[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 98 of about 98
1. Gregory TK, Wald D, Chen Y, Vermaat JM, Xiong Y, Tse W: Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics. J Hematol Oncol; 2009;2:23
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] Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.
  • Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation.
  • In approximately 60% of cases, specific recurrent chromosomal aberrations can be identified by modern cytogenetic techniques.
  • Currently, favorable risk AML patients are usually treated with contemporary chemotherapy while poor risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist.
  • The largest subgroup of AML patients (aproximately 40%) have no identifiable cytogenetic abnormalities and are classified as intermediate risk.
  • Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic AML (NC-AML).
  • Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q.
  • Further prospective studies are needed to confirm if poorer risk NC-AML patients have improved clinical outcomes after more aggressive therapy.
  • [MeSH-major] Genetic Markers. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cytogenetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Neoplasm, Residual. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Prognosis. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / physiology



2. Gupta M, Raghavan M, Gale RE, Chelala C, Allen C, Molloy G, Chaplin T, Linch DC, Cazier JB, Young BD: Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia. Genes Chromosomes Cancer; 2008 Sep;47(9):729-39
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 regions of acquired uniparental disomy discovered in acute myeloid leukemia.
  • The acquisition of uniparental disomy (aUPD) in acute myeloid leukemia (AML) results in homozygosity for known gene mutations.
  • We therefore aimed to develop a map of the regions of aUPD in AML.
  • Here, we have analyzed a large set of diagnostic AML samples (n = 454) from young adults (age: 15-55 years) using genotype arrays.
  • Novel recurrent regions of aUPD were uncovered at 2p, 17p, 2q, 17q, 1p, and Xq.
  • This study demonstrates aUPD is a frequent and significant finding in AML and pinpoints regions that may contain novel mutational targets.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Uniparental Disomy / genetics
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 13 / genetics. DNA Mutational Analysis. Humans. Middle Aged. Models, Genetic. Mutation

  • 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
  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18506749.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



3. Peniket A, Wainscoat J, Side L, Daly S, Kusec R, Buck G, Wheatley K, Walker H, Chatters S, Harrison C, Boultwood J, Goldstone A, Burnett A: Del (9q) AML: clinical and cytological characteristics and prognostic implications. Br J Haematol; 2005 Apr;129(2):210-20
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] Del (9q) AML: clinical and cytological characteristics and prognostic implications.
  • Del (9q) is a recurrent cytogenetic abnormality in acute myeloid leukaemia (AML).
  • We report an analysis of 81 patients with del(9q) as a diagnostic karyotypic abnormality entered into the Medical Research Council AML trials 10, 11 and 12.
  • It is likely that the deletion of single or multiple tumour suppressor genes located in this region may underlie the pathogenesis of del (9q) AML.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Disease-Free Survival. Female. Genetic Markers. Humans. Male. Middle Aged. Survival Rate. Translocation, Genetic

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Br J Haematol. 2005 Sep;130(6):969; author reply 969 [16156871.001]
  • (PMID = 15813849.001).
  • [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 / Genetic Markers
  •  go-up   go-down



Advertisement
4. Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Isolated extramedullary relapse presenting as autologous lymphocyte response. Am J Hematol; 2008 Jun;83(6):512-4
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.
  • Isolated EMR in the CNS is a relatively rare form of recurrent leukemia.
  • We report here a case of a 38-year-old man with inv(16) acute myeloid leukemia (AML, M2) who suffered a central nervous system (CNS) relapse after allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor.
  • His leukemia relapsed in the CNS 2.5 years after the allogeneic BMT.
  • Lumbar puncture revealed 780/muL white blood cells with 67.3% leukemia cells and 32.7% mature lymphocytes.
  • Fluorescent in situ hybridization (FISH) using a probe for the Y chromosome demonstrated that both leukemia cells and lymphocytes in the cerebrospinal fluid (CSF) were derived from the recipient, although the bone marrow cells were from the donor.
  • No leukemia cells with inv(16) were detected by FISH in the bone marrow.
  • This is the first report to clarify the chimerism of lymphocytes in the CSF of patients with isolated EMR in the CNS after allogeneic SCT, in which analysis revealed that autologous immunologic cells rather than donor lymphocytes responded to the recurrent isolated leukemic cells in CNS.
  • This observation suggests that the CNS is a "sanctuary" site not only from chemotherapy but also from the graft-versus-leukemia effect.
  • The present case contributes to our understanding of the possibility of immunological escape phenomenon of recurrent leukemia cells in extramedullary sites.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Bone Marrow Transplantation / methods. Humans. Male. Recurrence. Sarcoma, Myeloid. Transplantation Chimera

  • 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 2008 Wiley-Liss, Inc.
  • (PMID = 18306363.001).
  • [ISSN] 1096-8652
  • [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



5. Rau R, Brown P: Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity. Hematol Oncol; 2009 Dec;27(4):171-81
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] Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity.
  • Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in adult acute myeloid leukaemia (AML), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK) AML.
  • In children, NPM1 mutations are far less frequent, occurring in 8-10% of all AML cases, and in approximately 25% of those with a NK.
  • NPM1 mutations lead to aberrant localization of the NPM protein into the cytoplasm, thus the designation, NPMc+ AML.
  • NPMc+ AML is seen predominantly in patients with a NK and is essentially mutually exclusive of recurrent chromosomal translocations.
  • NPMc+ AML is also characterized by a unique gene expression signature and microRNA signature.
  • NPMc+ AML has important prognostic significance, as NPMc+ AML, in the absence of a coexisting FLT3-ITD mutation, is associated with a favourable outcome.
  • Given its distinctive biologic and clinical features and its clear clinical relevance, NPMc+ AML is included as a provisional entity in the 2008 WHO classifications.
  • Further, it represents a potential therapeutic target warranting research aimed at identifying novel small molecules with activity in NPMc+ AML.

  • 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
  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • [Cites] Leukemia. 2007 Jul;21(7):1564-6 [17410190.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1566-70 [17443224.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6230-7 [17616680.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2000-9 [17597811.001]
  • [Cites] Int J Hematol. 2007 Aug;86(2):143-6 [17875528.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]
  • [Cites] Leukemia. 2008 Jan;22(1):195-8 [17637812.001]
  • [Cites] J Biol Chem. 2008 Feb 29;283(9):5728-37 [18165222.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1234-40 [18401421.001]
  • [Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]
  • [Cites] J Pathol. 1996 Jan;178(1):48-52 [8778315.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]
  • [Cites] Cell. 1997 Nov 28;91(5):649-59 [9393858.001]
  • [Cites] J Soc Gynecol Investig. 1997 Nov-Dec;4(6):298-304 [9408885.001]
  • [Cites] FEBS Lett. 1997 Dec 22;420(1):25-7 [9450543.001]
  • [Cites] Nat Cell Biol. 1999 May;1(1):20-6 [10559859.001]
  • [Cites] Cell. 2000 Sep 29;103(1):127-40 [11051553.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • [Cites] FEBS Lett. 2001 Oct 12;506(3):272-6 [11602260.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1053-68 [12040437.001]
  • [Cites] Nat Cell Biol. 2002 Jul;4(7):529-33 [12080348.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Biosci Biotechnol Biochem. 2002 Oct;66(10):2239-42 [12450141.001]
  • [Cites] Mol Cell. 2003 Feb;11(2):415-24 [12620229.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1738-52 [12970773.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):985-96 [14729947.001]
  • [Cites] Science. 2004 Apr 23;304(5670):594-6 [15105502.001]
  • [Cites] Cancer Cell. 2004 May;5(5):465-75 [15144954.001]
  • [Cites] Genes Dev. 2004 Aug 1;18(15):1862-74 [15289458.001]
  • [Cites] J Biol Chem. 2004 Aug 20;279(34):35726-34 [15190079.001]
  • [Cites] FEBS Lett. 2004 Sep 24;575(1-3):112-8 [15388344.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]
  • [Cites] Haematologica. 2008 Mar;93(3):439-42 [18268276.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] Leuk Lymphoma. 2007 Nov;48(11):2141-4 [17990177.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3859-62 [18212245.001]
  • [Cites] Oncogene. 2008 Apr 10;27(17):2382-9 [17968318.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Leukemia. 2008 May;22(5):1075-8 [17972951.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1285-9 [18059485.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9327-38 [15485902.001]
  • [Cites] Cell. 1989 Feb 10;56(3):379-90 [2914325.001]
  • [Cites] J Biol Chem. 1990 Oct 25;265(30):18227-33 [2211699.001]
  • [Cites] Cancer Res. 1992 Jun 15;52(12):3372-7 [1596895.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Biol Chem. 1994 Dec 9;269(49):30994-8 [7527039.001]
  • [Cites] Cancer Res. 1995 Apr 15;55(8):1625-8 [7712464.001]
  • [Cites] Nucleic Acids Res. 1995 Oct 11;23(19):3974-9 [7479045.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Oncogene. 2006 Jul 20;25(31):4376-80 [16501600.001]
  • [Cites] J Cell Biol. 2008 Jul 14;182(1):19-26 [18625840.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2041-7 [18668134.001]
  • [Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]
  • [Cites] Nucleic Acids Res. 1998 Oct 1;26(19):4508-15 [9742256.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3706-11 [10097101.001]
  • [Cites] Protein Sci. 1999 Apr;8(4):905-12 [10211837.001]
  • [Cites] Prostate. 1999 Jun 1;39(4):298-304 [10344220.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):10988-96 [15644315.001]
  • [Cites] Biochem J. 2005 May 15;388(Pt 1):7-15 [15737070.001]
  • [Cites] Blood. 2005 Aug 1;106(3):899-902 [15831697.001]
  • [Cites] Nat Cell Biol. 2005 Aug;7(8):823-30 [16041368.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(17):7534-45 [16107701.001]
  • [Cites] Nature. 2005 Sep 1;437(7055):147-53 [16007073.001]
  • [Cites] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • [Cites] Cell Cycle. 2005 Nov;4(11):1593-8 [16205118.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3044-50 [16540653.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]
  • [Cites] Mol Cell Biol. 2006 May;26(10):3798-809 [16648475.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Br J Haematol. 2006 Jun;133(6):638-41 [16704439.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4514-23 [16455950.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1147-8 [16870548.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Leuk Res. 2007 Jan;31(1):109-11 [16678898.001]
  • [Cites] Trends Mol Med. 2006 Dec;12(12):580-7 [17071139.001]
  • [Cites] Nature. 2006 Nov 30;444(7119):638-42 [17136094.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4146-55 [16926285.001]
  • [Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]
  • [Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]
  • [Cites] Leuk Res. 2007 Apr;31(4):427-34 [17161457.001]
  • [Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]
  • [Cites] Leukemia. 2007 May;21(5):998-1004 [17361227.001]
  • [Cites] APMIS. 2007 Apr;115(4):341-6 [17504301.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1307 [17315018.001]
  • (PMID = 19569254.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111728-05; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / K23 CA111728-05
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Number-of-references] 102
  • [Other-IDs] NLM/ NIHMS234930; NLM/ PMC3069851
  •  go-up   go-down



6. Kuwahara E, Otsuji Y, Iguro Y, Ueno T, Zhu F, Mizukami N, Kubota K, Nakashiki K, Yuasa T, Yu B, Uemura T, Takasaki K, Miyata M, Hamasaki S, Kisanuki A, Levine RA, Sakata R, Tei C: Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase after surgical annuloplasty: importance of augmented posterior leaflet tethering. Circulation; 2006 Jul 4;114(1 Suppl):I529-34
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] Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase after surgical annuloplasty: importance of augmented posterior leaflet tethering.
  • BACKGROUND: Surgical annuloplasty can potentially hoist the posterior annulus anteriorly, exaggerate posterior leaflet (PML) tethering, and lead to recurrent ischemic/functional mitral regurgitation (MR).
  • METHODS AND RESULTS: In 30 patients with surgical annuloplasty for ischemic MR and 20 controls, the anterior leaflet (AML) and PML tethering angles relative to the line connecting annuli, posterior and apical displacement of the coaptation and the MR grade were measured by echocardiography before, early after, and late after surgery.
  • Early after surgery, grade of MR and AML tethering generally decreased (P<0.01), whereas PML tethering significantly worsened (P<0.01).
  • Nine of the 30 patients showed recurrent/persistent MR late after surgery.
  • CONCLUSIONS: Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to recurrent/persistent ischemic/functional MR late after surgical annuloplasty.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chronic Disease. Coronary Artery Bypass. Female. Humans. Incidence. Male. Middle Aged. Motion. Papillary Muscles / pathology. Recurrence. Treatment Failure

  • COS Scholar Universe. author profiles.
  • 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 = 16820632.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



7. Grandics P: Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy. J Altern Complement Med; 2006 Apr;12(3):311-5
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] Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy.
  • OBJECTIVES: The aim of this study was to determine the possible clinical benefit of molasses-based dietary compositions (designated as MSQ 13, MSQ 15, and MSQ 18) in a case of both primary and recurrent adult AML.
  • OUTCOME MEASURES: Clinical improvement and regression of AML were the outcome measures.
  • CONCLUSIONS: Treatment with the MSQ dietary compositions resulted in disease regression and the reversal of clinical manifestations over two episodes of AML.
  • Therefore, further studies are warranted to evaluate the utility of this approach for the clinical management of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diet therapy. Molasses. Nutrition Therapy / methods
  • [MeSH-minor] Adult. Female. Humans. Remission Induction. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16646731.001).
  • [ISSN] 1075-5535
  • [Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)
  • [ISO-abbreviation] J Altern Complement Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down



8. Andersson BS, de Lima M, Thall PF, Madden T, Russell JA, Champlin RE: Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S11-5
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] Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia.
  • We hypothesized that standardized systemic drug delivery would improve treatment safety and provide better leukemia control.
  • We used a Bayesian method to compare the outcomes of 67 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) patients who received intravenous busulfan-cyclophosphamide (BuCy2) with 148 subsequent AML/MDS patients who received busulfan-fludarabine (Bu-Flu).
  • Overall, the data support replacing BuCy2 with or without antithymocyte globulin (ATG) with Bu-Flu with or without rabbit-ATG for AML or MDS.
  • We further suggest that the high level of safety and fast recovery from conditioning therapy-related side effects after the Bu-Flu regimen makes it a suitable platform technology for testing additional adjuncts for improved posttransplant immune recovery and long-term disease control in patients who are at high risk of rapidly recurrent disease after alloSCT.
  • The extremely low one-year treatment-related mortality as well as high overall and event-free survival of patients in the Bu-Flu group indicate that it is time to revisit the value of alloSCT compared with conventional maintenance chemotherapy for patients in first complete remission of AML/MDS.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • 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
  • [Cites] Transplant Proc. 1996 Dec;28(6):3101 [8962201.001]
  • [Cites] Bone Marrow Transplant. 2000 May;25(9):915-24 [10800057.001]
  • [Cites] Bone Marrow Transplant. 1998 Sep;22(5):439-43 [9733266.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2208-14 [15753460.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):348-57 [10637249.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jun;14(6):672-84 [18489993.001]
  • [Cites] Blood. 2001 Feb 1;97(3):631-7 [11157478.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Aug;48 Suppl 1:S53-8 [11587368.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3569-74 [11739158.001]
  • [Cites] Clin Pharmacokinet. 2002;41(2):93-103 [11888330.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(3):145-54 [11939604.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(9):477-85 [12374452.001]
  • [Cites] Blood. 2003 Mar 1;101(5):2043-8 [12406916.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1352-8 [12663726.001]
  • [Cites] Bone Marrow Transplant. 2004 Jun;33(12):1191-9 [15122310.001]
  • [Cites] Blood. 2004 Aug 1;104(3):857-64 [15073038.001]
  • [Cites] N Engl J Med. 1983 Dec 1;309(22):1347-53 [6355849.001]
  • [Cites] Blood. 1987 Nov;70(5):1382-8 [3311203.001]
  • [Cites] Blood. 1993 Apr 15;81(8):2187-93 [8471778.001]
  • [Cites] Cancer Chemother Pharmacol. 1996;37(5):401-8 [8599861.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Feb;14(2):220-8 [18215782.001]
  • [Cites] N Engl J Med. 1997 Mar 27;336(13):897-904 [9070469.001]
  • (PMID = 19561406.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS588342; NLM/ PMC4037323
  •  go-up   go-down



9. Kornblau SM, McCue D, Singh N, Chen W, Estrov Z, Coombes KR: Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia. Blood; 2010 Nov 18;116(20):4251-61
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] Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia.
  • We hypothesized that comprehensive profiling of C&Ckine expression in leukemia would provide greater insight compared with individual analyses.
  • We used multiplex array technology to simultaneously measure the level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndrome (MDS) patients and 19 normal controls.
  • C&Ckine levels in AML and MDS differed significantly from normal controls (5 higher, 13 lower) but were similar to each other for 24 of 27 analytes, with interleukin-8 and interleukin-13 higher in AML and vascular endothelial growth factor A higher in MDS.
  • Levels did not correlate with age, gender, infection, or blood counts; however, 3 correlated with specific cytognetic abnormalities in AML.
  • In newly diagnosed AML, 8 C&Ckine signatures, distinct from the normal control signature, were observed.
  • These patterns suggest specific therapeutic interventions to investigate in subsets of AML patients.
  • In conclusion, C&Ckine expression in AML and MDS differs from normal, is similar with one another, and forms recurrent patterns of expression with prognostic relevance.
  • [MeSH-major] Chemokines / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cluster Analysis. Cytogenetic Analysis. Female. Humans. Male. Middle Aged. Multivariate Analysis. Principal Component Analysis. Prognosis. Survival Analysis. Treatment Outcome. Young Adult



10. Fujieda A, Masuya M, Kitano S, Miyazaki K, Yazaki A, Sugimoto Y, Usui E, Miyata E, Shibasaki T, Yamamura K, Ohishi K, Nishii K, Nakase K, Takeuchi T, Katayama N: Deletion of chromosome arm 15q in a case of minimally differentiated hypoplastic AML-M0. Cancer Genet Cytogenet; 2008 Jul;184(1):57-61
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] Deletion of chromosome arm 15q in a case of minimally differentiated hypoplastic AML-M0.
  • Deletion of the long arm of chromosome 15 is known as a rare but recurrent chromosomal abnormality in myeloid malignancies.
  • We report a novel case of minimally differentiated hypoplastic acute myeloid leukemia (AML M0) in a patient who initially had a normal karyotype, but clonal interstitial deletion of chromosome 15, del(15)(q11.2q22), coincided with increment of leukemic cells a year later.
  • We also summarize 18 published cases with myeloid malignancies and this chromosomal abnormality.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Recurrence

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18558291.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down



11. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
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] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.
  • [MeSH-minor] Abdomen / pathology. Adult. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors



12. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
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] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • Therefore, we screened the AmL patients for known specific genetic abnormalities that could lead to more definitive prognoses.
  • METHODS: A total of 113 AML patients were evaluated at diagnosis based on routine morphology and cytochemistry and classified according to the WHO criteria.
  • The distribution of AML subtypes was M1(1), M2(32), M3(57), M4(14), M5(1), M6(1) and seven cases where morphological subtype could not be classified.
  • FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other AML subtypes (17.5 vs. 8.9%), the frequency greater in patients with bcr3 isoform (70%) than in those with in bcr1 isoform (30%).
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

  • 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 = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down



13. Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS: Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up. Chang Gung Med J; 2006 Sep-Oct;29(5):532-7
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 myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
  • Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.
  • AML with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.
  • It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).
  • [MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis
  • [MeSH-minor] Adult. Bone Marrow Examination. Flow Cytometry. Humans. Immunohistochemistry. Male

  • Genetic Alliance. consumer health - Acute Myelomonocytic 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 = 17214400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  •  go-up   go-down



14. Mansour S, Connell F, Steward C, Ostergaard P, Brice G, Smithson S, Lunt P, Jeffery S, Dokal I, Vulliamy T, Gibson B, Hodgson S, Cottrell S, Kiely L, Tinworth L, Kalidas K, Mufti G, Cornish J, Keenan R, Mortimer P, Murday V, Lymphoedema Research Consortium: Emberger syndrome-primary lymphedema with myelodysplasia: report of seven new cases. Am J Med Genet A; 2010 Sep;152A(9):2287-96
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.
  • Four reports have been published on an association between acute myeloid leukaemia (AML) and primary lymphedema, with or without congenital deafness.
  • The AML is often preceded by pancytopenia or myelodysplasia with a high incidence of monosomy 7 in the bone marrow (five propositi and two relatives).
  • Associated anomalies included hypotelorism, epicanthic folds, long tapering fingers and/or neck webbing (four patients), recurrent cellulitis in the affected limb (four patients), generalized warts (two patients), and congenital, high frequency sensorineural deafness (one patient).
  • [MeSH-minor] Abnormalities, Multiple. Adolescent. Adult. Child. Child, Preschool. Chromosomes, Human, Pair 7. Female. Genitalia / abnormalities. Humans. Infant. Infant, Newborn. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Lower Extremity Deformities, Congenital. Male. Monosomy. Young Adult

  • Genetic Alliance. consumer health - Lymphedema.
  • MedlinePlus Health Information. consumer health - Lymphedema.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • (PMID = 20803646.001).
  • [ISSN] 1552-4833
  • [Journal-full-title] American journal of medical genetics. Part A
  • [ISO-abbreviation] Am. J. Med. Genet. A
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / / PG/10/58/28477; United Kingdom / British Heart Foundation / /
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



15. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
  •  go-up   go-down



16. Bedekovics J, Rejto L, Telek B, Udvardy M, Ujfalusi A, Oláh E, Hevessy Z, Kappelmayer J, Kajtár B, Méhes G: [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression]. Orv Hetil; 2009 May 31;150(22):1031-5
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] [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].
  • [Transliterated title] Mutáns nucleophosmin fehérje kimutatása akut myeloid leukaemiában: az NPMc+ AML biológiai és klinikai jellemzôi.
  • The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in acute myeloid leukemia (AML).
  • Due to the high frequency and the obvious impact on disease outcome, the current WHO classification also defines the new (tentative) entity of "AML with NPM mutation".
  • The present study focused on further biological and clinical characterization of NPMc+ AML determined by histological and cytological preparations of the bone marrow.
  • 41 adult AML cases were investigated in our center between 2005 and 2008, 6/41 cases were presented with cytoplasmic NPM immunostaining (14.6%).
  • All but one were female patients, and were diagnosed as de novo AML with no recurrent cytogenetic aberrations (6/23, 26.1%).
  • In conclusion, immunohistochemistry is well applicable for the identification of NPM mutated AML in the daily hematopathology practice.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19465351.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  •  go-up   go-down



17. Gil L, Styczynski J, Dytfeld D, Debski R, Kazmierczak M, Kolodziej B, Rafinska B, Kubicka M, Nowicki A, Komarnicki M, Wysocki M: Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia. Anticancer Res; 2007 Nov-Dec;27(6B):4021-5
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] Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia.
  • AIM: The aim of the study was the analysis of in vitro drug resistance to bortezomib and other anticancer drugs in de novo and relapsed adult acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: The leukemic cells of 46 adult patients with AML were tested for the in vitro drug resistance profile.
  • The group included 20 de novo and 26 relapsed AML patients, among whom, 12 relapsed after allogeneic hematopoietic stem cell transplantation (HSCT) and 4 after autologous HSCT.
  • RESULTS: No significant differences in drug resistance were found for all tested drugs between de novo and relapsed AML samples, while expression of PGP, MRP1 and LRP was higher in relapsed patients.
  • Patients with refractory or relapsed disease, had higher resistance of myeloblasts to cyclophosphamide (RR = 2.4, p = 0.050), and better sensitivity to busulfan (RR = 0.4, p = 0.054) and topotecan (RR = 0.4, p = 0.031).
  • Those who have died due to refractory/relapsed disease (n = 16) had better sensitivity to bortezomib (RR = 0.6, p = 0.046) and treosulfan (RR = 0.1, p = 0.018).
  • CONCLUSION: In vitro drug resistance in relapsed adult AML is comparable to that in de novo disease.
  • Activity in vitro of bortezomib might be a rationale for its use in refractory/relapsed AML adult patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Leukemia, Myeloid / drug therapy. Pyrazines / pharmacology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bortezomib. Drug Resistance, Neoplasm. Female. Flow Cytometry. HL-60 Cells. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / biosynthesis. Vault Ribonucleoprotein Particles / metabolism

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • 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 = 18225565.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Pyrazines; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 69G8BD63PP / Bortezomib
  •  go-up   go-down



18. Olesen LH, Aggerholm A, Andersen BL, Nyvold CG, Guldberg P, Nørgaard JM, Hokland P: Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling. Br J Haematol; 2005 Nov;131(4):457-67
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] Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling.
  • Although a number of molecular aberrations have been described in acute myeloid leukaemia (AML), no study has yet determined their relative prognostic importance.
  • We have analysed blast cells from 250 adult patients treated at the same institution during a 15-year period.
  • Compared with normal bone marrow, the chemotherapy resistance protein MRP1 and apoptosis related genes BAX and CASPASE3 were found to be overexpressed in AML blasts.
  • From these data, which are the first to compare these molecular aberrations directly, we conclude that, when a battery of molecular changes is evaluated for upfront significance in AML, recurrent translocations are of prime importance for treatment outcome.
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid / genetics. Tandem Repeat Sequences / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA, Neoplasm / genetics. Gene Expression Profiling. Genes, MDR. Humans. Middle Aged. Neoplasm Proteins / genetics. Promoter Regions, Genetic / genetics. Proportional Hazards Models. Retrospective Studies. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics

  • COS Scholar Universe. author profiles.
  • 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 = 16281935.001).
  • [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 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down



19. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
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] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • AML patients were negative for common mutations of FLT3, NRAS, NPM1, KIT, MLL and JAK2; one patient revealed a splice mutation of RUNX1 exon 7.
  • We conclude that all eosinophilia-associated hematological malignancies should be screened for the presence of the FIP1L1-PDGFRA fusion gene as they are excellent candidates for treatment with tyrosine kinase inhibitors even if they present with an aggressive phenotype such as AML.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods



20. Yasar D, Karadogan I, Alanoglu G, Akkaya B, Luleci G, Salim O, Timuragaoglu A, Toruner GA, Berker-Karauzum S: Array comparative genomic hybridization analysis of adult acute leukemia patients. Cancer Genet Cytogenet; 2010 Mar;197(2):122-9
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] Array comparative genomic hybridization analysis of adult acute leukemia patients.
  • We have performed a retrospective array-based comparative hybridization (array-CGH) study on 41 acute leukemia samples [n=17 acute lymphoblastic leukemia (ALL) patients only at diagnosis, n=3 ALL patients both at diagnosis and relapse; n=20 acute myeloid leukemia (AML) patients only at diagnosis and n=1 AML patient both at diagnosis and relapse] using an Agilent 44K array.
  • In addition to previously detected cytogenetic aberrations, we observed cryptic aberrations in 95% of ALL and 90.5% of AML cases.
  • ALL-specific recurrent abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions; AML-specific recurrent abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).
  • Recurrent duplication of the ELK1 oncogene was observed in both ALL (n=2) and AML (n=3) cases.
  • [MeSH-major] Comparative Genomic Hybridization / methods. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Mutation. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

  • 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 = 20193845.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down



21. Garçon L, Libura M, Delabesse E, Valensi F, Asnafi V, Berger C, Schmitt C, Leblanc T, Buzyn A, Macintyre E: DEK-CAN molecular monitoring of myeloid malignancies could aid therapeutic stratification. Leukemia; 2005 Aug;19(8):1338-44
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] DEK-CAN molecular monitoring of myeloid malignancies could aid therapeutic stratification.
  • The t(6;9)(p23;q34) is a recurrent chromosomal abnormality observed in 1% of acute myelogenous leukemia (AML), which generates a fusion transcript between DEK and CAN/NUP214 genes.
  • We conclude that DEK-CAN molecular monitoring by RQ-PCR in t(6;9) malignancies is a useful tool for individual patient management and that molecular negativity is indispensable for survival, but should not be a prerequisite for allografting in this rare, poor prognosis, subset of AML.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Molecular Diagnostic Techniques. Oncogene Proteins / analysis. Recombinant Fusion Proteins / analysis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction. Prognosis. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Leukemia (2005) 1344.19, 1338- doi
  • (PMID = 15973457.001).
  • [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 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins
  •  go-up   go-down



22. Wakui M, Kuriyama K, Miyazaki Y, Hata T, Taniwaki M, Ohtake S, Sakamaki H, Miyawaki S, Naoe T, Ohno R, Tomonaga M: Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol. Int J Hematol; 2008 Mar;87(2):144-51
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] Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.
  • We reviewed and categorized 638 of 809 patients who were registered in the Japan Adult Leukemia Study Group acute myeloid leukemia (AML)-97 protocol using morphological means.
  • According to the WHO classification, 171 patients (26.8%) had AML with recurrent genetic abnormalities, 133 (20.8%) had AML with multilineage dysplasia (MLD), 331 (51.9%) had AML not otherwise categorized, and 3 (0.5%) had acute leukemia of ambiguous lineage.
  • The platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in AML with MLD than in the other WHO categories.
  • Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with AML, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged



23. Sino US Leukemia Cooperative Group of Shanghai: [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):444-8
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] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
  • OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.
  • METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.
  • A total of 572 adult AL cases were diagnosed and classified according to WHO and FAB classification.
  • RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).
  • The AML and ALL percentage ratio was 3.66: 1.
  • AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.
  • The percentage of therapy-related AML in Shanghai was lower than that in the Western.
  • According to FAB classification, AML-M4 was the most (38.5%) common subtype.
  • The percentage of AML-M3 and M4 in Shanghai were higher than that in the Western, but that of AML-M, was lower.
  • The incidence of karyotypic abnormalities in AML was 60.8%.
  • The incidence of AML with t (15;17) was higher than that in the Western.
  • Favorable cytogenetic risk group accounted for 30.6%, intermediate group for 51.5%, unfavorable group for 17.9% of AML.
  • CONCLUSIONS: The percentages of AML with t (15;17) and AML-M4 in Shanghai and the incidence of cytogenetic favorable group were higher than that in the Western.
  • It was different in WHO classification and karyotypic abnormalities of AML between Shanghai and the Western.
  • Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.
  • [MeSH-major] Leukemia / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18072625.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down



24. Wang Y, Xue Y, Chen S, Wu Y, Pan J, Zhang J, Shen J: [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Feb;27(1):34-7
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] [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)].
  • OBJECTIVE: To explore the clinical and laboratory features of 6 cases of acute myeloid leukemia (AML) with t(6;9)(p23;q34).
  • CONCLUSION: The t(6;9)(p23;q34) is a rare recurrent abnormity.
  • AML with t(6;9)(p23;q34) has unique clinical and laboratory features and its prognosis is poor in most cases.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antigens, CD / genetics. Antigens, CD13 / genetics. Antigens, CD34 / genetics. Antigens, Differentiation, Myelomonocytic / genetics. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins c-kit / genetics. Sialic Acid Binding Ig-like Lectin 3

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 20140864.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down



25. Cunningham I: Extramedullary sites of leukemia relapse after transplant. Leuk Lymphoma; 2006 Sep;47(9):1754-67
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] Extramedullary sites of leukemia relapse after transplant.
  • Recurrent or residual leukemia found in extramedullary sites after intensive treatments adversely affects prognosis.
  • The most commonly reported sites are soft tissue in acute leukemias and bone in CML.
  • Extramedullary relapse occurred typically within 2 years in ALL, but later in one-third of myeloid leukemias.
  • Most testicular relapses reported in AML followed non-TBI conditioning.
  • Intensive therapy has produced lengthy remissions in cases of acute leukemias involving various sites, whereas CML cases, particularly involving bone, were most resistant to treatment.
  • [MeSH-major] Bone Neoplasms / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid, Acute / pathology. Neoplasm Recurrence, Local / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Soft Tissue Neoplasms / pathology. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged



26. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down



27. Pan J, Xue Y, Qiu H, Chen S, Zhang J, Wu Y, Shen J, Wang Y: A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):333-40
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 pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia.
  • A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive leukemia patients, including 3 with chronic myeloid leukemia (CML) in chronic phase and 1 with acute myeloid leukemia (AML) in our hospital since 2004.
  • FISH also found a deletion of partial sequence of BCR on der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) in 67.5% of bone marrow cells in the AML patient, but did not detect the deletion of the sequence of ASS/9q34 in these four patients.
  • Reverse transcriptase-polymerase chain reaction revealed a b3a2 type of BCR/ABL1 fusion transcript in all of them, proving their disease to be Ph-positive leukemia.
  • On reviewing the literature, only two solitary Ph-positive leukemia patients have been noticed to have the inv(9)(p22q34) anomaly.
  • These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but recurrent secondary chromosomal abnormality for Ph-positive leukemia.
  • Despite receiving hydroxyurea therapy (n = 3 patients), combined chemotherapy (n = 2), even imatinib treatment (n = 1), three patients, including one with AML and two with CML (one of whom progressed into the lymphoblastic blast phase), died with survival times of 28 days, 13 months, and 34 months, respectively.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Bone Marrow Cells / cytology. Chromosome Aberrations. Disease Progression. Female. Gene Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Chronic 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
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156255.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down



28. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion
  • [MeSH-minor] Adult. Aged. Chromosome Banding. Fatal Outcome. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
  •  go-up   go-down



29. Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T: Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia. Cancer Genet Cytogenet; 2009 Oct;194(1):38-43
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] Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
  • Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia.
  • We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2).
  • A 35-year-old man was diagnosed as having de novo AML with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
  • These results suggest that the idic(21)(p11.2) could be implicated also in the pathogenesis of AML through amplification of genes including RUNX1 located on 21q.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19737652.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down



30. Sakamaki H: [The role of gemtuzumab ozogamicin in the treatment of acute myeloid leukemia patients]. Gan To Kagaku Ryoho; 2008 Sep;35(9):1629-34
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 role of gemtuzumab ozogamicin in the treatment of acute myeloid leukemia patients].
  • Gemtuzumab Ozogamicin (GO) targets leukemia cells expressing CD33 by means of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin.
  • GO has been approved in Japan as monotherapy for the treatment of patients with relapsed/refractory acute myeloid leukemia (AML)since 2005.
  • GO administered as a single agent has resulted in overall response rates of about 30% in previously relapsed adult AML.
  • Although caution is advised when administering GO within 115 days of a stem cell transplantation (SCT) procedure because of veno-occlusive disease, recent clinical studies overseas suggest that GO can be integrated into reduced-intensity conditioning therapy before allogeneic SCT in patients with relapsed AML.
  • [MeSH-major] Aminoglycosides / immunology. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / immunology. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / immunology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18799927.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
  •  go-up   go-down



31. Bao L, Wang X, Ryder J, Ji M, Chen Y, Chen H, Sun H, Yang Y, Du X, Kerzic P, Gross SA, Yao L, Lv L, Fu H, Lin G, Irons RD: Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations. Eur J Haematol; 2006 Jul;77(1):35-45
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] Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations.
  • We report a prospective study of 174 unselected adult de novo acute myeloid leukemia (AML) cases diagnosed using the WHO classification.
  • Of those, 57 (33%) were AML with recurrent cytogenetic abnormalities, 41 were (24%) AML with multilineage dysplasia, 74 (42%) were AML not otherwise categorized, and two were acute leukemias of ambiguous lineage.
  • Clonal cytogenetic abnormalities were detected in 64% of the WHO AML cases with t(15;17) (15%), t(8;21) (12%), +8 (11%), -7/del7q (8%) and del9q (5%) being the most common ones.
  • The FLT3/ITD mutations (FMS-like tyrosine kinase 3/internal tandem duplication) were observed in 12% of the WHO AML cases, which is much lower than ones in the literature, while the 6% incidence of the FLT3-activating loop mutations (either FLT3/D835 or FLT3/I836) was comparable with others.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Classification. Cytogenetic Analysis. Female. Humans. Leukocytosis / genetics. Male. Middle Aged. Prospective Studies. World Health Organization

  • 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 = 16573742.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down



32. Biggio V, Renneville A, Nibourel O, Philippe N, Terriou L, Roumier C, Amouyel P, Cottel D, Castaigne S, Dombret H, Thomas X, Fenaux P, Preudhomme C, French alfa group: Recurrent in-frame insertion in C/EBPalpha TAD2 region is a polymorphism without prognostic value in AML. Leukemia; 2008 Mar;22(3):655-7
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] Recurrent in-frame insertion in C/EBPalpha TAD2 region is a polymorphism without prognostic value in AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic / statistics & numerical data. Disease-Free Survival. Female. Humans. Male. Middle Aged. Mutagenesis, Insertional. Prognosis. Protein Structure, Tertiary. Risk. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17851556.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Neoplasm Proteins
  •  go-up   go-down



33. Carnicer MJ, Lasa A, Buschbeck M, Serrano E, Carricondo M, Brunet S, Aventin A, Sierra J, Di Croce L, Nomdedeu JF: K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML). Ann Hematol; 2008 Oct;87(10):819-27
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] K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML).
  • The CEBPA gene codes for a transcription factor that has a pivotal role in controlling proliferation and differentiation of myeloid progenitors.
  • Acquired CEBPA mutations have been found in acute myeloid leukemias (AML) with a good prognosis, and most of these patients have a normal karyotype.
  • All four had an AML-M1 with CD7 positivity and T-cell receptor gamma chain (TCR-gamma) rearrangement.
  • K313dup seems to be selected in leukemic cells, and its frequency in other AML series could be determined using the screening method reported in this paper.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18587575.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Receptors, Antigen, T-Cell, gamma-delta
  •  go-up   go-down



34. Lee MY, Tan TD, Feng AC: Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype. J Chin Med Assoc; 2007 Jul;70(7):269-73
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] Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype.
  • BACKGROUND: Most acute leukemias are classified as lymphoid or myeloid lineages by standard microscopic morphology, cytochemistry and a panel of immunologic markers.
  • The World Health Organization classification of acute leukemia incorporates morphologic, cytogenetic, immunologic and clinical features to define the entities that are biologically homogeneous and that have clinical relevance.
  • The purpose of this study was to determine the clinicopathologic characteristics of acute myeloid leukemia (AML) in Taiwan.
  • The median age at onset of disease was 49 years (range, 2-78 years), which was younger in biphenotypic AML (23.5 years) and older in multilineage dysplasia-related AML (61 years).
  • There were 9 cases (13%) with recurrent cytogenetic abnormality, 7 (10%) multilineage dysplasia-related, 7 (10%) therapy-related, 39 (56%) not other categorized and 8 (11%) of ambiguous lineage.
  • The 2- and 5-year overall survival rates of AML were 26.5% and 20.6%, respectively.
  • The median survivals of therapyrelated, multilineage dysplasia-related and biphenotypic AML were 2 months, 9 months and 30.5 months, respectively.
  • CONCLUSION: This was a clinicopathologic study of AML in Taiwan.
  • Multilineage dysplasia- and therapy-related AML have worse prognosis.
  • Biphenotypic AML may not be an aggressive subtype.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Myelodysplastic Syndromes / pathology. Phenotype



35. Bullinger L, Krönke J, Schön C, Radtke I, Urlbauer K, Botzenhardt U, Gaidzik V, Carió A, Senger C, Schlenk RF, Downing JR, Holzmann K, Döhner K, Döhner H: Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis. Leukemia; 2010 Feb;24(2):438-49
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] Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis.
  • As acute myeloid leukemia (AML) represents a genetically heterogeneous disease, this technology might prove helpful, especially for cytogenetically normal AML (CN-AML) cases.
  • Thus, we performed high-resolution SNP analyses in 157 adult cases of CN-AML.
  • Furthermore, we identified two cases with a cryptic t(6;11) as well as several non-recurrent aberrations pointing to leukemia-relevant regions.
  • These data show the potential of high-resolution SNP analysis for identifying genomic regions of potential pathogenic and clinical relevance in AML.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy / genetics
  • [MeSH-minor] Adolescent. Adult. CCAAT-Enhancer-Binding Proteins / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 6 / genetics. Female. Gene Expression Regulation, Leukemic. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Nuclear Proteins / genetics. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 20016533.001).
  • [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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  •  go-up   go-down



36. Verhaak RG, Valk PJ: Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia. Cancer Treat Res; 2010;145:67-83
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] Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia.
  • The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision making in acute myeloid leukemia (AML).
  • The World Health Organization (WHO) has recognized this important information by including, besides clinical, cytological, cytochemical, and immunophenotypical features, recurrent cytogenetic abnormalities in its classification (Table 1).
  • In addition, novel molecular approaches in genomics, like monitoring the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities for further refinement of prognostication of AML.
  • Gene expression profiling in AML is already well established and has proven to be valuable to recognize various cytogenetic subtypes, discover novel AML subclasses, and predict clinical outcome.
  • The current advances made in molecular understanding of AML will ultimately lead to a further refinement of prognostics of AML.
  • [MeSH-major] Genes, Neoplasm. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Chromosome Aberrations. Gene Expression Profiling. Humans. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Oligonucleotide Array Sequence Analysis. Prognosis. Treatment Outcome



37. Tullu MS, Date NB, Ghildiyal RG, Modi CJ: Acute myelogenous leukemia in a child with HIV infection. Eur J Pediatr; 2010 May;169(5):629-31
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 myelogenous leukemia in a child with HIV infection.
  • The occurrence of acute myelogenous leukemia (AML) in HIV-infected patients is extremely rare with only adult patients reported so far.
  • The child also had recurrent parotid swellings, melena, and purulent otitis media.
  • The patient's bone marrow aspiration and biopsy suggested AML, and the leukemia panel 1 study showed CD13, CD33, CD34, and HLA DR-positive AML with CD7 expression.
  • AML can occur in pediatric patients with HIV infection.
  • This is the first HIV-infected pediatric patient (<12 years) with AML reported in the medical literature.
  • [MeSH-major] HIV Infections / complications. Leukemia, Myeloid, Acute / complications



38. Chelghoum Y, Vey N, Raffoux E, Huguet F, Pigneux A, Witz B, Pautas C, de Botton S, Guyotat D, Lioure B, Fegueux N, Garban F, Saad H, Thomas X: Acute leukemia during pregnancy: a report on 37 patients and a review of the literature. Cancer; 2005 Jul 1;104(1):110-7
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 leukemia during pregnancy: a report on 37 patients and a review of the literature.
  • BACKGROUND: Acute leukemia (AL) requiring cytotoxic treatment occurring during pregnancy poses a very difficult therapeutic dilemma.
  • RESULTS: Thirty-one patients had acute myeloid leukemia (AML), and 6 patients had acute lymphoblastic leukemia (ALL).
  • Ten patients developed recurrent disease.
  • Overall, 12 of 37 pregnant women died from leukemia.
  • [MeSH-major] Leukemia / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pregnancy Complications, Neoplastic
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Leukemia, Myeloid / drug therapy. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters. Remission Induction

  • Genetic Alliance. consumer health - Pregnancy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Tumors and Pregnancy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15912518.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 13
  •  go-up   go-down



39. Kothary N, Soulen MC, Clark TW, Wein AJ, Shlansky-Goldberg RD, Crino PB, Stavropoulos SW: Renal angiomyolipoma: long-term results after arterial embolization. J Vasc Interv Radiol; 2005 Jan;16(1):45-50
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 study was conducted to evaluate the long-term efficacy of AML embolization.
  • Of these, 10 patients had tuberous sclerosis (TS) with multiple AMLs and nine patients had a solitary sporadic AML.
  • Recurrence was defined as an increase in tumor size of greater than 2 cm on follow-up imaging and/or recurrent symptoms that required repeat embolization.
  • AML recurrence was noted in 31.6% of patients (n = 19) and for 30% of lesions overall (n = 9).
  • Six of 10 patients in the TS group had AML recurrences.
  • No recurrences occurred in the patients with sporadic AML.
  • Six lesions in four patients had to be reembolized because of recurrent symptoms, including one hemorrhage, and three lesions in two patients required repeat embolization because of a greater than 2 cm increase in size.
  • However, long-term follow-up revealed a high AML recurrence rate in patients with TS.
  • Lifelong surveillance for recurrence after AML embolization is essential in patients with TS.
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Hemorrhage / prevention & control. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Treatment Outcome. Tuberous Sclerosis / complications

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Vasc Interv Radiol. 2005 Aug;16(8):1153-4; author reply 1154 [16105930.001]
  • (PMID = 15640409.001).
  • [ISSN] 1051-0443
  • [Journal-full-title] Journal of vascular and interventional radiology : JVIR
  • [ISO-abbreviation] J Vasc Interv Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down



40. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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 balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.
  • INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
  • Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • 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 = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down



41. Zhang L, Alsabeh R, Mecucci C, La Starza R, Gorello P, Lee S, Lill M, Schreck R: Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature. Cancer Genet Cytogenet; 2007 Oct 1;178(1):42-8
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] Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature.
  • Balanced chromosome rearrangements are the hallmark of therapy-related leukemia that develops in patients treated with topoisomerase II inhibitors.
  • Many of these rearrangements involve recurrent chromosomal sites and associated genes (11q23/MLL, 21q22.3/AML1, and 11p15/NUP98), which can interact with a variety of partner genes.
  • With time, the patient's disorder progressed to acute myelomonocytic leukemia with cytogenetic evidence of clonal evolution.
  • To our knowledge, this is the first report of a patient presenting with a myelodysplastic syndrome with isolated t(1;11) (q23;p15), which evolved into therapy-related acute myeloid leukemia (t-AML).
  • This patient is the third reported with this cytogenetic rearrangement and t-AML, and is compared with the other two reports of t(1;11)(q23;p15).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Myelomonocytic, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neutrophils / metabolism



42. Schnittger S, Kohl TM, Haferlach T, Kern W, Hiddemann W, Spiekermann K, Schoch C: KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival. Blood; 2006 Mar 1;107(5):1791-9
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] KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival.
  • Mutations in codon D816 of the KIT gene represent a recurrent genetic alteration in acute myeloid leukemia (AML).
  • To clarify the biologic implication of activation loop mutations of the KIT gene, 1940 randomly selected AML patients were analyzed.
  • In contrast, other activating mutations like FLT3 and NRAS mutations were very rarely detected in AML1-rearranged leukemia.
  • Our findings clearly indicate that activating mutations of receptor tyrosine kinases are associated with distinct genetic subtypes in AML.
  • The KIT-D816 mutations confer a poor prognosis to AML1-ETO-positive AML and should therefore be included in the diagnostic workup.
  • Patients with KIT-D816-positive/AML1-ETO-positive AML might benefit from early intensification of treatment or combination of conventional chemotherapy with KIT PTK inhibitors.
  • [MeSH-major] Amino Acid Substitution. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Point Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adult. Aged. Cell Line. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Codon / genetics. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression / genetics. Humans. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Retrospective Studies. Translocation, Genetic / 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16254134.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down



43. Chamberlain MC, Raizer J: Extended exposure to alkylator chemotherapy: delayed appearance of myelodysplasia. J Neurooncol; 2009 Jun;93(2):229-32
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.
  • OBJECTIVE: A case series of gliomas treated with alkylator-based chemotherapy who subsequently developed myelodysplastic syndrome (tMDS) or acute myelocytic leukemia (AML).
  • Three patients were diagnosed with AML as well (in two determined by bone marrow and one at autopsy).
  • Interval from last chemotherapy exposure to diagnosis of tMDS/AML ranged from 3 to 31 months (median 24 months).
  • Five patients have died, 2 as a consequence of recurrent brain tumor, 1 as a complication of transplantation, and 2 due to AML.
  • CONCLUSIONS: Although rare, induction of tMDS/AML following extended use of alkylator-based chemotherapy may become more relevant with the evolving practice to treat gliomas for protracted periods.
  • [MeSH-minor] Adult. Aged. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Follow-Up Studies. Humans. Male. Middle Aged. Nitrosourea Compounds / therapeutic use. Reoperation / statistics & numerical data. Survival Analysis. Survivors. Time Factors

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • 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
  • [Cites] Ann Oncol. 2001 Feb;12 (2):259-66 [11300335.001]
  • [Cites] Neurology. 2001 Jul 24;57(2):340-2 [11468326.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):509-18 [11208845.001]
  • [Cites] J Neurooncol. 2001 May;53(1):55-9 [11678432.001]
  • [Cites] J Clin Oncol. 2004 Aug 1;22(15):3133-8 [15284265.001]
  • [Cites] J Neurooncol. 2005 Feb;71(3):315-8 [15735923.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3389-95 [10550132.001]
  • [Cites] N Engl J Med. 1985 Aug 29;313(9):579 [3894973.001]
  • [Cites] Neurology. 2001 Jan 9;56(1):118-20 [11148250.001]
  • [Cites] Neurology. 2004 Jun 8;62(11):2113-5 [15184628.001]
  • [Cites] Oncology. 2002;63(1):38-41 [12187069.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2525-8 [12829671.001]
  • [Cites] J Clin Oncol. 2003 Feb 15;21(4):646-51 [12586801.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Feb;18(2):321-4 [2154418.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] J Neurooncol. 1998 Oct;40(1):39-46 [9874184.001]
  • [Cites] Neurol Med Chir (Tokyo). 2002 Apr;42(4):170-4 [12013670.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]
  • [Cites] Neuro Oncol. 2006 Jul;8(3):280-3 [16728498.001]
  • [Cites] Semin Oncol. 2000 Jun;27(3 Suppl 6):27-34 [10866347.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):987-96 [15758009.001]
  • (PMID = 19099199.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Nitrosourea Compounds; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
  •  go-up   go-down



44. Fagnoni P, Limat S, Hintzy-Fein E, Martin F, Deconinck E, Cahn JY, Arveux P, Dussaucy A, Woronoff-Lemsi MC: [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification]. Bull Cancer; 2006 Aug;93(8):813-9
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] [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification].
  • The confrontation of the macro- and micro-economic approaches of hospital costs is a recurrent question, in particular for pathologies where length of stay is highly variable, like acute myeloid leukemias (AML).
  • This monocentric and retrospective study compares direct hospital medical costs of induction and relapse treatment sequences for AML, valued according to four different approaches: the analytic accounting system of our hospital, the French Diagnosis Related Group (DRG) cost databases of hospital discharges (readjusted, or not, to actual hospital stay duration), and official tariffs from the new French DRG prospective payment system.
  • The average cost of hospital AML care valued by the analytic accounting system of our hospital is 61,248 euros for the induction phase and 91,702 euros for the relapse phase.
  • [MeSH-major] Hospital Costs. Leukemia, Myeloid / economics. Prospective Payment System / economics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Diagnosis-Related Groups / economics. Female. France. Humans. Length of Stay / economics. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16935786.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down



45. Ley TJ, Ding L, Walter MJ, McLellan MD, Lamprecht T, Larson DE, Kandoth C, Payton JE, Baty J, Welch J, Harris CC, Lichti CF, Townsend RR, Fulton RS, Dooling DJ, Koboldt DC, Schmidt H, Zhang Q, Osborne JR, Lin L, O'Laughlin M, McMichael JF, Delehaunty KD, McGrath SD, Fulton LA, Magrini VJ, Vickery TL, Hundal J, Cook LL, Conyers JJ, Swift GW, Reed JP, Alldredge PA, Wylie T, Walker J, Kalicki J, Watson MA, Heath S, Shannon WD, Varghese N, Nagarajan R, Westervelt P, Tomasson MH, Link DC, Graubert TA, DiPersio JF, Mardis ER, Wilson RK: DNMT3A mutations in acute myeloid leukemia. N Engl J Med; 2010 Dec 16;363(25):2424-33
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] DNMT3A mutations in acute myeloid leukemia.
  • BACKGROUND: The genetic alterations responsible for an adverse outcome in most patients with acute myeloid leukemia (AML) are unknown.
  • METHODS: Using massively parallel DNA sequencing, we identified a somatic mutation in DNMT3A, encoding a DNA methyltransferase, in the genome of cells from a patient with AML with a normal karyotype.
  • We sequenced the exons of DNMT3A in 280 additional patients with de novo AML to define recurring mutations.
  • CONCLUSIONS: DNMT3A mutations are highly recurrent in patients with de novo AML with an intermediate-risk cytogenetic profile and are independently associated with a poor outcome. (Funded by the National Institutes of Health and others.).



46. Niparuck P, Chuncharunee S, Ungkanont A, Udomtrupayakul U, Aungchaisuksiri P, Rerkamnuatchoke B, Jootar S, Atichartakarn V: Long-term outcomes of de novo acute myeloid leukemia in Thai patients. J Med Assoc Thai; 2009 Sep;92(9):1143-9
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] Long-term outcomes of de novo acute myeloid leukemia in Thai patients.
  • BACKGROUND: Acute myeloid leukemia (AML) is the heterogeneous disease.
  • As per previous reports, there are some differences in clinical features and cytogenetic biomarkers of AML among different ethnic backgrounds.
  • Therefore, we conducted a retrospective study to analyze clinical outcomes and predictive factors of Thai AML patients receiving chemotherapy treatment.
  • MATERIAL AND METHOD: The authors performed a retrospective analysis of 106 adults with newly diagnosed de novo AML at Ramathibodi Hospital between 2003 and 2007.
  • Of 101 patients with non- M3 subtype, the patients received induction and consolidation chemotherapy with anthracyclin plus cytarabine based regimens (3 + 7).
  • AML with recurrent cytogenetic translocations, complex chromosome, trisomy 8, polyploidy, del 5q and del 7q were found in 16.8, 6.3, 5.3, 5.3, 2.1 and 3.2%, respectively.
  • CONCLUSION: The overall complete remission rate of Thai AML patients is in 60%.
  • Only a small proportion of the presented patients have long-term DFS and OS, the significant factor for predicting survival of Thai AML patients is the complete remission status.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Cohort Studies. Disease-Free Survival. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Thailand. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19772172.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down



47. Ando T, Mitani N, Matsui K, Yamashita K, Nomiyama J, Tsuru M, Yujiri T, Tanizawa Y: Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity. Int J Hematol; 2009 Oct;90(3):374-7
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] Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.
  • Isolated extramedullary (EM) relapse of acute myelogenous leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is rare.
  • We describe an AML patient showing the chromosomal abnormality t(8;21) and CD56 expression who experienced a unique EM relapse after allo-HSCT.
  • These findings suggest that the graft-versus-leukemia effect may preferentially maintain marrow remission rather than prevent EM relapse.
  • In addition, our findings show that extended survival is possible after EM relapse following allo-HSCT in patients with marrow hematopoiesis of donor origin, and that augmentation of the graft-versus-leukemia effect may be useful.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute. Stomach Neoplasms. Translocation, Genetic
  • [MeSH-minor] Antigens, CD56 / metabolism. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gastric Mucosa / pathology. Humans. Male. Recurrence. Transplantation, Homologous. Young Adult



48. Tibes R, Keating MJ, Ferrajoli A, Wierda W, Ravandi F, Garcia-Manero G, O'Brien S, Cortes J, Verstovsek S, Browning ML, Faderl S: Activity of alemtuzumab in patients with CD52-positive acute leukemia. Cancer; 2006 Jun 15;106(12):2645-51
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] Activity of alemtuzumab in patients with CD52-positive acute leukemia.
  • BACKGROUND: Alemtuzumab is a humanized monoclonal antibody directed against the cell surface antigen CD52 and has demonstrated activity in chronic lymphocytic leukemia and other CD52-positive lymphoproliferative disorders.
  • Because CD52 also is expressed on acute leukemic blasts, the authors investigated the safety and efficacy of alemtuzumab in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
  • METHODS: Fifteen patients with CD52-positive (> or = 20%), recurrent or refractory acute leukemia (9 patients with AML and 6 patients with ALL) received alemtuzumab at a dose of 30 mg intravenously given 3 times a week (dose escalation during Week 1) for a total of 4 to 12 weeks.
  • CONCLUSIONS: Single-agent alemtuzumab was found to have limited activity in recurrent or refractory acute leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Bacteremia / diagnosis. Bacteremia / etiology. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Fungemia / diagnosis. Fungemia / etiology. Humans. Male. Middle Aged. Pneumonia / diagnosis. Pneumonia / etiology. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16688777.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down



49. Parkin B, Ouillette P, Wang Y, Liu Y, Wright W, Roulston D, Purkayastha A, Dressel A, Karp J, Bockenstedt P, Al-Zoubi A, Talpaz M, Kujawski L, Liu Y, Shedden K, Shakhan S, Li C, Erba H, Malek SN: NF1 inactivation in adult acute myelogenous leukemia. Clin Cancer Res; 2010 Aug 15;16(16):4135-47
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] NF1 inactivation in adult acute myelogenous leukemia.
  • PURPOSE: This study was conducted to identify novel genes with importance to the biology of adult acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: We analyzed DNA from highly purified AML blasts and paired buccal cells from 95 patients for recurrent genomic microdeletions using ultra-high density Affymetrix single nucleotide polymorphism 6.0 array-based genomic profiling.
  • Sequence analysis of all NF1 coding exons in the 11 AML cases with NF1 copy number changes identified acquired truncating frameshift mutations in two patients.
  • Subsequent expression analysis of NF1 mRNA in the entire AML cohort using fluorescence-activated cell sorting sorted blasts as a source of RNA identified six patients (one with a NF1 mutation) with absent NF1 expression.
  • The NF1 null states were associated with increased Ras-bound GTP, and short hairpin RNA-mediated NF1 suppression in primary AML blasts with wild-type NF1 facilitated colony formation in methylcellulose.
  • Primary AML blasts without functional NF1, unlike blasts with functional NF1, displayed sensitivity to rapamycin-induced apoptosis, thus identifying a dependence on mammalian target of rapamycin (mTOR) signaling for survival.
  • Finally, colony formation in methylcellulose ex vivo of NF1 null CD34+/CD38- cells sorted from AML bone marrow samples was inhibited by low-dose rapamycin.
  • CONCLUSIONS: NF1 null states are present in 7 of 95 (7%) of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin-directed therapeutics.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • 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
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1012-21 [18281475.001]
  • [Cites] N Engl J Med. 1997 Jun 12;336(24):1713-20 [9180088.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Blood. 2008 Aug 1;112(3):814-21 [18490517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11921-6 [18697940.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1993-2003 [18436738.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4603-9 [18559876.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Cancer Cell. 2009 Jul 7;16(1):44-54 [19573811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12950-5 [19651600.001]
  • [Cites] Clin Cancer Res. 2009 Nov 1;15(21):6732-9 [19843663.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):181-8 [10620616.001]
  • [Cites] Leukemia. 2000 Mar;14(3):513-7 [10720153.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]
  • [Cites] Blood. 1991 Mar 1;77(5):925-9 [1704804.001]
  • [Cites] Am J Clin Pathol. 1993 Nov;100(5):534-40 [8249893.001]
  • [Cites] N Engl J Med. 1994 Mar 3;330(9):597-601 [8302341.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50874-85 [15371411.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3217-24 [15867216.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8573-8 [15937108.001]
  • [Cites] Biogerontology. 2005;6(3):185-92 [16041622.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):337-48 [16226708.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] J Biol Chem. 2005 Nov 25;280(47):39524-33 [16169856.001]
  • [Cites] Leukemia. 2006 Apr;20(4):635-44 [16467864.001]
  • [Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]
  • [Cites] Cancer Cell. 2006 Sep;10(3):179-90 [16959610.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]
  • [Cites] Clin Cancer Res. 2007 Aug 15;13(16):4777-85 [17699855.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1584-93 [17971485.001]
  • [Cites] Leukemia. 2008 Feb;22(2):240-8 [18200041.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4322-8 [18172006.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):144-8 [8563751.001]
  • [CommentOn] Clin Cancer Res. 2010 Aug 15;16(16):4074-6 [20587590.001]
  • (PMID = 20505189.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA136537; United States / NCI NIH HHS / CA / 1R01 CA136537-01; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R01 CA136537-02; United States / NCI NIH HHS / CA / CA136537-02
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS210184; NLM/ PMC2921448
  •  go-up   go-down



50. Owen C, Fitzgibbon J, Paschka P: The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia. Hematol Oncol; 2010 Mar;28(1):13-9
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] The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia.
  • Recurrent genetic aberrations are important predictors of outcome in acute myeloid leukaemia (AML).
  • WT1 mutations occur in approximately 10% of adult AML patients at diagnosis and are most frequent in the cytogenetically normal (CN) AML subgroup.
  • Herein, we discuss the importance of WT1 mutations in AML.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics. Mutation / genetics
  • [MeSH-minor] Adult. Humans. Prognosis. WT1 Proteins / genetics. WT1 Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20013787.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0700052; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / WT1 Proteins
  • [Number-of-references] 75
  •  go-up   go-down



51. De Stefano V, Sorà F, Rossi E, Chiusolo P, Laurenti L, Fianchi L, Zini G, Pagano L, Sica S, Leone G: The risk of thrombosis in patients with acute leukemia: occurrence of thrombosis at diagnosis and during treatment. J Thromb Haemost; 2005 Sep;3(9):1985-92
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] The risk of thrombosis in patients with acute leukemia: occurrence of thrombosis at diagnosis and during treatment.
  • BACKGROUND: Thromboembolism can occur during acute leukemia, especially acute lymphoid leukemia (ALL) treated with L-asparaginase.
  • Yet, most reports are anecdotical and scarce data are available on the risk of thrombosis in acute myeloid leukemia (AML).
  • OBJECTIVES: To evaluate the risk of thrombosis in patients with acute leukemia.
  • PATIENTS AND METHODS: Three-hundred and seventy-nine consecutive adult patients with newly diagnosed acute leukemia were recruited in an observational cohort study conducted from January 1994 to December 2003.
  • Diagnosis was ALL in 69 patients, acute promyelocytic leukemia (APL; FAB subtype M3) in 31, and non-M3 AML in 279.
  • All first or recurrent symptomatic thromboembolic events objectively diagnosed were recorded.
  • At diagnosis, thrombosis was a presenting manifestation in 13 cases (3.4% of the whole cohort): 1.4% in ALL, 9.6% in APL, and 3.2% in non-M3 AML patients.
  • At 6 months from diagnosis, the cumulative incidence of thrombosis was 10.6% in ALL, 8.4% in APL, and 1.7% in non-M3 AML patients.
  • CONCLUSIONS: In patients with acute leukemia, the risk of thrombosis is not negligible.
  • Thombosis can be a presenting symptom at diagnosis in a significant portion of cases with APL (9.6%) and non-M3 AML (3.2%); a similar rate of thrombosis can occur during the subsequent course of the disease.
  • [MeSH-major] Leukemia / complications. Thrombosis / etiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Asparaginase / adverse effects. Female. Follow-Up Studies. Genetic Predisposition to Disease. Humans. Incidence. Male. Middle Aged. Risk

  • Genetic Alliance. consumer health - Thrombosis.
  • MedlinePlus Health Information. consumer health - Blood Clots.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16102104.001).
  • [ISSN] 1538-7933
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.5.1.1 / Asparaginase
  •  go-up   go-down



52. Erkeland SJ, Verhaak RG, Valk PJ, Delwel R, Löwenberg B, Touw IP: Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia. Cancer Res; 2006 Jan 15;66(2):622-6
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] Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with a variable response to treatment.
  • Recurrent cytogenetic defects and acquired mutations in regulatory genes are associated with AML subtypes and prognosis.
  • Recently, gene expression profiling (GEP) has been applied to further risk stratify AML.
  • Here, we show that mouse leukemia genes identified by retroviral insertion mutagenesis are more frequently differentially expressed in distinct subclasses of adult and pediatric AML than randomly selected genes or genes located more distantly from a virus integration site.
  • The candidate proto-oncogenes showing discriminative expression in primary AML could be placed in regulatory networks mainly involved in signal transduction and transcriptional control.
  • Our data support the validity of retroviral insertion mutagenesis in mice for human disease and indicate that combining these murine screens for potential proto-oncogenes with GEP in human AML may help to identify critical disease genes and novel pathogenetic networks in leukemia.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid / genetics. Mutagenesis, Insertional. Proto-Oncogenes
  • [MeSH-minor] Acute Disease. Adult. Animals. Child. Humans. Mice. Retroviridae / genetics. Signal Transduction. Transcription, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16423987.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



53. Falini B, Mecucci C, Saglio G, Lo Coco F, Diverio D, Brown P, Pane F, Mancini M, Martelli MP, Pileri S, Haferlach T, Haferlach C, Schnittger S: NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia. Haematologica; 2008 Mar;93(3):439-42
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] NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.
  • Acute myeloid leukemia carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+) acute myeloid leukemia) represents one-third of adult AML (50-60% of all acute myeloid leukemia with normal karyotype) and shows distinct biological, pathological and clinical features.
  • We confirm in 2562 patients with acute myeloid leukemia our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities.
  • Taken together, these findings make NPMc+ acute myeloid leukemia a good candidate for inclusion in the upcoming World Health Organization classification.
  • [MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18268276.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin
  •  go-up   go-down



54. Ahmad F, Dalvi R, Mandava S, Das BR: Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2). Am J Hematol; 2007 Jul;82(7):676-8
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] Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2).
  • Acute Myelogeneous Leukemia (AML) is a heterogeneous disease with respect to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis.
  • In this study, we report a case whose clinical features were suggestive of AML-M1 subtype with t(14;17) (q32; q11.2) karyotype involving rearrangement of chromosomal segments 17q11.2 and 14q32.
  • This is the first report of novel chromosomal translocation in this subset of AML and has not yet been reported elsewhere.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Female. Humans. Karyotyping

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17177193.001).
  • [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



55. Sindt A, Deau B, Brahim W, Staal A, Visanica S, Villarese P, Rault JP, Macintyre E, Delabesse E: Acute monocytic leukemia with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9. Genes Chromosomes Cancer; 2006 Jun;45(6):575-82
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.
  • [Title] Acute monocytic leukemia with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9.
  • The t(9;22)(q34;q11) translocation occurs in chronic myeloid leukemia (CML) and adult B-cell acute lymphoblastic leukemia (ALL), leading to fusion of BCR to ABL1 and constitutive activation of ABL1 tyrosine kinase activity.
  • The latter is found in almost all cases of CML and in one third of the cases of t(9;22)-positive adult B-ALL.
  • P190 BCR-ABL1 is found in the remaining two thirds of t(9;22)-positive adult B-ALL cases but only exceptionally in CML.
  • We describe here the first case of t(9;22)(q34;q11) associated with t(10;11)(p13;q14) in acute monocytic leukemia.
  • The recurrent t(10;11)(p13;q14) translocation, usually found in acute myeloid leukemia (AML) and T-ALL, merges PICALM to MLLT10.
  • RT-PCR enabled identification of PICALM-MLLT10 and BCR-ABL1 e1-a2 fusion transcripts; in the context of chronic and acute myeloid leukemia, the latter usually has a monocytic presentation.
  • We also identified overexpression of HOXA9, a gene essential to myeloid differentiation that is expressed in PICALM-MLLT10 and MLL-rearranged acute leukemias.
  • This case fits with and extends a recently proposed multistage AML model in which constitutive activation of tyrosine kinases by mutations (BCR-ABL1) are associated with deregulation of transcription factors central to myeloid differentiation (HOXA9 secondary to PICALM-MLLT10).
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / metabolism. Leukemia, Monocytic, Acute / genetics. Oncogene Proteins, Fusion / metabolism

  • 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
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16518848.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / PICALM-MLLT10 fusion protein, human; 0 / Transcription Factors; 0 / homeobox protein HOXA9; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down



56. Landrette SF, Kuo YH, Hensen K, Barjesteh van Waalwijk van Doorn-Khosrovani S, Perrat PN, Van de Ven WJ, Delwel R, Castilla LH: Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. Blood; 2005 Apr 1;105(7):2900-7
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] Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11.
  • Recurrent chromosomal rearrangements are associated with the development of acute myeloid leukemia (AML).
  • This fusion protein inhibits the core-binding factor (CBF), resulting in a block of hematopoietic differentiation, and induces leukemia upon the acquisition of additional mutations.
  • In this study, we demonstrate that Plag1 and Plagl2 independently cooperate with CBF beta-SMMHC in vivo to efficiently trigger leukemia with short latency in the mouse.
  • Finally, PLAG1 and PLAGL2 expression was increased in 20% of human AML samples.
  • Interestingly, PLAGL2 was preferentially increased in samples with chromosome 16 inversion, suggesting that PLAG1 and PLAGL2 may also contribute to human AML.
  • Overall, this study shows that Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Animals. Female. G1 Phase / immunology. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Male. Mice. Mice, Mutant Strains. Middle Aged. Mutagenesis, Insertional. Retroviridae / genetics. S Phase / immunology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. HGNC: Data: Gene Annotation .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15585652.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096983-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / PLAG1 protein, human; 0 / PLAGL2 protein, human; 0 / RNA-Binding Proteins; 0 / Transcription Factors
  •  go-up   go-down



57. Shali W, Hélias C, Fohrer C, Struski S, Gervais C, Falkenrodt A, Leymarie V, Lioure B, Raby P, Herbrecht R, Lessard M: Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH. Cancer Genet Cytogenet; 2006 Jul 15;168(2):133-45
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] Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.
  • We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or acute myeloid leukemias (t-AML) observed for 6 years.
  • Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/AML.
  • A considerable proportion of recurrent balanced translocations characterized t-AML secondary to therapy.
  • Compared to other series, recurrent translocations appeared to be more numerous (25%), probably reflecting an evolution of therapeutic modalities.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Gene Amplification. Gene Deletion. Humans. Karyotyping. Male. Middle Aged. Translocation, Genetic



58. Katsanos K, Sabharwal T, Ahmad F, Dourado R, Adam A: Onyx embolization of sporadic angiomyolipoma. Cardiovasc Intervent Radiol; 2009 Nov;32(6):1291-5
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.
  • We present what is to our knowledge the first case of successful embolization of a solitary sporadic AML with the use of a new nonadhesive liquid embolic agent (ethylene vinyl alcohol copolymer; Onyx).
  • Short-term follow-up magnetic resonance imaging showed complete tumor necrosis without any recurrent pathologic vessels.
  • The specific features, potential advantages in AML treatment, and technical limitations of this new liquid embolic agent are discussed.
  • [MeSH-minor] Adult. Angiography. Contrast Media. Female. Humans. Magnetic Resonance Imaging

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • Hazardous Substances Data Bank. DIMETHYL SULFOXIDE .
  • 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 = 19083054.001).
  • [ISSN] 1432-086X
  • [Journal-full-title] Cardiovascular and interventional radiology
  • [ISO-abbreviation] Cardiovasc Intervent Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Onyx copolymer; 0 / Polyvinyls; YOW8V9698H / Dimethyl Sulfoxide
  •  go-up   go-down



59. Boissel N, Nibourel O, Renneville A, Gardin C, Reman O, Contentin N, Bordessoule D, Pautas C, de Revel T, Quesnel B, Huchette P, Philippe N, Geffroy S, Terre C, Thomas X, Castaigne S, Dombret H, Preudhomme C: Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group. J Clin Oncol; 2010 Aug 10;28(23):3717-23
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] Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group.
  • PURPOSE: Recently, whole-genome sequencing in acute myeloid leukemia (AML) identified recurrent isocitrate dehydrogenase enzyme isoform (IDH1) mutations (IDH1m), previously reported to be involved in gliomas as well as IDH2 mutations (IDH2m).
  • The prognosis of both IDH1m and IDH2m in AML remains unclear.
  • PATIENTS AND METHODS: The prevalence and the prognostic impact of R132 IDH1 and R172 IDH2 mutations were evaluated in a cohort of 520 adults with AML homogeneously treated in the French Acute Leukemia French Association (ALFA) -9801 and -9802 trials.
  • In patients with CN-AML, IDH1m were associated with NPM1m (P = .008), but exclusive of CEBPAm (P = .03).
  • In CN-AML patients, IDH1m were found in 19% of favorable genotype ([NPM1m or CEBPAm] without fms-related tyrosine kinase 3 [FLT3] internal tandem duplication [ITD]) and were associated with a higher risk of relapse (RR) and a shorter overall survival (OS).
  • Favorable genotype in CN-AML could thus be defined by the association of NPM1m or CEBPAm with neither FLT3-ITD nor IDH1m.
  • In IDH2m CN-AML patients, we observed a higher risk of induction failure, a higher RR and a shorter OS.
  • CONCLUSION: Contrarily to what is reported in gliomas, IDH1m and IDH2m in AML are associated with a poor prognosis.
  • Screening of IDH1m could help to identify high-risk patients within the subset of CN-AML with a favorable genotype.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Humans. Middle Aged. Mutation. Prevalence. Prognosis. Protein Isoforms / genetics. Randomized Controlled Trials as Topic. Retrospective Studies. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • 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 = 20625116.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00880243/ NCT00931138
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
  •  go-up   go-down



60. Mulrooney DA, Dover DC, Li S, Yasui Y, Ness KK, Mertens AC, Neglia JP, Sklar CA, Robison LL, Davies SM, Childhood Cancer Survivor Study: Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study. Cancer; 2008 May 1;112(9):2071-9
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] Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study.
  • BACKGROUND: Limited data exist on the comprehensive assessment of late medical and social effects experienced by survivors of childhood and young adult acute myeloid leukemia (AML).
  • METHODS: This analysis included 272 5-year AML survivors who participated in the Childhood Cancer Survivor Study (CCSS).
  • The cumulative incidence of recurrent AML was 6.6% at 10 years (95% CI, 3.7%-9.6%) and 8.6% at 20 years (95% CI, 5.1%-12.1%).
  • CONCLUSIONS: Long-term survival from childhood AML > or =5-years after diagnosis was favorable.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18327823.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / K12 RR023247; United States / NCI NIH HHS / CA / U24 CA055727; United States / NCRR NIH HHS / RR / 1 K12 RR 023247; United States / NCI NIH HHS / CA / U24 CA 55727
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Robison LL; Hudson M; Armstrong G; Perkins J; O'Leary M; Friedman D; Pendergrass T; Greffe B; Odom L; Ruccione K; Mulvihill J; Ginsberg J; Meadows A; Tersak J; Ritchey A; Blatt J; Reaman G; Packer R; Davies S; Bhatia S; Qualman S; Hammond S; Termuhlen A; Ruymann F; Diller L; Grier H; Li F; Meacham L; Mertens A; Leisenring W; Potter J; Greenberg M; Nathan PC; Boice J; Rodriguez V; Smithson WA; Gilchrist G; Sklar C; Oeffinger K; Finklestein J; Anderson B; Inskip P; Vik TA; Weetman R; Green DM; Hayashi R; Vietti T; Marina N; Donaldson SS; Link MP; Dreyer Z; Whelan K; Sande J; Berkow R; Yasui Y; Casallis J; Zeltzer L; Goldsby R; Ablin A; Hutchinson R; Neglia J; Deapen D; Breslow N; Bowers D; Tomlinson G; Buchanan GR; Strong L; Stovall M
  •  go-up   go-down



61. Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party: Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study. Leukemia; 2007 Nov;21(11):2324-31
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 375 patients (54%) developed recurrent lymphoma, 10-year progression-free survival (PFS) being 31%.
  • Thirty-nine patients developed secondary myelodysplastic syndrome/acute myeloid leukaemia (MDS/AML), in 34 cases having received TBI as the conditioning regimen.
  • The 5-year non-relapse mortality (NRM) was 9%.
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / cytology. Bone Marrow Transplantation. Disease-Free Survival. Female. Humans. Male. Middle Aged. Registries. Remission Induction. Stem Cells / cytology. Transplantation, Autologous. Treatment Outcome



62. Bacher U, Kern W, Schnittger S, Hiddemann W, Haferlach T, Schoch C: Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia. Haematologica; 2005 Nov;90(11):1502-10
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] Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: It is well known that the different cytogenetic subgroups of acute myeloid leukemia (AML) show different age-specific frequencies.
  • For example, balanced translocations tend to be found in younger patients while complex aberrant karyotypes are usually found in elderly patients with AML.
  • DESIGN AND METHODS: We evaluated the population-based age-specific incidences of different cytogenetic subgroups in 2555 patients with AML between 21 and 70 years of age.
  • There were also different age-specific incidences of some recurrent molecular mutations.
  • INTERPRETATION AND CONCLUSIONS: These results are suggestive of different mechanisms in the pathogenesis of AML.
  • [MeSH-major] Cytogenetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Age Factors. Aged. Female. Genetic Markers / genetics. Genetics, Population. Humans. Incidence. Male. Middle Aged. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 16266897.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down



63. Walter MJ, Payton JE, Ries RE, Shannon WD, Deshmukh H, Zhao Y, Baty J, Heath S, Westervelt P, Watson MA, Tomasson MH, Nagarajan R, O'Gara BP, Bloomfield CD, Mrózek K, Selzer RR, Richmond TA, Kitzman J, Geoghegan J, Eis PS, Maupin R, Fulton RS, McLellan M, Wilson RK, Mardis ER, Link DC, Graubert TA, DiPersio JF, Ley TJ: Acquired copy number alterations in adult acute myeloid leukemia genomes. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12950-5
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] Acquired copy number alterations in adult acute myeloid leukemia genomes.
  • Cytogenetic analysis of acute myeloid leukemia (AML) cells has accelerated the identification of genes important for AML pathogenesis.
  • To complement cytogenetic studies and to identify genes altered in AML genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86 adult patients with de novo AML using 1.85 million feature SNP arrays.
  • A total of 201 somatic CNAs were found in the 86 AML genomes (mean, 2.34 CNAs per genome), with French-American-British system M6 and M7 genomes containing the most changes (10-29 CNAs per genome).
  • Twenty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were recurrent.
  • The mRNA expression levels of 57 genes were significantly altered in 27 of 50 recurrent CNA regions <5 megabases in size.
  • Collectively, 34 of 86 AML genomes (40%) contained alterations not found with cytogenetics, and 98% of these regions contained genes.
  • In this study of 86 adult AML genomes, the use of an unbiased high-resolution genomic screen identified many genes not previously implicated in AML that may be relevant for pathogenesis, along with many known oncogenes and tumor suppressor genes.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Jun 1;97(11):3581-8 [11369654.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1820-4 [10477709.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jan;36(1):90-8 [12461753.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2244-7 [12931227.001]
  • [Cites] Blood. 1993 Dec 1;82(11):3241-9 [8241496.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4129-37 [15806161.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2355-8 [16239911.001]
  • [Cites] Leukemia. 2006 Apr;20(4):696-706 [16467868.001]
  • [Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Leukemia. 2007 Mar;21(3):571-4 [17268525.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1648-55 [17494858.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Nat Genet. 2008 Jun;40(6):722-9 [18438408.001]
  • [Cites] Nature. 2008 Nov 6;456(7218):66-72 [18987736.001]
  • [Cites] Leukemia. 2009 Jan;23(1):85-94 [18818702.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1741-8 [19109227.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • (PMID = 19651600.001).
  • [ISSN] 1091-6490
  • [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
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL083012; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHLBI NIH HHS / HL / T32 HL007088; United States / NCI NIH HHS / CA / U10 CA101140
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / NSD1 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Nup98 protein, human
  • [Other-IDs] NLM/ PMC2716381
  •  go-up   go-down



64. Park HK, Zhang S, Wong MK, Kim HL: Clinical presentation of epithelioid angiomyolipoma. Int J Urol; 2007 Jan;14(1):21-5
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.
  • OBJECTIVE: Epithelioid angiomyolipomas (AML) of the kidney are malignant tumors with aggressive clinical behavior.
  • METHODS: We reviewed cases of epithelioid AML recently diagnosed at our institution to highlight the spectrum of clinical presentations.
  • The diagnosis of epithelioid AML was established by positive staining for melanoma and smooth muscle cell markers, and presence of perivascular epithelioid cells.
  • Two patients developed recurrent, metastatic disease following nephrectomy.
  • One patient with tuberous sclerosis and multiple, bilateral AML developed an enhancing renal tumor that did not contain any fat densities.
  • A partial nephrectomy was performed and pathology revealed epithelioid AML adjacent to conventional AML.
  • Epithelioid AML may be locally aggressive and metastasize.
  • [MeSH-minor] Adult. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17199855.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Duplicate Publication; Journal Article
  • [Publication-country] Australia
  •  go-up   go-down



65. Cornely OA, Böhme A, Reichert D, Reuter S, Maschmeyer G, Maertens J, Buchheidt D, Paluszewska M, Arenz D, Bethe U, Effelsberg J, Lövenich H, Sieniawski M, Haas A, Einsele H, Eimermacher H, Martino R, Silling G, Hahn M, Wacker S, Ullmann AJ, Karthaus M, Multinational Case Registry of the Infectious Diseases Working Party of the German Society for Hematology and Oncology: Risk factors for breakthrough invasive fungal infection during secondary prophylaxis. J Antimicrob Chemother; 2008 Apr;61(4):939-46
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.
  • Secondary prophylaxis of IFI is widely administered, but reliable data on outcome and risk factors for recurrent IFI during subsequent chemotherapy are not available.
  • This study determines risk factors for recurrent IFI in leukaemia patients.
  • METHODS: From 25 European cancer centres, 166 consecutive patients with acute myelogenous leukaemia (AML) and a recent history of proven or probable pulmonary IFI were included.
  • Recurrent IFI occurred in 26 patients (15.7%).
  • Multiple logistic regressions yielded predisposing factors: duration of neutropenia [per additional day; odds ratio (OR) 1.043, confidence interval (CI) 1.008-1.078], high-dose cytarabine (OR 3.920, CI 1.120-12.706), number of antibiotics (per antibiotic; OR 1.504, CI 1.089-2.086), partial response as outcome of prior IFI (OR 4.037, CI 1.301-12.524) and newly diagnosed AML (OR 3.823, CI 0.953-15.340).
  • CONCLUSIONS: Duration of neutropenia, high-dose cytarabine, prior antibiotic therapy and a partial response to the first IFI therapy were risk factors for recurrent IFI and should be considered in AML patients with prior pulmonary IFI undergoing further chemotherapy.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemoprevention. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Logistic Models. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18272515.001).
  • [ISSN] 1460-2091
  • [Journal-full-title] The Journal of antimicrobial chemotherapy
  • [ISO-abbreviation] J. Antimicrob. Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents
  •  go-up   go-down



66. Davis CJ, Barton JH, Sesterhenn IA: Cystic angiomyolipoma of the kidney: a clinicopathologic description of 11 cases. Mod Pathol; 2006 May;19(5):669-74
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.
  • This report deals with 11 examples of renal angiomyolipomas (AML) which appear to include an epithelial element as a part of the neoplasm in the form of gross or microscopic cysts-usually both.
  • Three of these were known to be symptomatic: intermittent flank pain and gross hematuria for 2 months; recurrent hematuria both before and after flank trauma and a third patient with acute abdomen due to a ruptured tumor blood vessel.
  • [MeSH-minor] Actins / analysis. Adult. Aged. Antigens, Neoplasm. Desmin / analysis. Female. Humans. Immunohistochemistry. MART-1 Antigen. Male. Melanoma-Specific Antigens. Middle Aged. Muscle, Smooth / chemistry. Neoplasm Proteins / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16528375.001).
  • [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 / Actins; 0 / Antigens, Neoplasm; 0 / Desmin; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
  •  go-up   go-down



67. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Zhang Y, Liu YR, Shi HL, Lu DP: Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22). Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Oct;13(5):733-40
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] Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22).
  • q22) frequently associated with additional chromosomal aberrations is one of the most recurrent chromosomal abnormalities in AML.
  • Clinically, this type of AML usually shows some specific characteristics and has a good response to chemotherapy with a high remission rate and a relatively long median survival.
  • On the other hand, some reports also showed poor prognosis in AML patients with t (8; 21), and the associated bad-prognosis factors have not been strongly established to date.
  • 21) AML in China, 75 Chinese AML patients with t (8;.
  • Cytogenetically, 62.5% cases had additional chromosomal abnormalities, and the main associated recurrent additional abnormalities were loss of a sex chromosome (LOS), trisomy 4, del (9q) and trisomy 8.
  • With a follow-up of 1 to 96 months, 19 cases relapsed at a median time of 10.5 months (range 3 to 42 months).
  • In multivariate analyses of prognostic factors, karyotype, extramedullary leukemia, age and post-remission therapy were of prognostic value for OS.
  • Extramedullary leukemia was an adverse prognostic factor (P = 0.012).
  • It is concluded that Chinese AML patients with t (8;.
  • 21) had some different characteristics as compared with patients from other countries, a relatively poor outcome was observed in our patients, especially in those with extramedullary leukemia or additional chromosomal abnormalities.
  • 21) AML in China, especially to those with adverse prognostic factors.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16277833.001).
  • [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] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
  •  go-up   go-down



68. Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E: del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality. Eur J Haematol; 2006 Sep;77(3):245-50
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] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
  • OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.
  • In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
  • RESULTS: A diagnosis of AML-M2 was confirmed in both patients by morphological and immunophenotyping studies.
  • The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Chromosomal Proteins, Non-Histone / genetics. Cytogenetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Oncogene Proteins / genetics. Oncogenes. Recurrence

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16856925.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
  •  go-up   go-down



69. Maserati E, Pressato B, Valli R, Minelli A, Sainati L, Patitucci F, Marletta C, Mastronuzzi A, Poli F, Lo Curto F, Locatelli F, Danesino C, Pasquali F: The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies. Br J Haematol; 2009 Apr;145(2):190-7
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] The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.
  • An investigation of 22 new patients with Shwachman-Diamond syndrome (SDS) and the follow-up of 14 previously reported cases showed that (i) clonal chromosome changes of chromosomes 7 and 20 were present in the bone marrow (BM) of 16 out of 36 cases, but if non-clonal changes were taken into account, the frequency of anomalies affecting these chromosomes was 20/36: a specific SDS karyotype instability was thus confirmed;.
  • (ii) the recurrent isochromosome i(7)(q10) did not include short arm material, whereas it retained two arrays of D7Z1 alphoid sequences;.
  • (iii) the deletion del(20)(q11) involved the minimal region of deletion typical of myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML);.
  • We conclude that karyotype instability is part of the natural history of SDS through a specific mutator effect, linked to lacking SBDS protein, with consequent clonal anomalies of chromosomes 7 and 20 in BM, which may eventually promote MDS/AML with the patients' ageing.
  • [MeSH-major] Aging / genetics. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Human, Pair 20. Chromosomes, Human, Pair 7. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Humans. In Situ Hybridization, Fluorescence. Isochromosomes. Karyotyping. Male. Proteins / genetics. Young Adult



70. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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.
  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • Here we review the differing technologies employed in generation of GEM of AML.
  • We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis



71. Trubia M, Albano F, Cavazzini F, Cambrin GR, Quarta G, Fabbiano F, Ciambelli F, Magro D, Hernandezo JM, Mancini M, Diverio D, Pelicci PG, Coco FL, Mecucci C, Specchia G, Rocchi M, Liso V, Castoldi G, Cuneo A: Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia. Leukemia; 2006 Jan;20(1):48-54
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] Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia.
  • Six patients with de novo acute myeloid leukemia (AML) and a t(2;3)(p15-21;q26-27) were identified among approximately 1000 cases enrolled in the GIMEMA trial.
  • The patients showed dysplasia of at least two myeloid cell lineages in all cases; they had a low-to-normal platelet count and displayed an immature CD34+ CD117+ immunophenotype.
  • We arrived at the following conclusions: (a) the t(2;3) is a recurrent translocation having an approximate 0.5% incidence in adult AML;.
  • [MeSH-major] Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Cytogenetic Analysis / methods. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Trisomy

  • COS Scholar Universe. author profiles.
  • 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 = 16619048.001).
  • [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
  •  go-up   go-down



72. Park SH, Chi HS, Park SJ, Jang S, Park CJ: [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes]. Korean J Lab Med; 2010 Jun;30(3):231-8
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] [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes].
  • BACKGROUND: AML with myelodysplasia related changes (AML MRC) is known to show a poor prognosis compared with de novo AML, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC.
  • We investigated the prognostic impact of MLD in AML MRC.
  • METHODS: A total of 357 patients newly diagnosed as AML at Asan Medical Center from January 2001 to December 2005 were analyzed.
  • They were diagnosed and classified as AML with recurrent genetic abnormalities, AML MRC, and AML not otherwise specified (AML NOS).
  • RESULTS: AML MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than AML NOS patients.
  • Patients with MLD among AML MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than AML NOS patients.
  • However, among AML MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD.
  • CONCLUSIONS: AML MRC patients showed a lower CR rate and shorter OS and EFS than AML NOS patients.
  • AML MRC patients with MLD showed similar results and their prognosis was not different from those without MLD.
  • MLD findings among AML MRC could be an independent poor prognostic factor in de novo AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Data Interpretation, Statistical. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis



73. Tang JM, Meng FY, Chen AW: [Gene expression profile of refractory acute myeloid leukemia (M2a)]. Ai Zheng; 2005 Jun;24(6):676-9
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] [Gene expression profile of refractory acute myeloid leukemia (M2a)].
  • BACKGROUND & OBJECTIVE: Recurrence is the major cause of treatment failure of acute myeloid leukemia (AML).
  • Drug resistance, the main cause of refractoriness of AML, is related to abnormal genes expression.
  • This study was to detect differential expression of genes in naive and recurrent/refractory AML, and explore potential mechanisms of recurrent/refractory AML.
  • METHODS: Differential gene expressions of bone marrow mononuclear cells between naive and recurrent/refractory diseases in 5 self-paired patients with AML-M(2a) were detected by DNA microarray.
  • RESULTS: In 925 tested genes, 14 were differentially expressed between naive and recurrent/refractory diseases in the 5 self-paired patients.
  • Of the 14 genes, 12 (involved in signal transduction, DNA replication, regulation of transcription, RNA processing, and regulation of cell cycle) were obviously up-regulated in recurrent diseases, and up-regulation of RRM1 (involved in DNA replication) was the most obvious.
  • CONCLUSIONS: Development of recurrent/refractory AML-M(2a) is concerned with various genes.
  • Up-regulation of these genes suggests that proliferation of recurrent/refractory AML-M(2a) blasts may be higher than that of naive AML-M(2a) blasts.
  • [MeSH-major] Gene Expression Profiling. Immunophenotyping. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / metabolism. Cell Proliferation. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Tumor Suppressor Proteins / metabolism. Up-Regulation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15946477.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins
  •  go-up   go-down



74. Kaya M, Nagoya S, Sasaki M, Kukita Y, Yamashita T: Primary total hip arthroplasty with Asian-type AML total hip prosthesis: follow-up for more than 10 years. J Orthop Sci; 2008 Jul;13(4):324-7
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] Primary total hip arthroplasty with Asian-type AML total hip prosthesis: follow-up for more than 10 years.
  • BACKGROUND: We retrospectively reviewed 137 consecutive total hip arthroplasties performed with AML-A stems and Tri-Lock cups to see whether design modifications made to these components would achieve durable biological fixation in the Japanese population in whom developmental dysplasia of the hip (DDH) is relatively common.
  • METHODS: Between April 1988 and June 1994, we performed 137 total hip arthroplasties using the AML-A prosthesis for the patients with osteoarthritis of the hip joint.
  • Another seven hips underwent revision surgery for recurrent dislocation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged. Reoperation. Young Adult

  • MedlinePlus Health Information. consumer health - Hip Replacement.
  • 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 = 18696190.001).
  • [ISSN] 0949-2658
  • [Journal-full-title] Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
  • [ISO-abbreviation] J Orthop Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down



75. Horton TM, Thompson PA, Berg SL, Adamson PC, Ingle AM, Dolan ME, Delaney SM, Hedge M, Weiss HL, Wu MF, Blaney SM, Children's Oncology Group Study: Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study. J Clin Oncol; 2007 Nov 1;25(31):4922-8
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] Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study.
  • PURPOSE: To determine the tolerability, pharmacokinetics, and mechanisms of temozolomide resistance in children with relapsed or refractory leukemia.
  • Pretreatment leukemia cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tumor and plasma MGMT promoter methylation, and microsatellite instability (MSI) were examined in 14 of 16 study patients and in tissue bank samples from children with acute leukemia not treated with temozolomide (MGMT, n = 67; MSI, n = 65).
  • RESULTS: Sixteen patients (nine female, seven male; acute lymphoblastic leukemia [ALL], n = 8; acute myeloid leukemia [AML], n = 8), median age 11 years (range, 1 to 19 years), received either 200 mg/m2/d (nine enrolled, three assessable for toxicity) or 260 mg/m2/d (seven enrolled, three assessable for toxicity) of temozolomide.
  • MGMT activity in leukemia cells was quite variable and was highest in patients with relapsed ALL.
  • CONCLUSION: Temozolomide was well tolerated at doses as high as 260 mg/m2/d for 5 days in children with relapsed or refractory leukemia.
  • Increased MGMT activity may account for the temozolomide resistance in children with relapsed leukemia.
  • Leukemia cell MGMT activity was higher in pediatric ALL than AML (P < .0001).
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacokinetics. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / genetics. Leukemia / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Female. Humans. Infant. Male. Microsatellite Instability. Tumor Suppressor Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17971589.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12CA90433; United States / NCI NIH HHS / CA / P30 CA14599; United States / NCI NIH HHS / CA / U01CA63187; United States / NCI NIH HHS / CA / UO1-CA97452
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down



76. Yamamoto K, Yakushijin K, Kawamori Y, Minagawa K, Katayama Y, Matsui T: Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jul 1;176(1):61-6
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] Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for acute myeloblastic leukemia.
  • Reciprocal translocations involving the long arm of chromosome 7 are relatively rare cytogenetic aberrations in myelodysplastic syndrome (MDS) and acute myeloblastic leukemia (AML).
  • A 44-year-old woman was initially given a diagnosis of de novo AML M6A with a normal karyotype.
  • Considering two other such reported cases of AML, the t(7;9)(q22;q34) may be a novel recurrent translocation in myeloid malignancies.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Female. Humans. Spectral Karyotyping



77. Lu SH, Hou YY, Tan YS, Xu JF, Zeng HY, Sujie AK, Wang XD, Bai CX: Clinical and histopathological alterations of lymphangioleiomyomatosis in 14 Chinese patients. Chin Med J (Engl); 2009 Aug 20;122(16):1895-900
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 LAM is characterized by progressive dyspnea on exertion, recurrent pneumothorax, and chylous fluid collections.
  • Extrapulmonary findings such as renal angiomyolipoma (AML), enlarged abdominal lymph nodes, liver AML and retroperitoneal lymphangioleiomyoma were seen in 21.4%, 14.3%, 7.14% and 7.14% in 14 cases respectively, which is remarkably lower than in the previously reported.
  • CONCLUSIONS: Women with unexplained recurrent pneumothorax, tuberous sclerosis, or a diagnosis of primary spontaneous pneumothorax or emphysema in the setting of limited or absent tobacco use should undergo high-resolution computed tomography (HRCT) scan screening for LAM.
  • [MeSH-minor] Adolescent. Adult. Aged. Contraceptives, Oral, Synthetic. Female. Humans. Immunohistochemistry. Medroxyprogesterone / therapeutic use. Middle Aged. Ovariectomy. Progesterone / therapeutic use. Progestins / therapeutic use. Young Adult

  • Genetic Alliance. consumer health - Lymphangioleiomyomatosis.
  • Hazardous Substances Data Bank. MEDROXYPROGESTERONE .
  • Hazardous Substances Data Bank. PROGESTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19781367.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Synthetic; 0 / Progestins; 4G7DS2Q64Y / Progesterone; HSU1C9YRES / Medroxyprogesterone
  •  go-up   go-down



78. de Lima M, Giralt S, Thall PF, de Padua Silva L, Jones RB, Komanduri K, Braun TM, Nguyen HQ, Champlin R, Garcia-Manero G: Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study. Cancer; 2010 Dec 01;116(23):5420-31
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] Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study.
  • BACKGROUND: Recurrence is a major cause of treatment failure after allogeneic transplantation for acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), and treatment options are very limited.
  • Azacitidine is a DNA methyltransferase inhibitor with activity in myeloid disease.
  • CONCLUSIONS: Azacitidine at 32 mg/m2 given for 5 days is safe and can be administered after allogeneic transplant for at least 4 cycles to heavily pretreated AML/MDS patients.
  • [MeSH-major] Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Adult. Aged. DNA Methylation. Disease-Free Survival. Drug Administration Schedule. Female. Graft vs Host Disease / epidemiology. Humans. Male. Middle Aged. Recurrence. Transplantation, Homologous



79. Graziano A, Santangelo M, Umana DS: Clinical evaluation of epithelioid angiomyolipoma. Ann Ital Chir; 2008 Mar-Apr;79(2):135-8
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.
  • OBJECTIVE: Epithelioid angiomyolipomas (AML) of the kidney are malignant tumors with aggressive clinical behavior.
  • The diagnosis of epithelioid AML was established by positive staining for melanoma and smooth muscle cell markers, and presence of perivascular epithelioid cells.
  • Two patients developed recurrent, metastatic disease following nephrectomy.
  • Epithelioid AML, may be locally aggressive and metastasized.
  • [MeSH-minor] Adult. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Kidney / pathology. Male. Middle Aged. Nephrectomy. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18727277.001).
  • [ISSN] 0003-469X
  • [Journal-full-title] Annali italiani di chirurgia
  • [ISO-abbreviation] Ann Ital Chir
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  •  go-up   go-down



80. Arnaud B, Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Banzakour S, Bourquard P, Morice P, Le Calvez G, Marion V, Abgrall JF, Berthou C, De Braekeleer M: Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with acute myeloblastic leukemia. Cancer Genet Cytogenet; 2005 Sep;161(2):110-5
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] Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with acute myeloblastic leukemia.
  • A large number of abnormalities involving the MLL gene have been associated with hematological malignancies, including acute myeloblastic leukemias (AML).
  • Given the overall unfavorable prognosis of AML with an MLL abnormality, its reliable and accurate detection is needed for informed treatment decision.
  • We therefore investigated the occurrence of MLL abnormalities in 239 unselected consecutive AML patients, using conventional cytogenetic and fluorescent in situ hybridization (FISH) analyses.
  • MLL abnormalities were more frequently found in AML-M5 and M4, mainly as rearrangements, and in AML-M2, mainly as overrepresentation.
  • All M2, M4, and M5 AML patients without known recurrent translocations, such as t(8;21) and inv(16), should be investigated by FISH with an MLL probe because it allows the detection of MLL rearrangement that would go undetected by conventional cytogenetics and because it has the ability of detecting multiple copies of the MLL gene in, for example, marker chromosomes and double minutes.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant, Newborn. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16102580.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down



81. Yang L, Zhang Y, Zhang MR, Xiao ZJ: [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations]. Zhonghua Yi Xue Za Zhi; 2005 Aug 31;85(33):2312-6
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] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
  • OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.
  • METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.
  • RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.
  • The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.
  • 21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.
  • 17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.
  • CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene and t (15;.
  • [MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. NAD(P)H Dehydrogenase (Quinone) / genetics. Translocation, Genetic. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 16321221.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
  •  go-up   go-down



82. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics



83. Marcucci G, Maharry K, Wu YZ, Radmacher MD, Mrózek K, Margeson D, Holland KB, Whitman SP, Becker H, Schwind S, Metzeler KH, Powell BL, Carter TH, Kolitz JE, Wetzler M, Carroll AJ, Baer MR, Caligiuri MA, Larson RA, Bloomfield CD: IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study. J Clin Oncol; 2010 May 10;28(14):2348-55
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] IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study.
  • PURPOSE To analyze the frequency and associations with prognostic markers and outcome of mutations in IDH genes encoding isocitrate dehydrogenases in adult de novo cytogenetically normal acute myeloid leukemia (CN-AML).
  • IDH2 mutations, previously unreported in AML, were detected in 69 patients (19%; 13 with R172 and 56 with R140).
  • The highest expressed gene and microRNAs in R172 IDH2-mutated patients compared with the IDH1/IDH2wt patients were APP (previously associated with complex karyotype AML) and miR-1 and miR-133 (involved in embryonal stem-cell differentiation), respectively.
  • CONCLUSION IDH1 and IDH2 mutations are recurrent in CN-AML and have an unfavorable impact on outcome.
  • The R172 IDH2 mutations, previously unreported in AML, characterize a novel subset of CN-AML patients lacking other prognostic mutations and associate with unique gene- and microRNA-expression profiles that may lead to the discovery of novel, therapeutically targetable leukemogenic mechanisms.

  • 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 .
  • 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] N Engl J Med. 1995 Jun 22;332(25):1671-7 [7760868.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4290-301 [15514371.001]
  • [Cites] Genomics. 1996 Oct 1;37(1):140-1 [8921382.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):55-9 [9426057.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):482-93 [15534356.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Nat Cell Biol. 2005 Mar;7(3):255-61 [15723050.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Leukemia. 2006 Mar;20(3):426-32 [16424866.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] J Immunol. 2006 Jul 15;177(2):1078-84 [16818764.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Am J Hematol. 2006 Oct;81(10):779-86 [16838325.001]
  • [Cites] J Clin Oncol. 2009 Oct 20;27(30):5031-8 [19752345.001]
  • [Cites] Inflamm Res. 2009 Dec;58(12):909-19 [19603257.001]
  • [Cites] Nature. 2009 Dec 10;462(7274):739-44 [19935646.001]
  • [Cites] Blood. 2010 Jan 21;115(3):453-74 [19880497.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] J Inherit Metab Dis. 2008 Apr;31(2):226-9 [18392745.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):896-903 [8078551.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5164-7 [17341662.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3337-43 [17577018.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1552-9 [17940205.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5371-9 [18378853.001]
  • [Cites] Int J Oncol. 2008 Aug;33(2):239-44 [18636143.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):336-45 [18692684.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):346-55 [18692685.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4934-9 [18591543.001]
  • [Cites] J Exp Med. 2008 Oct 27;205(11):2499-506 [18936236.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):813-5 [19228626.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6215-24 [18955566.001]
  • [Cites] J Clin Oncol. 2009 Jul 1;27(19):3198-204 [19451432.001]
  • [Cites] Circ J. 2009 Aug;73(8):1492-7 [19521018.001]
  • [Cites] Best Pract Res Clin Haematol. 2009 Jun;22(2):239-48 [19698931.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] Blood. 2009 Oct 1;114(14):2993-3000 [19643984.001]
  • [Cites] J Clin Oncol. 1999 Sep;17(9):2831-9 [10561359.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Hypertens Res. 2002 Jan;25(1):135-40 [11924719.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):415-23 [12077272.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1940-51 [15217827.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1418-25 [8640834.001]
  • (PMID = 20368543.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / CA140158; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / R21 CA129657; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U24 CA114725; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA129657; United States / NCI NIH HHS / CA / CA114725; United States / NCI NIH HHS / CA / CA31946
  • [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 / MicroRNAs; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
  • [Other-IDs] NLM/ PMC2881719
  •  go-up   go-down



84. Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, La Starza R, Diverio D, Colombo E, Santucci A, Bigerna B, Pacini R, Pucciarini A, Liso A, Vignetti M, Fazi P, Meani N, Pettirossi V, Saglio G, Mandelli F, Lo-Coco F, Pelicci PG, Martelli MF, GIMEMA Acute Leukemia Working Party: Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med; 2005 Jan 20;352(3):254-66
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] Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
  • METHODS: We used immunohistochemical methods to study the subcellular localization of NPM in bone marrow-biopsy specimens from 591 patients with primary acute myelogenous leukemia (AML).
  • RESULTS: Cytoplasmic NPM was detected in 208 (35.2 percent) of the 591 specimens from patients with primary AML but not in 135 secondary AML specimens or in 980 hematopoietic or extrahematopoietic neoplasms other than AML.
  • It was associated with a wide spectrum of morphologic subtypes of the disease, a normal karyotype, and responsiveness to induction chemotherapy, but not with recurrent genetic abnormalities.
  • There was a high frequency of FLT3 internal tandem duplications and absence of CD34 and CD133 in AML specimens with a normal karyotype and cytoplasmic dislocation of NPM, but not in those in which the protein was restricted to the nucleus.
  • AML specimens with cytoplasmic NPM carried mutations of the NPM gene that were predicted to alter the protein at its C-terminal; this mutant gene caused cytoplasmic localization of NPM in transfected cells.
  • CONCLUSIONS: Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
  • [MeSH-major] Bone Marrow / pathology. Cytoplasm / chemistry. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Nucleolus. DNA Mutational Analysis. Humans. Karyotyping. Middle Aged. Remission Induction. Transfection. Translocation, Genetic



85. Nimer SD: Is it important to decipher the heterogeneity of "normal karyotype AML"? Best Pract Res Clin Haematol; 2008 Mar;21(1):43-52
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] Is it important to decipher the heterogeneity of "normal karyotype AML"?
  • Almost half of adult acute myelogenous leukemia (AML) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.
  • The finding of recurrent cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.
  • Yet "normal karyotype AML" lacks such obvious abnormalities, but has a variety of prognostically important genetic abnormalities.
  • Although resistance to treatment is associated with specific mutations, the degree to which the leukemia resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.
  • Although usually all of the circulating leukemia cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.
  • Increased understanding of the biological consequences of at least some of these mutations in "normal karyotype AML" is leading to more targeted approaches to develop more effective treatments for this disease.

  • 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
  • [Cites] Cancer Genet Cytogenet. 1989 Jul 15;40(2):203-16 [2766244.001]
  • [Cites] Blood. 1989 Dec;74(8):2668-73 [2479427.001]
  • [Cites] Clin Lab Med. 1990 Dec;10(4):755-67 [2272173.001]
  • [Cites] Am J Med Genet Suppl. 1990;7:251-61 [2149958.001]
  • [Cites] EMBO J. 1993 Dec;12(12):4481-7 [8223458.001]
  • [Cites] Nat Genet. 1994 Feb;6(2):146-51 [8162068.001]
  • [Cites] Cancer Genet Cytogenet. 1994 Mar;73(1):1-7 [8174068.001]
  • [Cites] J Clin Invest. 1994 Aug;94(2):489-96 [8040301.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1423-30 [7731694.001]
  • [Cites] Leuk Res. 2004 Jan;28(1):43-8 [14630079.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Nature. 1970 Jun 27;226(5252):1209-11 [4316300.001]
  • [Cites] Nature. 1970 Jun 27;226(5252):1211-3 [4316301.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1975;39 Pt 1:1-7 [50905.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Feb;74(2):560-4 [265521.001]
  • [Cites] Br J Cancer. 1977 Mar;35(3):265-72 [322689.001]
  • [Cites] Arch Intern Med. 1983 Sep;143(9):1726-31 [6577818.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 May;83(9):2934-8 [3458254.001]
  • [Cites] Prog Clin Biol Res. 1995;393:169-76 [8545449.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]
  • [Cites] Am J Clin Pathol. 1997 Jun;107(6):653-60 [9169661.001]
  • [Cites] Leuk Lymphoma. 1997 Aug;26(5-6):589-93 [9389365.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3635-44 [10207087.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11370-5 [10500183.001]
  • [Cites] J Natl Cancer Inst. 1961 Nov;27:1013-35 [14480645.001]
  • [Cites] Trans Assoc Am Physicians. 1955;68:78-81 [13299314.001]
  • [Cites] Leuk Res. 2006 Aug;30(8):1037-42 [16303180.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Mol Cell Biol. 2006 Sep;26(17):6395-402 [16914725.001]
  • [Cites] Br J Haematol. 2006 Sep;134(6):616-9 [16938118.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]
  • [Cites] Haematologica. 2006 Dec;91(12):1653-61 [17145602.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3509-12 [17179228.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5164-7 [17341662.001]
  • [Cites] Oncogene. 2007 Jul 5;26(31):4596-9 [17237811.001]
  • [Cites] J Clin Pathol. 2007 Nov;60(11):1238-43 [17259299.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 24;276(2):673-9 [11027530.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]
  • [Cites] Leukemia. 2001 Aug;15(8):1161-4 [11480556.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] J Biol Chem. 2001 Nov 2;276(44):40373-6 [11568179.001]
  • [Cites] Science. 2002 Feb 22;295(5559):1523-5 [11809937.001]
  • [Cites] Cancer Immunol Immunother. 2002 Aug;51(6):299-310 [12111118.001]
  • [Cites] Cell Growth Differ. 2002 Jun;13(6):275-83 [12114217.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Leukemia. 2002 Oct;16(10):1974-83 [12357348.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jul;37(3):237-51 [12759922.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 1:263-73 [3472723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6131-5 [3476934.001]
  • [Cites] Science. 1956 Jul 20;124(3212):127-9 [13337365.001]
  • [Cites] Acta Paediatr Suppl. 1963;:SUPPL146:77-91 [14043522.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]
  • [Cites] Oncogene. 2005 May 26;24(23):3847-52 [15750627.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]
  • [Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3958-61 [16081693.001]
  • [Cites] Haematologica. 2005 Dec;90(12):1617-25 [16330434.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Leukemia. 2006 Feb;20(2):212-7 [16357841.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):175-87 [16530702.001]
  • [Cites] Pediatr Res. 2006 Apr;59(4 Pt 2):59R-64R [16549550.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3737-46 [16585200.001]
  • (PMID = 18342811.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS44325; NLM/ PMC2654590
  •  go-up   go-down



86. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
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] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
  • Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.
  • Here, we demonstrate in 893 newly diagnosed cases of AML mutations in the IDH1 (6%) and IDH2 (11%) genes.
  • Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).
  • In AML, IDH1 and IDH2 mutations are more common among AML with normal karyotype and NPM1(mutant) genotypes.
  • Thus, IDH1 and IDH2 mutations are common genetic aberrations in AML, and IDH1 mutations may carry prognostic value in distinct subtypes of AML.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Hematologic Diseases. Humans. Janus Kinase 2 / genetics. Male. Middle Aged. Prevalence. Prognosis. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 20538800.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 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



87. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
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.
  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without AML who was refractory to G-CSF treatment.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.
  • [MeSH-minor] Adult. Cells, Cultured. Dimerization. Drug Resistance. Female. Gene Expression. Humans. Infant, Newborn. Ligands. Male. Parents. Point Mutation. Signal Transduction / drug effects. Signal Transduction / immunology

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down



88. Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF: Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation. Blood; 2010 Apr 8;115(14):2749-54
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] Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.
  • Recent genome-wide screening also revealed IDH1 mutation as a recurrent event in acute myeloid leukemia (AML), but its clinical implications in AML are largely unknown.
  • We analyzed 493 adult Chinese AML patients in Taiwan and found 27 patients (5.5%) harboring this mutation.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics
  • [MeSH-minor] Adult. Aged. Antigens, CD13 / biosynthesis. Antigens, CD13 / genetics. Antigens, CD14 / biosynthesis. Antigens, CD14 / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Genome-Wide Association Study. HLA-DR Antigens / biosynthesis. HLA-DR Antigens / genetics. Humans. Male. Middle Aged. Recurrence. Remission Induction. Taiwan

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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
  • [CommentIn] Blood. 2010 Jul 22;116(3):495-6 [20651083.001]
  • (PMID = 20097881.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down



89. Camera A, Rinaldi CR, Palmieri S, Cantore N, Mele G, Mettivier V, Miraglia E, Mastrullo L, Grimaldi F, Luciano L, Guerriero A, Rotoli B, Ferrara F: Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or relapsed adult acute myeloid leukemia patients. Ann Hematol; 2009 Feb;88(2):151-8
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] Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or relapsed adult acute myeloid leukemia patients.
  • A large proportion of adult patients with acute myeloid leukemia (AML) relapse after treatment, and some of them are resistant to primary induction chemotherapy.
  • Sixty-one patients from seven hematological centers with poor-risk AML, primary refractory (n = 16), or relapsed (n = 45) were treated with a salvage regimen, including fludarabine (2 days) and cytarabine (3 days) in a sequential continuous infusion, associated with liposomal daunorubicin (3 days) (FLAD).
  • Complete response rate was 44% and 56% for refractory and relapsed patients, respectively, with an overall response rate of 52% (32 of 61).
  • Twenty patients (62.5%) relapsed after this treatment in a median of 7.3 months; ten patients relapsed after a SCT procedure.
  • A better response rate was obtained in the subgroup of relapsed patients, compared to patients treated for refractory disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Daunorubicin / administration & dosage. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Liposomes. Male. Middle Aged. Recurrence. Salvage Therapy. Stem Cell Transplantation. Survival Rate. Time Factors



90. Shearer BM, Knudson RA, Flynn HC, Ketterling RP: Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia. Leukemia; 2005 Jan;19(1):126-31
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] Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia.
  • The t(6;9)(p23;q34)-DEK/CAN fusion occurs with an incidence of 1-5% in adult patients with acute myelogenous leukemia (AML) and tends to have an unfavorable prognosis at diagnosis.
  • Unfortunately, no commercial or previously published fluorescence in situ hybridization (FISH) strategies exist for this recurrent anomaly.
  • The development of this sensitive D-FISH strategy for the detection of the t(6;9)(p23;q34) adds to the AML FISH testing repertoire, and is effective in the detection of low-level disease in post-treatment samples in these patients.
  • [MeSH-major] Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins / genetics. Recombinant Fusion Proteins / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15510206.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins
  •  go-up   go-down



91. Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T: Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience. Eur J Haematol; 2005 May;74(5):418-23
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] Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
  • The actual utility of a new classification system of acute myeloid leukemia (AML) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
  • In this study, we evaluated long-term outcomes of unselected AML patients categorized according to the new WHO classification.
  • Between 1990 and 2002, 109 adult AML cases were referred to our hospital.
  • AML with recurrent genetic abnormalities accounted for 26%, AML with multilineage dysplasia for 29%, therapy-related AML for 13%, and AML not otherwise categorized for 32% of classifiable cases.
  • These results indicate that outcomes for AML patients appear to be distinguished on the basis of the WHO classification, but the prognostic significance of multilineage dysplasia and prior therapy is lost after adjusting for cytogenetic risk and age.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Humans. Middle Aged. Palliative Care. Retrospective Studies. Survival Analysis. Survivors. Treatment Outcome. World Health Organization

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15813916.001).
  • [ISSN] 0902-4441
  • [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



92. Sperr WR, Mitterbauer M, Mitterbauer G, Kundi M, Jäger U, Lechner K, Valent P: Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse. Clin Cancer Res; 2005 Sep 15;11(18):6536-43
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] Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.
  • PURPOSE: Recent data suggest that tryptase is produced by blast cells in a group of patients with acute myeloid leukemia (AML).
  • PATIENTS: In this study, we examined the value of tryptase as a marker of minimal residual AML.
  • In 61 patients with de novo AML exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.
  • Thus, AML relapses occurred in 15 of 29 patients with CR + BR (52%) and in 12 of 13 patients with CR without BR (92%), resulting in a significantly reduced probability of continuous CR for patients with CR without BR (P < 0.05).
  • In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a recurrent elevation of tryptase in CR was invariably followed by a hematologic relapse.
  • CONCLUSION: A persistently elevated tryptase level in AML in CR is indicative of minimal residual AML and associated with a high risk of relapse.
  • [MeSH-major] Leukemia, Myeloid / pathology. Neoplasm, Residual / pathology. Serine Endopeptidases / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Recurrence, Local. Oncogene Proteins, Fusion / genetics. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Analysis. Time Factors. Tryptases

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16166430.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
  •  go-up   go-down



93. Inaba H, Stewart CF, Crews KR, Yang S, Pounds S, Pui CH, Rubnitz JE, Razzouk BI, Ribeiro RC: Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia. Cancer; 2010 Jan 1;116(1):98-105
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] Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia.
  • BACKGROUND: The prognosis after recurrence of pediatric acute myeloid leukemia (AML) is poor, and effective salvage regimens are urgently needed.
  • METHODS: In phase 1 and pilot studies, the authors evaluated the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of a 5-day course of cladribine followed by topotecan in pediatric patients with recurrent/refractory AML.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Topotecan .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Cancer Society.
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):633-40 [12576429.001]
  • [Cites] J Clin Oncol. 2003 Aug 1;21(15):2940-7 [12885813.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Nov;9(11):706-13 [14652854.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4377-85 [14645428.001]
  • [Cites] Cancer Res. 1973 Nov;33(11):2834-6 [4748440.001]
  • [Cites] Biometrics. 1989 Sep;45(3):925-37 [2790129.001]
  • [Cites] J Clin Invest. 1990 Nov;86(5):1480-8 [1700795.001]
  • [Cites] J Clin Oncol. 1992 Mar;10(3):364-70 [1346800.001]
  • [Cites] J Clin Oncol. 1992 Oct;10(10):1514-8 [1357107.001]
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1235-9 [7906999.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2098-104 [9058732.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2233-7 [9626225.001]
  • [Cites] Clin Cancer Res. 1996 Dec;2(12):1921-30 [9816150.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3051-7 [15632206.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1):1-25 [17222748.001]
  • [Cites] Br J Haematol. 2007 Jan;136(2):229-236 [17278259.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] J Clin Oncol. 2002 Mar 15;20(6):1617-24 [11896112.001]
  • (PMID = 19885837.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 7M7YKX2N15 / Topotecan
  • [Other-IDs] NLM/ NIHMS151111; NLM/ PMC2920745
  •  go-up   go-down



94. Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I: Phenotypic quantitative features of patients with acute myeloid leukemia. Neoplasma; 2006;53(2):155-60
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] Phenotypic quantitative features of patients with acute myeloid leukemia.
  • The recent WHO classification for acute myeloid leukemias (AML) separates entities by recurrent cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
  • We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo AML, using a 3-color two-step panel.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 16575472.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
  •  go-up   go-down



95. Hijiya N, Ness KK, Ribeiro RC, Hudson MM: Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer; 2009 Jan 1;115(1):23-35
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 leukemia as a secondary malignancy in children and adolescents: current findings and issues.
  • Secondary acute leukemia is a devastating complication in children and adolescents who have been treated for cancer.
  • Secondary acute lymphoblastic leukemia (s-ALL) was rarely reported previously but can be distinguished today from recurrent primary ALL by comparison of immunoglobulin and T-cell receptor rearrangement.
  • Secondary acute myeloid leukemia (s-AML) is much more common, and some cases actually may be second primary cancers.
  • Treatment-related and host-related characteristics and their interactions have been identified as risk factors for s-AML.
  • A high cumulative dose of alkylating agents is well known to predispose to s-AML.
  • The prevalence of alkylator-associated s-AML has diminished among pediatric oncology patients with the reduction of cumulative alkylator dose and limited use of the more leukemogenic alkylators.
  • The best-documented topoisomerase II inhibitor-associated s-AML is s-AML associated with epipodophyllotoxins.
  • The risk of s-AML in these cases is influenced by the schedule of drug administration and by interaction with other antineoplastic agents but is not consistently found to be related to cumulative dose.
  • The unpredictable risk of s-AML after epipodophyllotoxin therapy may discourage the use of these agents, even in patients at a high risk of disease recurrence, although the benefit of recurrence prevention may outweigh the risk of s-AML.
  • Studies in survivors of adult cancers suggest that, contrary to previous beliefs, the outcome of s-AML is not necessarily worse than that of de novo AML when adjusted for cytogenetic features.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PODOFILOX .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • [Cites] Lancet. 1996 Feb 3;347(8997):295-7 [8569364.001]
  • [Cites] N Engl J Med. 1996 Mar 21;334(12):745-51 [8592547.001]
  • [Cites] J Natl Cancer Inst. 1996 Dec 18;88(24):1840-7 [8961974.001]
  • [Cites] Cancer. 1997 Mar 1;79(5):1049-54 [9041170.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2247-53 [9196137.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3617-23 [10339466.001]
  • [Cites] Blood. 1999 Jul 15;94(2):803-7 [10397748.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3221-5 [10506622.001]
  • [Cites] Bone Marrow Transplant. 1999 Oct;24(7):735-9 [10516676.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4926-33 [15611507.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):926-7 [15681547.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Leukemia. 2006 Feb;20(2):239-46 [16341039.001]
  • [Cites] Oncogene. 2006 Sep 25;25(43):5875-84 [16998502.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2020-6 [17057028.001]
  • [Cites] Blood. 2007 Jan 1;109(1):46-51 [16985182.001]
  • [Cites] Bone Marrow Transplant. 2007 Jan;39(2):59-70 [17143301.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):292-300 [17159192.001]
  • [Cites] J Natl Cancer Inst. 2007 Feb 7;99(3):196-205 [17284714.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):493-500 [17290056.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Mar;20(1):29-37 [17336252.001]
  • [Cites] JAMA. 2007 Mar 21;297(11):1207-15 [17374815.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1431-5 [17460701.001]
  • [Cites] Ophthalmology. 2007 Jul;114(7):1378-83 [17613328.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1379-87 [17488876.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3871-6 [17664457.001]
  • [Cites] J Pediatr Hematol Oncol. 2007 Sep;29(9):646-8 [17805043.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):233-55 [9748598.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13176-81 [9789061.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3880-9 [9850034.001]
  • [Cites] Bone Marrow Transplant. 1999 Jan;23(1):21-5 [10037046.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):569-77 [10080601.001]
  • [Cites] Pediatr Hematol Oncol. 1999 May-Jun;16(3):267-70 [10326227.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2128-36 [17673902.001]
  • [Cites] Haematologica. 2007 Oct;92(10):1389-98 [17768113.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:453-9 [18024664.001]
  • [Cites] J Clin Oncol. 2008 Mar 1;26(7):1106-11 [18309945.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Med Pediatr Oncol. 1989;17(6):477-84 [2586362.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Leukemia. 2000 Feb;14(2):232-7 [10673738.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1588-93 [10688812.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):947-55 [10694543.001]
  • [Cites] Br J Haematol. 2000 Apr;109(1):13-23 [10848777.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):91-4 [10883674.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(15):2836-42 [10920131.001]
  • [Cites] Ann Oncol. 2000 Oct;11(10):1289-94 [11106118.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2205-22 [11187912.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2234-9 [11187914.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2240-6 [11187915.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2276-85 [11187919.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2295-306 [11187921.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2307-20 [11187922.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):109-17 [11225603.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):525-35 [11340607.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):536-40 [11340608.001]
  • [Cites] Leukemia. 2001 Jun;15(6):963-70 [11417484.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11592-7 [11553769.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):429-36 [11905737.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2002 Jul 15;100(2):427-34 [12091332.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1972-6 [12200354.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):605-11 [12439220.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1074-81 [12637473.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1195-204 [12663705.001]
  • [Cites] Blood. 2003 May 15;101(10):3862-7 [12531808.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2123-37 [12775738.001]
  • [Cites] Leukemia. 2004 Jan;18(1):120-5 [14586477.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2675-80 [15102670.001]
  • [Cites] Int J Hematol. 2004 Apr;79(3):229-34 [15168589.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2510-1 [15197216.001]
  • [Cites] Blood. 2004 Aug 1;104(3):822-8 [15090454.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1581-6 [15356657.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Apr;3(4):532-8 [2984346.001]
  • [Cites] Blood. 1987 Nov;70(5):1412-7 [2822173.001]
  • [Cites] Cancer. 1988 Oct 1;62(7):1364-70 [3046737.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):432-7 [1999712.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1682-7 [1944468.001]
  • [Cites] J Clin Oncol. 1992 Jan;10(1):156-63 [1309379.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):209-17 [8426196.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1039-45 [8388919.001]
  • [Cites] Leukemia. 1993 Dec;7(12):1975-86 [8255096.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1680-4 [7564509.001]
  • [Cites] Leukemia. 1996 Jan;10(1):27-31 [8558933.001]
  • (PMID = 19072983.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] L36H50F353 / Podophyllotoxin
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS135594; NLM/ PMC2767267
  •  go-up   go-down



96. La Starza R, Matteucci C, Gorello P, Brandimarte L, Pierini V, Crescenzi B, Nofrini V, Rosati R, Gottardi E, Saglio G, Santucci A, Berchicci L, Arcioni F, Falini B, Martelli MF, Sambani C, Aventin A, Mecucci C: NPM1 deletion is associated with gross chromosomal rearrangements in leukemia. PLoS One; 2010;5(9):e12855
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] NPM1 deletion is associated with gross chromosomal rearrangements in leukemia.
  • BACKGROUND: NPM1 gene at chromosome 5q35 is involved in recurrent translocations in leukemia and lymphoma.
  • It also undergoes mutations in 60% of adult acute myeloid leukemia (AML) cases with normal karyotype.
  • The incidence and significance of NPM1 deletion in human leukemia have not been elucidated.
  • METHODOLOGY AND PRINCIPAL FINDINGS: Bone marrow samples from 145 patients with myelodysplastic syndromes (MDS) and AML were included in this study.
  • NPM1 deletion was an uncommon event in the "5q- syndrome" but occurred in over 40% of cases with high risk MDS/AML with complex karyotypes and 5q loss.
  • CONCLUSIONS AND SIGNIFICANCE: NPM1/5q35 deletion is a consistent event in MDS/AML with a 5q-/-5 in complex karyotypes.
  • NPM1 deletion and NPM1 exon 12 mutations appear to be mutually exclusive and are associated with two distinct cytogenetic subsets of MDS and AML.
  • [MeSH-major] Gene Deletion. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 5 / metabolism. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Young Adult

  • 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
  • [Cites] Leukemia. 2006 Feb;20(2):319-21 [16341035.001]
  • [Cites] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867.001]
  • [Cites] Cancer Genet Cytogenet. 2006 May;167(1):66-9 [16682289.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1943-9 [16990778.001]
  • [Cites] J Mol Histol. 2006 Sep;37(5-7):239-51 [16855788.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jul 1;176(1):1-21 [17574959.001]
  • [Cites] Haematologica. 2008 Jul;93(7):976-82 [18591623.001]
  • [Cites] Leukemia. 2009 Jan;23(1):203-6 [18596741.001]
  • [Cites] PLoS One. 2009;4(2):e4583 [19240791.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1252-6 [19322210.001]
  • [Cites] Oncogene. 2009 Oct 1;28(39):3429-41 [19597464.001]
  • [Cites] Nat Med. 2010 Jan;16(1):49-58 [19898489.001]
  • [Cites] Nat Med. 2010 Jan;16(1):59-66 [19966810.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4638-41 [12036901.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Haematologica. 2004 Mar;89(3):281-5 [15020265.001]
  • [Cites] Cell Cycle. 2004 Aug;3(8):976-9 [15254398.001]
  • [Cites] Nature. 1974 Oct 4;251(5474):437-8 [4421285.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Biochim Biophys Acta. 2005 Jul 25;1755(2):71-89 [15921859.001]
  • [Cites] Nature. 2005 Sep 1;437(7055):147-53 [16007073.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • (PMID = 20877721.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC2943467
  •  go-up   go-down



97. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down



98. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • Similarly, the frequency of other recurrent FAB associated abnormalities viz.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. India. Infant. Karyotyping. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down