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1. 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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  • [Cites] Blood. 2007 Aug 1;110(3):986-93 [17473062.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3495-503 [12393681.001]
  • [Cites] Br Med J. 1963 Aug 24;2(5355):472-7 [14043710.001]
  • [Cites] N Engl J Med. 2005 Feb 10;352(6):549-57 [15703420.001]
  • [Cites] Mod Pathol. 2005 May;18(5):603-14 [15578075.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1158-64 [16609064.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):513-21 [15173958.001]
  • (PMID = 21274282.001).
  • [ISSN] 1687-9635
  • [Journal-full-title] Case reports in medicine
  • [ISO-abbreviation] Case Rep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3026984
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2. Geron I, Abrahamsson AE, Barroga CF, Kavalerchik E, Gotlib J, Hood JD, Durocher J, Mak CC, Noronha G, Soll RM, Tefferi A, Kaushansky K, Jamieson CH: Selective inhibition of JAK2-driven erythroid differentiation of polycythemia vera progenitors. Cancer Cell; 2008 Apr;13(4):321-30
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  • [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.
  • [MeSH-major] Cell Differentiation / drug effects. Erythroid Precursor Cells / enzymology. Erythroid Precursor Cells / pathology. Janus Kinase 2 / antagonists & inhibitors. Polycythemia Vera / enzymology. Polycythemia Vera / pathology. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] Adult. Aged. Amino Acid Substitution. Animals. Base Sequence. Female. Humans. Male. Mice. Middle Aged. Molecular Sequence Data. Phenylalanine / genetics. Signal Transduction / drug effects. Stem Cell Transplantation. Valine / genetics


3. Kawagoe H, Grosveld GC: Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9. Blood; 2005 Dec 15;106(13):4269-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9.
  • Expression of MN1-TEL enhanced the growth of myeloid progenitors in an interleukin 3/stem cell factor (IL-3/SCF)-dependent manner in vitro whereas 10% of MN1-TEL-expressing mice developed altered myelopoiesis with severe anemia after long latency.
  • Coexpression of MN1-TEL and IL-3, but not SCF, rapidly caused a fatal myeloproliferative disease rather than acute myeloid leukemia (AML).
  • Thus, the leukemogenic effect of MN1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome.

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  • [Cites] J Leukoc Biol. 1999 Feb;65(2):217-31 [10088605.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Oncogene. 2000 Feb 3;19(5):608-16 [10698505.001]
  • [Cites] Mol Cell Biol. 2000 May;20(9):3274-85 [10757811.001]
  • [Cites] Int J Hematol. 2000 Jun;71(4):301-8 [10905048.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(24):9281-93 [11094079.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Feb;23(2):122-5 [11216704.001]
  • [Cites] Exp Hematol. 2001 Jul;29(7):856-63 [11438208.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Int Immunol. 2002 Jul;14(7):813-22 [12096041.001]
  • [Cites] Oncogene. 2003 Feb 6;22(5):699-709 [12569362.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5428-37 [14500378.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):1256-69 [14729970.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2522-9 [14630789.001]
  • [Cites] Biotechnol Bioeng. 2004 Apr 20;86(2):174-87 [15052637.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6091-100 [15342392.001]
  • [Cites] Genes Dev. 2004 Oct 1;18(19):2336-41 [15371326.001]
  • [Cites] EMBO J. 1989 Jan;8(1):133-6 [2653809.001]
  • [Cites] Blood. 1991 Dec 1;78(11):3012-20 [1954386.001]
  • [Cites] Hematol Oncol Clin North Am. 1992 Jun;6(3):571-86 [1613007.001]
  • [Cites] EMBO J. 1993 Oct;12(10):3835-46 [8104786.001]
  • [Cites] Leuk Lymphoma. 1993 Oct;11(3-4):197-205 [8260894.001]
  • [Cites] Cell. 1994 Apr 22;77(2):307-16 [8168137.001]
  • [Cites] Oncogene. 1995 Apr 20;10(8):1511-9 [7731705.001]
  • [Cites] Oncogene. 1995 Apr 20;10(8):1521-8 [7731706.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):516-26 [7734349.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1427-9 [7660125.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):159-67 [8563754.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4804-8 [8639852.001]
  • [Cites] J Immunol Methods. 1996 Oct 16;197(1-2):139-50 [8890901.001]
  • [Cites] Int J Biochem Cell Biol. 1997 Dec;29(12):1371-87 [9570133.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Genes Dev. 1998 Aug 15;12(16):2475-87 [9716401.001]
  • [Cites] Leukemia. 1999 Jan;13(1):6-13 [10049061.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4278-86 [16081688.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12804-9 [10536003.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1761-72 [10477702.001]
  • (PMID = 16105979.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA217G; United States / NCI NIH HHS / CA / CA72999-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / Mn1 protein, mouse; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; 0 / homeobox protein HOXA9
  • [Other-IDs] NLM/ PMC1895240
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4. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera (PV) is a chronic myeloproliferative neoplasm (MPN) characterized by excessive production of red blood cells.
  • Patients with PV are at a risk of thrombosis, bleeding, and transformation to myelofibrosis or acute myeloid leukemia.
  • Therapy for PV is based on the use of phlebotomy, aspirin, and in high-risk patients, cytoreductive agents such as hydroxyurea.
  • 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.
  • [MeSH-major] Piperazines / administration & dosage. Polycythemia Vera / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Benzamides. Female. Humans. Imatinib Mesylate. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Male. Middle Aged. Mutation, Missense. Proto-Oncogene Proteins c-abl / antagonists & inhibitors. Proto-Oncogene Proteins c-abl / genetics. Proto-Oncogene Proteins c-kit / genetics. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Platelet-Derived Growth Factor / genetics. Time Factors

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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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5. Reuss CS, Wilansky S: Images in cardiovascular medicine. Eosinophilic heart disease in acute myeloproliferative disorder. Circulation; 2007 Jun 12;115(23):e614-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Images in cardiovascular medicine. Eosinophilic heart disease in acute myeloproliferative disorder.
  • [MeSH-major] Eosinophilia / complications. Heart Diseases / etiology. Myeloproliferative Disorders / complications

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  • (PMID = 17562961.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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6. Ngirabacu MC, Ravoet C, Dargent JL, Meuleman N, Ahmad I, Ysebrant L, Bennani J, André M, Bron D: Long-term follow-up of autologous peripheral blood stem cell transplantation in the treatment of a patient with acute panmyelosis with myelofibrosis. Haematologica; 2006 Dec;91(12 Suppl):ECR53
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  • [Title] Long-term follow-up of autologous peripheral blood stem cell transplantation in the treatment of a patient with acute panmyelosis with myelofibrosis.
  • [MeSH-major] Leukemia, Myeloid / surgery. Peripheral Blood Stem Cell Transplantation. Primary Myelofibrosis / surgery
  • [MeSH-minor] Acute Disease. Anemia, Refractory / drug therapy. Anemia, Refractory / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cytarabine / administration & dosage. Erythropoietin / therapeutic use. Etoposide / administration & dosage. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Mitoxantrone / administration & dosage. Postoperative Complications / drug therapy. Postoperative Complications / etiology. Recombinant Proteins. Transplantation Conditioning / adverse effects. Transplantation, Autologous. Whole-Body Irradiation / adverse effects

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  • (PMID = 17194659.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; YL5FZ2Y5U1 / Methotrexate
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7. 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.
  • Myelosuppressive drugs can reduce the rate of thromboses and hemorrhages, but there is concern that their use accelerates the rate of leukemic transformation.
  • Cytotoxic agents are recommended in high-risk cases and hydroxyurea is the drug of choice in most patients.
  • [MeSH-major] Cardiovascular Diseases / etiology. Polycythemia Vera / drug therapy. Thrombocythemia, Essential / drug therapy
  • [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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8. 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.
  • Myelosuppressive drugs can reduce the rate of thromboses and hemorrhages, but there is concern that their use accelerates the rate of leukemic transformation.
  • Cytotoxic agents are recommended in high-risk patients and hydroxyurea is the drug of choice in most patients.
  • 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.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Aspirin / administration & dosage. Humans. Risk Factors

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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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9. Español I, Romagosa V, Berlanga J, Domingo A, Losa F, Heras L, Janáriz J: Zoledronate-induced remission of acute panmyelosis with myelofibrosis. Eur J Haematol; 2004 Sep;73(3):215-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zoledronate-induced remission of acute panmyelosis with myelofibrosis.
  • Acute panmyelosis with myelofibrosis is a rare and aggressive form of acute myeloid leukemia.
  • We describe a new case with a huge proliferation of megakaryocytes, blast cells and reticulin fibers.
  • Ten months after the diagnosis, the patient is still in healthy condition.
  • [MeSH-major] Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Blood Cell Count. Blood Transfusion. Bone Marrow Examination. Humans. Male. Remission Induction / methods

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  • [Copyright] Copyright Blackwell Munksgaard 2004.
  • (PMID = 15287920.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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10. Naoe T: Developing target therapy against oncogenic tyrosine kinase in myeloid maliganacies. Curr Pharm Biotechnol; 2006 Oct;7(5):331-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fusion genes involving ABL, ARG, PDGFRs, JAK2, SYK, TRKC, and FGFRs, and gain-of-function mutations of FLT3, KIT and JAK2 have been detected at various rates in myeloproliferative disease and acute myeloid leukemia.
  • These gene products are constitutively activated and potentially transform hematopoietic cells by augmentation of proliferation and enhanced viability.
  • 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.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems / methods. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Neoplasm Proteins / metabolism. Protein Kinase Inhibitors / administration & dosage. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Drug Design. Humans. Treatment Outcome

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  • (PMID = 17076649.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 111
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11. Gangat N, Tefferi A: Pharmacotherapy of essential thrombocythemia. Expert Opin Pharmacother; 2008 Jul;9(10):1679-85
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  • BACKGROUND: The natural history of essential thrombocythemia is characterized by an increased incidence of thrombotic and hemorrhagic events and, in the long-term, a tendency for disease transformation to myelofibrosis or acute leukemia.
  • Advanced age and a prior history of thrombosis are the major predictors of thrombotic complications.
  • 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.
  • Hydroxycarbamide is the agent of choice in most patients: however, interferon-alpha is a reasonable alternative in young patients, pregnancy or those intolerant of hydroxycarbamide.
  • 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-major] Platelet Aggregation Inhibitors / therapeutic use. Thrombocythemia, Essential / drug therapy
  • [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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12. 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.
  • [Transliterated title] Maladie de Vaquez.
  • 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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13. Di Venuti G, Nawgiri R, Foss F: Denileukin diftitox and hyper-CVAD in the treatment of human T-cell lymphotropic virus 1-associated acute T-cell leukemia/lymphoma. Clin Lymphoma; 2003 Dec;4(3):176-8
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  • [Title] Denileukin diftitox and hyper-CVAD in the treatment of human T-cell lymphotropic virus 1-associated acute T-cell leukemia/lymphoma.
  • We report a case of human T-cell lymphotropic virus 1 (HTLV-1)-associated adult T cell leukemia/lymphoma (ATL) in clinical remission > 1 year after therapy with denileukin diftitox and hyper-CVAD (hyperfractionated cyclophosphamide/doxorubicin/vincristine/decadron).
  • The patient presented with leukocytosis, anemia, and thrombocytopenia, and bone marrow biopsy demonstrated extensive myelofibrosis and infiltration with leukemic T cells.
  • Initial therapy with 4 cycles of denileukin diftitox resulted in restoration of normal hematopoiesis and a reduction in bone marrow myelofibrosis.
  • After disease progression, 4 cycles of hyper-CVAD were administered and a complete clinical remission was achieved.
  • The patient remains free of disease with normal hematopoiesis and has continued maintenance therapy with denileukin diftitox for 1 year.
  • This case demonstrates clinical improvement of myelofibrosis and acute T-cell leukemia after denileukin diftitox administration, suggesting that denileukin diftitox may affect the paracrine secretion of HTLV-1-associated clinical manifestations of ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Interleukin-2 / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Adult. Biopsy. Bone Marrow / metabolism. Bone Marrow Cells / drug effects. Female. Humans. Remission Induction. Time Factors. Treatment Outcome

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  • (PMID = 14715100.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
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14. 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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  • 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.
  • Initial therapy was begun with imatinib mesylate at 400 mg a day and two dose escalations, one to 600 and second to 800 mg a day, were allowed for patients not achieving a target hematocrit of 44 or less; or a platelet count of less than 600,000/mm(3).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Piperazines / administration & dosage. Polycythemia Vera / drug therapy. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Aged. Benzamides. Dose-Response Relationship, Drug. Female. Gastrointestinal Diseases / blood. Gastrointestinal Diseases / chemically induced. Hematocrit. Humans. Imatinib Mesylate. Male. Middle Aged. Platelet Count. Remission Induction. Skin Diseases / blood. Skin Diseases / chemically induced

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  • [Cites] Exp Hematol. 2007 Jun;35(6):931-8 [17533047.001]
  • [Cites] Hematology. 2000;4(5):381-395 [11399580.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] J Biol Chem. 1997 Mar 14;272(11):6850-3 [9054369.001]
  • [Cites] Blood. 1997 May 15;89(10):3574-81 [9160662.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3370-7 [9345019.001]
  • [Cites] Semin Hematol. 1986 Apr;23(2):132-43 [3704665.001]
  • [Cites] Br J Haematol. 1994 Nov;88(3):497-505 [7529530.001]
  • [Cites] Am J Med Sci. 2003 Mar;325(3):149-52 [12640290.001]
  • [Cites] J Biol Chem. 2005 Jun 17;280(24):22788-92 [15863514.001]
  • [Cites] Am J Hematol. 1984;17(4):329-34 [6496458.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1710-4 [1371882.001]
  • [Cites] Exp Hematol. 2007 Jan;35(1):32-8 [17198871.001]
  • [Cites] Ann Intern Med. 2006 Feb 21;144(4):257-61 [16490911.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1186-7 [12764388.001]
  • [Cites] Biochem J. 1997 Oct 1;327 ( Pt 1):73-80 [9355737.001]
  • [Cites] Int J Hematol. 1992 Apr;55(2):111-5 [1511160.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Br J Haematol. 1994 Jan;86(1):12-21 [7516694.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Transfusion. 2003 Oct;43(10):1366-73 [14507266.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2240-2 [12763928.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Jul 5;791(1-2):39-44 [12798163.001]
  • [Cites] Leukemia. 1994 Apr;8(4):631-7 [7512174.001]
  • (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] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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15. Harrison CN: Essential thrombocythaemia: challenges and evidence-based management. Br J Haematol; 2005 Jul;130(2):153-65
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  • This condition is dominated by thrombotic and haemorrhagic complications and, in the long-term, by risk of transformation to myelofibrosis and/or acute leukaemia.
  • Here, a review of current concepts in disease aetiology and management is offered with reference to recent focused reviews where appropriate.
  • In addition, five specific areas are discussed in detail: the role of the trephine biopsy, the disease entity prefibrotic myelofibrosis; the recently described Janus kinase 2 (JAK2) mutations; the leukaemogenicity of hydroxyurea (hydroxycarbamide); and lastly, the implications of the results of the Medical Research Council Primary Thrombocythaemia 1 study are explored.
  • [MeSH-major] Thrombocythemia, Essential / drug therapy
  • [MeSH-minor] Evidence-Based Medicine. Humans. Randomized Controlled Trials as Topic

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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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16. Hoffman R: Quality of life issues in patients with essential thrombocythemia and polycythemia vera. Semin Oncol; 2002 Jun;29(3 Suppl 10):3-9
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  • Essential thrombocythemia and polycythemia vera are both chronic progressive myeloproliferative disorders of insidious onset.
  • However, the clinical course of these patients can be complicated by a variety of events, including thrombotic episodes, bleeding episodes, arthropathies, pruritus, weakness, weight loss, neurologic impairment, erythromelalgia, fever, abdominal pain, and the life-threatening consequences of progression to myelofibrosis and/or acute leukemia.
  • Effective control of hematopoiesis by phlebotomy or a variety of therapeutic agents has resulted in a reduction or elimination of many of these clinical events, but has not altered the evolution to myelofibrosis or acute leukemia.
  • Use of each of these therapeutic strategies is also associated with a range of adverse events.
  • Monitoring overall survival or a reduction in the frequency of clinical events has previously served as a means of assessing the results of these therapeutic interventions.
  • Quality-of-life instruments have not been applied in a systematic fashion to the evaluation of outcomes in patients with these chronic myeloproliferative disorders.
  • Quality-of-life assessments evaluate not only the state of well-being of a patient that results from an assessment of the individual's ability to perform everyday activities, which are reflective of physical, psychological, and social well-being, but also patient satisfaction with the control of disease and/or treatment-related symptoms.
  • Quality-of-life instruments have been used to assess the clinical course of patients suffering from a variety of disorders, ranging from cancer to renal failure to chronic fatigue syndrome.
  • Information about quality-of-life outcomes can contribute to the evaluation of variations in dose and timing of administration of therapeutic agents.
  • It is possible that the side effects of a particular therapy may outweigh the disease regression achieved with a particular therapy.

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  • [Copyright] Copyright 2002, Elsevier Science (USA). All rights reserved.
  • (PMID = 12096351.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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17. Finazzi G, Harrison C: Essential thrombocythemia. Semin Hematol; 2005 Oct;42(4):230-8
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  • Significant progress in our understanding of the molecular pathogenesis of essential thrombocythemia (ET) and the other Philadelphia (Ph) chromosome-negative myeloproliferative disorders (MPDs) has recently been achieved.
  • Unfortunately, the diagnosis of ET still relies on a set of exclusion criteria developed years ago, as recent advances have yet to be evaluated for this purpose.
  • The clinical course of ET is characterized by an increased incidence of thrombotic and hemorrhagic complications and an inherent tendency to progress into myelofibrosis or acute myeloid leukemia (AML).
  • Myelosuppressive agents are not recommended in low-risk patients, whereas controlled studies support the therapeutic value of hydroxyurea (HU) plus aspirin in high-risk cases.
  • [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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18. 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-major] Antihypertensive Agents / therapeutic use. Portal Vein / radiography. Venous Thrombosis / drug therapy
  • [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


19. Petrides PE: [Primary thrombocythemia: diagnosis and therapy]. Med Klin (Munich); 2006 Aug 15;101(8):624-34
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  • [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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20. 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.
  • Evaluation of long-term leukemogenic risk of currently available drugs, therefore, is crucial.
  • 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.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Hydroxyurea / therapeutic use. Pipobroman / therapeutic use. Polycythemia Vera / drug therapy. Thrombocythemia, Essential / drug therapy
  • [MeSH-minor] Drug Therapy, Combination. Female. Humans. Interferon-alpha / adverse effects. Interferon-alpha / therapeutic use. Janus Kinase 2. Leukemia / chemically induced. Leukemia / etiology. Male. Mutation. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / etiology. Prospective Studies. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Randomized Controlled Trials as Topic. Retrospective Studies. Time Factors

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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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21. Barbui T, Finazzi G: Evidence-based management of polycythemia vera. Best Pract Res Clin Haematol; 2006;19(3):483-93
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  • The clinical course of polycythemia vera is marked by significant thrombotic complications and a variable risk of the disease turning either into myeloid metaplasia with myelofibrosis or into acute myeloid leukemia.
  • However, there is concern that certain myelosuppressive drugs accelerate the disease progression to acute leukemia.
  • This chapter provides updated estimates of the risk of thrombosis and disease progression and evaluates the various randomized and observational studies in polycythemia vera, according to an evidence-based approach.
  • [MeSH-minor] Evidence-Based Medicine. Humans. Hydroxyurea / therapeutic use. Interferon-alpha / therapeutic use. Middle Aged. Platelet Aggregation Inhibitors / therapeutic use

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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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22. Gilbert HS: Modern treatment strategies in polycythemia vera. Semin Hematol; 2003 Jan;40(1 Suppl 1):26-9
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  • Polycythemia vera (PV), one of the chronic myeloproliferative disorders (MPD), is characterized by predominant erythroid proliferation and secondary platelet proliferation, and by progression from a proliferative stage to a metastatic phase and finally a malignant phase.
  • These characteristics expose patients to increased risk for thrombohemorrhagic complications, myeloid metaplasia, myelofibrosis, and acute leukemic conversion irrespective of treatments.
  • Currently, there are three agents-hydroxyurea (HU), interferon-alfa (IFN-alpha), and anagrelide-that differ in mechanisms of action and in treating specific phenotypic manifestations of PV, suggesting a potential role for combination therapy.
  • Because of the differing risks for long-term complications associated with these agents, age is an important variable in selecting treatments.
  • [MeSH-major] Polycythemia Vera / drug therapy. Polycythemia Vera / therapy
  • [MeSH-minor] Age Factors. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Drug Therapy, Combination. Humans. Hydroxyurea / therapeutic use. Interferon-alpha / therapeutic use. Phlebotomy. Platelet Aggregation Inhibitors / therapeutic use. Quinazolines / therapeutic use. Risk Factors

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  • [Copyright] Copyright 2003 Elsevier Inc. All rights reserved.
  • (PMID = 12682879.001).
  • [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 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 40
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23. 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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  • 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.
  • However, the expectation that these drugs could selectively target mutant cells and cause a molecular remission, similar to the experience with imatinib in chronic myelogenous leukemia, has been largely unmet.

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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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24. 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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  • [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.
  • The improved diagnostic certainty these molecular markers provide have resulted in the modification, and simplification, of the World Health Organization (WHO) diagnostic algorithms for MPDs.
  • No current medical therapy has altered the natural trend of the MPDs to lead to overt severe myelofibrosis or acute leukemia.
  • Investigations into targeted therapies for MPDs are proceeding at a brisk pace with agents aimed at immunomodulation, decreasing marrow stromal reaction to the aberrant clone, DNA hypomethylation, or the inhibition of tyrosine kinases.
  • 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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25. Paydas S, Disel U, Yavuz S, Ergin M: Fludarabine as the possible cause of acute myelofibrosis. Hematol J; 2004;5(3):283-4
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fludarabine as the possible cause of acute myelofibrosis.

  • Genetic Alliance. consumer health - Myelofibrosis.
  • Hazardous Substances Data Bank. FLUDARABINE .
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  • (PMID = 15167919.001).
  • [ISSN] 1466-4860
  • [Journal-full-title] The hematology journal : the official journal of the European Haematology Association
  • [ISO-abbreviation] Hematol. J.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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26. Takabayashi M, Sakai R, Kanamori H, Ishigatsubo Y: Successful treatment with intermediate dose cytosine arabinoside for myelodysplastic syndrome with acute myelofibrosis. Leuk Lymphoma; 2003 May;44(5):891-2
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with intermediate dose cytosine arabinoside for myelodysplastic syndrome with acute myelofibrosis.
  • [MeSH-major] Cytarabine / administration & dosage. Myelodysplastic Syndromes / drug therapy. Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Acute Disease. Humans. Male. Middle Aged. Remission Induction / methods. Treatment Outcome






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