiosis who was immunosuppressed by virtue of a myeloproliferative disorder.
  • [MeSH-minor] Aged. Anti-Infective Agents / administration & dosage. Anti-Infective Agents / therapeutic use. Biopsy, Needle. Bronchoscopy. Follow-Up Studies. Humans. Immunocompromised Host. Lung / microbiology. Lung / pathology. Male. Neural Tube Defects / complications. Neural Tube Defects / drug therapy. Primary Myelofibrosis / complications. Primary Myelofibrosis / drug therapy. Radiography, Thoracic. Time Factors. Tomography, X-Ray Computed. Treatment Outcome. Trimethoprim, Sulfamethoxazole Drug Combination / administration & dosage. Trimethoprim, Sulfamethoxazole Drug Combination / therapeutic use

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  • (PMID = 16734042.001).
  • [ISSN] 0023-0294
  • [Journal-full-title] The Journal of the Kentucky Medical Association
  • [ISO-abbreviation] J Ky Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 8064-90-2 / Trimethoprim, Sulfamethoxazole Drug Combination
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63. Hultdin M, Sundström G, Wahlin A, Lundström B, Samuelsson J, Birgegård G, Engström-Laurent A: Progression of bone marrow fibrosis in patients with essential thrombocythemia and polycythemia vera during anagrelide treatment. Med Oncol; 2007;24(1):63-70
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  • Anagrelide is a second-line option for reduction of thrombocythemia in patients with chronic myeloproliferative disorders (CMPDs).
  • A multicenter, open, phase II study of anagrelide treatment in 60 patients during 2 yr was performed by the Swedish Myeloproliferative Disorder Study Group.
  • Adequate bone marrow biopsies were obtained from 53 of the CMPD patients [36 essential thrombocythemia (ET), 16 polycythemia vera (PV), 1 chronic idiopathic myelofibrosis (CIMF)] before treatment and compared with biopsies from 30 healthy volunteers and 34 patients with acute myeloid leukemia (AML).
  • [MeSH-major] Fibrinolytic Agents / therapeutic use. Polycythemia Vera / complications. Primary Myelofibrosis / etiology. Quinazolines / therapeutic use. Thrombocythemia, Essential / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Hyaluronic Acid / metabolism. Male. Middle Aged. Prognosis. Prospective Studies. Reticulin / metabolism. Thrombocytosis

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  • (PMID = 17673813.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibrinolytic Agents; 0 / Quinazolines; 0 / Reticulin; 0 / anagrelide; 9004-61-9 / Hyaluronic Acid
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64. Harrison CN: Essential thrombocythaemia: challenges and evidence-based management. Br J Haematol; 2005 Jul;130(2):153-65
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  • This condition is dominated by thrombotic and haemorrhagic complications and, in the long-term, by risk of transformation to myelofibrosis and/or acute leukaemia.
  • Here, a review of current concepts in disease aetiology and management is offered with reference to recent focused reviews where appropriate.
  • In addition, five specific areas are discussed in detail: the role of the trephine biopsy, the disease entity prefibrotic myelofibrosis; the recently described Janus kinase 2 (JAK2) mutations; the leukaemogenicity of hydroxyurea (hydroxycarbamide); and lastly, the implications of the results of the Medical Research Council Primary Thrombocythaemia 1 study are explored.

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  • [ErratumIn] Br J Haematol. 2005 Aug;130(3):465
  • (PMID = 16029444.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 121
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65. Wu MY, Eldin KW, Beaudet AL: Identification of chromatin remodeling genes Arid4a and Arid4b as leukemia suppressor genes. J Natl Cancer Inst; 2008 Sep 3;100(17):1247-59
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  • These sick Arid4a(-/-) mice showed bone marrow failure with myelofibrosis associated with splenomegaly and hepatomegaly.
  • Five of 42 Arid4a(-/-) mice and 10 of 12 Arid4a(-/-)Arid4b(+/-) mice progressed to acute myeloid leukemia (AML) and had rapid further increases of leukocyte counts.
  • CONCLUSIONS: Arid4a-deficient mice initially display ineffective hematopoiesis, followed by transition to chronic myelomonocytic leukemia (CMML)-like myelodysplastic/myeloproliferative disorder, and then transformation to AML.
  • The disease processes in the Arid4a-deficient mice are very similar to the course of events in humans with CMML and AML.

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  • [Cites] Leukemia. 2001 Jun;15(6):987-9 [11417488.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1275-86 [17570480.001]
  • [Cites] Oncogene. 2001 Sep 6;20(39):5440-8 [11571641.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):910-7 [12459729.001]
  • [Cites] Mol Cell Biol. 2003 May;23(10):3456-67 [12724404.001]
  • [Cites] Mol Cell Biol. 2003 Jun;23(11):3872-83 [12748289.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1823-8 [12897052.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1870-81 [12897054.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):1562-9 [14581478.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1136-45 [15247124.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R28-49 [17613546.001]
  • [Cites] Trends Mol Med. 2007 Sep;13(9):363-72 [17822958.001]
  • [Cites] Curr Opin Immunol. 2007 Oct;19(5):583-8 [17703930.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):2764-9 [10850410.001]
  • [Cites] Am J Hematol. 2000 Oct;65(2):111-8 [10996827.001]
  • [Cites] J Clin Invest. 2000 Dec;106(12):R75-81 [11120765.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):18-20 [11137992.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):20-1 [11137993.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):68-73 [11138001.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):116-20 [11242053.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):120-4 [11242054.001]
  • [Cites] Mol Cell Biol. 2001 Apr;21(8):2918-32 [11283269.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Oct 29;323(4):1216-22 [15451426.001]
  • [Cites] Nature. 1991 Jul 18;352(6332):251-4 [1857421.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10735-9 [1720549.001]
  • [Cites] Mol Cell Biol. 1993 Jan;13(1):351-7 [8093327.001]
  • [Cites] Oncogene. 1993 Nov;8(11):3149-56 [8414517.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5434-43 [7565694.001]
  • [Cites] Blood. 1997 Sep 1;90(5):1840-9 [9292516.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4573-8 [9539779.001]
  • [Cites] Oncogene. 1999 Mar 25;18(12):2091-100 [10321733.001]
  • [Cites] Breast Cancer Res Treat. 1999 Feb;53(3):279-90 [10369074.001]
  • [Cites] Mol Cell Biol. 1999 Oct;19(10):6632-41 [10490602.001]
  • [Cites] Br J Cancer. 1999 Sep;81(2):342-9 [10496363.001]
  • [Cites] Cell. 2004 Nov 24;119(5):603-14 [15550243.001]
  • [Cites] Curr Biol. 2004 Nov 23;14(22):2063-9 [15556871.001]
  • [Cites] Nucleic Acids Res. 2005;33(1):66-80 [15640446.001]
  • [Cites] Nature. 2005 Jan 27;433(7024):434-8 [15647753.001]
  • [Cites] Genomics. 2005 Aug;86(2):242-51 [15922553.001]
  • [Cites] Exp Hematol. 2006 Feb;34(2):167-78 [16459185.001]
  • [Cites] Mol Cell Biol. 2006 Mar;26(5):1917-31 [16479010.001]
  • [Cites] Science. 2006 May 5;312(5774):748-51 [16601153.001]
  • [Cites] Genes Dev. 2006 Oct 15;20(20):2859-70 [17043311.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):85-9 [17255784.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):865-8 [17404613.001]
  • [Cites] Nature. 2007 Apr 5;446(7136):685-9 [17377532.001]
  • [Cites] Nat Immunol. 2007 May;8(5):457-62 [17440451.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 1;93(15):1159-65 [11481388.001]
  • (PMID = 18728284.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD-37283
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arid4a protein, mouse; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Rbbp1l1 protein, mouse; 0 / Retinoblastoma-Binding Protein 1
  • [Other-IDs] NLM/ PMC2528019
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66. Metzgeroth G, Reiter A, Back W, Anders M, Hehlmann R, Hastka J: Peritoneal haematopoiesis in acute panmyelosis with myelofibrosis. Br J Haematol; 2005 Jul;130(1):1
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  • [Title] Peritoneal haematopoiesis in acute panmyelosis with myelofibrosis.
  • [MeSH-major] Bone Marrow Cells / pathology. Hematopoiesis, Extramedullary. Myelodysplastic Syndromes / pathology. Peritoneum. Primary Myelofibrosis / pathology

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  • (PMID = 15982337.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reticulin
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67. Ngirabacu MC, Ravoet C, Dargent JL, Meuleman N, Ahmad I, Ysebrant L, Bennani J, André M, Bron D: Long-term follow-up of autologous peripheral blood stem cell transplantation in the treatment of a patient with acute panmyelosis with myelofibrosis. Haematologica; 2006 Dec;91(12 Suppl):ECR53
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  • [Title] Long-term follow-up of autologous peripheral blood stem cell transplantation in the treatment of a patient with acute panmyelosis with myelofibrosis.
  • [MeSH-major] Leukemia, Myeloid / surgery. Peripheral Blood Stem Cell Transplantation. Primary Myelofibrosis / surgery
  • [MeSH-minor] Acute Disease. Anemia, Refractory / drug therapy. Anemia, Refractory / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cytarabine / administration & dosage. Erythropoietin / therapeutic use. Etoposide / administration & dosage. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Mitoxantrone / administration & dosage. Postoperative Complications / drug therapy. Postoperative Complications / etiology. Recombinant Proteins. Transplantation Conditioning / adverse effects. Transplantation, Autologous. Whole-Body Irradiation / adverse effects

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  • (PMID = 17194659.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; YL5FZ2Y5U1 / Methotrexate
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68. Reuss CS, Wilansky S: Images in cardiovascular medicine. Eosinophilic heart disease in acute myeloproliferative disorder. Circulation; 2007 Jun 12;115(23):e614-6
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  • [Title] Images in cardiovascular medicine. Eosinophilic heart disease in acute myeloproliferative disorder.
  • [MeSH-major] Eosinophilia / complications. Heart Diseases / etiology. Myeloproliferative Disorders / complications

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  • (PMID = 17562961.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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69. Crystal SC, Leonidas J, Jakubowski A, Di Rocco A: Thalidomide induced acute worsening of Parkinson's disease. Mov Disord; 2009 Sep 15;24(12):1863-4
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  • [Title] Thalidomide induced acute worsening of Parkinson's disease.
  • [MeSH-major] Immunosuppressive Agents / adverse effects. Parkinson Disease / etiology. Thalidomide / adverse effects
  • [MeSH-minor] Aged. Humans. Male. Primary Myelofibrosis / complications. Primary Myelofibrosis / drug therapy

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  • (PMID = 19606491.001).
  • [ISSN] 1531-8257
  • [Journal-full-title] Movement disorders : official journal of the Movement Disorder Society
  • [ISO-abbreviation] Mov. Disord.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
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