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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. 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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5. 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.


6. Mesa RA, Li CY, Ketterling RP, Schroeder GS, Knudson RA, Tefferi A: Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases. Blood; 2005 Feb 1;105(3):973-7
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  • [Title] Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases.
  • Among 2333 consecutive patients with myelofibrosis with myeloid metaplasia (MMM) seen at our institution, 91 fulfilled the World Health Organization (WHO) criteria for leukemic transformation (LT).
  • All episodes of LT were myeloid in origin (acute myeloid leukemia [AML]) with all French-American-British (FAB) subtypes represented except M3; the most frequent subtypes were M7 (25.4%), M0 (22.4%), and M2 (17.9%).
  • Cytogenetic studies during LT were available in 56 patients and revealed a clonal abnormality in 51 (91%): 30 patients had complex karyotype, 2 had core-binding factor gene lesions, and 18 had abnormalities of chromosome 5 or 7.
  • Twenty-four patients received AML-like induction chemotherapy that resulted in no complete remission: 41% reverted into chronic-phase disease and the incidence of treatment-related mortality was 33%.
  • The outcome of LT in MMM with current therapies is dismal and either supportive care alone or appropriate clinical trials should be considered.
  • [MeSH-major] Leukemia / drug therapy. Leukemia / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Myelodysplastic Syndromes / pathology. Primary Myelofibrosis / pathology


7. Neben-Wittich MA, Brown PD, Tefferi A: Successful treatment of severe extremity pain in myelofibrosis with low-dose single-fraction radiation therapy. Am J Hematol; 2010 Oct;85(10):808-10
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  • [Title] Successful treatment of severe extremity pain in myelofibrosis with low-dose single-fraction radiation therapy.
  • Myelofibrosis (MF) is characterized by cytopenias/cytoses, leukoerythroblastic blood picture, bone marrow fibrosis, and extramedullary hematopoiesis.
  • No patients reported any acute or late side effects from radiation.Bone involvement in MF can cause disabling pain, but single-fraction low-dose radiation is a safe and effective treatment, often leading to a durable response.
  • [MeSH-major] Pain, Intractable / radiotherapy. Primary Myelofibrosis / complications

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  • (PMID = 20799357.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics
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8. Huang SC, Wu VC, Chou G, Huang TY, Lin SY, Sheu WH: Benign parathyroid adenoma presenting with unusual parathyroid crisis, anemia and myelofibrosis. J Formos Med Assoc; 2007 Feb;106(2 Suppl):S13-6
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  • [Title] Benign parathyroid adenoma presenting with unusual parathyroid crisis, anemia and myelofibrosis.
  • Although the clinical symptoms of patients with benign parathyroid adenoma are usually nonspecific and benign, a malignant presentation of the benign disease may sometimes occur.
  • Acute hypercalcemic crisis manifested and primary hyperparathyroidism was diagnosed together with myelofibrosis on account of the result of bone marrow biopsy.
  • These findings suggested that benign parathyroid adenoma may mimic the clinical presentation of parathyroid carcinoma, releasing excess parathyroid hormone and resulting in hyperparathyroid crisis.
  • In addition, primary hyperparathyroidism can be associated with anemia and myelofibrosis.

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  • (PMID = 17493890.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


10. 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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11. Elpek GO, Bozova S, Erdoğan G, Temizkan K, Oğüş M: Extramedullary hematopoiesis mimicking acute appendicitis: a rare complication of idiopathic myelofibrosis. Virchows Arch; 2006 Aug;449(2):258-61
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  • [Title] Extramedullary hematopoiesis mimicking acute appendicitis: a rare complication of idiopathic myelofibrosis.
  • We report a case with a previous history of idiopathic myelofibrosis, which presented with clinical findings of acute appendicitis that necessitate appendectomy after the relief of his anemia.
  • The histopathological features of acute appendicitis were not observed.
  • Although in gastrointestinal system, obstruction and bleeding are the most common symptomatic manifestations, this case emphasizes that EMH might also present clinically as acute appendicitis.
  • The absence of histopathological features of acute appendicitis raises the possibility that local production of some mediators from hematopoietic precursor cells might contribute to this clinical presentation.
  • [MeSH-major] Appendicitis / diagnosis. Hematopoiesis, Extramedullary. Primary Myelofibrosis / complications
  • [MeSH-minor] Acute Disease. Humans. Male. Middle Aged

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  • (PMID = 16738896.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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12. 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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13. Naik SG, Negrin R, Laport G, Miklos D, Shizuru J, Arai S, Blume K, Wong R, Lowsky R, Johnston L: Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All pts were treated with a uniform preparatory regimen: busulfan 16.0 mg/kg (d-8 to-5), etoposide 60mg/kg (d-4), cyclophosphamide 60mg/kg (d-2), and graft-versus-host-disease (GVHD) prophylaxis of cyclosporine and prednisone.
  • Disease status at transplantation was induction failure (IF) acute myeloid leukemia (AML) (n = 10), HR AML in 1st complete remission (CR1) n = 11, in CR2 (n = 5), in CR3 (n = 2), relapsed refractory (RR) AML (n = 14), chronic myeloid leukemia (CML) in second chronic phase (n = 6), blast crisis (n = 2), myelofibrosis (n = 6), myeloproliferative disorders (n = 2), and MDS (n = 38).
  • With a median follow up of 5.6 yrs (1.6-14.6 yrs) actuarial 5-year overall survival (OS) was 32% (95% CI 22-42%) and 5-year probability for freedom from progression (FFP) was 64% (95% CI 52%-76%).
  • Cumulative incidence of acute (grade 3-4) and chronic GVHD was 28% (95% CI 19%-37%) and 38% (95% CI 24%-52%), respectively.
  • Relapse and acute GVHD remain significant causes of mortality.

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  • (PMID = 27961395.001).
  • [ISSN] 1527-7755
  • [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
  • [Publication-country] United States
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14. Cvetković ZP, Cvetković BR, Celeketić D, Milenković D, Perunicić-Peković G: Bilateral ureteral obstruction due to primary myelofibrosis caused hyperuricaemia. Acta Chir Iugosl; 2010;57(2):79-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral ureteral obstruction due to primary myelofibrosis caused hyperuricaemia.
  • Extreme hiperuricaemia is seen in cancer patients with tumour lysis syndrome (TLS) which is classically associated with haematological malignancies with rapid tumour growth rates such as acute lymphoid leukaemia and high grade lymphomas.
  • Primary melofibrosis (Agnogenic myeloid metaplasia-AMM) is a chronic myeloproliferative disease characterized by splenomegaly, a leukoerythroblastic blood picture, teardrop poikilocytosis and varying degrees of marrow fibrosis.
  • In this paper we present a case of a 47-year-old male patient who was admitted to the hospital with symptoms of fatigue and small amount of urine, and clinical signs of plethora and enlarged spleen.
  • The bone marrow biopsy was also performed and histopathological diagnosis was: Hypercellulary phase of AMM.
  • [MeSH-major] Hyperuricemia / etiology. Primary Myelofibrosis / complications. Ureteral Obstruction / etiology

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  • (PMID = 20949707.001).
  • [ISSN] 0354-950X
  • [Journal-full-title] Acta chirurgica Iugoslavica
  • [ISO-abbreviation] Acta Chir Iugosl
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Serbia
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15. Wakita S, Yamaguchi H, Okabe M, Takeuchi J, Tamai H, Nakamura K, Tajika K, Inokuchi K, Dan K: [Low dose whole lung irradiation for intractable pleural effusion due to idiopathic myelofibrosis]. Rinsho Ketsueki; 2006 Jun;47(6):526-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Low dose whole lung irradiation for intractable pleural effusion due to idiopathic myelofibrosis].
  • A 63-year-old man with idiopathic myelofibrosis, diagnosed on Sept.
  • However, bilateral pleural effusion appeared only 2 weeks later, which was thought to be extramedullary hematopoiesis or acute transformation.
  • [MeSH-major] Hydroxyurea / therapeutic use. Lung / radiation effects. Pleural Effusion / radiotherapy. Primary Myelofibrosis / complications

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  • (PMID = 16862981.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] X6Q56QN5QC / Hydroxyurea
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16. Bai J, Xue YP, Ye L, Yao JF, Zhou CL, Qian LS, Yang RC, Li HY, Zhang HY, Shao ZH: [The risk factors for thrombosis, myelofibrosis and leukemia transformation in patients with polycythemia vera]. Zhonghua Xue Ye Xue Za Zhi; 2007 Oct;28(10):685-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The risk factors for thrombosis, myelofibrosis and leukemia transformation in patients with polycythemia vera].
  • OBJECTIVE: To reassess the natural history of polycythemia vera (PV) in Chinese and evaluate the relationship between the incidence of thrombosis, post-polycythaemic myelofibrosis with myeloid metaplasia( PPMM) , leukemia transformation and the therapeutic outcome and prognostic factors.
  • METHODS: The clinical manifestations, laboratory parameters and treatment were retrospectively analyzed in 287 patients with PV.
  • Most of these episodes occurred either at presentation or in the 2 years before diagnosis.
  • CONCLUSION: The incidence of thromboembolism is higher and the time to myelofibrosis was shorter in Chinese PV patients than in western PV patients.
  • [MeSH-major] Leukemia / etiology. Polycythemia Vera / complications. Primary Myelofibrosis / etiology. Thromboembolism / etiology
  • [MeSH-minor] Acute Disease. Female. Follow-Up Studies. Humans. Male. Prognosis. Risk Factors

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  • (PMID = 18399175.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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17. 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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18. 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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19. 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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20. Kröger N, Thiele J, Zander A, Schwerdtfeger R, Kobbe G, Bornhäuser M, Bethge W, Schubert J, de Witte T, Kvasnicka HM, MDS-Subcommittee of the Chronic Leukaemia Working Party of the European Group for Blood and Marrow Transplantation: Rapid regression of bone marrow fibrosis after dose-reduced allogeneic stem cell transplantation in patients with primary myelofibrosis. Exp Hematol; 2007 Nov;35(11):1719-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid regression of bone marrow fibrosis after dose-reduced allogeneic stem cell transplantation in patients with primary myelofibrosis.
  • OBJECTIVE: To investigate the effect of a busulfan/fludarabine-based reduced intensity conditioning followed by allogeneic stem cell transplantation on regression of bone marrow fibrosis in patients with myelofibrosis.
  • METHODS: Twenty-four patients (male, n = 16; female, n = 8) with a median age of 52 years (range, 32-63 years) were included.
  • Diagnosis was primary myelofibrosis in 18 patients and secondary myelofibrosis in 6 patients; in 4 of them, primary myelofibrosis evolved from polycythemia vera, and in 2 of them from essential thrombocythemia.
  • No correlation between occurrence of acute graft-vs-host disease and fibrosis regression on day +180 was observed.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Primary Myelofibrosis / therapy
  • [MeSH-minor] Adult. Bone Marrow Examination. Busulfan / administration & dosage. Female. Graft vs Host Disease. Humans. Kinetics. Male. Middle Aged. Remission Induction / methods. Severity of Illness Index. Transplantation Conditioning / methods. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17976523.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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21. TAHARA K, YOKOHAMA A, HANDA H, SAITOH T, UCHIUMI H, SEKIGAMI T, TOYAMA K, MAWATARI M, OSAKI Y, MATSUSHIMA T, KARASAWA M, MURAKAMI H, TSUKAMOTO N, NOJIMA Y: Successful treatment with reduced-intensity stem cell transplantation for secondary myelofibrosis following polycythemia vera. Rinsho Ketsueki; 2009 Nov;50(11):1630-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with reduced-intensity stem cell transplantation for secondary myelofibrosis following polycythemia vera.
  • Ten years after being diagnosed with polycythemia vera, a 55-year-old woman required frequent blood transfusion due to secondary myelofibrosis.
  • At day 73, she developed acute graft-versus-host disease of the liver, while simultaneous resolution of splenomegaly occurred and complete donor chimerism in the peripheral blood was achieved.
  • Thus, RIST for an older patient with secondary myelofibrosis was successful without severe treatment-related morbidity.
  • This case suggests that RIST could be an effective treatment modality for secondary myelofibrosis.
  • [MeSH-major] Polycythemia Vera / complications. Primary Myelofibrosis / etiology. Primary Myelofibrosis / therapy. Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Female. Graft vs Host Disease / prevention & control. Humans. Janus Kinase 2 / genetics. Melphalan / administration & dosage. Middle Aged. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 20009439.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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22. 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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23. Barugola G, Cavallini A, Lipari G, Armatura G, Mantovani W, Baggio E: The role of splenectomy in myelofibrosis with myeloid metaplasia. Minerva Chir; 2010 Dec;65(6):619-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of splenectomy in myelofibrosis with myeloid metaplasia.
  • AIM: In this paper we retrospectively analyzed prospectively-collected data on our myelofibrosis with myeloid metaplasia (MMM) patients who underwent splenectomy.
  • Postoperative work-up consisting in laboratory tests and clinical evaluation performing a quality of life (QoL) test based on EORTC QLQ-C30 questionnaire.
  • Acute complications are almost exclusively limited to respiratory tract.
  • [MeSH-major] Primary Myelofibrosis / complications. Primary Myelofibrosis / surgery. Splenectomy

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  • (PMID = 21224796.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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24. Thepot S, Itzykson R, Seegers V, Raffoux E, Quesnel B, Chait Y, Sorin L, Dreyfus F, Cluzeau T, Delaunay J, Sanhes L, Eclache V, Dartigeas C, Turlure P, Harel S, Salanoubat C, Kiladjian JJ, Fenaux P, Adès L, Groupe Francophone des Myelodysplasies (GFM): Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM). Blood; 2010 Nov 11;116(19):3735-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM).
  • Transformation of Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) to myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) is associated with poor response to chemotherapy and short survival.
  • Fifty-four patients with Ph-negative MPN (including 21 essential thrombocythemia [ET], 21 polycythemia vera [PV], 7 primary myelofibrosis, and 5 unclassified MPN) who had progressed to AML (n = 26) or MDS (n = 28) were treated with azacitidine in a patient-named program.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / etiology. Myeloproliferative Disorders / complications. Myeloproliferative Disorders / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. France / epidemiology. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Philadelphia Chromosome. Prognosis. Treatment Outcome


25. Suzuki R, Onizuka M, Kojima M, Shimada M, Tsuboi K, Ogawa Y, Kawada H, Ando K: Infrequent hypermethylation of WIF-1 promoter in BCR/ABL-negative myeloproliferative disorders. Tokai J Exp Clin Med; 2007 Dec;32(4):131-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infrequent hypermethylation of WIF-1 promoter in BCR/ABL-negative myeloproliferative disorders.
  • Wnt inhibitory factor-1 (WIF-1) is a negative regulator of Wnt signaling that is frequently downregulated by hypermethylation of the WIF-1 promoter in acute promyelocytic leukemia (APL) and other malignancies.
  • This is the first study to examine the relationship between WIF-1 methylation and the existence of JAK2V617F mutation in the pathogenesis of BCR/ABL-negative myeloproliferative disorders (MPD) including polycythemia vera, essential thrombocythemia, idiopathic myelofibrosis, and chronic myeloproliferative disease, unclassifiable.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Janus Kinase 2 / genetics. Myeloproliferative Disorders / enzymology. Myeloproliferative Disorders / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Chronic Disease. Cohort Studies. CpG Islands / genetics. Female. Fusion Proteins, bcr-abl. Humans. Male. Methylation. Middle Aged. Molecular Sequence Data. Mutation. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 21318952.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Repressor Proteins; 0 / WIF1 protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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26. Taki T, Taniwaki M: Chromosomal translocations in cancer and their relevance for therapy. Curr Opin Oncol; 2006 Jan;18(1):62-8
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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: Recurring chromosomal abnormalities are considered the primary genetic change in oncogenesis as well as an important indicator for tumor phenotype and clinical outcome.
  • Observation of high frequencies of mutations in NOTCH1, NPM and JAK2 in T-cell acute lymphoblastic leukemia, acute myeloid leukemia with normal karyotype and myeloproliferative disorders (polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis) have provided important suggestions for a better understanding of chromosomal translocations.

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  • (PMID = 16357566.001).
  • [ISSN] 1040-8746
  • [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] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 46
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27. Nagata K, Shimoda K: [Myeloproliferative diseases caused by JAK2 mutation]. Rinsho Byori; 2009 Apr;57(4):357-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Myeloproliferative diseases caused by JAK2 mutation].
  • Polycythemia vera (PV), essential thrombocythemia(ET), and primary myelofibrosis (PMF) share common clinical features, being clonal disorders of multipotent progenitors.
  • This may suggest that the expression levels of JAK2 V617F directly determine which cell lineages increase, possibly leading to the diversity of myeloproliferative diseases.
  • Although only V617F JAK2 may cause myeloproliferative disease (MPD), clonogenic assay, analysis of familial MPD patients, and examination of JAK2 mutation in acute leukemia patients transformed from MPD show that there are additional somatic mutations which contribute to the pathogenesis of V617F JAK2 positive PV, ET, and PMF.
  • [MeSH-major] Janus Kinase 2 / genetics. Janus Kinase 2 / physiology. Mutation. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Humans. Polycythemia Vera / genetics. Polycythemia Vera / pathology. Primary Myelofibrosis / genetics. Primary Myelofibrosis / pathology. Thrombocythemia, Essential / genetics. Thrombocythemia, Essential / pathology

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  • (PMID = 19489438.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 22
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28. 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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29. 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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30. 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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31. 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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  • 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


32. Kröger N, Holler E, Kobbe G, Bornhäuser M, Schwerdtfeger R, Baurmann H, Nagler A, Bethge W, Stelljes M, Uharek L, Wandt H, Burchert A, Corradini P, Schubert J, Kaufmann M, Dreger P, Wulf GG, Einsele H, Zabelina T, Kvasnicka HM, Thiele J, Brand R, Zander AR, Niederwieser D, de Witte TM: Allogeneic stem cell transplantation after reduced-intensity conditioning in patients with myelofibrosis: a prospective, multicenter study of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation. Blood; 2009 Dec 17;114(26):5264-70
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic stem cell transplantation after reduced-intensity conditioning in patients with myelofibrosis: a prospective, multicenter study of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation.
  • From 2002 to 2007, 103 patients with primary myelofibrosis or postessential thrombocythemia and polycythemia vera myelofibrosis and a median age of 55 years (range, 32-68 years) were included in a prospective multicenter phase 2 trial to determine efficacy of a busulfan (10 mg/kg)/fludarabine (180 mg/m(2))-based reduced-intensity conditioning regimen followed by allogeneic stem cell transplantation from related (n = 33) or unrelated donors (n = 70).
  • Acute graft-versus-host disease grade 2 to 4 occurred in 27% and chronic graft-versus-host disease in 43% of the patients.
  • Cumulative incidence of nonrelapse mortality at 1 year was 16% (95% confidence interval, 9%-23%) and significantly lower for patients with a completely matched donor (12% vs 38%; P = .003).
  • [MeSH-major] Primary Myelofibrosis / surgery. Stem Cell Transplantation / methods. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Aged. Busulfan / therapeutic use. Disease-Free Survival. Female. Graft vs Host Disease / epidemiology. Humans. Male. Middle Aged. Myeloablative Agonists / therapeutic use. Recurrence. Transplantation, Homologous. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • (PMID = 19812383.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00599547
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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33. Okabayash S, Ohno C, Yasutomi Y: Acute megakaryocytic leukaemia (AMKL)-like disease in a cynomolgus monkey (Macaca fascicularis). J Comp Pathol; 2009 Feb-Apr;140(2-3):212-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute megakaryocytic leukaemia (AMKL)-like disease in a cynomolgus monkey (Macaca fascicularis).
  • A 5-year-old male cynomolgus monkey (Macaca fascicularis) with a clinical history of bleeding tendency, severe anaemia, thrombocytopenia and elevated serum concentration of liver-related enzymes was examined post mortem.
  • Microscopically, numerous atypical cells resembling myeloid cells were observed in the bone marrow, and myelofibrosis was present.
  • A diagnosis of acute megakaryocytic leukaemia (AMKL)-like disease was made.
  • This would appear to be the first report of AMKL-like disease in non-human primates.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Megakaryoblastic, Acute / veterinary. Monkey Diseases / pathology

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  • (PMID = 19159898.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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34. 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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35. Brière JB: Essential thrombocythemia. Orphanet J Rare Dis; 2007;2:3
Genetic Alliance. consumer health - Essential Thrombocythemia.

  • [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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  • (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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36. Al-Ghazaly J, Al-Selwi AH, Abdullah M, Al-Jahafi AK, Al-Dubai W, Al-Hashdi A: Pattern of haematological diseases diagnosed by bone marrow examination in Yemen: a developing country experience. Clin Lab Haematol; 2006 Dec;28(6):376-81
MedlinePlus Health Information. consumer health - Blood Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A total of 159 patients had Acute myeloid leukaemia, 75 had acute lymphocytic leukaemia, 87 had chronic myeloid leukaemia, 36 chronic lymphocytic leukaemia, eight had multiple myeloma, 13 myelodysplastic syndromes, seven myelofibrosis, seven polycythaemia vera, three primary thrombocythaemia, two hairy cell leukaemia, two metastases, 36 aplastic anaemia, 29 immune thrombocytopenic purpura (ITP), nine autoimmune haemolytic anaemia, three pernicious anaemia, 65 iron deficiency anaemia, 57 megaloblastic anaemia and malaria, 18 mixed deficiencies, and 11 patients had visceral leishmaniasis.
  • In conclusion, the leukaemias were the most frequently encountered diagnosis followed by iron deficiency anaemia, megaloblastic anaemia and malaria, aplastic anaemia and ITP respectively.
  • [MeSH-major] Hematologic Diseases / diagnosis. Hematologic Diseases / epidemiology

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  • (PMID = 17105490.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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37. Schwarz J, Pytlík R, Doubek M, Brychtová Y, Dulícek P, Campr V, Kren L, Penka M: Analysis of risk factors: the rationale of the guidelines of the Czech Hematological Society for diagnosis and treatment of chronic myeloproliferative disorders with thrombocythemia. Semin Thromb Hemost; 2006 Apr;32(3):231-45
Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of risk factors: the rationale of the guidelines of the Czech Hematological Society for diagnosis and treatment of chronic myeloproliferative disorders with thrombocythemia.
  • The rationale of the Czech Hematological Society guidelines for diagnosis and treatment of Philadelphia chromosome-negative myeloproliferative disorders with thrombocythemia (MPD-T) is reviewed.
  • For diagnosis of MPD-T, the classification according to the World Health Organization or to the Rotterdam criteria is preferred because they distinguish true essential thrombocythemia from prefibrotic or early fibrotic idiopathic myelofibrosis and prepolycythemic polycythemia vera.
  • The histopathology-based nosological distinction provided by these classifications yields valuable information on prognosis (including the risks of transition into secondary acute myeloid leukemia and myelofibrosis).
  • Another serious complication in MPD-T is thrombosis (arterial or venous), the main risk factors of which are age, previous thrombosis, platelet counts 350 to 2,200 x 10 (9)/L (peak at approximately 900 x 10 (9)/L) and the presence of additional thrombophilic risk factors (hereditary thrombophilia, any hypercoagulable state, cardiovascular disease).
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Practice Guidelines as Topic. Thrombocytosis / diagnosis
  • [MeSH-minor] Chronic Disease. Czechoslovakia. Humans. Risk Factors. Societies, Medical

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  • (PMID = 16673277.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. 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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39. Finazzi G, Gregg XT, Barbui T, Prchal JT: Idiopathic erythrocytosis and other non-clonal polycythemias. Best Pract Res Clin Haematol; 2006;19(3):471-82
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Its diagnosis is based on the exclusion of polycythemia vera (PV), secondary acquired polycythemias and various congenital primary and secondary polycythemias.
  • IE is a stable disease with a low thrombotic risk and a low, if any, tendency to spontaneous progression to acute leukemia or myelofibrosis.
  • Myelosuppressive drugs should be avoided since their use is associated with evolution into acute leukemia in about 10% of patients.

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  • (PMID = 16781484.001).
  • [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
  • [Number-of-references] 35
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40. 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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41. Levine RL, Loriaux M, Huntly BJ, Loh ML, Beran M, Stoffregen E, Berger R, Clark JJ, Willis SG, Nguyen KT, Flores NJ, Estey E, Gattermann N, Armstrong S, Look AT, Griffin JD, Bernard OA, Heinrich MC, Gilliland DG, Druker B, Deininger MW: The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood; 2005 Nov 15;106(10):3377-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.
  • Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
  • We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B-lineage acute lymphoblastic leukemia (ALL), T-cell ALL, and chronic lymphocytic leukemia (CLL).
  • We did not identify the JAK2V617F disease allele in B-lineage ALL (n = 83), T-cell ALL (n = 93), or CLL (n = 45).
  • These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies.


42. Passamonti F, Rumi E, Pietra D, Elena C, Boveri E, Arcaini L, Roncoroni E, Astori C, Merli M, Boggi S, Pascutto C, Lazzarino M, Cazzola M: A prospective study of 338 patients with polycythemia vera: the impact of JAK2 (V617F) allele burden and leukocytosis on fibrotic or leukemic disease transformation and vascular complications. Leukemia; 2010 Sep;24(9):1574-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prospective study of 338 patients with polycythemia vera: the impact of JAK2 (V617F) allele burden and leukocytosis on fibrotic or leukemic disease transformation and vascular complications.
  • We studied the relationship between JAK2 (V617F) mutant allele burden and clinical phenotype, disease progression and survival in patients with polycythemia vera (PV).
  • During the study period, eight patients progressed to post-PV myelofibrosis (MF) (all carrying >50% mutant alleles), while 10 patients developed acute myeloid leukemia (AML).
  • The mutant allele burden was significantly related to the risk of developing myelofibrosis (P=0.029) and retained its significant effect also in multivariable analysis (P=0.03).
  • [MeSH-major] Alleles. Cell Transformation, Neoplastic / genetics. Janus Kinase 2 / genetics. Leukemia / genetics. Leukocytosis / genetics. Polycythemia Vera / genetics. Primary Myelofibrosis / genetics. Vascular Diseases / complications

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  • (PMID = 20631743.001).
  • [ISSN] 1476-5551
  • [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] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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43. Hellmann A: Myeloproliferative syndromes: diagnosis and therapeutic options. Pol Arch Med Wewn; 2008 Dec;118(12):756-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloproliferative syndromes: diagnosis and therapeutic options.
  • Myeloproliferative syndromes (MPS) are clonal proliferation of hematopoietic progenitor cells characterized by proliferation of 1 or a few cell lines such as granulocytic, erythroid, megakaryocytic or mastocytic.
  • These syndromes include: chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, chronic eosinophilic leukemia/hypereosinophilic syndrome, chronic neutrophilic leukemia and systemic mastocytosis.
  • Diagnosis of MPS is often difficult due to need of differential diagnosis with reactive proliferation caused by primarily non-hematological factors.
  • Differentiation of individual MPS forms is also difficult because of overlapping of particular clinical or laboratory adnormalities.
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / therapy
  • [MeSH-minor] Bone Marrow. Diagnosis, Differential. Humans. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Erythroblastic, Acute / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Neutrophilic, Chronic / diagnosis. Leukemia, Neutrophilic, Chronic / therapy. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / therapy. Risk Factors. Thrombocytosis / diagnosis. Thrombocytosis / therapy

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  • (PMID = 19202955.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 19
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44. 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
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [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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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. Pardanani AD, Levine RL, Lasho T, Pikman Y, Mesa RA, Wadleigh M, Steensma DP, Elliott MA, Wolanskyj AP, Hogan WJ, McClure RF, Litzow MR, Gilliland DG, Tefferi A: MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients. Blood; 2006 Nov 15;108(10):3472-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients.
  • Recently, a gain-of-function MPL mutation, MPLW515L, was described in patients with JAK2V617F-negative myelofibrosis with myeloid metaplasia (MMM).
  • To gain more information on mutational frequency, disease specificity, and clinical correlates, genomic DNA from 1182 patients with myeloproliferative and other myeloid disorders and 64 healthy controls was screened for MPL515 mutations, regardless of JAK2V617F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leukemia (AML).
  • The diagnosis of patients with mutant MPL alleles at the time of molecular testing was de novo MMM in 12 patients, ET in 4, post-ET MMM in 1, and MMM in blast crisis in 3.
  • Furthermore, MPL mutations may occur concurrently with the JAK2V617F mutation, suggesting that these alleles may have functional complementation in myeloproliferative disease.
  • [MeSH-major] Janus Kinase 2 / genetics. Mutation, Missense. Myeloproliferative Disorders / genetics. Receptors, Thrombopoietin / genetics

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  • (PMID = 16868251.001).
  • [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 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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47. 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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48. 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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49. Bernardini P, Giannandrea F, Voso MT, Sica S: [Myeloproliferative disorders due to the use of gasoline as a solvent: report of three cases]. Med Lav; 2005 Mar-Apr;96(2):119-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Myeloproliferative disorders due to the use of gasoline as a solvent: report of three cases].
  • OBJECTIVES: To describe three recent cases of severe haematological disease presumably induced by an occupational exposure to benzene.
  • METHODS: Clinical diagnosis was performed using standard immuno-phenotypic and morphological criteria; the hypothesis of an occupational origin was derived from analysis of the occupational histories.
  • RESULTS: The first case was a 59 year-old blacksmith suffering from acute myeloid leukaemia (AML) FAB M2, who had used petrol for 36 years to degrease the forged metal parts before painting them.
  • The third was an 82 year-old car mechanic suffering from idiopathic myelofibrosis since the age of 75, who had used petrol to degrease mechanical car motor parts for 42 years.
  • Latency of the disease was between 30-50 years from start of exposure, and between 3-17 years following cessation of exposure.
  • If it cannot, how many cases of benzene-related diseases escape aetiological diagnosis?
  • Furthermore, in all cases of haematological disease potentially related to benzene, any form of contact with petrol, even if uncommon, should be carefully researched.
  • [MeSH-major] Gasoline / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Promyelocytic, Acute / chemically induced. Metallurgy. Motor Vehicles. Occupational Diseases / chemically induced. Primary Myelofibrosis / chemically induced. Solvents / adverse effects
  • [MeSH-minor] Aged. Aged, 80 and over. Alleles. Cytochrome P-450 CYP1A1 / analysis. Cytochrome P-450 CYP1A1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / analysis. Guideline Adherence. Humans. Inhalation Exposure. Italy / epidemiology. Male. Middle Aged. Occupational Health. Suction

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  • [CommentIn] Med Lav. 2005 Sep-Oct;96(5):447-51 [16711648.001]
  • [ErratumIn] Med Lav. 2005 Sep-Oct;96(5):418
  • (PMID = 16001511.001).
  • [ISSN] 0025-7818
  • [Journal-full-title] La Medicina del lavoro
  • [ISO-abbreviation] Med Lav
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Gasoline; 0 / Solvents; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.5.1.18 / glutathione transferase T1-1, human
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50. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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51. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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52. 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


53. Wolanskyj AP, Lasho TL, Schwager SM, McClure RF, Wadleigh M, Lee SJ, Gilliland DG, Tefferi A: JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance. Br J Haematol; 2005 Oct;131(2):208-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance.
  • Clinical correlates and long-term prognostic relevance of the JAK2(V617F) mutation was studied in 150 patients with essential thrombocythaemia (ET) from a single institution and followed for a median of 11.4 years.
  • During this period, thrombotic complications were documented in 62 patients (41.3%) and transformation into acute myeloid leukaemia (AML), polycythaemia vera (PV), or myelofibrosis with myeloid metaplasia (MMM) occurred in 4 (2.7%), 8 (5.3%), and 15 (10%) patients, respectively.
  • Parameters at diagnosis that were significantly associated with the presence of JAK2(V617F) included advanced age and higher counts of both haemoglobin and leucocytes.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Hemoglobins / analysis. Humans. Janus Kinase 2. Leukemia, Myeloid, Acute / genetics. Leukocyte Count. Male. Middle Aged. Multivariate Analysis. Polycythemia Vera / genetics. Primary Myelofibrosis / genetics. Risk Factors. Thrombosis / complications

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  • (PMID = 16197451.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; 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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54. Vannucchi AM, Guglielmelli P, Pieri L, Antonioli E, Bosi A: Treatment options for essential thrombocythemia and polycythemia vera. Expert Rev Hematol; 2009 Feb;2(1):41-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera and essential thrombocythemia are the most common chronic myeloproliferative neoplasms; their molecular basis has been appreciated only recently and is briefly discussed in this article.
  • Major causes of morbidity and mortality are represented by arterial and venous thrombosis, as well as by evolution to myelofibrosis or transformation to acute leukemia.
  • However, results of clinical trials with interferon, and the expected effects of novel drugs selectively targeting the abnormal pathways that are involved in the clonal myeloproliferation, are pushing therapeutic goals from disease control only to cure.

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  • (PMID = 21082994.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
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55. Kuriyama K: [Classification of myeloid leukemias]. Nihon Rinsho; 2009 Oct;67(10):1853-62
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  • The myeloid neoplasms are composed of six categories, which are 1) myeloproliferative neoplasms (MPN), a new category of 2) myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1, 3) myelodysplastic syndrome (MDS)/MPN, 4) MDS, 5) acute myeloid leukemia (AML) and related precursor neoplasms, and 6) acute leukemias of ambiguous lineage.
  • In MPNs without chronic myelogenous leukemia, the genetic marker of JAK2 V617F is added to the diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis.
  • [MeSH-minor] Eosinophilia. Humans. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. World Health Organization

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  • (PMID = 19860179.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Number-of-references] 14
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56. Hussein K, Ketterling RP, Hulshizer RL, Kuffel DG, Wiktor AE, Hanson CA, Tefferi A, Van Dyke DL: Peripheral blood cytogenetic studies in hematological neoplasms: predictors of obtaining metaphases for analysis. Eur J Haematol; 2008 Apr;80(4):318-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A total of 242 PB cytogenetic studies from adult patients were performed: clinical diagnosis was a myeloid neoplasm in 169 patients (70%), lymphoid or plasma cell neoplasm in 50 (21%), and a benign/reactive cytopenia or leukocytosis in 23 (9%).
  • PB cytogenetic studies resulted in at least two analyzable metaphases in 142 of the 242 study cases (59%); in univariate analysis, this was predicted by the specific clinical diagnosis (P < 0.0001), presence and degree of circulating myeloid progenitor cells or blasts of any lineage (P < 0.0001), higher leukocyte count (P < 0.001), lower platelet count (P = 0.003), lower hemoglobin level (P = 0.002), and presence of palpable splenomegaly (P = 0.002).
  • In multivariable analysis, only the presence of circulating myeloid progenitor cells or blasts sustained significance and this was consistent with the high yield rates seen in primary myelofibrosis (PMF) (80%), post-PV/ET PMF (85%), acute myeloid leukemia (76%), and acute lymphoblastic leukemia (80%) in contrast with the low rates seen in ET (0%) and PV (2%).

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  • (PMID = 18088399.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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57. 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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  • [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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58. Dan K, Yamada T, Kimura Y, Usui N, Okamoto S, Sugihara T, Takai K, Masuda M, Mori M, Japanese Elderly Leukemia and Lymphoma Study Group: Clinical features of polycythemia vera and essential thrombocythemia in Japan: retrospective analysis of a nationwide survey by the Japanese Elderly Leukemia and Lymphoma Study Group. Int J Hematol; 2006 Jun;83(5):443-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features of polycythemia vera and essential thrombocythemia in Japan: retrospective analysis of a nationwide survey by the Japanese Elderly Leukemia and Lymphoma Study Group.
  • We conducted the first nationwide survey to clarify the clinical features, treatment methods, and prognoses for polycythemia vera (PV) and essential thrombocythemia (ET).
  • Thrombotic events at diagnosis and during follow-up occurred at rates of 15.4% and 8.5%, respectively, in PV cases and 17.6% and 8.7% in ET cases.
  • The rates of transformation to myelofibrosis were 2.6% in both PV and ET cases, and acute leukemia was noted in 1.1% of PV patients and 2.9% of ET patients.
  • The present study clearly demonstrated clinical differences between Japanese and Western patients for PV and ET.
  • [MeSH-minor] Adolescent. Age Factors. Aged. Aged, 80 and over. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Guidelines as Topic. Humans. Japan. Male. Middle Aged. Primary Myelofibrosis / blood. Primary Myelofibrosis / etiology. Primary Myelofibrosis / mortality. Retrospective Studies. Risk Factors. Survival Rate. Thrombosis / blood. Thrombosis / etiology. Thrombosis / mortality

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  • (PMID = 16787877.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
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59. Gangat N, Tefferi A, Thanarajasingam G, Patnaik M, Schwager S, Ketterling R, Wolanskyj AP: Cytogenetic abnormalities in essential thrombocythemia: prevalence and prognostic significance. Eur J Haematol; 2009 Jul;83(1):17-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: In the current study we describe cytogenetic findings as well as clinical correlates and long-term prognostic relevance of abnormal cytogenetics at the time of diagnosis of essential thrombocythemia (ET).
  • PATIENTS AND METHODS: The study cohort consisted of a consecutive group of patients with ET who fulfilled the World Health Organization diagnostic criteria, and in whom cytogenetic analysis was performed at diagnosis.
  • The prevalence of abnormal cytogenetics at diagnosis was 7% (28 of 402).
  • Parameters at diagnosis that were significantly associated with abnormal cytogenetics included palpable splenomegaly (P = 0.03), current tobacco use (P = 0.04); venous thrombosis (P = 0.02), and anemia with a hemoglobin of <10 g/dL (P = 0.02); but did not include JAK2V617F mutation status, or advanced age.
  • During follow up, patients with abnormal cytogenetics did not have shorter survival, or increased transformation to acute leukemia or myelofibrosis.
  • CONCLUSION: Cytogenetic anomalies at diagnosis are relatively uncommon in ET, and do not predict evolution into more aggressive myeloid disorders, or inferior survival.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Cohort Studies. Female. Humans. Janus Kinase 2 / genetics. Karyotyping. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Mutation. Primary Myelofibrosis / etiology. Primary Myelofibrosis / genetics. Prognosis. Trisomy. Young Adult

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  • (PMID = 19236446.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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60. Pieri L, Guglielmelli P, Vannucchi AM: Chronic myeloproliferative neoplasms: a collaborative approach. Mediterr J Hematol Infect Dis; 2010;2(2):e2010017

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  • [Title] Chronic myeloproliferative neoplasms: a collaborative approach.
  • The classic chronic myeloproliferative neoplasms (MPN) include different entities that pose significant challenges for their optimal diagnosis, treatment and overall management.
  • Polycythemia Vera and Essential Thrombocythemia are the most common among chronic myeloproliferative neoplasms (MPNs); major causes of morbidity and mortality are represented by arterial and venous thrombosis, as well as evolution to myelofibrosis or transformation to acute leukemia.
  • On the other hand, survival is significantly reduced in primary myelofibrosis, and the clinical manifestations may be disabling.
  • In the absence of therapies with the potential of curing the disease, a careful risk-oriented approach is employed for stratifying patients to the most appropriate, currently available, therapeutic options.
  • In this brief review, we will discuss some of the key issues that can arise along the clinical course of MPNs and require an integrated, strictly patient-oriented, approach.

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  • (PMID = 21415968.001).
  • [ISSN] 2035-3006
  • [Journal-full-title] Mediterranean journal of hematology and infectious diseases
  • [ISO-abbreviation] Mediterr J Hematol Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3033142
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61. Tripodi J, Hoffman R, Najfeld V, Weinberg R: Frequency of heterozygous TET2 deletions in myeloproliferative neoplasms. Cancer Manag Res; 2010 Sep 17;2:219-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of heterozygous TET2 deletions in myeloproliferative neoplasms.
  • The Philadelphia chromosome (Ph)-negative myeloproliferative neoplasms (MPNs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis, are a group of clonal hematopoietic stem cell disorders with overlapping clinical and cytogenetic features and a variable tendency to evolve into acute leukemia.

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  • (PMID = 21188113.001).
  • [ISSN] 1179-1322
  • [Journal-full-title] Cancer management and research
  • [ISO-abbreviation] Cancer Manag Res
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108671
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3004566
  • [Keywords] NOTNLM ; TET2 / cytogenetics / fluorescence in situ hybridization / myeloproliferative neoplasms
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62. Wang SA, Pozdnyakova O, Jorgensen JL, Medeiros LJ, Stachurski D, Anderson M, Raza A, Woda BA: Detection of paroxysmal nocturnal hemoglobinuria clones in patients with myelodysplastic syndromes and related bone marrow diseases, with emphasis on diagnostic pitfalls and caveats. Haematologica; 2009 Jan;94(1):29-37
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  • DESIGN AND METHODS: By using multiparameter flow cytometry immunophenotypic analysis with antibodies specific for four glycosylphosphatidylinositol-anchored proteins (CD55, CD59, CD16, CD66b) and performing an aerolysin lysis confirmatory test in representative cases, we assessed the paroxysmal nocturnal hemoglobinuria-phenotype granulocytes in 110 patients with myelodysplastic syndrome, 15 with myelodysplastic/myeloproliferative disease, 5 with idiopathic myelofibrosis and 6 with acute myeloid leukemia.
  • CONCLUSIONS: These results show that routine screening for paroxysmal nocturnal hemoglobinuria clones in patients with an intrinsic bone marrow disease who show no clinical evidence of hemolysis has an appreciable yield in patients with low grade myelodysplastic syndromes.
  • The recognition of diagnostic caveats and pitfalls associated with the underlying intrinsic bone marrow disease is essential in interpreting paroxysmal nocturnal hemoglobinuria testing correctly.
  • [MeSH-major] Bone Marrow Diseases / complications. Bone Marrow Diseases / diagnosis. Hemoglobinuria, Paroxysmal / complications. Hemoglobinuria, Paroxysmal / diagnosis. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / diagnosis


63. Manola KN, Sambani C, Karakasis D, Kalliakosta G, Harhalakis N, Papaioannou M: Leukemias associated with Turner syndrome: report of three cases and review of the literature. Leuk Res; 2008 Mar;32(3):481-6
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  • Here we report three TS patients with leukemia including one case of T-large granular lymphocyte leukemia (T-LGL), one rare case of coexistence of chronic lymphocytic leukemia (CLL) and idiopathic myelofibrosis (IMF) and one case of a patient with AML-M2 who received autologous stem cell transplantation (SCT).
  • Our cases and the limited data of previously reported leukemia patients with TS suggest that TS is not associated with a specific type of leukemia and that presentation, clinical course and response to treatment are similar to that of the non-TS leukemia patients.
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Large Granular Lymphocytic / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Myeloid, Acute / complications. Middle Aged. Monosomy. Treatment Outcome

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  • (PMID = 17669490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
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64. Jekarl DW, Han SB, Kim M, Lim J, Oh EJ, Kim Y, Kim HJ, Min WS, Han K: JAK2 V617F mutation in myelodysplastic syndrome, myelodysplastic syndrome/myeloproliferative neoplasm, unclassifiable, refractory anemia with ring sideroblasts with thrombocytosis, and acute myeloid leukemia. Korean J Hematol; 2010 Mar;45(1):46-50
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  • [Title] JAK2 V617F mutation in myelodysplastic syndrome, myelodysplastic syndrome/myeloproliferative neoplasm, unclassifiable, refractory anemia with ring sideroblasts with thrombocytosis, and acute myeloid leukemia.
  • BACKGROUND: The JAK2 V617F mutation has been noted in the cases of polycythemia vera, essential thrombocythemia, and primary myelofibrosis patients.
  • This mutation occurs less frequently in acute myeloid leukemia (AML) and other hematologic diseases, such as myelodysplastic syndrome (MDS); myelodysplatic syndrome/myeloproliferative neoplasm, unclassifiable (MDS/MPN-U); and refractory anemia with ring sideroblasts with thrombocytosis (RARS-T).
  • Data obtained from JAK2 V617F mutation analysis and cytogenetic study as well as complete blood count and clinical data were analyzed.

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  • (PMID = 21120162.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983014
  • [Keywords] NOTNLM ; AML / JAK2 V617F / MDS / MDS/MPN-U / RARS-T
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65. Spivak JL: Narrative review: Thrombocytosis, polycythemia vera, and JAK2 mutations: The phenotypic mimicry of chronic myeloproliferation. Ann Intern Med; 2010 Mar 2;152(5):300-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The myeloproliferative disorders polycythemia vera, essential thrombocytosis, and primary myelofibrosis are clonal disorders arising in a pluripotent hematopoietic stem cell, causing an unregulated increase in the number of erythrocytes, leukocytes, or platelets, alone or in combination; eventual marrow dominance by the progeny of the involved stem cell; and a tendency to arterial or venous thrombosis, marrow fibrosis, splenomegaly, or transformation to acute leukemia, albeit at widely varying frequencies.
  • The discovery of an activating mutation (V617F) in the gene for JAK2 (Janus kinase 2), a tyrosine kinase utilized by hematopoietic cell receptors for erythropoietin, thrombopoietin, and granulocyte colony-stimulating factor, provided an explanation for the shared clinical features of these 3 disorders.
  • Because the erythropoietin, thrombopoietin, and granulocyte colony-stimulating factor receptors are all constitutively activated, polycythemia vera is the potential ultimate clinical phenotype of the JAK2 V617F mutation and, as a corollary, is the most common of the 3 disorders.
  • The number of cells expressing the JAK2 V617F mutation (the allele burden) seems to correlate with the clinical phenotype.
  • Preliminary results of clinical trials with agents that inhibit the mutated kinase indicate a reduction in splenomegaly and alleviation of night sweats, fatigue, and pruritus.
  • [MeSH-major] Janus Kinase 2 / genetics. Polycythemia Vera / genetics. Primary Myelofibrosis / genetics. Thrombocytosis / genetics
  • [MeSH-minor] Chronic Disease. Hematopoiesis. Humans. Mutation. Phenotype. Signal Transduction

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  • (PMID = 20194236.001).
  • [ISSN] 1539-3704
  • [Journal-full-title] Annals of internal medicine
  • [ISO-abbreviation] Ann. Intern. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA108671
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 59
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66. Andrikovics H, Szilvási A, Meggyesi N, Király V, Halm G, Lueff S, Nahajevszky S, Mikala G, Sipos A, Lovas N, Csukly Z, Mátrai Z, Tamáska J, Tordai A, Masszi T: [Role of the activating mutation Val617Phe of Janus kinase 2 gene in myeloproliferative diseases and significance of its detection]. Orv Hetil; 2007 Feb 4;148(5):203-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Role of the activating mutation Val617Phe of Janus kinase 2 gene in myeloproliferative diseases and significance of its detection].
  • The Val617Phe point mutation of Janus kinase 2 gene is believed to participate in the pathogenesis of myeloproliferative syndrome characterised by the clonal alteration of hematopoietic stem cells.
  • According to current results, the frequency of Val617Phe activating mutation is around 80% in polycythaemia vera, 35% in essential thrombocythemia, and 50% in chronic idiopathic myelofibrosis.
  • The diagnoses of polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis were so far based on the exclusion of secondary factors as well as bone marrow biopsy histology.
  • The goal of the present work was to establish simple molecular genetic techniques for the routine testing of Janus kinase 2 gene Val617Phe mutation, and to compare the clinical phenotypes of Val617Phe mutation positive and negative myeloproliferative syndromes.
  • We employed the allele specific polymerase chain technique for detection of Val617Phe mutation in 252 patients with myeloproliferative syndrome.
  • We measured Val617Phe frequency as 85,4% (117/137) in polycythemia vera, 56,6% (56/99) in essential thrombocythemia, and 87,5% (14/16) in idiopathic myelofibrosis.
  • We found significantly elevated hemoglobin levels and white blood cell counts (measured at the time of diagnosis) in Val617Phe-positive polycythemia vera and essential thrombocythemia patient groups compared to Val617Phe-negative patients.
  • However, the frequencies of splenomegaly and other complications (thrombosis, bleeding, transformation to acute leukemia) were not significantly different between the mutation-positive and negative groups.
  • In conclusion, the non-invasive mutation analysis of the Janus kinase 2 Val617Phe is suitable for routine laboratory application and helps the differential diagnosis of myeloproliferative syndrome.
  • [MeSH-major] Janus Kinase 2 / genetics. Myeloproliferative Disorders / genetics. Point Mutation
  • [MeSH-minor] Adult. Aged. Biopsy. Bone Marrow / pathology. Female. Gene Expression Regulation. Gene Frequency. Humans. Male. Middle Aged. Phenotype. Phenylalanine. Polycythemia Vera / genetics. Polymerase Chain Reaction. Primary Myelofibrosis / genetics. Thrombocytosis / genetics. Valine

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  • (PMID = 17344140.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 47E5O17Y3R / Phenylalanine; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; HG18B9YRS7 / Valine
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67. Gibbins J, Pankhurst T, Murray J, McCafferty I, Baiden-Amissahk K, Shafeek S, Lipkin GW: Extramedullary haematopoiesis in the kidney: a case report and review of literature. Clin Lab Haematol; 2005 Dec;27(6):391-4
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  • We report a 47-year-old man with myelofibrosis who presented with bilateral nephromegaly secondary to extramedullary haematopoiesis.
  • We discuss diagnosis and treatment of this rare case and review the literature.
  • [MeSH-major] Hematopoiesis, Extramedullary. Kidney Diseases / diagnosis. Primary Myelofibrosis / diagnosis
  • [MeSH-minor] Cell Transformation, Neoplastic. Humans. Hypertrophy / etiology. Leukemia, Myeloid, Acute. Male. Middle Aged

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  • (PMID = 16307541.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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68. 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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69. Mesa RA: Tipifarnib: farnesyl transferase inhibition at a crossroads. Expert Rev Anticancer Ther; 2006 Mar;6(3):313-9
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  • Tipifarnib has displayed the most interesting activity in the myeloid malignancies of myelodysplastic syndrome, myelofibrosis with myeloid metaplasia and elderly/high-risk acute myeloid leukemia.
  • Overall clinical response rates of approximately 20-30% have been reported in myelodysplastic syndrome and acute myeloid leukemia patients who have few alternative therapeutic options.
  • US FDA approval for tipifarnib awaits results of subsequent Phase III trials of the agent in elderly acute leukemia.
  • [MeSH-minor] Clinical Trials as Topic. Drug Administration Schedule. Humans. Neoplasms / drug therapy. Treatment Outcome

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  • (PMID = 16503848.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase
  • [Number-of-references] 54
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70. Prentice HG, Sacchi S, Russell N: Future directions in haematology: beyond multiple myeloma. Acta Haematol; 2005;114 Suppl 1:27-32
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  • The European Collaboration Group on Myelofibrosis with Myeloid Metaplasia reviewed patients who received at least four weeks' thalidomide treatment, in doses ranging from 50 mg/day to 400 mg/day.
  • Data on thalidomide and acute myeloblastic leukaemia (AML) are conflicting: a recently published study indicated that thalidomide does not have a role in the management of acute myeloblastic leukaemia (AML), while other studies suggest some patients may respond because of thalidomide's ability to activate natural killer cells and cytotoxic T-lymphocytes.
  • [MeSH-minor] Animals. Blood Transfusion. Clinical Trials, Phase II as Topic. Cytokines / metabolism. Disease-Free Survival. European Union. Hemoglobins / metabolism. Humans. Killer Cells, Natural / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Lymphocyte Activation / drug effects. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Organ Size / drug effects. Remission Induction. Spleen / metabolism. Spleen / pathology. T-Lymphocytes / metabolism. Waldenstrom Macroglobulinemia / metabolism. Waldenstrom Macroglobulinemia / mortality. Waldenstrom Macroglobulinemia / pathology. Waldenstrom Macroglobulinemia / therapy

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  • [Copyright] Copyright 2005 S. Karger AG, Basel
  • (PMID = 16166770.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / Hemoglobins; 4Z8R6ORS6L / Thalidomide
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71. Tefferi A: Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1. Leukemia; 2010 Jun;24(6):1128-38
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  • [Title] Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1.
  • Myeloproliferative neoplasms (MPNs) originate from genetically transformed hematopoietic stem cells that retain the capacity for multilineage differentiation and effective myelopoiesis.
  • Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs.
  • JAK2 and MPL mutations appear to exert a phenotype-modifying effect and are distinctly associated with polycythemia vera, essential thrombocythemia and primary myelofibrosis; the corresponding mutational frequencies are approximately 99, 55 and 65% for JAK2 and 0, 3 and 10% for MPL mutations.
  • The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1).
  • However, it is not clear as to whether and how these abnormalities contribute to disease initiation, clonal evolution or blastic transformation.
  • [MeSH-major] Biomarkers, Tumor / genetics. Mutation / genetics. Myeloproliferative Disorders / genetics. Neoplasm Proteins / genetics

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  • (PMID = 20428194.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Thrombopoietin; 0 / Repressor Proteins; 0 / TET2 protein, human; 143641-95-6 / MPL protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 171
  • [Other-IDs] NLM/ PMC3035972
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72. Harrison CN, Campbell PJ, Buck G, Wheatley K, East CL, Bareford D, Wilkins BS, van der Walt JD, Reilly JT, Grigg AP, Revell P, Woodcock BE, Green AR, United Kingdom Medical Research Council Primary Thrombocythemia 1 Study: Hydroxyurea compared with anagrelide in high-risk essential thrombocythemia. N Engl J Med; 2005 Jul 7;353(1):33-45
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  • As compared with hydroxyurea plus aspirin, anagrelide plus aspirin was associated with increased rates of arterial thrombosis (P=0.004), serious hemorrhage (P=0.008), and transformation to myelofibrosis (P=0.01) but with a decreased rate of venous thromboembolism (P=0.006).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Drug Therapy, Combination. Female. Follow-Up Studies. Hemorrhage / etiology. Hemorrhage / mortality. Humans. Leukemia, Myeloid, Acute / etiology. Male. Middle Aged. Platelet Count. Primary Myelofibrosis / etiology. Primary Myelofibrosis / prevention & control. Thrombosis / etiology. Thrombosis / mortality

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  • [Copyright] Copyright 2005 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2005 Jul 7;353(1):85-6 [16000360.001]
  • (PMID = 16000354.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 088340
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide; R16CO5Y76E / Aspirin; X6Q56QN5QC / Hydroxyurea
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73. 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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  • (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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74. Daskalakis M, Blagitko-Dorfs N, Hackanson B: Decitabine. Recent Results Cancer Res; 2010;184:131-57
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  • Multiple clinical trials have shown the promising activity of low-dose decitabine in AML, MDS, CML, and hemoglobinopathies, whereas its efficacy in solid tumors is rather limited.Clinical responses appear to be induced by both epigenetic alterations and the induction of cell-cycle arrest and/or apoptosis.
  • Recent clinical trials have been investigating new dosing schedules, routes of administration, and combination of decitabine with other agents, including histone deacetylase (HDAC) inhibitors.
  • [MeSH-minor] Animals. Humans. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Primary Myelofibrosis / drug therapy. Stem Cell Transplantation. Transplantation, Homologous

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  • (PMID = 20072836.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Number-of-references] 161
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75. Tefferi A, Skoda R, Vardiman JW: Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics. Nat Rev Clin Oncol; 2009 Nov;6(11):627-37
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  • [Title] Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics.
  • Myeloid neoplasms are now classified into five categories: acute myeloid leukemia, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN, and myeloid and/or lymphoid malignancies associated with eosinophilia and PDGFR or FGFR1 rearrangements.
  • MPN are subclassified into eight separate entities: chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, primary myelofibrosis, systemic mastocytosis, chronic eosinophilic leukemia not otherwise specified, chronic neutrophilic leukemia, and unclassifiable MPN.
  • The diagnosis of chronic myelogenous leukemia requires the presence of BCR-ABL1, while its absence is required for all other MPN.
  • JAK2 V617F is found in most patients with polycythemia vera, essential thrombocythemia, or primary myelofibrosis and is, therefore, useful as a clonal marker in those settings.
  • In systemic mastocytosis, presence of KIT D816V is expected but not essential for diagnosis.
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Algorithms. Biomarkers, Tumor / genetics. Fusion Proteins, bcr-abl / genetics. Humans. Janus Kinase 2 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / genetics. Polycythemia Vera / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / genetics. World Health Organization

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  • (PMID = 19806146.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 77
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76. Scott BL, Storer BE, Greene JE, Hackman RC, Appelbaum FR, Deeg HJ: Marrow fibrosis as a risk factor for posttransplantation outcome in patients with advanced myelodysplastic syndrome or acute myeloid leukemia with multilineage dysplasia. Biol Blood Marrow Transplant; 2007 Mar;13(3):345-54
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  • [Title] Marrow fibrosis as a risk factor for posttransplantation outcome in patients with advanced myelodysplastic syndrome or acute myeloid leukemia with multilineage dysplasia.
  • We performed a retrospective analysis in 471 patients with MDS or acute myeloid leukemia with multilineage dysplasia arising from MDS, 113 with and 358 without marrow fibrosis, who received myeloablative allogeneic HCT.
  • However, among patients with advanced disease (int-2 or high-risk disease by the International Prognostic Scoring System), OS (P = .03), RFS (P = .04), and NRM (P = .04) were inferior when marrow fibrosis was present.
  • Given that marrow fibrosis is a poor prognostic factor for patients with MDS, and that it does not appear to affect outcome of transplantation in patients with earlier-stage disease but has a negative impact on outcome for patients with advanced disease, patients with earlier-stage MDS and marrow fibrosis might be considered for HCT earlier than their disease stage would normally dictate.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / complications. Myelodysplastic Syndromes / complications. Primary Myelofibrosis / mortality

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  • (PMID = 17317588.001).
  • [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 / CA15704; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL084054; United States / NHLBI NIH HHS / HL / HL36444; United States / NHLBI NIH HHS / HL / HL82941
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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77. 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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78. Vannucchi AM: Insights into the pathogenesis and management of thrombosis in polycythemia vera and essential thrombocythemia. Intern Emerg Med; 2010 Jun;5(3):177-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The classic myeloproliferative neoplasms (MPNs) include polycythemia vera and essential thrombocythemia; their molecular basis has been described only recently with the demonstration of recurrent mutations in JAK2 or MPL.
  • While life expectancy may not be significantly shortened, arterial and venous thrombosis constitute the major causes of morbidity and mortality, together with disease evolution to myelofibrosis or transformation to acute leukemia.
  • Better knowledge in the pathophysiology of these disorders, and the introduction of molecularly targeted drugs in clinical trials, anticipate the possibility of more specific and efficacious treatment of classic MPN, particularly as concerns the reduction of risk associated with vascular events.

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  • (PMID = 19789961.001).
  • [ISSN] 1970-9366
  • [Journal-full-title] Internal and emergency medicine
  • [ISO-abbreviation] Intern Emerg Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Platelet Aggregation Inhibitors; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; R16CO5Y76E / Aspirin
  • [Number-of-references] 50
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79. Weiss DJ: Sideroblastic anemia in 7 dogs (1996-2002). J Vet Intern Med; 2005 May-Jun;19(3):325-8
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  • Historical, clinical, and clinicopathologic findings were reviewed to determine whether the condition was idiopathic or associated with disease conditions or drug or toxin exposure.
  • Associated diseases were identified in 6 affected dogs and included acute hepatitis, pancreatitis, acute hepatitis and pancreatitis, inflammatory disease, glomerulonephritis, and myelofibrosis.
  • One dog had no evidence of associated disease.
  • Regardless of the associated disease condition, sideroblastic anemia was characterized by moderate to severe nonregenerative and frequently hypochromic anemia with prominent dysplastic features in bone marrow that were most prominent in the erythroid series.
  • Identification of large numbers of siderocytes or sideroblasts in blood or bone marrow is inconsistent with a diagnosis of iron deficiency and should prompt a search for inflammatory disease conditions, including hepatitis, pancreatitis, and glomerulonephritis.

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  • (PMID = 15954546.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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80. Vannucchi AM, Guglielmelli P, Rambaldi A, Bogani C, Barbui T: Epigenetic therapy in myeloproliferative neoplasms: evidence and perspectives. J Cell Mol Med; 2009 Aug;13(8A):1437-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic therapy in myeloproliferative neoplasms: evidence and perspectives.
  • The classic Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs), which include polycythaemia vera, essential thrombocythaemia and primary myelofibrosis, originate from a stem cell-derived clonal myeloproliferation that manifests itself with variable haematopoietic cell lineage involvement; they are characterized by a high degree of similarities and the chance to transform each to the other and to evolve into acute leukaemia.
  • Their molecular pathogenesis has been associated with recurrent acquired mutations in janus kinase 2 (JAK2) and myeloproliferative leukemia virus oncogene (MPL).
  • These discoveries have simplified the diagnostic approach and provided a number of clues to understanding the phenotypic expression of MPNs; furthermore, they represented a framework for developing and/or testing in clinical trials small molecules acting as tyrosine kinase inhibitors.
  • The first clinical trials with epigenetic drugs have been completed recently, whereas others are still ongoing; results have been variable and at present do not allow any firm conclusion.
  • [MeSH-major] Epigenesis, Genetic. Leukemia / drug therapy. Leukemia / genetics. Myeloproliferative Disorders / drug therapy. Myeloproliferative Disorders / genetics

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  • (PMID = 19522842.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 175
  • [Other-IDs] NLM/ PMC3828857
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81. 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.


82. 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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83. 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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84. 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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85. 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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86. 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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87. Riley RS, Idowu M, Chesney A, Zhao S, McCarty J, Lamb LS, Ben-Ezra JM: Hematologic aspects of myeloablative therapy and bone marrow transplantation. J Clin Lab Anal; 2005;19(2):47-79
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  • Since the recipient is profoundly ill during the initial treatment period, laboratory data is critical for monitoring engraftment, detecting residual/recurrent disease, and identifying problems that may delay bone marrow reconstitution or lead to other medical complications.
  • The potential complications of bone marrow transplantation include engraftment failure and delayed engraftment, infection, residual bone marrow disease, acute and chronic graft versus host disease, myelofibrosis, therapy-related acute leukemia, post-transplant lympho-proliferative disorders, and toxic myelopathy.


88. 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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  • [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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89. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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90. Walz C, Cross NC, Van Etten RA, Reiter A: Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disorders. Leukemia; 2008 Jul;22(7):1320-34
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  • [Title] Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disorders.
  • Constitutively activated mutants of the non-receptor tyrosine kinases (TK) ABL1 (Abelson murine leukemia viral (v-abl) homolog (1) protein) and JAK2 (JAnus Kinase 2 or Just Another Kinase 2) play a central role in the pathogenesis of clinically and morphologically distinct chronic myeloproliferative disorders but are also found in some cases of de novo acute leukemia and lymphoma.
  • Specific abnormalities are correlated with clinical phenotype, although some are broad and encompass several World Health Organization-defined entities.
  • TKs are excellent drug targets as exemplified by the activity of imatinib in BCR-ABL1-positive disease, particularly chronic myeloid leukemia.
  • Selective and non-selective inhibitors of JAK2 are currently being developed, and encouraging data from pre-clinical experiments and initial phase-I studies regarding efficacy and potential toxicity of these compounds have already been reported.

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  • (PMID = 18528425.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL089747; United States / NHLBI NIH HHS / HL / HL089747
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / PCM1 protein, human; 0 / Protein Kinase Inhibitors; 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/ NIHMS417174; NLM/ PMC3490192
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91. Yee KW, Zeng Z, Konopleva M, Verstovsek S, Ravandi F, Ferrajoli A, Thomas D, Wierda W, Apostolidou E, Albitar M, O'Brien S, Andreeff M, Giles FJ: Phase I/II study of the mammalian target of rapamycin inhibitor everolimus (RAD001) in patients with relapsed or refractory hematologic malignancies. Clin Cancer Res; 2006 Sep 1;12(17):5165-73
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  • RESULTS: Twenty-seven patients (9 acute myelogenous leukemia, 5 myelodysplastic syndrome, 6 B-chronic lymphocytic leukemia, 4 mantle cell lymphoma, 1 myelofibrosis, 1 natural killer cell/T-cell leukemia, and 1 T-cell prolymphocytic leukemia) received everolimus.
  • Phosphorylation of downstream targets of mTOR, eukaryotic initiation factor 4E-binding protein 1, and/or, p70 S6 kinase, was inhibited in six of nine patient samples, including those from the patient with a major platelet response.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Myelodysplastic Syndromes / drug therapy. Sirolimus / analogs & derivatives

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  • (PMID = 16951235.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Phosphoproteins; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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92. 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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93. Kaune KM, Baumgart M, Schmitke E, Haase D, Middel P, Ghadimi BM, Bertsch HP, Neumann C, Emmert S: Papular exanthem discloses acute myeloid leukaemia: interphase fluorescence in situ hybridization revealed deletion of p53 and gain at 8q22/8q24/Tel8q without trisomy 8. Clin Exp Dermatol; 2010 Mar;35(2):160-4
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  • [Title] Papular exanthem discloses acute myeloid leukaemia: interphase fluorescence in situ hybridization revealed deletion of p53 and gain at 8q22/8q24/Tel8q without trisomy 8.
  • Previous attempts to taking bone-marrow biopsies had resulted in a 'dry tap', with no material collected, suggesting idiopathic myelofibrosis.
  • Histological examination of skin biopsies showed dermal infiltration of monocytoid cells, resulting in a diagnosis of acute myeloid leukaemia (French-American-British M5 morphology) with leukaemia cutis (LC).
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Genes, p53 / genetics. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Trisomy / genetics

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  • (PMID = 19438543.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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94. Norén-Nyström U, Roos G, Bergh A, Botling J, Lönnerholm G, Porwit A, Heyman M, Forestier E: Bone marrow fibrosis in childhood acute lymphoblastic leukemia correlates to biological factors, treatment response and outcome. Leukemia; 2008 Mar;22(3):504-10
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  • [Title] Bone marrow fibrosis in childhood acute lymphoblastic leukemia correlates to biological factors, treatment response and outcome.
  • We retrospectively evaluated reticulin fiber density (RFD) in 166 diagnostic bone marrow (BM) biopsies and 62 biopsies obtained at treatment day 29 from children with acute lymphoblastic leukemia (ALL).
  • In BCP-ALL patients, RFD at diagnosis correlated to the levels of minimal residual disease (MRD) analyzed by flow cytometry on treatment day 29 (P=0.001).
  • Accordingly, patients with MRD > or = 10(-4) presented higher RFD at diagnosis compared to patients with MRD < 10(-4) (P=0.003).
  • BCP-ALL patients with low RFD at diagnosis and a rapid reduction of RFD on day 29 had a favorable outcome compared to patients with the same baseline RFD level at diagnosis but a slow RFD reduction (P=0.041).
  • Expanded use of BM biopsy both at diagnosis and during follow-up is suggested.
  • [MeSH-major] Bone Marrow Examination. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Primary Myelofibrosis / pathology. Reticulin / analysis


95. Fröhling S, Scholl C, Gilliland DG, Levine RL: Genetics of myeloid malignancies: pathogenetic and clinical implications. J Clin Oncol; 2005 Sep 10;23(26):6285-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetics of myeloid malignancies: pathogenetic and clinical implications.
  • Recent advances in our understanding of the genetic basis of myeloid malignancies have provided important insights into the pathogenesis of acute myeloid leukemia (AML) and myeloproliferative diseases (MPD) and have led to the development of novel therapeutic approaches.
  • In this review, we describe our current state of understanding of the genetic basis of AML and MPD, with a specific focus on pathogenetic and therapeutic significance.
  • Specific examples discussed include RAS mutations, KIT mutations, FLT3 mutations, and core binding factor rearrangements in AML, and JAK2 mutations in polycythemia vera, essential thrombocytosis, and chronic idiopathic myelofibrosis.
  • [MeSH-major] Genetic Predisposition to Disease / epidemiology. Genetic Therapy / methods. Hematologic Neoplasms / genetics. Hematologic Neoplasms / therapy
  • [MeSH-minor] Female. Forecasting. Gene Transfer Techniques. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Male. Molecular Biology. Myeloproliferative Disorders / genetics. Myeloproliferative Disorders / pathology. Myeloproliferative Disorders / therapy. Prognosis. Risk Assessment. Severity of Illness Index. Survival Analysis. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2006 Apr 1;24(10):1647 [16575017.001]
  • (PMID = 16155011.001).
  • [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] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 189
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96. Tefferi A, Spivak JL: Polycythemia vera: scientific advances and current practice. Semin Hematol; 2005 Oct;42(4):206-20
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  • 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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97. Ueda T, Ito Y, Maeda M, Fukunaga Y: Massive periosteal reaction a presenting feature of acute megakaryocytic leukemia. Pediatr Int; 2007 Dec;49(6):1015-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Massive periosteal reaction a presenting feature of acute megakaryocytic leukemia.
  • Acute megakaryoblastic leukemia (AML M7) is a biologically heterogeneous form of acute myeloid leukemia accounting for 14.6% of cases.
  • In many instances in the past, AML M7 has been classified as undifferentiated leukemia, myelodysplasia, myelofibrosis or some other disease because of its complex clinical presentation or the difficulty of obtaining and interpreting bone marrow samples.
  • Here we report on a 14-month-old girl who presented with a massive periosteal reaction of the extremities and clavicles associated with myelofibrosis, a presenting feature of AML M7.
  • [MeSH-major] Hyperostosis / etiology. Leukemia, Megakaryoblastic, Acute / complications. Paraneoplastic Syndromes. Periosteum / pathology. Primary Myelofibrosis / etiology

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  • (PMID = 18045316.001).
  • [ISSN] 1328-8067
  • [Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society
  • [ISO-abbreviation] Pediatr Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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98. 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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99. Verstovsek S, Tefferi A, Cortes J, O'Brien S, Garcia-Manero G, Pardanani A, Akin C, Faderl S, Manshouri T, Thomas D, Kantarjian H: Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis. Clin Cancer Res; 2008 Jun 15;14(12):3906-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis.
  • PURPOSE: Molecular characterization of Philadelphia chromosome-negative (Ph-) chronic myeloproliferative disorders, such as systemic mastocytosis (SM), has provided a clear rationale for investigating novel targeted therapies.
  • Only two patients, one with SM-myelofibrosis and one with SM-chronic eosinophilic leukemia, achieved complete response (elimination of mastocytosis) lasting for 5 and 16 months, respectively.
  • Complete responses were achieved in two other patients (acute myeloid leukemia and hypereosinophilic syndrome).
  • No responses were observed among patients with myelodysplastic syndromes and primary myelofibrosis.
  • CONCLUSION: These data show that dasatinib therapy may benefit a selected group of SM patients, primarily by improving their symptoms, but it does not eliminate the disease in the patients with KIT-D816V mutation.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Mastocytosis, Systemic / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 18559612.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS814210; NLM/ PMC5018899
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100. 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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