[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 230
1. Steensma DP, Gibbons RJ, Mesa RA, Tefferi A, Higgs DR: Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia. Eur J Haematol; 2005 Jan;74(1):47-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia.
  • OBJECTIVE: Acquired somatic point mutations in RUNX1/CBFA2/AML1 have recently been described in a subset of patients with myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML).
  • Given the importance of core-binding factor in megakaryocytic differentiation and platelet production, as well as the central role of megakaryocytes in the pathophysiology of myelofibrosis with myeloid metaplasia (MMM), we hypothesised that RUNX1 gene mutations might be common in MMM.
  • In addition, it is unclear whether patients with MDS-associated acquired alpha thalassaemia (ATMDS), a special subgroup with a very high incidence of point mutations in the ATRX gene, have an especially high incidence of RUNX1 mutations.
  • [MeSH-major] DNA-Binding Proteins / genetics. Myelodysplastic Syndromes / genetics. Point Mutation. Primary Myelofibrosis / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics


2. Mesa RA, Quintás-Cardama A, Verstovsek S: Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia. Curr Hematol Malig Rep; 2007 Feb;2(1):25-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia.
  • Myelofibrosis with myeloid metaplasia (MMM) is currently classified as a classic (ie, BCR-ABL-negative) myeloproliferative disorder characterized by anemia, multiorgan extramedullary hematopoiesis, constitutional symptoms, and premature death from either leukemic transformation or other disease complications.
  • Current pharmacologic therapy has been beneficial mainly in terms of palliating disease-associated cytopenias, constitutional symptoms, splenomegaly, and other organ damage from excess myeloproliferation.
  • [MeSH-major] Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Aged. Alkylating Agents / therapeutic use. Anemia / drug therapy. Anemia / etiology. Antimetabolites, Antineoplastic / therapeutic use. Blood Coagulation Disorders / drug therapy. Blood Coagulation Disorders / etiology. Disease Progression. Drug Delivery Systems. Drugs, Investigational / therapeutic use. Erythropoietin / therapeutic use. Hematopoiesis, Extramedullary / drug effects. Humans. Immunologic Factors / therapeutic use. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / drug therapy. Middle Aged. Mutation, Missense. Palliative Care. Point Mutation. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Signal Transduction / drug effects. Thrombocytopenia / drug therapy. Thrombocytopenia / etiology

  • Genetic Alliance. consumer health - Myelofibrosis.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Med Hypotheses. 2003 Aug;61(2):244-7 [12888313.001]
  • [Cites] Eur J Haematol. 1988 Oct;41(4):375-81 [3197824.001]
  • [Cites] Br J Haematol. 1994 Mar;86(3):654-6 [8043450.001]
  • [Cites] Br J Haematol. 1994 Sep;88(1):1-8 [7803229.001]
  • [Cites] Mayo Clin Proc. 2003 Oct;78(10):1223-33 [14531481.001]
  • [Cites] Blood. 2001 Mar 15;97(6):1896 [11263440.001]
  • [Cites] Br J Haematol. 2001 Jul;114(1):78-83 [11472348.001]
  • [Cites] Scand J Haematol. 1984 Nov;33(5):453-9 [6515328.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4714-6 [12595304.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1013-8 [8704209.001]
  • [Cites] Eur J Haematol. 2005 Mar;74(3):273-4 [15693801.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):1071-9 [10071302.001]
  • [Cites] J Immunol. 1995 Jun 1;154(11):6040-7 [7751646.001]
  • [Cites] Br J Haematol. 2002 Mar;116(3):576-81 [11849213.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Jul 5;14(13):3581-4 [15177479.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]
  • [Cites] Eur J Haematol. 2001 May;66(5):324-7 [11422412.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2534-41 [12517815.001]
  • [Cites] Nat Rev Drug Discov. 2005 May;Suppl:S6-7 [15962522.001]
  • [Cites] Blood. 2005 May 15;105(10):4115-9 [15671439.001]
  • [Cites] J Med Chem. 2002 Feb 28;45(5):999-1001 [11855979.001]
  • [Cites] Blood. 2002 May 15;99(10):3854-6 [11986248.001]
  • [Cites] Cancer Res. 2000 Apr 15;60(8):2178-89 [10786682.001]
  • [Cites] Blood. 1987 Oct;70(4):1014-9 [3115331.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3948-56 [15883410.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3665-7 [11369668.001]
  • [Cites] Haematologica. 1998 Jul;83(7):616-21 [9718866.001]
  • [Cites] Br J Haematol. 1990 May;75(1):4-9 [2375922.001]
  • [Cites] Blood. 2005 Feb 1;105(3):986-93 [15459012.001]
  • [Cites] Blood. 2003 Jun 15;101(12):5087-8; author reply 5088-9 [12788793.001]
  • [Cites] Nat Rev Drug Discov. 2004 Dec;3(12):1011-22 [15573100.001]
  • [Cites] J Med Chem. 2004 Aug 26;47(18):4494-506 [15317461.001]
  • [Cites] Br J Haematol. 2005 Nov;131(3):320-8 [16225651.001]
  • [Cites] Cancer. 2003 Apr 15;97(8):1920-8 [12673719.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2226-33 [10733489.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2319-27 [9116275.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1699-705 [15471948.001]
  • [Cites] Br J Haematol. 1997 Nov;99(2):352-7 [9375753.001]
  • [Cites] J Immunol. 2000 Aug 15;165(4):2271-7 [10925316.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7954-61 [15520202.001]
  • [Cites] N Engl J Med. 2000 Apr 27;342(17):1255-65 [10781623.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1158-64 [16609064.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2252-4 [11877307.001]
  • [Cites] Curr Pharm Des. 2006;12(3):387-94 [16454752.001]
  • [Cites] Blood. 2005 Feb 1;105(3):973-7 [15388582.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] Blood. 2003 May 1;101(9):3597-605 [12531805.001]
  • [Cites] Br J Haematol. 2001 Jul;114(1):111-3 [11472354.001]
  • [Cites] Haematologica. 2000 Jun;85(6):595-9 [10870115.001]
  • [Cites] Eur J Haematol. 2005 Feb;74(2):117-20 [15654901.001]
  • [Cites] Bioorg Med Chem Lett. 1999 Jun 7;9(11):1625-30 [10386948.001]
  • [Cites] Am J Hematol. 1999 May;61(1):10-5 [10331505.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] J Clin Oncol. 2004 Feb 1;22(3):424-31 [14752066.001]
  • [Cites] Histol Histopathol. 2004 Oct;19(4):1245-60 [15375769.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3281-9 [15833861.001]
  • [Cites] Ann Hematol. 2001 Feb;80(2):79-82 [11261329.001]
  • [Cites] Br J Haematol. 2004 Nov;127(4):399-403 [15521916.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Mol Cell Biol. 1999 Mar;19(3):1831-40 [10022870.001]
  • [Cites] Br J Haematol. 1998 Aug;102(3):684-90 [9722294.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3912-8 [12920019.001]
  • [Cites] Leuk Lymphoma. 2002 Dec;43(12):2301-7 [12613516.001]
  • [Cites] Cancer. 2006 Feb 1;106(3):623-30 [16369987.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Jun;305(3):1222-32 [12649301.001]
  • (PMID = 20425385.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antimetabolites, Antineoplastic; 0 / Drugs, Investigational; 0 / Immunologic Factors; 0 / Protein Kinase Inhibitors; 11096-26-7 / Erythropoietin; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 76
  •  go-up   go-down


3. Weitzman G, Schamberg NJ, Lake-Bakaar G: Synergism between hepatocellular injury and shunting in portosystemic encephalopathy (PSE): case report of acute brittle TIPS-induced PSE. Dig Dis Sci; 2007 Nov;52(11):3270-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergism between hepatocellular injury and shunting in portosystemic encephalopathy (PSE): case report of acute brittle TIPS-induced PSE.
  • [MeSH-major] Hepatic Encephalopathy / etiology. Portasystemic Shunt, Transjugular Intrahepatic / adverse effects. Primary Myelofibrosis / complications
  • [MeSH-minor] Acute Disease. Aged. Biopsy. Fatal Outcome. Female. Humans. Postoperative Complications. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Surg Oncol. 2001 May;77(1):42-8 [11344482.001]
  • [Cites] Semin Liver Dis. 1986 May;6(2):97-106 [3529410.001]
  • [Cites] World J Gastroenterol. 2005 Aug 28;11(32):5053-6 [16124065.001]
  • [Cites] N Engl J Med. 1995 May 4;332(18):1192-7 [7700312.001]
  • [Cites] Liver. 2001 Oct;21(5):361-4 [11589774.001]
  • [Cites] Hepatology. 1994 Jul;20(1 Pt 1):46-55 [8020904.001]
  • [Cites] Lancet. 2005 Apr 16-22;365(9468):1384-5; author reply 1385-6 [15836879.001]
  • [Cites] Am J Gastroenterol. 1999 Jul;94(7):1918-22 [10406260.001]
  • [Cites] J Vasc Interv Radiol. 1997 Jan-Feb;8(1 Pt 1):129-32 [9025052.001]
  • [Cites] Blood. 1979 Mar;53(3):515-8 [760865.001]
  • [Cites] J Gastroenterol Hepatol. 2002 Dec;17 Suppl 3:S260-7 [12472947.001]
  • [Cites] Am J Clin Pathol. 1980 Nov;74(5):693-6 [7446477.001]
  • [Cites] Am J Med. 1966 Sep;41(3):360-8 [5914111.001]
  • [Cites] J Vasc Interv Radiol. 1996 Mar-Apr;7(2):263-7 [9007808.001]
  • [Cites] Hepatogastroenterology. 2002 Nov-Dec;49(48):1645-8 [12397754.001]
  • [Cites] Hum Pathol. 1972 Jun;3(2):265-76 [5028623.001]
  • [Cites] Liver. 1998 Apr;18(2):73-89 [9588766.001]
  • [Cites] J Biol Chem. 1980 Jan 25;255(2):627-31 [6766129.001]
  • [Cites] Dig Dis Sci. 2003 Mar;48(3):542-50 [12757168.001]
  • [Cites] Hepatology. 2003 Mar;37(3):558-61 [12601353.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2226-33 [10733489.001]
  • [Cites] J Am Coll Nutr. 1995 Apr;14(2):152-8 [7790689.001]
  • [Cites] Ann Intern Med. 1969 Apr;70(4):763-71 [5771533.001]
  • [Cites] Am J Med. 1962 May;32:758-64 [13911166.001]
  • [Cites] Lancet. 2005 Jan 29-Feb 4;365(9457):431-3 [15680459.001]
  • [Cites] Am J Gastroenterol. 2001 Jul;96(7):1968-76 [11467622.001]
  • [Cites] Gastroenterol Clin North Am. 1988 Jun;17(2):265-87 [3049345.001]
  • [Cites] Can Med Assoc J. 1977 Oct 8;117(7):771-2 [907949.001]
  • [Cites] Clin Nucl Med. 1999 Jul;24(7):507-10 [10402004.001]
  • [Cites] Gastroenterology. 1998 Jun;114(6):1296-303 [9609767.001]
  • [Cites] Acta Haematol. 1991;85(4):184-8 [1677228.001]
  • [Cites] J Gastroenterol Hepatol. 1998 Sep;13(9):907-13 [9794189.001]
  • [Cites] Scand J Haematol. 1978 Aug;21(2):81-93 [308689.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4246-7 [12043694.001]
  • [Cites] Gut. 1999 May;44(5):754-8 [10205219.001]
  • [Cites] J Hepatol. 2000;32(1 Suppl):171-80 [10728803.001]
  • [Cites] Wien Klin Wochenschr. 2001 Mar 15;113(5-6):208-11 [11293952.001]
  • [Cites] AJR Am J Roentgenol. 1997 Dec;169(6):1727-31 [9393198.001]
  • [Cites] Clin Sci. 1970 Jan;38(1):73-84 [5411484.001]
  • [Cites] Am J Gastroenterol. 1993 Dec;88(12 ):2095-7 [8249979.001]
  • (PMID = 17638078.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


Advertisement
4. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Myelofibrosis.
  • Genetic Alliance. consumer health - Transplantation.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


5. Kornblihtt LI, Vassalllu PS, Heller PG, Lago NR, Alvarez CL, Molinas FC: Primary myelofibrosis in a patient who developed primary biliary cirrhosis, autoimmune hemolytic anemia and fibrillary glomerulonephritis. Ann Hematol; 2008 Dec;87(12):1019-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary myelofibrosis in a patient who developed primary biliary cirrhosis, autoimmune hemolytic anemia and fibrillary glomerulonephritis.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / complications. Glomerulonephritis / complications. Liver Cirrhosis, Biliary / complications. Primary Myelofibrosis / complications
  • [MeSH-minor] Aged. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / complications


6. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - Stroke.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


7. Goh BK, Chen JJ, Tan HK, Yong WS, Chan WH: Acute variceal bleed in a patient with idiopathic myelofibrosis successfully treated with endoscopic variceal band ligation. Dig Dis Sci; 2007 Jan;52(1):173-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute variceal bleed in a patient with idiopathic myelofibrosis successfully treated with endoscopic variceal band ligation.
  • [MeSH-major] Esophageal and Gastric Varices / surgery. Gastrointestinal Hemorrhage / complications. Primary Myelofibrosis / complications
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Dilatation, Pathologic. Endoscopy, Gastrointestinal. Humans. Ligation. Male. Splenic Vein / pathology. Splenomegaly / diagnostic imaging. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Myelofibrosis.
  • MedlinePlus Health Information. consumer health - Gastrointestinal Bleeding.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Gastroenterol. 1965 Dec;44(6):536-44 [5891822.001]
  • [Cites] Dig Dis Sci. 2001 Apr;46(4):915-9 [11330433.001]
  • [Cites] J Gastroenterol. 1996 Apr;31(2):260-2 [8680548.001]
  • [Cites] Hepatology. 1995 Jun;21(6):1517-22 [7768494.001]
  • [Cites] Cardiovasc Intervent Radiol. 2000 Nov-Dec;23 (6):491-2 [11232905.001]
  • [Cites] Ann Intern Med. 1962 Sep;57:419-40 [14478106.001]
  • [Cites] Gastroenterology. 1974 Mar;66(3):429-32 [4813509.001]
  • [Cites] J Gastroenterol Hepatol. 1999 Apr;14(4):370-5 [10207788.001]
  • [Cites] Gastroenterology. 1987 Apr;92(4):1067-72 [3493936.001]
  • [Cites] Hepatology. 1993 Feb;17(2):246-50 [8428721.001]
  • [Cites] Wien Klin Wochenschr. 2001 Mar 15;113(5-6):208-11 [11293952.001]
  • (PMID = 17195922.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Acute Erythroleukemia.
  • Genetic Alliance. consumer health - Myelofibrosis.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


9. Bock O, Büsche G, Koop C, Schröter S, Buhr T, Kreipe H: Detection of the single hotspot mutation in the JH2 pseudokinase domain of Janus kinase 2 in bone marrow trephine biopsies derived from chronic myeloproliferative disorders. J Mol Diagn; 2006 May;8(2):170-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of the single hotspot mutation in the JH2 pseudokinase domain of Janus kinase 2 in bone marrow trephine biopsies derived from chronic myeloproliferative disorders.
  • The recent discovery of a single point mutation in the JH2 pseudokinase domain of Janus kinase 2 (JAK2) in a considerable fraction of patients has shed light on the molecular pathomechanism in Philadelphia chromosome-negative chronic myeloproliferative disorders (Ph- CMPDs).
  • In a series of proven Ph- CMPDs classified according to World Health Organization criteria (n = 79), we detected the JAK2 mutation in 90% of polycythemia vera, 22% of cellular prefibrotic chronic idiopathic myelofibrosis, 60% of advanced chronic idiopathic myelofibrosis, and 27% of essential thrombocythemia.
  • JAK2 mutation was not detected in Ph+ chronic myeloid leukemia (n = 5), acute myeloid leukemia (n = 10), acute lymphoblastic leukemia (n = 10), secondary erythrocytosis (n = 10), or normal bone marrow (n = 10).
  • Besides providing support in the differential diagnosis of reactive versus neoplastic myeloproliferations, this newly developed assay reveals considerable overlaps between histologically different disease entities, indicating that additional genetic alterations might be responsible for the established differences of CMPD subentities.
  • [MeSH-major] Bone Marrow / metabolism. Myeloproliferative Disorders / enzymology. Myeloproliferative Disorders / genetics. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Base Sequence. Biopsy. Chronic Disease. Fusion Proteins, bcr-abl / genetics. Hematopoiesis. Humans. Janus Kinase 2. Molecular Sequence Data. Mutation / genetics. Neoplasms. RNA, Messenger / genetics. Restriction Mapping

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mol Diagn. 2003 Feb;5(1):54-60 [12552081.001]
  • [Cites] Am J Clin Pathol. 2003 Jan;119(1):152-8 [12520711.001]
  • [Cites] Diagn Mol Pathol. 2003 Sep;12(3):119-23 [12960692.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4187-90 [15817681.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] N Engl J Med. 2000 Apr 27;342(17):1255-65 [10781623.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3387-95 [10779328.001]
  • [Cites] Int J Hematol. 2001 Feb;73(2):170-6 [11372728.001]
  • [Cites] Anal Biochem. 2001 Aug 1;295(1):116-7 [11476553.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3334-58 [12032773.001]
  • [Cites] Int J Hematol. 2002 Aug;76(2):133-45 [12215011.001]
  • [Cites] Int J Hematol. 2002 Aug;76 Suppl 2:6-8 [12430892.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1869-71 [12730106.001]
  • (PMID = 16645202.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Protein-Tyrosine Kinases; 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
  • [Other-IDs] NLM/ PMC1867581
  •  go-up   go-down


10. Sundström G, Hultdin M, Engström-Laurent A, Dahl IM: Bone marrow hyaluronan and reticulin in patients with malignant disorders. Med Oncol; 2010 Sep;27(3):618-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow hyaluronan and reticulin in patients with malignant disorders.
  • Myelofibrosis is commonly seen in patients with chronic myeloproliferative diseases and sometimes in myelodysplastic syndrome, acute leukaemia and lymphoproliferative diseases.
  • Earlier studies have shown that there is a positive correlation between hyaluronan and reticulin staining in healthy volunteers and in patients with de novo acute myeloid leukaemia.
  • In this study bone marrow biopsies from 43 patients with a malignant disease involving the bone marrow were compared with 18 patients with a malignant disease not involving the bone marrow.
  • The intensity of hyaluronan grading was significantly higher in the patients with disease involving the bone marrow compared to the healthy controls but not compared to the patients without disease involving the bone marrow.
  • The staining intensity of reticulin in the bone marrow was significantly higher in the patients with disease involving the bone marrow, compared to those without disease involving the bone marrow and to the controls.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Extracellular Matrix / chemistry. Female. Humans. Male. Middle Aged. Primary Myelofibrosis / etiology. Primary Myelofibrosis / metabolism. Primary Myelofibrosis / pathology

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. HYALURONIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4581-4 [11717316.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4593-6 [11717318.001]
  • [Cites] Med Oncol. 2007;24(1):63-70 [17673813.001]
  • [Cites] Cell Stem Cell. 2008 Mar 6;2(3):198-200 [18371444.001]
  • [Cites] Leuk Res. 1993 May;17(5):421-7 [8501969.001]
  • [Cites] Anal Cell Pathol. 1991 Jul;3(4):225-31 [1883746.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]
  • [Cites] J Intern Med. 1997 Jul;242(1):27-33 [9260563.001]
  • [Cites] Semin Cancer Biol. 2008 Aug;18(4):288-95 [18468453.001]
  • [Cites] Eur J Haematol. 1992 Apr;48(4):208-14 [1592101.001]
  • [Cites] Haematologica. 2005 Aug;90(8):1128-32 [16079113.001]
  • [Cites] Med Oncol. 2005;22(1):71-8 [15750199.001]
  • [Cites] Biochem J. 1986 May 1;235(3):903 [16744177.001]
  • [Cites] Eur J Haematol. 2002 Apr;68(4):194-202 [12071934.001]
  • [Cites] Cancer. 1974 May;33(5):1399-410 [4823484.001]
  • [Cites] Med Oncol. 2004;21(4):325-31 [15579916.001]
  • [Cites] Blood. 1958 Jul;13(7):609-30 [13560561.001]
  • [Cites] Br J Haematol. 1979 Oct;43(2):185-90 [508627.001]
  • [Cites] Leuk Lymphoma. 1994;14 Suppl 1:1-12 [7820038.001]
  • [Cites] Biochim Biophys Acta. 1979 Jun 19;578(2):281-9 [486527.001]
  • [Cites] Blood. 2003 Feb 1;101(3):856-62 [12393456.001]
  • [Cites] J Intern Med. 1997 Jul;242(1):35-40 [9260564.001]
  • [Cites] N Engl J Med. 1984 Jan 5;310(1):15-8 [6689734.001]
  • [Cites] Cancer Sci. 2008 Sep;99(9):1720-5 [18564137.001]
  • [Cites] Blood Rev. 1997 Dec;11(4):233-42 [9481452.001]
  • [Cites] N Engl J Med. 2005 Jul 7;353(1):33-45 [16000354.001]
  • [Cites] Am J Clin Pathol. 1971 Jul;56(1):24-31 [5556211.001]
  • [Cites] Eur J Haematol. 1990 Jan;44(1):33-8 [2307218.001]
  • (PMID = 19548126.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reticulin; 9004-61-9 / Hyaluronic Acid
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.


12. Charafeddine KM, Mahfouz RA, Zaatari GS, Ibrahim GY, Muwakkit SA, Najm ND, Farra CG: Essential thrombocythemia with myelofibrosis transformed into acute myeloid leukemia with der(1;15)(q10;q10): case report and literature review. Cancer Genet Cytogenet; 2010 Jul 1;200(1):28-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Essential thrombocythemia with myelofibrosis transformed into acute myeloid leukemia with der(1;15)(q10;q10): case report and literature review.
  • We herein report the first case in the literature, to our knowledge, of a 44-year-old female with essential thrombocythemia and severe myelofibrosis who developed acute myeloid leukemia (AML-M4) with der(1;15)(q10;q10) after 13 years of treatment.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Primary Myelofibrosis / genetics. Thrombocythemia, Essential / genetics


13. Thiele J, Kvasnicka HM: Is it justified to perform a bone marrow biopsy examination in sustained erythrocytosis? Curr Hematol Malig Rep; 2006 Jun;1(2):87-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Significantly extending former descriptions of bone marrow features, a trilineage myeloproliferation (panmyelosis) with a pleomorphous appearance (differences in size) of megakaryopoiesis is a characteristic histopathologic finding in PV.
  • Advanced stages (spent phases) of PV show an increased left-shifted granulocytic proliferation accompanied by reduction of erythroid precursors and progressive myelofibrosis (postpolycythemic myeloid metaplasia).
  • [MeSH-major] Bone Marrow Cells / pathology. Bone Marrow Examination. Polycythemia / pathology. Polycythemia Vera / diagnosis
  • [MeSH-minor] Aged. Blast Crisis / pathology. Cell Lineage. Cohort Studies. Diagnosis, Differential. Disease Progression. Female. Fibrosis. Humans. Iron / analysis. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Sensitivity and Specificity. Single-Blind Method. Stromal Cells / pathology. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / pathology. Unnecessary Procedures

  • Hazardous Substances Data Bank. IRON, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Res Pract. 1993 Mar;189(2):121-32 [8321741.001]
  • [Cites] Am J Clin Pathol. 1993 Apr;99(4):513-25 [8475918.001]
  • [Cites] Ann Hematol. 2004 Jun;83(6):364-70 [15034760.001]
  • [Cites] Ann Hematol. 1999 Nov;78(11):495-506 [10602893.001]
  • [Cites] Int J Hematol. 2002 Aug;76(2):133-45 [12215011.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4272-90 [12393615.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):29-39 [9025160.001]
  • [Cites] Histol Histopathol. 2005 Apr;20(2):633-44 [15736066.001]
  • [Cites] Ann Hematol. 1999 May;78(5):219-22 [10391102.001]
  • [Cites] Pathol Annu. 1979;14 Pt 1:383-403 [390480.001]
  • [Cites] Semin Hematol. 2005 Oct;42(4):206-20 [16210034.001]
  • [Cites] Semin Hematol. 2005 Oct;42(4):184-95 [16210032.001]
  • [Cites] Histol Histopathol. 2005 Jan;20(1):317-28 [15578448.001]
  • [Cites] Eur J Haematol. 1994 Sep;53(3):163-7 [7925859.001]
  • [Cites] Baillieres Clin Haematol. 1998 Dec;11(4):695-720 [10640213.001]
  • [Cites] Eur J Haematol. 1992 Jan;48(1):20-6 [1730276.001]
  • [Cites] Blood. 1994 Feb 1;83(3):744-8 [8298136.001]
  • [Cites] Leuk Lymphoma. 1999 Apr;33(3-4):207-18 [10221501.001]
  • [Cites] Acta Haematol. 2005;113(4):213-9 [15983426.001]
  • [Cites] Clin Lab Haematol. 1999 Oct;21(5):309-16 [10646073.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2862-4 [15985544.001]
  • [Cites] Semin Hematol. 1975 Oct;12(4):433-44 [1198128.001]
  • [Cites] Am J Hematol. 1987 Jun;25(2):191-201 [3605067.001]
  • [Cites] Haematologica. 2005 Aug;90(8):1128-32 [16079113.001]
  • [Cites] Ann Hematol. 1992 Jun;64(6):286-91 [1637884.001]
  • [Cites] Semin Hematol. 1975 Oct;12(4):339-51 [1198126.001]
  • [Cites] Am J Hematol. 1981;10(2):129-36 [6940439.001]
  • [Cites] Clin Lab Haematol. 1979;1(3):189-96 [535313.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:15-29 [8951769.001]
  • [Cites] Semin Hematol. 1986 Apr;23(2):144-55 [3704666.001]
  • [Cites] Ann Intern Med. 1995 Nov 1;123(9):656-64 [7574220.001]
  • [Cites] Ann Hematol. 2005 Jun;84(6):362-7 [15803315.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1144-9 [11830459.001]
  • [Cites] Semin Oncol. 1995 Aug;22(4):307-26 [7638629.001]
  • [Cites] Haematologica. 2001 Apr;86(4):368-74 [11325641.001]
  • [Cites] Acta Haematol. 2005;113(2):137-43 [15802893.001]
  • [Cites] Baillieres Clin Haematol. 1998 Dec;11(4):721-49 [10640214.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;413(5):407-17 [3140482.001]
  • [Cites] Pathol Res Pract. 2001;197(2):77-84 [11261821.001]
  • [Cites] Semin Hematol. 2001 Jan;38(1 Suppl 2):21-4 [11242598.001]
  • [Cites] Semin Hematol. 1999 Jan;36(1 Suppl 2):9-13 [9930551.001]
  • [Cites] Ann Intern Med. 2003 Sep 16;139(6):470-5 [13679323.001]
  • [Cites] Eur J Haematol. 1993 Jan;50(1):41-52 [8436214.001]
  • [Cites] Eur J Haematol. 2000 Jan;64(1):32-41 [10680703.001]
  • (PMID = 20425337.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] E1UOL152H7 / Iron
  • [Number-of-references] 47
  •  go-up   go-down


14. Cornetta K, Laughlin M, Carter S, Wall D, Weinthal J, Delaney C, Wagner J, Sweetman R, McCarthy P, Chao N: Umbilical cord blood transplantation in adults: results of the prospective Cord Blood Transplantation (COBLT). Biol Blood Marrow Transplant; 2005 Feb;11(2):149-60
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Secondary end points included engraftment, graft-versus-host disease, relapse, and long-term survival.
  • Eligibility criteria for malignant and nonmalignant diseases were specified.
  • Subjects with active central nervous system disease, Karnofsky performance status <70%, grade 3 or 4 or primary myelofibrosis, or suitable related donors were excluded.
  • Thirty-four subjects were entered, with a median age of 34.5 years (range, 18.2-55 years).
  • Diagnoses at transplantation included acute myelogenous leukemia (n = 19), acute lymphoblastic leukemia (n = 9), chronic myelogenous leukemia (n = 3), myelodysplastic syndrome (n = 1), paroxysmal nocturnal hemoglobinuria (PNH) (n = 1), and non-Hodgkin lymphoma (n = 1); 94% were classified as poor risk according to National Marrow Donor Program criteria.
  • The findings of high treatment-related mortality and slow engraftment kinetics indicate that CBT should continue to be performed in specialized centers with a research focus on cord blood cells.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Graft vs Host Disease / mortality. Hematologic Neoplasms / mortality
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Female. Graft Survival. Histocompatibility Testing. Humans. Male. Middle Aged. Retrospective Studies. Risk Factors. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15682076.001).
  • [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
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


16. Metzgeroth G, Reiter A, Back W, Anders M, Hehlmann R, Hastka J: Peritoneal haematopoiesis in acute panmyelosis with myelofibrosis. Br J Haematol; 2005 Jul;130(1):1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peritoneal haematopoiesis in acute panmyelosis with myelofibrosis.
  • [MeSH-major] Bone Marrow Cells / pathology. Hematopoiesis, Extramedullary. Myelodysplastic Syndromes / pathology. Peritoneum. Primary Myelofibrosis / pathology

  • Genetic Alliance. consumer health - Myelofibrosis.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15982337.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reticulin
  •  go-up   go-down


17. Rain JD: [Polycythemia vera]. Rev Prat; 2005 Oct 15;55(15):1659-68
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Polycythemia vera.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


18. Lee JW, Kim YG, Soung YH, Han KJ, Kim SY, Rhim HS, Min WS, Nam SW, Park WS, Lee JY, Yoo NJ, Lee SH: The JAK2 V617F mutation in de novo acute myelogenous leukemias. Oncogene; 2006 Mar 2;25(9):1434-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The JAK2 V617F mutation in de novo acute myelogenous leukemias.
  • A missense somatic mutation in JAK2 gene (JAK2 V617F) has recently been reported in chronic myeloproliferative disorders, including polycythemia vera, essential thrombocythemia and myelofibrosis with myeloid metaplasia, strongly suggesting its role in the pathogenesis of myeloid disorders.
  • As activation of JAK2 signaling is occurred in other malignancies as well, we have analysed 558 tissues from common human cancers, including colon, breast and lung carcinomas, and 143 acute adulthood leukemias by polymerase chain reaction -- single strand conformation polymorphism analysis.
  • We found three JAK2 mutations in the 113 acute myelogenous leukemias (AMLs) (2.7%), but none in other cancers.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16247455.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [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
  •  go-up   go-down


19. Daskalakis M, Blagitko-Dorfs N, Hackanson B: Decitabine. Recent Results Cancer Res; 2010;184:131-57
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


20. Brière JB: Essential thrombocythemia. Orphanet J Rare Dis; 2007;2:3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1996 Jun;93(4):962-5 [8703834.001]
  • [Cites] Clin Lab Haematol. 1995 Sep;17(3):217-20 [8719893.001]
  • [Cites] Am J Hematol. 1996 Sep;53(1):6-10 [8813089.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:15-29 [8951769.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:31-40 [8951770.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):577-83 [10997967.001]
  • [Cites] Haematologica. 2000 Nov;85(11):1126-34 [11064463.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4261-6 [11110700.001]
  • [Cites] Mayo Clin Proc. 2001 Jan;76(1):22-8 [11155408.001]
  • [Cites] Br J Haematol. 2000 Dec;111(3):943-53 [11122159.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:149-60 [8951786.001]
  • [Cites] Blood. 1997 Jan 1;89(1):128-34 [8978285.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):29-39 [9025160.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):51-4 [9025162.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):179-84 [9136963.001]
  • [Cites] Br J Haematol. 1997 May;97(2):453-6 [9163613.001]
  • [Cites] Semin Thromb Hemost. 1997;23(4):371-7 [9263354.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3370-7 [9345019.001]
  • [Cites] Blood. 1997 Nov 15;90(10):4031-8 [9354672.001]
  • [Cites] Am J Hematol. 1997 Nov;56(3):168-72 [9371529.001]
  • [Cites] Blood. 1998 Jan 15;91(2):616-22 [9427717.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1091-6 [9694695.001]
  • [Cites] Br J Haematol. 1998 Dec;103(3):772-7 [9858229.001]
  • [Cites] Blood. 1999 Jan 15;93(2):417-24 [9885203.001]
  • [Cites] Leukemia. 1999 Feb;13(2):150-4 [10025886.001]
  • [Cites] Br J Haematol. 1999 Mar;104(4):929 [10192463.001]
  • [Cites] Ann Hematol. 1999 May;78(5):219-22 [10391102.001]
  • [Cites] Ann Hematol. 1999 Sep;78(9):389-92 [10525825.001]
  • [Cites] Am J Med. 2004 Nov 15;117(10):755-61 [15541325.001]
  • [Cites] Am J Obstet Gynecol. 2004 Dec;191(6):2016-20 [15592285.001]
  • [Cites] Br J Haematol. 2005 Feb;128(3):275-90 [15667529.001]
  • [Cites] Br J Haematol. 2005 Mar;128(5):583-92 [15725078.001]
  • [Cites] Leuk Res. 2005 May;29(5):481-91 [15755500.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] Br J Haematol. 2005 May;129(3):293-306 [15842653.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Br J Haematol. 2005 May;129(4):553-60 [15877740.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4187-90 [15817681.001]
  • [Cites] N Engl J Med. 2005 Jul 7;353(1):33-45 [16000354.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:57-63 [8951773.001]
  • [Cites] Blood. 2006 Sep 15;108(6):2037-40 [16709929.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3548-55 [16873677.001]
  • [Cites] Leukemia. 2007 Feb;21(2):277-80 [17251900.001]
  • [Cites] Br J Haematol. 2002 Apr;117(1):47-53 [11918532.001]
  • [Cites] Thromb Haemost. 2002 May;87(5):802-7 [12038780.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1596-601 [12176877.001]
  • [Cites] Br J Haematol. 2002 Sep;118(3):786-90 [12181046.001]
  • [Cites] Am J Hematol. 2002 Sep;71(1):1-6 [12221665.001]
  • [Cites] Leukemia. 2002 Oct;16(10):2078-83 [12357360.001]
  • [Cites] Ann Hematol. 2003 Mar;82(3):148-52 [12634946.001]
  • [Cites] Best Pract Res Clin Haematol. 2003 Jun;16(2):227-42 [12763489.001]
  • [Cites] Clin Appl Thromb Hemost. 1999 Apr;5(2):131-5 [10725994.001]
  • [Cites] Clin Appl Thromb Hemost. 1999 Oct;5(4):247-51 [10726022.001]
  • [Cites] Haematologica. 2000 May;85(5):492-5 [10800165.001]
  • [Cites] Eur J Haematol. 2000 Aug;65(2):132-9 [10966175.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):153-65 [16029444.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1847-9 [16079890.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):208-13 [16197451.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2862-4 [15985544.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:201-8 [16304381.001]
  • [Cites] Lancet. 2005 Dec 3;366(9501):1945-53 [16325696.001]
  • [Cites] Br J Haematol. 2006 Jan;132(2):244-5 [16398659.001]
  • [Cites] Haematologica. 2006 Feb;91(2):169-75 [16461300.001]
  • [Cites] Blood. 2006 May 1;107(9):3676-82 [16373657.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):171-3 [16673273.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):174-207 [16673274.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):219-30 [16673276.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):231-45 [16673277.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):246-50 [16673278.001]
  • [Cites] Semin Thromb Hemost. 2006 Apr;32(3):251-9 [16673279.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4214-22 [16484586.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1181-3 [16598303.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2397-405 [16639737.001]
  • [Cites] Blood. 2006 Jul 1;108(1):346-52 [16537803.001]
  • [Cites] Semin Thromb Hemost. 2006 Jun;32(4 Pt 2):381-98 [16810614.001]
  • [Cites] Ann Hematol. 1999 Oct;78(10):437-44 [10550553.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Ann Hematol. 1999 Dec;78(12):539-43 [10647877.001]
  • [Cites] Ann Hematol. 2000 Jan;79(1):40-2 [10663620.001]
  • [Cites] Cancer. 2003 Jul 1;98(1):100-9 [12833462.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1869-71 [12730106.001]
  • [Cites] Am J Hematol. 2003 Sep;74(1):26-31 [12949887.001]
  • [Cites] Haematologica. 2003 Oct;88(10):1130-8 [14555309.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:200-24 [14633783.001]
  • [Cites] N Engl J Med. 2004 Jan 8;350(2):114-24 [14711910.001]
  • [Cites] Haematologica. 2004 Feb;89(2):215-32 [15003898.001]
  • [Cites] Hematol J. 2004;5(2):161-7 [15048067.001]
  • [Cites] Ann Hematol. 2004 Jun;83(6):364-70 [15034760.001]
  • [Cites] Pathol Biol (Paris). 2004 Jun;52(5):267-74 [15217712.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):504-12 [15164229.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):495-7 [15175894.001]
  • [Cites] J Clin Oncol. 1990 Mar;8(3):556-62 [2307991.001]
  • [Cites] Cancer. 1991 May 15;67(10):2658-63 [2015567.001]
  • [Cites] Br J Haematol. 1993 Feb;83(2):198-203 [8457467.001]
  • [Cites] Acta Haematol. 1994;91(2):84-8 [8023650.001]
  • [Cites] Ann Hematol. 2001 Feb;80(2):74-8 [11261328.001]
  • [Cites] Exp Hematol. 2001 Jun;29(6):670-6 [11378261.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):855-61 [11886392.001]
  • [Cites] Haematologica. 1993 Nov-Dec;78(6 Suppl 2):18-21 [8039753.001]
  • [Cites] N Engl J Med. 1995 Apr 27;332(17):1132-6 [7700286.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):748-56 [7772511.001]
  • (PMID = 17210076.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hematologic Agents; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 108
  • [Other-IDs] NLM/ PMC1781427
  •  go-up   go-down


21. Lichtman MA: Chronic megakaryocytic leukemia, misnamed chronic idiopathic myelofibrosis, has neoplastic not hyperplastic megakaryocytopoiesis. Blood; 2007 Oct 15;110(8):3085-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic megakaryocytic leukemia, misnamed chronic idiopathic myelofibrosis, has neoplastic not hyperplastic megakaryocytopoiesis.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Megakaryocytes / pathology. Primary Myelofibrosis / pathology. Terminology as Topic
  • [MeSH-minor] Chronic Disease. Humans. Hyperplasia

  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Blood. 2007 Aug 1;110(3):986-93 [17473062.001]
  • (PMID = 17916755.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  •  go-up   go-down


22. Kröger N, Zabelina T, Schieder H, Panse J, Ayuk F, Stute N, Fehse N, Waschke O, Fehse B, Kvasnicka HM, Thiele J, Zander A: Pilot study of reduced-intensity conditioning followed by allogeneic stem cell transplantation from related and unrelated donors in patients with myelofibrosis. Br J Haematol; 2005 Mar;128(5):690-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study of reduced-intensity conditioning followed by allogeneic stem cell transplantation from related and unrelated donors in patients with myelofibrosis.
  • A prospective pilot study was performed to evaluate the effect of reduced-intensity conditioning with busulphan (10 mg/kg), fludarabine (180 mg/qm) and anti-thymocyte globulin followed by allogeneic stem cell transplantation from related (n = 8) and unrelated donors (n = 13) in 21 patients with myelofibrosis.
  • Acute graft-versus-host disease (GvHD) grades II-IV and III/IV occurred in 48% and 19% of cases and 55% of the patients had chronic GvHD.
  • Haematological response was seen in 100% and complete histopathological remission was observed in 75% of the patients and 25% of the patients showed partial histopathological remission with a continuing decline in the grade of fibrosis.
  • After a median follow-up of 22 months (range, 4-59), the 3-year estimated overall and disease-free survival was 84% (95% CI: 67-100%).
  • [MeSH-major] Blood Transfusion, Autologous. Lymphocyte Transfusion. Primary Myelofibrosis / surgery. Stem Cell Transplantation / methods. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Antilymphocyte Serum / administration & dosage. Busulfan / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / prevention & control. Humans. Immunosuppressive Agents / administration & dosage. Male. Middle Aged. Pilot Projects. Prospective Studies. Survival Rate. Transplantation Chimera

  • Genetic Alliance. consumer health - Myelofibrosis.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15725091.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  •  go-up   go-down


23. McMullin MF: A review of the therapeutic agents used in the management of polycythaemia vera. Hematol Oncol; 2007 Jun;25(2):58-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The acquired clonal disorder Polycythaemia Vera leads to increased erythropoiesis, myelopoiesis and megakaryopoeisis.
  • These anomalies result in an increased incidence of thromboembolic events, transformation to acute leukaemia and myelofibrosis.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. PIPOBROMAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2007 John Wiley & Sons, Ltd.
  • (PMID = 17352450.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 6Q99RDT97R / Pipobroman; 9008-11-1 / Interferons; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 72
  •  go-up   go-down


24. Poitras JL, Dal Cin P, Aster JC, Deangelo DJ, Morton CC: Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia. Genes Chromosomes Cancer; 2008 Oct;47(10):884-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia.
  • Activating mutations in JAK2 are found in virtually all patients with polycythemia vera, and about half of those with essential thrombocythemia and primary myelofibrosis.
  • In addition, less common aberrations (particularly gene fusions) involving JAK2 have been described in acute leukemias.
  • With the advent of JAK2 inhibitor trials in myeloproliferative disorders, tumors with JAK2 mutations or rearrangements have become candidates for targeted therapy.
  • In this report, we identify SSBP2 as a new JAK2 fusion partner in a patient with pre-B cell acute lymphocytic leukemia.
  • This finding adds to the expanding compendium of JAK2 aberrations found in various hematopoietic malignancies, as well as the potential need for a diagnostic FISH analysis in the appropriate clinical setting.
  • [MeSH-minor] Acute Disease. Adult. Humans. In Situ Hybridization, Fluorescence. Male. Mutation. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18618714.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA066996-11A1
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / SSBP2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


25. Sanchez PV, Perry RL, Sarry JE, Perl AE, Murphy K, Swider CR, Bagg A, Choi JK, Biegel JA, Danet-Desnoyers G, Carroll M: A robust xenotransplantation model for acute myeloid leukemia. Leukemia; 2009 Nov;23(11):2109-17
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A robust xenotransplantation model for acute myeloid leukemia.
  • Xenotransplantation of human acute myeloid leukemia (AML) in immunocompromised animals has been critical for defining leukemic stem cells.
  • [MeSH-major] Disease Models, Animal. Leukemia, Myeloid, Acute / pathology. Mice, Inbred NOD. Neoplasm Transplantation / methods. Transplantation, Heterologous / methods
  • [MeSH-minor] Animals. Humans. Mice. Mice, SCID. Point Mutation. Primary Myelofibrosis / pathology. Receptors, Interleukin-2 / genetics. Severity of Illness Index. T-Lymphocytes, Cytotoxic / pathology. fms-Like Tyrosine Kinase 3 / genetics


26. Shimada A, Hayashi Y, Ogasawara M, Park MJ, Katoh M, Minakami H, Kitoh T, Kojima S, Kawa K, Kimura H: Pro-inflammatory cytokinemia is frequently found in Down syndrome patients with hematological disorders. Leuk Res; 2007 Sep;31(9):1199-203
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Down syndrome (DS) patients are frequently complicated with infections, autoimmune phenomena and hematological disorders, including transient abnormal myelopoiesis (TAM) in infancy and acute megakaryoblastic leukaemia (AMKL) in later life.
  • These abnormal cytokinemia may have a role in the pathophysiology of TAM, MDS and AMKL in DS, especially in liver fibrosis or myelofibrosis.
  • [MeSH-major] Cytokines / blood. Down Syndrome / blood. Hematologic Diseases / immunology. Leukemia, Megakaryoblastic, Acute / blood. Myelodysplastic Syndromes / blood
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Humans. Infant. Infant, Newborn. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / immunology


27. Di Nisio M, Barbui T, Di Gennaro L, Borrelli G, Finazzi G, Landolfi R, Leone G, Marfisi R, Porreca E, Ruggeri M, Rutjes AW, Tognoni G, Vannucchi AM, Marchioli R, European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Investigators: The haematocrit and platelet target in polycythemia vera. Br J Haematol; 2007 Jan;136(2):249-59
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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 whose major morbidity and mortality are thrombohaemorragic events and progression to acute leukaemia or myelofibrosis.
  • High platelet count was associated with a lower progression rate to acute leukaemia/myelofibrosis, whereas it had no significant relationship with thrombotic events or mortality.
  • [MeSH-minor] Aged. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Disease Progression. Female. Follow-Up Studies. Hematocrit. Hemorrhage / etiology. Humans. Leukemia / blood. Male. Middle Aged. Platelet Count. Primary Myelofibrosis / blood. Prognosis. Proportional Hazards Models. Prospective Studies. Thrombosis / etiology


28. Corella F, Barnadas MA, Bordes R, Curell R, Espinosa I, Vergara C, Alomar A: [A case of cutaneous extramedullary hematopoiesis associated with idiopathic myelofibrosis]. Actas Dermosifiliogr; 2008 May;99(4):297-300
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of cutaneous extramedullary hematopoiesis associated with idiopathic myelofibrosis].
  • [Transliterated title] Hematopoyesis extramedular cutánea en mielofibrosis idiopática: a propósito de un caso.
  • Cutaneous extramedullary hematopoiesis is a rare manifestation of chronic myeloproliferative processes, mainly chronic idiopathic myelofibrosis.
  • The lesions usually appear soon after diagnosis and the possibility of a relationship between splenectomy and the appearance of extramedullary foci of hematopoiesis is still debated.
  • Diagnosis is based on histopathology showing an infiltrate with different combinations of myeloid and erythroid cell precursors and megakaryocytes.
  • Symptomatic treatment is provided alongside treatment of the underlying disease.
  • We report a new case associated with chronic idiopathic myelofibrosis in which foci of cutaneous extramedullary hematopoiesis were observed 9 years after initial diagnosis.
  • The lesions were progressive and the patient went on to develop acute myeloid leukemia.
  • [MeSH-major] Hematopoiesis, Extramedullary. Primary Myelofibrosis / complications. Skin Physiological Phenomena

  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18394406.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


29. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


30. Pasqualucci L, Li S, Meloni G, Schnittger S, Gattenlohner S, Liso A, Di Ianni M, Martelli MP, Pescarmona E, Foa R, Haferlach T, Skoda RC, Falini B: NPM1-mutated acute myeloid leukaemia occurring in JAK2-V617F+ primary myelofibrosis: de-novo origin? Leukemia; 2008 Jul;22(7):1459-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1-mutated acute myeloid leukaemia occurring in JAK2-V617F+ primary myelofibrosis: de-novo origin?
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. Primary Myelofibrosis / genetics

  • Genetic Alliance. consumer health - Myelofibrosis.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18200037.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


31. Vannucchi AM, Guglielmelli P: Advances in understanding and management of polycythemia vera. Curr Opin Oncol; 2010 Nov;22(6):636-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Polycythemia vera.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


32. Tefferi A, Elliott MA, Pardanani A: Atypical myeloproliferative disorders: diagnosis and management. Mayo Clin Proc; 2006 Apr;81(4):553-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical myeloproliferative disorders: diagnosis and management.
  • The World Health Organization system for classification of tumors of the hematopoietic system divides myeloid disorders into acute myeloid leukemia and chronic myeloid disorders based on the presence or absence, respectively, of acute myeloid leukemia--defining morphological and cytogenetic features including the presence of 20% or more myeloblasts in either the bone marrow or the peripheral blood.
  • A recently proposed semimolecular classification system for chronic myeloid disorders recognizes 3 broad categories: the myelodysplastic syndrome, classic myeloproliferative disorders (MPD), and atypical MPD.
  • Classic MPD includes polycythemia vera, essential thrombocythemia, myelofibrosis with myeloid metaplasia, and chronic myeloid leukemia.
  • The current review focuses on the diagnosis and treatment of both molecularly defined and clinicopathologically assigned categories of atypical MPD: chronic myelomonocytic leukemia, juvenile myelomonocytic leukemia, chronic neutrophilic leukemia, chronic basophilic leukemia, chronic eosinophilic leukemia, idiopathic eosinophilia including hypereosinophilic syndrome, systemic mastocytosis, unclassified MPD, and eosinophilic/mast cell disorders associated with mutations of platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB), FGFR1, and KIT.
  • [MeSH-major] Myeloproliferative Disorders
  • [MeSH-minor] Biomarkers, Tumor / genetics. Bone Marrow / pathology. Diagnosis, Differential. Humans

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16610578.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 173
  •  go-up   go-down


33. Shaikh MA, Byrd RP Jr, Roy TM: Pulmonary nocardiosis: an unusual cause of a solitary pulmonary nodule. J Ky Med Assoc; 2006 May;104(5):184-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This infection may be transient and subclinical or may result in an acute or chronic bronchopulmonary process.
  • Although an unusual cause of pulmonary infection in immunocompentent individuals, human nocardiosis is now documented more often in patients whose cell-mediated immunity is compromised by immunosuppression from comorbid disease or as a result of modern medical intervention.
  • The diagnosis is often elusive unless a high index of suspicion is maintained.
  • We present a patient with localized pulmonary nocardiosis who was immunosuppressed by virtue of a myeloproliferative disorder.
  • [MeSH-minor] Aged. Anti-Infective Agents / administration & dosage. Anti-Infective Agents / therapeutic use. Biopsy, Needle. Bronchoscopy. Follow-Up Studies. Humans. Immunocompromised Host. Lung / microbiology. Lung / pathology. Male. Neural Tube Defects / complications. Neural Tube Defects / drug therapy. Primary Myelofibrosis / complications. Primary Myelofibrosis / drug therapy. Radiography, Thoracic. Time Factors. Tomography, X-Ray Computed. Treatment Outcome. Trimethoprim, Sulfamethoxazole Drug Combination / administration & dosage. Trimethoprim, Sulfamethoxazole Drug Combination / therapeutic use

  • Genetic Alliance. consumer health - Nocardiosis.
  • MedlinePlus Health Information. consumer health - Lung Diseases.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TRIMETHOPRIM/SULFAMETHOXAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16734042.001).
  • [ISSN] 0023-0294
  • [Journal-full-title] The Journal of the Kentucky Medical Association
  • [ISO-abbreviation] J Ky Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 8064-90-2 / Trimethoprim, Sulfamethoxazole Drug Combination
  •  go-up   go-down


34. Andrieux JL, Demory JL: Karyotype and molecular cytogenetic studies in polycythemia vera. Curr Hematol Rep; 2005 May;4(3):224-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The most frequent visible alteration is a 20q deletion, also characterized in other myeloproliferative diseases (MPD) and myeloid malignancies; among other chromosomal changes, trisomy 9 appears more common in PV than in other MPDs.
  • When a myelofibrosis complicates the course of the disease, cytogenetic anomalies become quite common with a striking frequency of partial duplication 1q; an evolution towards myelodysplasia or acute leukemia is almost always associated with nonspecific chromosomal aberrations.
  • [MeSH-minor] Cells, Cultured / ultrastructure. Chromosome Deletion. Chromosomes, Human, Pair 13 / ultrastructure. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 20 / ultrastructure. Chromosomes, Human, Pair 8. Chromosomes, Human, Pair 9 / genetics. Chromosomes, Human, Pair 9 / ultrastructure. Disease Progression. Genes. Humans. Middle Aged. Myeloid Cells / ultrastructure. Primary Myelofibrosis / genetics. Thrombophilia / etiology. Trisomy

  • Genetic Alliance. consumer health - Polycythemia vera.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15865876.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 47
  •  go-up   go-down


35. Amemiya S, Akahane M, Takita J, Igarashi T, Ohtomo K: Imaging findings of upper abdominal involvement by acute megakaryoblastic leukaemia. Pediatr Radiol; 2008 Apr;38(4):457-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imaging findings of upper abdominal involvement by acute megakaryoblastic leukaemia.
  • Acute megakaryoblastic leukaemia (AMKL), a relatively rare type of acute myeloid leukaemia, is characterized by frequent involvement of the liver, spleen and lymph nodes in addition to myelofibrosis in children.
  • Diagnosis is difficult both clinically and pathologically, and the hepatic or lymph node involvement is not uncommonly misinterpreted as solid tumour.
  • With the association of splenic lesion and lymphadenopathy, the imaging findings were considered indicative of a haematological disorder.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / diagnosis. Liver Neoplasms / diagnosis
  • [MeSH-minor] Contrast Media. Diagnosis, Differential. Fatal Outcome. Humans. Infant. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed. Ultrasonography

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2000 Jan;14(1):216-8 [10637500.001]
  • [Cites] Radiographics. 1994 Nov;14 (6):1291-307 [7855342.001]
  • [Cites] AJR Am J Roentgenol. 1999 Oct;173(4):1063-4 [10511179.001]
  • [Cites] Histopathology. 1995 Apr;26(4):311-21 [7607619.001]
  • [Cites] Am J Clin Pathol. 1992 Aug;98(2):214-21 [1510033.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1495-6 [15920489.001]
  • (PMID = 18172635.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
  •  go-up   go-down


36. Phekoo KJ, Richards MA, Møller H, Schey SA, South Thames Haematology Specialist Committee: The incidence and outcome of myeloid malignancies in 2,112 adult patients in southeast England. Haematologica; 2006 Oct;91(10):1400-4
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There is a paucity of epidemiological data on chronic myeloproliferative disorders and myelodysplastic syndromes (MDS), while subtypes of acute myeloid leukemia (AML) are rarely defined.
  • The incidence (European standard population) of AML was 3.00/100,000, that of MDS 3.47/100,000, chronic myelomonocytic leukemia (CMML) 0.46/100,000, idiopathic myelofibrosis (IMF) 0.37/100,000, polycythemia vera (PV) 1.08/100,000, primary thrombocythemia (PT) 1.65/100,000 and chronic myeloid leukemia (CML) 1.09/100,000.
  • [MeSH-major] Myelodysplastic Syndromes / mortality. Myeloproliferative Disorders / mortality


37. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • Genetic Alliance. consumer health - Myelofibrosis.
  • Genetic Alliance. consumer health - Thrombosis.
  • MedlinePlus Health Information. consumer health - Blood Clots.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. MELPHALAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


38. Poiraud C, Gagey-Caron V, Barbarot S, Durant C, Ayari S, Stalder JF: [Cutaneous, mucosal and systemic pyoderma gangrenosum]. Ann Dermatol Venereol; 2010 Mar;137(3):212-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Examination revealed vegetative legions with a purple edge on the lower lip and tongue.
  • Histological examination of the skin and mucosal biopsy samples was consistent with a diagnosis of PG.
  • A chest-abdomen CT scan showed mesenteric panniculitis and interstitial lung disease.
  • The bone marrow sample revealed an appearance of chronic myelomonocytic leukaemia with myelofibrosis and excessively high blast levels.
  • The patient presented secondary worsening of his acute myeloid leukaemia type-IV requiring bone marrow rescue.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Mouth Mucosa / pathology. Pyoderma Gangrenosum / pathology

  • Genetic Alliance. consumer health - Pyoderma gangrenosum.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20227565.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


39. Barbui T, Finazzi G: Evidence-based management of polycythemia vera. Best Pract Res Clin Haematol; 2006;19(3):483-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Polycythemia vera.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


40. Rondelli D, Barosi G, Bacigalupo A, Prchal JT, Popat U, Alessandrino EP, Spivak JL, Smith BD, Klingemann HG, Fruchtman S, Hoffman R, Myeloproliferative Diseases-Research Consortium: Allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning in intermediate- or high-risk patients with myelofibrosis with myeloid metaplasia. Blood; 2005 May 15;105(10):4115-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning in intermediate- or high-risk patients with myelofibrosis with myeloid metaplasia.
  • A total of 21 patients with myelofibrosis with myeloid metaplasia (MMM), with a median age of 54 years (range, 27-68 years), were prepared with a reduced-intensity conditioning (RIC) regimen.
  • Acute graft-versus-host disease (GVHD) grades II to IV was observed in 7 patients, grades III to IV in 2, and extensive chronic GVHD in 8 of 18 evaluable patients.
  • There were 3 patients who died from acute GVHD, infection, and relapse.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Primary Myelofibrosis / complications. Primary Myelofibrosis / therapy. Transplantation Conditioning
  • [MeSH-minor] Adult. Aged. Female. Graft vs Host Disease / immunology. Humans. Male. Middle Aged. Retrospective Studies. Risk Factors. Survival Rate. Time Factors. Transplantation, Homologous


41. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Myelofibrosis.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


42. Nguyen-Khac F, Lesty C, Eclache V, Couronné L, Kosmider O, Andrieux J, Collonge-Rame MA, Penther D, Lafage M, Bilhou-Nabera C, Chapiro E, Mozziconacci MJ, Mugneret F, Gachard N, Nadal N, Lippert E, Struski S, Dastugue N, Cabrol C, Bernard OA, Groupe Francophone de Cytogénétique Hématologique: Chromosomal abnormalities in transformed Ph-negative myeloproliferative neoplasms are associated to the transformation subtype and independent of JAK2 and the TET2 mutations. Genes Chromosomes Cancer; 2010 Oct;49(10):919-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal abnormalities in transformed Ph-negative myeloproliferative neoplasms are associated to the transformation subtype and independent of JAK2 and the TET2 mutations.
  • Evolution to myelofibrosis (MF), acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) may occur over time in myeloproliferative neoplasms (MPN) patients most likely due to the acquisition of additional mutations.
  • Significantly more -7/del(7q) (P = 0.004) and -5/del(5q) (P = 0.03) were found in AML/MDS with a higher incidence of dup1q (P = 0.01) in MF.
  • In multivariate analysis, two factors were independently associated with an inferior overall survival (OS); AML/MDS transformation (P < 0.0001) and -5/del(5q) abnormality (P = 0.02).
  • The mutated and wild-type forms of the genes were not found to be associated with a specific chromosomal abnormality.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20629097.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [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 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


43. O'Malley DP, Orazi A, Wang M, Cheng L: Analysis of loss of heterozygosity and X chromosome inactivation in spleens with myeloproliferative disorders and acute myeloid leukemia. Mod Pathol; 2005 Dec;18(12):1562-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of loss of heterozygosity and X chromosome inactivation in spleens with myeloproliferative disorders and acute myeloid leukemia.
  • Neoplastic myeloid proliferations are seen in the spleens of some patients with acute and chronic myeloproliferative disorders.
  • Both acute myeloid leukemia (AML) and chronic myeloproliferative disorders have a variety of underlying cytogenetic defects that can be evaluated by loss of heterozygosity (LOH) studies.
  • We evaluated the spleens in AML and chronic myeloproliferative disorders with neoplastic myeloid proliferations for the presence of LOH at several chromosome loci, and X-chromosome inactivation.
  • A total of 17 spleens were evaluated (chronic myelogenous leukemia = 6; chronic idiopathic myelofibrosis = 6; essential thrombocythemia = 1; AML arising from previous chronic myeloproliferative disorders = 4).
  • We examined LOH loci 7q (D7S2554), 8q (D8S263), 9p (D9S157, D9S161), 13q (D13S319), common sites of genetic abnormality in chronic myeloproliferative disorders, and TP53.
  • Our results show that allelic losses were common in the neoplastic extramedullary hematopoiesis found in spleens of chronic myeloproliferative disorders and AML.
  • [MeSH-major] Chromosomes, Human, X. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myeloproliferative Disorders / genetics. Spleen / pathology. X Chromosome Inactivation / genetics
  • [MeSH-minor] Bone Marrow Cells / pathology. Chronic Disease. Clone Cells. DNA, Neoplasm / analysis. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Microdissection. Polymerase Chain Reaction. Primary Myelofibrosis / genetics. Primary Myelofibrosis / pathology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16118625.001).
  • [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 / DNA, Neoplasm
  •  go-up   go-down


44. Adamus M: [Substance P as a regulatory peptide of hematopoiesis and blood cell functions]. Postepy Hig Med Dosw (Online); 2009 Mar 02;63:106-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SP seems to be important in the neoplastic transformation of bone marrow, leading to the development of acute leukaemia in children; myelofibrosis and also metastases to bone marrow of solid tumors in early stages of these diseases.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19252469.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Interleukin-3; 0 / Interleukin-6; 33507-63-0 / Substance P; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 87
  •  go-up   go-down


45. Condat B, Valla D: Nonmalignant portal vein thrombosis in adults. Nat Clin Pract Gastroenterol Hepatol; 2006 Sep;3(9):505-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT.
  • Acute PVT usually presents as abdominal pain.
  • Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy.
  • Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease.
  • Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively.
  • A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT.
  • Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.
  • [MeSH-minor] Adult. Clinical Trials as Topic. Humans. Hypertension, Portal / diagnosis. Hypertension, Portal / drug therapy. Hypertension, Portal / etiology. Risk Factors. Tomography, X-Ray Computed. Ultrasonography, Doppler, Color


46. Kirsammer G, Jilani S, Liu H, Davis E, Gurbuxani S, Le Beau MM, Crispino JD: Highly penetrant myeloproliferative disease in the Ts65Dn mouse model of Down syndrome. Blood; 2008 Jan 15;111(2):767-75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Highly penetrant myeloproliferative disease in the Ts65Dn mouse model of Down syndrome.
  • We discovered that Ts65Dn mice display persistent macrocytosis and develop a myeloproliferative disease (MPD) characterized by profound thrombocytosis, megakaryocyte hyperplasia, dysplastic megakaryocyte morphology, and myelofibrosis.
  • Of the 104 trisomic genes in Ts65Dn mice, Aml1/Runx1 attracts considerable attention as a candidate oncogene in DS-acute megakaryoblastic leukemia (DS-AMKL).
  • Surprisingly, trisomy for Aml1/Runx1 is not required for megakaryocyte hyperplasia and myelofibrosis, suggesting that trisomy for one or more of the remaining genes can promote this disease.

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11598-602 [8524811.001]
  • [Cites] Nat Genet. 1995 Oct;11(2):177-84 [7550346.001]
  • [Cites] Clin Genet. 1996 Jan;49(1):15-9 [8721566.001]
  • [Cites] Methods Mol Biol. 1997;68:53-76 [9055250.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):296-308 [10460585.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):613-9 [15895080.001]
  • [Cites] J Biol Chem. 2005 Jun 17;280(24):22788-92 [15863514.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7596-602 [16140924.001]
  • [Cites] J Pediatr. 2005 Dec;147(6):744-7 [16356423.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6224-9 [16603627.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):807-12 [16783379.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] C R Biol. 2006 Sep;329(9):726-32 [16945839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14146-51 [16966598.001]
  • [Cites] Mamm Genome. 2006 Oct;17(10):1005-12 [17019652.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2452-66 [17151367.001]
  • [Cites] Dev Dyn. 2000 Feb;217(2):137-45 [10706138.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):512-24 [10997960.001]
  • [Cites] Am J Med Genet. 2002 Feb 1;107(4):317-24 [11840489.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] Lancet. 2003 May 10;361(9369):1617-20 [12747884.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4298-300 [12560215.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2960-8 [12816863.001]
  • [Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1588-9 [15317736.001]
  • [Cites] Science. 2004 Oct 22;306(5696):687-90 [15499018.001]
  • [Cites] Cancer. 1990 May 15;65(10):2178-84 [2189548.001]
  • [Cites] Am J Med Genet. 1993 Jun 15;46(5):510-2 [8322810.001]
  • [Cites] Prog Clin Biol Res. 1993;384:117-33 [8115398.001]
  • [Cites] Blood. 1995 Jul 1;86(1):1-14 [7795214.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • (PMID = 17901249.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-06; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-06
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ PMC2200841
  •  go-up   go-down


47. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • Genetic Alliance. consumer health - Polycythemia vera.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


48. Pardanani A, Hood J, Lasho T, Levine RL, Martin MB, Noronha G, Finke C, Mak CC, Mesa R, Zhu H, Soll R, Gilliland DG, Tefferi A: TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations. Leukemia; 2007 Aug;21(8):1658-68
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations.
  • JAK2V617F and MPLW515L/K represent recently identified mutations in myeloproliferative disorders (MPD) that cause dysregulated JAK-STAT signaling, which is implicated in MPD pathogenesis.
  • In a human JAK2V617F-expressing acute myeloid leukemia cell line, TG101209-induced cell cycle arrest and apoptosis, and inhibited phosphorylation of JAK2V617F, STAT5 and STAT3.
  • [MeSH-major] Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Janus Kinase 2 / antagonists & inhibitors. Mutation / genetics. Myeloproliferative Disorders / drug therapy. Pyrimidines / pharmacology. Receptors, Thrombopoietin / antagonists & inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Colony-Forming Units Assay. Humans. Janus Kinase 3 / antagonists & inhibitors. Janus Kinase 3 / genetics. Janus Kinase 3 / metabolism. Mice. Mice, SCID. Phosphorylation / drug effects. Polycythemia Vera / drug therapy. Polycythemia Vera / genetics. Polycythemia Vera / metabolism. Primary Myelofibrosis / drug therapy. Primary Myelofibrosis / genetics. Primary Myelofibrosis / metabolism. STAT Transcription Factors / metabolism. Stem Cells / drug effects. Thrombopoietin / metabolism. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17541402.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Pyrimidines; 0 / Receptors, Thrombopoietin; 0 / STAT Transcription Factors; 0 / Sulfonamides; 0 / TG101209; 143641-95-6 / MPL protein, human; 9014-42-0 / Thrombopoietin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3
  •  go-up   go-down


49. Leleu X, Micol JB, Guieze R, Berthon C, Kuhnovsky F, Terriou L, Moreau AS, Yakoub-Agha I, Bauters F, Facon T: [Thalidomide: mechanisms of action and new insights in hematology]. Rev Med Interne; 2005 Feb;26(2):119-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Purpose. - Thalidomide, a major teratogen drug, was rehabilitated mainly in malignant hemopathy.
  • Multiple trials are ongoing, however, the main indication remain multiple myeloma with a response rate of 30% in relapsed patients.
  • The IMiDs, which mechanism is based on stimulation of T lymphopoiesis rather than inhibition of tumour necrosis factor-alpha, are under clinical trials in multiple myeloma with interesting results.

  • MedlinePlus Health Information. consumer health - Blood Disorders.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15710258.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / Immunologic Factors; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Number-of-references] 91
  •  go-up   go-down


50. Wulfert M, Küpper AC, Tapprich C, Bottomley SS, Bowen D, Germing U, Haas R, Gattermann N: Analysis of mitochondrial DNA in 104 patients with myelodysplastic syndromes. Exp Hematol; 2008 May;36(5):577-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Analysis included 104 patients with MDS (24 refractory anemia, 32 refractory anemia with ringed sideroblasts, 34 refractory anemia with excess of blasts, 7 refractory anemia with excess of blasts in transformation to acute leukemia, and 7 chronic myelo-monocytic leukemia), 3 patients with acute myeloid leukemia from MDS, and 36 patients with myeloproliferative disease (23 chronic myeloid leukemia, 9 polycythemia vera, 4 idiopathic myelofibrosis).
  • RESULTS: Heteroplasmic mtDNA mutations, mostly transitions, were identified in 56% of MDS and 44% of myeloproliferative disorders patients.
  • In MDS, mutation frequency increased with age and more-advanced disease.
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Bone Marrow / pathology. Chromatography, High Pressure Liquid / methods. DNA Mutational Analysis. Disease Progression. Humans. Middle Aged. Mutation. Polymerase Chain Reaction / methods. Sensitivity and Specificity


51. Hasselbalch HC, Birgens H, Dufva IH, Dalseg AM, Brown Pde N, Jensen MK, Vangsted A: [Novel medical treatment modalities in hematology]. Ugeskr Laeger; 2008 Jun 9;170(24):2115-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Today several monoclonal antibodies, including the anti-CD20 antibody (rituximab), the anti-CD52 antibody (alemtuzumab) and the anti-CD33 antibody (gemtuzumab ozogamacin) are all integrated in the therapeutic armamentarium of patients with malignant lymphoma, chronic lymphocytic leukaemia and acute myelogenous leukaemia, respectively.
  • Thalidomide, lenalidomide and bortezomib have all been shown to be highly effective in multiple myeloma, and JAK2-inhibitors have entered phase II studies of patients with JAK2-positive primary myelofibrosis and related diseases.
  • [MeSH-minor] Aminoglycosides / therapeutic use. Anemia, Hemolytic / drug therapy. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Benzamides. Benzoates / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Carbazoles / therapeutic use. Carrier Proteins / therapeutic use. Cyclophosphamide / therapeutic use. Dasatinib. Humans. Hydrazines / therapeutic use. Imatinib Mesylate. Indoles / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Multiple Myeloma / drug therapy. Myelodysplastic Syndromes / drug therapy. Piperazines / therapeutic use. Purpura, Thrombocytopenic / drug therapy. Pyrazines / therapeutic use. Pyrazoles / therapeutic use. Pyrimidines / therapeutic use. Receptors, Fc / therapeutic use. Recombinant Fusion Proteins. Rituximab. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. Thiazoles / therapeutic use. Thrombopoietin. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

  • MedlinePlus Health Information. consumer health - Blood Disorders.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18565291.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzoates; 0 / Boronic Acids; 0 / Carbazoles; 0 / Carrier Proteins; 0 / Hydrazines; 0 / Immunologic Factors; 0 / Indoles; 0 / Piperazines; 0 / Pyrazines; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Receptors, Fc; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; 0 / eltrombopag; 0 / gemtuzumab; 0 / romiplostim; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide; 639089-54-6 / VX680; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; 9014-42-0 / Thrombopoietin; A3ULP0F556 / eculizumab; DO989GC5D1 / lestaurtinib; F0P408N6V4 / lenalidomide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; RBZ1571X5H / Dasatinib
  • [Number-of-references] 40
  •  go-up   go-down


52. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


53. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


54. Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP: JAK2 mutation 1849G&gt;T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia. Blood; 2005 Nov 15;106(10):3370-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.
  • An activating 1849G>T mutation of JAK2 (Janus kinase 2) tyrosine kinase was recently described in chronic myeloproliferative disorders (MPDs).
  • The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).
  • No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or acute lymphoblastic leukemia (20 patients).
  • We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the acute phase of these diseases and that it is generally rare in aggressive leukemias.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anal Biochem. 2000 Apr 10;280(1):103-10 [10805527.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1673-84 [12365015.001]
  • [Cites] Arch Pathol Lab Med. 2003 May;127(5):601-5 [12708906.001]
  • [Cites] Cell. 1993 Jul 30;74(2):227-36 [8343951.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]
  • [Cites] Cell. 1998 May 1;93(3):385-95 [9590173.001]
  • [Cites] Blood. 2005 Feb 1;105(3):973-7 [15388582.001]
  • [Cites] Curr Opin Hematol. 2005 Mar;12(2):112-6 [15725900.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2224-32 [15710945.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2662-7 [15805263.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] J Biol Chem. 2005 Jun 17;280(24):22788-92 [15863514.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] Blood. 2002 Feb 1;99(3):840-9 [11806985.001]
  • (PMID = 16037387.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [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
  • [Other-IDs] NLM/ PMC1895065
  •  go-up   go-down


55. Barbui T, Finazzi G: When and how to treat essential thrombocythemia. N Engl J Med; 2005 Jul 7;353(1):85-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Aspirin / therapeutic use. Drug Therapy, Combination. Hemorrhage / etiology. Hemorrhage / prevention & control. Humans. Leukemia, Myeloid, Acute / etiology. Primary Myelofibrosis / etiology. Risk Factors. Thrombosis / etiology. Thrombosis / prevention & control

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • MedlinePlus Health Information. consumer health - Blood Thinners.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] N Engl J Med. 2005 Jul 7;353(1):33-45 [16000354.001]
  • (PMID = 16000360.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide; R16CO5Y76E / Aspirin; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


56. Cervantes F, Passamonti F, Barosi G: Life expectancy and prognostic factors in the classic BCR/ABL-negative myeloproliferative disorders. Leukemia; 2008 May;22(5):905-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Life expectancy and prognostic factors in the classic BCR/ABL-negative myeloproliferative disorders.
  • Among the 'classic' BCR/ABL-negative chronic myeloproliferative disorders, primary myelofibrosis (PMF) is associated with a substantial life-expectancy reduction.
  • In this disease, initial haemoglobin level is the most important prognostic factor, whereas age, constitutional symptoms, low or high leukocyte counts, blood blast cells and cytogenetic abnormalities are also of value.
  • Several prognostic systems have been proposed to identify subgroups of patients with a different risk, which is especially important in younger individuals, who may benefit from therapies with curative potential.
  • With regard to PMF, the possible association of the mutation with shorter survival and higher acute transformation rate is currently being evaluated.
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / mortality

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18385755.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 113
  •  go-up   go-down


57. Hemminki K, Sundquist J, Bermejo JL: Associated cancers in parents and offspring of polycythaemia vera and myelofibrosis patients. Br J Haematol; 2009 Nov;147(4):526-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Associated cancers in parents and offspring of polycythaemia vera and myelofibrosis patients.
  • Polycythaemia vera (PV) and primary myelofibrosis (MF) show concordant familial clustering but limited population level data are available on the aggregation of other discordant neoplasms in these families.
  • Several discordant familial associations were found for PV (acute myeloid leukaemia, Hodgkin disease, prostate and bladder cancers) or for MF (chronic lymphatic leukaemia, colorectal, kidney and cervical cancers) or for both (nervous system, eye and endocrine tumours).
  • [MeSH-major] Polycythemia Vera / genetics. Primary Myelofibrosis / genetics
  • [MeSH-minor] Female. Genetic Predisposition to Disease. Humans. Male. Parents. Registries. Risk Assessment / methods. Siblings. Sweden / epidemiology

  • Genetic Alliance. consumer health - Myelofibrosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19754924.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


58. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


59. Dutta P, Hasan S, Bhattacharyya J, Kumar R, Mahapatra M, Saxena R, Tyagi S, Sazawal S, Pati HP: Acute promyelocytic leukemia with secondary myelofibrosis -- case report and review of the literature. Am J Hematol; 2006 Jun;81(6):476-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukemia with secondary myelofibrosis -- case report and review of the literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Primary Myelofibrosis / pathology


60. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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


61. Levine RL, Heaney M: New advances in the pathogenesis and therapy of essential thrombocythemia. Hematology Am Soc Hematol Educ Program; 2008;:76-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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).

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


62. Spanoudakis E, Tsatalas C: Hemopoiesis in Ph-negative chronic myeloproliferative disorders. Curr Stem Cell Res Ther; 2009 May;4(2):154-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemopoiesis in Ph-negative chronic myeloproliferative disorders.
  • Chronic myeloproliferative disorders (cMPDs) are clonal hemopoietic malignancies arising at the multipotent stem cell level.
  • Vascular events might complicate their course, and transformation to either acute leukemia or myelofibrosis can finally occur.
  • Among cMPDs, Polycythemia Vera (PV), Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF) belong to the group of Ph-negative cMPDs.
  • The mutation in JAK2 kinase is not an example of a genetic defect leading to a single disease, since it occurs in many other myeloid disorders, and probably represents a secondary hit in a multistep ongogenetic process.
  • [MeSH-major] Hematopoiesis / physiology. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / blood. Myeloproliferative Disorders / blood

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19442200.001).
  • [ISSN] 2212-3946
  • [Journal-full-title] Current stem cell research & therapy
  • [ISO-abbreviation] Curr Stem Cell Res Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / STAT Transcription Factors; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 116
  •  go-up   go-down


63. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


64. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


65. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


66. Orazi A: Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases. Pathobiology; 2007;74(2):97-114
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


67. Sever M, Kantarjian H, Pierce S, Jain N, Estrov Z, Cortes J, Verstovsek S: Cytogenetic abnormalities in essential thrombocythemia at presentation and transformation. Int J Hematol; 2009 Nov;90(4):522-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Their role in survival of patients and disease transformation is not extensively studied.
  • At presentation nine (5.2%) patients had cytogenetic abnormality and three (1.7%) additional patients acquired them during follow-up.
  • Five patients (2.9%) with normal karyotype transformed to myelofibrosis (MF) without developing new cytogenetic changes at transformation.
  • Two patients (1.2%) with normal karyotypes at presentation transformed to myelodysplastic syndrome and acute myeloid leukemia, respectively.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blood Cell Count. Chromosome Aberrations. Cytogenetic Analysis. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / genetics. Primary Myelofibrosis / blood. Primary Myelofibrosis / genetics. Young Adult

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Hematol. 2000 Jun;64(2):120-3 [10814992.001]
  • [Cites] Eur J Haematol. 2009 Jul;83(1):17-21 [19236446.001]
  • [Cites] Acta Haematol. 2002;108(2):55-65 [12187022.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] Cancer Genet Cytogenet. 1989 Nov;43(1):57-65 [2790773.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Jul 1;61(1):93-5 [1638486.001]
  • [Cites] Cancer Genet Cytogenet. 1993 Jun;67(2):150 [8330275.001]
  • [Cites] Leukemia. 1995 Mar;9(3):517-8 [7885050.001]
  • [Cites] Ann Hematol. 2005 Apr;84(4):250-7 [15692838.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Jul 1;160(1):76-8 [15949575.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1247-52 [16164981.001]
  • [Cites] Arch Intern Med. 2005 Dec 12-26;165(22):2651-8 [16344424.001]
  • [Cites] Mayo Clin Proc. 2006 Feb;81(2):159-66 [16471068.001]
  • [Cites] Leukemia. 2006 Jan;20(1):168-71 [16270039.001]
  • [Cites] In Vivo. 2006 May-Jun;20(3):381-4 [16724675.001]
  • [Cites] Eur J Haematol. 2006 Sep;77(3):210-6 [16923108.001]
  • [Cites] Leukemia. 2007 Feb;21(2):270-6 [17170720.001]
  • [Cites] Leukemia. 2007 May;21(5):992-7 [17315020.001]
  • [Cites] Leukemia. 2007 May;21(5):1097-9 [17315023.001]
  • [Cites] Leuk Res. 2007 Aug;31(8):1053-62 [17045648.001]
  • [Cites] Blood. 2007 Aug 1;110(3):840-6 [17379742.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1092-7 [17488875.001]
  • [Cites] Int J Hematol. 2007 Aug;86(2):130-6 [17875526.001]
  • [Cites] In Vivo. 2007 Sep-Oct;21(5):867-70 [18019426.001]
  • [Cites] Eur J Haematol. 2008 May;80(5):386-90 [18221390.001]
  • [Cites] Haematologica. 2008 Nov;93(11):1645-51 [18790799.001]
  • [Cites] J Appl Genet. 2009;50(1):73-6 [19193987.001]
  • [Cites] Hum Genet. 2000 Jun;106(6):669-70 [10942117.001]
  • (PMID = 19728024.001).
  • [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] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS635388; NLM/ PMC4209590
  •  go-up   go-down


68. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


69. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9.
  • Coexpression of MN1-TEL and IL-3, but not SCF, rapidly caused a fatal myeloproliferative disease rather than acute myeloid leukemia (AML).
  • Thus, the leukemogenic effect of MN1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • National BioResource Project. culture/stock collections - NBRP resources .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


70. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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%).

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


71. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Polycythemia vera.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


72. Ruiz-Argüelles GJ, Gomez-Almaguer D, Tarin-Arzaga LD, Morales-Toquero A, Cantu-Rodriguez OG, Manzano C: Second allogeneic peripheral blood stem cell transplants with reduced-intensity conditioning. Rev Invest Clin; 2006 Jan-Feb;58(1):34-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eight had a malignant condition (six acute leukemias, one myelofibrosis and one myelodysplasia), eleven individuals were allografted twice from the same donor and in one case, cells from two different umbilical cords were used.
  • Only three patients were successfully rescued with the second transplant, two with acute leukemia and one with aplastic anemia.
  • Seven patients are alive 10-41 months (median 35) after the second transplant, but only three (25%) remain disease-free.
  • [MeSH-minor] Acute Disease. Adult. Anemia, Aplastic / surgery. Child, Preschool. Cohort Studies. Disease-Free Survival. Female. Health Care Costs. Hospitals / statistics & numerical data. Hospitals, University / statistics & numerical data. Humans. Infant. Leukemia / surgery. Male. Mexico. Middle Aged. Neural Tube Defects / surgery. Osteopetrosis / surgery. Primary Myelofibrosis / surgery. Recurrence. Red-Cell Aplasia, Pure / surgery. Reoperation / statistics & numerical data. Survival Analysis. Thalassemia / surgery. Transplantation, Homologous / statistics & numerical data. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16789597.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Mexico
  •  go-up   go-down


73. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Occupational Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


74. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


75. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


76. Jones AV, Kreil S, Zoi K, Waghorn K, Curtis C, Zhang L, Score J, Seear R, Chase AJ, Grand FH, White H, Zoi C, Loukopoulos D, Terpos E, Vervessou EC, Schultheis B, Emig M, Ernst T, Lengfelder E, Hehlmann R, Hochhaus A, Oscier D, Silver RT, Reiter A, Cross NC: Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders. Blood; 2005 Sep 15;106(6):2162-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders.
  • The analysis of rare chromosomal translocations in myeloproliferative disorders has highlighted the importance of aberrant tyrosine kinase signaling in the pathogenesis of these diseases.
  • Of the 480 myeloproliferative disorder (MPD) samples, the proportion of positive cases per disease subtype was 30 (20%) of 152 for atypical or unclassified MPD, 2 of 134 (2%) for idiopathic hypereosinophilic syndrome, 58 of 72 (81%) for polycythemia vera, 24 of 59 (41%) essential thrombocythemia (ET), and 15 of 35 (43%) for idiopathic myelofibrosis.
  • V617F was not identified in patients with systemic mastocytosis (n = 28), chronic or acute myeloid leukemia (n = 35), secondary erythrocytosis (n = 4), or healthy controls (n = 160).
  • [MeSH-major] Mutation, Missense. Myeloproliferative Disorders / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Case-Control Studies. Chronic Disease. Female. Homozygote. Humans. Janus Kinase 2. Male. Microsatellite Repeats. Molecular Epidemiology. Prevalence. Signal Transduction / genetics

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Acta Haematol. 2016;136(2):123-8 [27410038.001]
  • (PMID = 15920007.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


77. Tamaki K, Otaka M, Sakamoto N, Matsumoto K, Yamashina S, Watanabe S: Acute variceal bleeding in a patient with idiopathic myelofibrosis successfully treated with endoscopic variceal band ligation and chemotherapy: a case report. J Med Case Rep; 2010;4:25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Intern Med. 2007;46(4):187-90 [17301514.001]
  • [Cites] Ann Intern Med. 1962 Sep;57:419-40 [14478106.001]
  • [Cites] Am J Gastroenterol. 1965 Dec;44(6):536-44 [5891822.001]
  • [Cites] Am J Clin Pathol. 1989 Mar;91(3):302-5 [2923095.001]
  • [Cites] Medicine (Baltimore). 1971 Sep;50(5):357-420 [4940717.001]
  • [Cites] J Gastroenterol. 1996 Apr;31(2):260-2 [8680548.001]
  • (PMID = 20181038.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2830976
  •  go-up   go-down


78. Toubai T, Tanaka J, Higa T, Ota S, Ibata M, Shono Y, Mashiko S, Miura Y, Umehara S, Kahata K, Toyoshima N, Morioka M, Asaka M, Kasai M, Imamura M: Long-term follow-up of a patient with idiopathic myelofibrosis associated with chromosome 11 and 13 abnormalities. Am J Hematol; 2005 Jan;78(1):67-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up of a patient with idiopathic myelofibrosis associated with chromosome 11 and 13 abnormalities.
  • A case of a leukemic transformation following a 27-year history of idiopathic myelofibrosis (IMF) is presented.
  • This patient's final diagnosis was acute micromegakaryocytic leukemia, and she died 1 month after leukemic transformation with an additional chromosomal abnormality, trisomy 8.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 13 / genetics. Primary Myelofibrosis / genetics
  • [MeSH-minor] Bone Marrow / pathology. Chromosomes, Human, Pair 8 / genetics. Fatal Outcome. Female. Follow-Up Studies. Gene Deletion. Humans. Leukemia, Megakaryoblastic, Acute / genetics. Middle Aged. Trisomy / genetics

  • Genetic Alliance. consumer health - Chromosome 11.
  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15609290.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


79. Mesa RA: Navigating the evolving paradigms in the diagnosis and treatment of myeloproliferative disorders. Hematology Am Soc Hematol Educ Program; 2007;:355-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


80. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


81. Hemminki K, Zhang H, Sundquist J, Lorenzo Bermejo J: Modification of risk for subsequent cancer after female breast cancer by a family history of breast cancer. Breast Cancer Res Treat; 2008 Sep;111(1):165-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SIRs for subsequent neoplasms in women who had a family history of breast cancer were increased for ovarian (2.0) and endometrial (1.8) cancers and for acute lymphoid leukemia (12.7) and myelofibrosis (9.4).
  • The remarkably high risks for second acute lymphoid leukemia and myelofibrosis, both characterized by chromosomal aberrations, in women with a family history of breast cancer may signal heritable defects in the ability to process DNA damage caused by ionizing radiation and chemotherapy.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Neoplasms, Second Primary / genetics

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17899363.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


82. Sakuma T, Hayashi Y, Kanomata N, Murayama T, Matsui T, Kajimoto K, Hanioka K, Chihara K, Maeda S: Histological and cytogenetic characterization of bone marrow in relation to prognosis and diagnosis of myelodysplastic syndromes. Pathol Int; 2006 Apr;56(4):191-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histological and cytogenetic characterization of bone marrow in relation to prognosis and diagnosis of myelodysplastic syndromes.
  • The cellularity in bone marrow histology is sometimes ineffective in the differential diagnosis of MDS and aplastic anemia (AA).
  • Hyperplastic marrow had a significantly high frequency of progress to acute myeloid leukemia (AML) and hypoplastic MDS had a lower rate of progress to AML.
  • Severe myelofibrosis had a significantly poor prognosis.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anemia, Aplastic / pathology. Cytogenetics. Diagnosis, Differential. Female. Humans. Leukemia / complications. Leukemia / epidemiology. Male. Middle Aged. Preleukemia / genetics. Preleukemia / mortality. Preleukemia / pathology. Prognosis. Retrospective Studies. Survival Analysis. Survival Rate


83. Reuss CS, Wilansky S: Images in cardiovascular medicine. Eosinophilic heart disease in acute myeloproliferative disorder. Circulation; 2007 Jun 12;115(23):e614-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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


84. Hsiao HH, Ito Y, Sashida G, Ohyashiki JH, Ohyashiki K: De novo appearance of der(1;7)(q10;p10) is associated with leukemic transformation and unfavorable prognosis in essential thrombocythemia. Leuk Res; 2005 Nov;29(11):1247-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Leukemic transformation or myelofibrosis is a major concern in managing patients with chronic myeloproliferative disorders, including essential thrombocythemia (ET).
  • We analyze the relationship between cytogenetic changes and the transformation in 89 patients with ET; 8 patients experienced transformation, including 2 patients with acute leukemia following myelofibrosis, 3 with acute leukemia, and 3 with myelofibrosis.
  • Among the eight patients showing transformation, two patients developing myelofibrosis derived from a group with normal cytogenetics, but the remaining six were categorized as showing de novo appearance of cytogenetic changes.
  • Two leukemia patients had de novo cytogenetic changes at the time of leukemia diagnosis, whereas two patients with acute leukemia following myelofibrosis showed der(1;7) during their myelofibrosis period.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Primary Myelofibrosis / genetics. Thrombocythemia, Essential / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Rate

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16164981.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


85. Kennedy JA, Barabé F, Patterson BJ, Bayani J, Squire JA, Barber DL, Dick JE: Expression of TEL-JAK2 in primary human hematopoietic cells drives erythropoietin-independent erythropoiesis and induces myelofibrosis in vivo. Proc Natl Acad Sci U S A; 2006 Nov 7;103(45):16930-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of TEL-JAK2 in primary human hematopoietic cells drives erythropoietin-independent erythropoiesis and induces myelofibrosis in vivo.
  • Activation of JAK2 by chromosomal translocation or point mutation is a recurrent event in hematopoietic malignancies, including acute leukemias and myeloproliferative disorders.
  • Here we report that expression of TEL-JAK2, a constitutively active variant of the JAK2 kinase, in lineage-depleted human umbilical cord blood cells results in erythropoietin-independent erythroid differentiation in vitro and induces the rapid development of myelofibrosis in an in vivo NOD/SCID xenotransplantation assay.
  • These studies provide functional evidence that activated JAK2 signaling in primitive human hematopoietic cells is sufficient to drive key processes implicated in the pathophysiology of polycythemia vera and idiopathic myelofibrosis.
  • Furthermore, they describe an in vivo model of myelofibrosis initiated with primary cells, highlighting the utility of the NOD/SCID xenotransplant system for the development of experimental models of human hematopoietic malignancies.
  • [MeSH-major] Erythropoiesis / physiology. Hematopoietic Stem Cells / metabolism. Oncogene Proteins, Fusion / metabolism. Primary Myelofibrosis / etiology

  • Genetic Alliance. consumer health - Myelofibrosis.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Mar 15;95(6):2076-83 [10706877.001]
  • [Cites] Blood. 2002 May 1;99(9):3197-204 [11964283.001]
  • [Cites] Nat Immunol. 2001 Jan;2(1):75-82 [11135582.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1438-48 [12149229.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3495-503 [12393681.001]
  • [Cites] Nat Med. 2003 Jul;9(7):959-63 [12796774.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):952-9 [14737125.001]
  • [Cites] Exp Hematol. 2004 Feb;32(2):179-87 [15102479.001]
  • [Cites] J Exp Med. 2004 Sep 6;200(5):623-35 [15353555.001]
  • [Cites] N Engl J Med. 1974 Jun 13;290(24):1382 [4827655.001]
  • [Cites] Hum Mol Genet. 1995 Feb;4(2):163-72 [7757063.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]
  • [Cites] Science. 1997 Nov 14;278(5341):1309-12 [9360930.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8239-44 [9653171.001]
  • [Cites] EMBO J. 1998 Sep 15;17(18):5321-33 [9736611.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4354-64 [10361134.001]
  • [Cites] Genome Biol. 2004;5(12):253 [15575979.001]
  • [Cites] Leuk Lymphoma. 2005 Feb;46(2):265-72 [15621811.001]
  • [Cites] Leukemia. 2005 Mar;19(3):442-8 [15674417.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2662-7 [15805263.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1259-61 [15878972.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1692-6 [16034466.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):329-33 [16001431.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14398-403 [16172394.001]
  • [Cites] Hum Pathol. 2005 Oct;36(10):1148-51 [16226118.001]
  • [Cites] Oncogene. 2005 Nov 3;24(48):7248-52 [16091753.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7 [16365288.001]
  • [Cites] Leukemia. 2006 Mar;20(3):536-7 [16424865.001]
  • [Cites] Hum Pathol. 2006 Apr;37(4):500; author reply 500-2 [16564930.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4274-81 [16478879.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1652-60 [16670266.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1551-4 [16684963.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2286-92 [11290589.001]
  • [Cites] J Biol Chem. 2001 Aug 31;276(35):32704-13 [11435425.001]
  • [Cites] Mol Cell. 2000 Sep;6(3):693-704 [11030348.001]
  • (PMID = 17077140.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Recombinant Proteins; 0 / TEL-JAK2 fusion protein, human; 11096-26-7 / Erythropoietin
  • [Other-IDs] NLM/ PMC1629449
  •  go-up   go-down


86. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


87. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Myelofibrosis.
  • MedlinePlus Health Information. consumer health - Anemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


88. Toms DR, Cannick L, Stuart RK, Jenrette JM, Terwiliger L: Helical tomotherapy for extramedullary hematopoiesis involving the pericardium in a patient with chronic myeloid leukemia. Jpn J Radiol; 2010 Jul;28(6):476-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The phenomenon occurs in a number of disease states, notably in myelofibrosis, thalassemia, immune thrombocytopenic purpura, sickle cell anemia, polycythemia vera, and myelodysplastic syndrome.
  • The present case report describes a patient with the diagnosis of atypical chronic myeloid leukemia and myelofibrosis who subsequently developed EMH of the pericardium with effusion and tamponade.
  • The patient tolerated treatment well without acute adverse effects.


89. Pardanani A, Lasho TL, Finke CM, Mai M, McClure RF, Tefferi A: IDH1 and IDH2 mutation analysis in chronic- and blast-phase myeloproliferative neoplasms. Leukemia; 2010 Jun;24(6):1146-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH1 and IDH2 mutation analysis in chronic- and blast-phase myeloproliferative neoplasms.
  • Bone marrow DNA was screened for isocitrate dehydrogenase (IDH) mutations in 200 patients with chronic (n=166) or blast (n=34) phase myeloproliferative neoplasms (MPN).
  • Included among the former were 77 patients with primary myelofibrosis (PMF), 47 essential thrombocythemia and 38 polycythemia vera (PV).
  • IDH mutations were seen in only 1 of 12 paired chronic-blast-phase samples and in none of 27 concurrently studied acute myeloid leukemia (AML) patients without antecedent MPN.
  • [MeSH-major] Blast Crisis / genetics. Isocitrate Dehydrogenase / genetics. Mutation / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Aged. Bone Marrow. Chronic Disease. Cohort Studies. Female. Genotype. Humans. Janus Kinase 2 / genetics. Male. Middle Aged. Receptors, Thrombopoietin / genetics

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20410924.001).
  • [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] 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


90. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


91. Sun XM: [Abnormal activation of tyrosine kinases and its role in the pathogenesis of hematological malignancies - review]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):657-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Other than the causative effect of PTK product of the bcr/abl fusion gene on chronic myelogenous leukemia (CML), more evidence suggests that mutated tyrosine kinases are pivotal in the pathogenesis of most of other chronic myeloproliferative disorders, such as chronic myelomonocytic leukemia (CMML) and hypereosinophilic syndrome (HES).
  • And the exciting results in several dependent groups in 2005 showed that a single nucleotide JAK2 somatic mutation (JAK2V617F mutation) was found to be involved in the pathogenesis of polycythemia vera (PV), essential thrombocythemia (ET) and chronic idiopathic myelofibrosis (CIMF).
  • In the leukogenesis of acute myeloid leukemias (AML), the losing of the control of the proliferation of hematopoietic progenitor cells was principally the results of the aberrant PTK activity, such as FLT3 and C-kit overexpression.
  • These upregulated PTK molecules represent attractive disease-specific targets, to which a new class of therapeutic agents are being developed.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17605888.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 15
  •  go-up   go-down


92. Crystal SC, Leonidas J, Jakubowski A, Di Rocco A: Thalidomide induced acute worsening of Parkinson's disease. Mov Disord; 2009 Sep 15;24(12):1863-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thalidomide induced acute worsening of Parkinson's disease.
  • [MeSH-major] Immunosuppressive Agents / adverse effects. Parkinson Disease / etiology. Thalidomide / adverse effects
  • [MeSH-minor] Aged. Humans. Male. Primary Myelofibrosis / complications. Primary Myelofibrosis / drug therapy

  • MedlinePlus Health Information. consumer health - Parkinson's Disease.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19606491.001).
  • [ISSN] 1531-8257
  • [Journal-full-title] Movement disorders : official journal of the Movement Disorder Society
  • [ISO-abbreviation] Mov. Disord.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
  •  go-up   go-down


93. Caramazza D, Hussein K, Siragusa S, Pardanani A, Knudson RA, Ketterling RP, Tefferi A: Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations. Eur J Haematol; 2010 Mar;84(3):191-200
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We show that chromosome 1 abnormalities are most frequent in BCR-ABL-negative classic myeloproliferative neoplasms (MPN): polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
  • Although occasionally seen in chronic phase MPN, unbalanced 1;7 translocations, e.g. der(1;7)(q10;p10), are usually seen in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and post-MPN AML/MDS.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics


94. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematol Pathol. 1992;6(3):161-7 [1429344.001]
  • [Cites] Cancer Genet Cytogenet. 1992 May;60(1):53-9 [1591707.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Nov;57(1):79-85 [1756488.001]
  • [Cites] Am J Hematol. 1997 Dec;56(4):224-9 [9395183.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1883-90 [8946926.001]
  • [Cites] Cancer Genet Cytogenet. 1994 Dec;78(2):181-8 [7828151.001]
  • [Cites] Eur J Haematol. 1988 Oct;41(4):341-6 [3197821.001]
  • (PMID = 23100969.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453485
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Ring chromosome 8 / Trisomy 8
  •  go-up   go-down


95. Infante PF, Tomatis L: Commentary to the paper by P. Bernardini et al "Malattie mieloproliferative da uso di benzina come solvente: descrizione di tre casi" Med Lav 2005; 96: 119-125. Med Lav; 2005 Sep-Oct;96(5):447-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Air Pollutants, Occupational / adverse effects. Benzene / adverse effects. Carcinogens, Environmental / adverse effects. Duty to Warn. Gasoline / adverse effects. Leukemia, Myeloid / chemically induced. Occupational Diseases / chemically induced. Occupational Health / legislation & jurisprudence. Primary Myelofibrosis / chemically induced. Solvents / adverse effects
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow / drug effects. Child. Environmental Exposure. Humans. Inhalation Exposure. Italy. Leukemia, Myeloid, Acute / chemically induced. Male. Metallurgy. Middle Aged. Occupational Exposure. United States

  • MedlinePlus Health Information. consumer health - Occupational Health.
  • Hazardous Substances Data Bank. BENZENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Med Lav. 2005 Mar-Apr;96(2):119-25 [16001511.001]
  • (PMID = 16711648.001).
  • [ISSN] 0025-7818
  • [Journal-full-title] La Medicina del lavoro
  • [ISO-abbreviation] Med Lav
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Air Pollutants, Occupational; 0 / Carcinogens, Environmental; 0 / Gasoline; 0 / Solvents; J64922108F / Benzene
  •  go-up   go-down


96. Tefferi A: Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era. Hematology Am Soc Hematol Educ Program; 2006;:240-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era.
  • JAK2V617F, a somatic gain-of-function mutation involving the JAK2 tyrosine kinase gene, occurs in nearly all patients with polycythemia vera (PV) but also in a variable proportion of patients with other myeloid disorders; mutational frequency is estimated at approximately 50% in both essential thrombocythemia (ET) and myelofibrosis (MF), up to 20% in certain subcategories of atypical myeloproliferative disorder (atypical MPD), less than 3% in de novo myelodysplastic syndrome (MDS) or acute myeloid leukemia, and 0% in chronic myeloid leukemia (CML).
  • Current information on disease-specific prognostic relevance of JAK2V617F is inconclusive and confounded by inter-study differences in the performance of mutation screening assays.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17124067.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 41
  •  go-up   go-down


97. Ozbudak IH, Shilo K, Hale S, Aguilera NS, Galvin JR, Franks TJ: Alveolar airspace and pulmonary artery involvement by extramedullary hematopoiesis: a unique manifestation of myelofibrosis. Arch Pathol Lab Med; 2008 Jan;132(1):99-103
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alveolar airspace and pulmonary artery involvement by extramedullary hematopoiesis: a unique manifestation of myelofibrosis.
  • Pulmonary extramedullary hematopoiesis is a rare manifestation of myelofibrosis.
  • Airspace foci were associated with acute and organizing alveolar hemorrhage, while within arteries the hematopoietic elements had a striking predilection for the vascular intima.
  • Extramedullary hematopoiesis should also be considered as a cause of pulmonary hemorrhage, especially in the setting of myelofibrosis.
  • [MeSH-major] Hematopoiesis, Extramedullary. Primary Myelofibrosis / pathology. Pulmonary Alveoli / pathology. Pulmonary Artery / pathology

  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18181682.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


98. Tefferi A, Spivak JL: Polycythemia vera: scientific advances and current practice. Semin Hematol; 2005 Oct;42(4):206-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Polycythemia vera (PV) is a clonal disorder of unknown etiology involving a multipotent hematopoietic progenitor cell that is characterized by the accumulation of phenotypically normal red blood cells, white blood cells, and platelets in the absence of a definable cause; extramedullary hematopoiesis, marrow fibrosis, and, in a few patients, transformation to acute leukemia can also occur.
  • First described in 1892, the cause of the disease remains unknown and no potentially curative therapy other than bone marrow transplantation is currently available.
  • It is commonly held that PV is a rare disorder, when in fact with a minimum incidence of 2.6 per 100,000 it is more common than chronic myelogenous leukemia (CML) and is particularly prevalent in persons of Ashkenazi Jewish ancestry.
  • However, the incidence of PV is not as high as that of erythrocytosis from other causes collectively, which poses a problem in differential diagnosis when PV presents as isolated erythrocytosis.
  • In current clinical practice, two different clinical approaches have been used to diagnose PV.
  • However, it is very clear that some patients with classical PV lack the JAK2 V617F mutation, while some patients with other chronic myeloproliferative disorders such as idiopathic myelofibrosis (IMF) and essential thrombocytosis (ET) also express the JAK2 V617F mutation.
  • Therefore, by necessity, any discussion of PV must take into consideration these companion myeloproliferative disorders, and since erythrocytosis is the single clinical feature that sets PV apart from IMF and ET, it is clear that the presence of the JAK2 V617F mutation cannot by itself establish a diagnosis of PV.

  • Genetic Alliance. consumer health - Polycythemia vera.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


99. Hussein K, Bock O, Theophile K, Schulz-Bischof K, Porwit A, Schlue J, Jonigk D, Kreipe H: MPLW515L mutation in acute megakaryoblastic leukaemia. Leukemia; 2009 May;23(5):852-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MPLW515L mutation in acute megakaryoblastic leukaemia.
  • The thrombopoietin receptor gene (MPL) is expressed in megakaryocytes and exhibits the gain of function point mutation W515K/L in approximately 5% of patients with primary myelofibrosis/idiopathic myelofibrosis (PMF) representing one subtype of the chronic myeloproliferative disorders (myeloproliferative neoplasm).
  • A series of primary and secondary acute myeloid leukaemias (AML) with megakaryoblastic phenotype and myelofibrosis unrelated to PMF (n=12) was analysed for the MPL(W515K/L) mutation by pyrosequencing.
  • We conclude that MPL(W515L) occurs in a considerable proportion of acute megakaryoblastic leukaemias with myelofibrosis unrelated to PMF.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation / genetics. Primary Myelofibrosis / genetics. Receptors, Thrombopoietin / genetics

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leukemia. 2009 Nov;23(11):2159-60 [19657363.001]
  • (PMID = 19194467.001).
  • [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] 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
  •  go-up   go-down


100. Brière J: [Essential thrombocythemia. Contribution of the V617F JAK2 mutation to the pathophysiology, diagnosis and outcome]. Bull Acad Natl Med; 2007 Mar;191(3):535-48
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Essential thrombocythemia. Contribution of the V617F JAK2 mutation to the pathophysiology, diagnosis and outcome].
  • Secondary thrombocytosis is a reactive process in relation with acute or chronic inflammatory diseases, or asplenia.
  • However, the most frequent causes of chronic thrombocytosis in adults are the so-called chronic myeloproliferative syndromes (chronic myelocytic leukaemia, polycythemia vera, primary myelofibrosis, essential thrombocytemia), and to a lesser extent, myelodysplastic syndromes.
  • In the course of these disorders, thrombocytosis is often the first recognized abnormality.
  • However, this mutation is neither specific nor constant in any of the Philadelphia negative myeloproliferative disorders, which outlines the importance of the WHO criteria of megakaryocytic abnormalities on bone marrow biopsy as the hallmark of Ph negative MPDs.
  • The exclusion of PV and of IMF, including pre fibrotic and early fibrotic forms is still required for the diagnosis of "true" ET.
  • Disease stratification and treatment strategy are targeted on the evaluation and prevention of vascular complications.
  • Acute leukaemia or myelodysplasia, and other clonal progressions like myelofibrotic transformation, are infrequent and delayed events.
  • [MeSH-minor] Adult. Biopsy. Bone Marrow / pathology. Cohort Studies. Diagnosis, Differential. Disease Progression. Female. Humans. Male. Middle Aged. Mutation. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics. Philadelphia Chromosome. Polycythemia Vera / diagnosis. Polycythemia Vera / genetics. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / genetics. Prognosis. Risk Factors. World Health Organization

  • Genetic Alliance. consumer health - Essential Thrombocythemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18072652.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 56
  •  go-up   go-down






Advertisement