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Items 1 to 36 of about 36
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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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. 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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  • [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


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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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  • (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. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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10. Gangat N, Tefferi A: Pharmacotherapy of essential thrombocythemia. Expert Opin Pharmacother; 2008 Jul;9(10):1679-85
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  • 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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11. 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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12. 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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  • 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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13. 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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14. Finazzi G, Harrison C: Essential thrombocythemia. Semin Hematol; 2005 Oct;42(4):230-8
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  • 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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15. 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


16. Petrides PE: [Primary thrombocythemia: diagnosis and therapy]. Med Klin (Munich); 2006 Aug 15;101(8):624-34
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [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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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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]
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  • (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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18. 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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  • (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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19. 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
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.


21. Finazzi G, Barbui T: Expertise-based management in essential thrombocythemia and polycythemia vera. Cancer J; 2007 Nov-Dec;13(6):372-6
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. 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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24. Vannucchi AM, Guglielmelli P: Advances in understanding and management of polycythemia vera. Curr Opin Oncol; 2010 Nov;22(6):636-41
Genetic Alliance. consumer health - Polycythemia vera.

  • [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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25. Harrison CN: Essential thrombocythaemia: challenges and evidence-based management. Br J Haematol; 2005 Jul;130(2):153-65

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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27. 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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28. Mesa RA: Navigating the evolving paradigms in the diagnosis and treatment of myeloproliferative disorders. Hematology Am Soc Hematol Educ Program; 2007;:355-62
COS Scholar Universe. author profiles.

  • [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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29. 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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  • (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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30. 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
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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31. 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
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [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 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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32. 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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33. Barbui T, Finazzi G: Evidence-based management of polycythemia vera. Best Pract Res Clin Haematol; 2006;19(3):483-93
Hazardous Substances Data Bank. HYDROXYUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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34. 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
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. 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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36. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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