[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 529
1. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
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] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics
  • [MeSH-minor] Child. Humans. Male. Molecular Sequence Data

  • 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 = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
  •  go-up   go-down


2. de Jonge HJ, Woolthuis CM, de Bont ES, Huls G: Paradoxical down-regulation of p16 mRNA with advancing age in acute myeloid leukemia. Aging (Albany NY); 2009 Nov;1(11):949-53
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] Paradoxical down-regulation of p16 mRNA with advancing age in acute myeloid leukemia.
  • We recently showed that, unlike healthy cells, acute myeloid leukemia (AML) derived blasts show a down-regulation of p16(INK4a) mRNA with increasing age.
  • [MeSH-major] Aging / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Down-Regulation / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3569-76 [10550156.001]
  • [Cites] Blood. 2009 Oct 1;114(14):2869-77 [19667402.001]
  • [Cites] Blood. 2001 May 1;97(9):2604-10 [11313248.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3500 [11732508.001]
  • [Cites] Nature. 2003 May 15;423(6937):255-60 [12714970.001]
  • [Cites] Nature. 2003 May 15;423(6937):302-5 [12714971.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5414-9 [14500376.001]
  • [Cites] Circ Res. 2003 Oct 3;93(7):604-13 [12958145.001]
  • [Cites] Nature. 2003 Oct 30;425(6961):962-7 [14574365.001]
  • [Cites] Kidney Int. 2004 Feb;65(2):510-20 [14717921.001]
  • [Cites] Circ Res. 2004 Mar 5;94(4):514-24 [14726476.001]
  • [Cites] Blood. 1982 May;59(5):1013-22 [6951613.001]
  • [Cites] Oncogene. 1997 Jul 10;15(2):203-11 [9244355.001]
  • [Cites] Lab Invest. 1999 Sep;79(9):1137-43 [10496532.001]
  • [Cites] J Clin Invest. 2004 Nov;114(9):1299-307 [15520862.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):720-4 [16079850.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13550-5 [16141321.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2419-30 [16760442.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):667-77 [16921403.001]
  • [Cites] Aging Cell. 2006 Oct;5(5):379-89 [16911562.001]
  • [Cites] Nature. 2006 Sep 28;443(7110):421-6 [16957735.001]
  • [Cites] Cell. 2006 Oct 20;127(2):265-75 [17055429.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3280-8 [16840728.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Cell. 2007 Jul 27;130(2):223-33 [17662938.001]
  • [Cites] PLoS Biol. 2007 Aug;5(8):e201 [17676974.001]
  • [Cites] Cell. 2008 Feb 22;132(4):681-96 [18295583.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3015-24 [18565887.001]
  • [Cites] Nature. 2000 Nov 9;408(6809):239-47 [11089981.001]
  • (PMID = 20157576.001).
  • [ISSN] 1945-4589
  • [Journal-full-title] Aging
  • [ISO-abbreviation] Aging (Albany NY)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2815746
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia / aging / p16INK4a / senescence
  •  go-up   go-down


3. Zhang JY, Lü T, Yang JC, Pan L, Luo JM, Yang L, Yao L, Dong ZR, Xu SR: Comparative study of expressions of cytoplasmic CD79a and other B-lymphoid immunomarkers in acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):954-8
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] Comparative study of expressions of cytoplasmic CD79a and other B-lymphoid immunomarkers in acute leukemic cells.
  • To evaluate the expression of cytoplasmic CD79a (CyCD79a) and other commonly used B-lymphoid immunomarkers including cytoplasmic CD22 (CyCD22), CD19, CD20 and CD10 in various acute leukemia cells and to define the most sensitive and specific markers in the diagnosis of precursor B-cell acute lymphoblastic leukemia (pB-ALL), the immunophenotypic data from 221 de novo adult and pediatric acute leukemia patients as studied using multi-parameter flow cytometry in addition to routine morphologic and enzyme cytochemical assay, were retrospectively analyzed.
  • Cytogenetic and/or molecular biological data in all 45 cases of acute promyelocytic leukemia (APL) and 13 cases of acute leukemia suspected as AML with the fusion genes such as AML1/ETO and CBFbeta/MYH11 were investigated.
  • At the same time, none (0%) of all 147 cases of acute myeloid leukemia (AML) and 15 cases of precursor T-cell acute leukemia (pT-ALL) was positive for CyCD22.
  • The conclusion is made that united detection of CyCD79a and CyCD22 is the optimal immune combination for the diagnosis pB-ALL and the distinguishing pB-ALL with AML and pT-ALL.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16403258.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD79; 0 / Biomarkers, Tumor; 0 / Sialic Acid Binding Ig-like Lectin 2
  •  go-up   go-down


Advertisement
4. Flotho C, Claus R, Batz C, Schneider M, Sandrock I, Ihde S, Plass C, Niemeyer CM, Lübbert M: The DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells. Leukemia; 2009 Jun;23(6):1019-28
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 DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells.
  • The three DNA methyltransferase (DNMT)-inhibiting cytosine nucleoside analogues, azacitidine, decitabine and zebularine, which are currently studied as nonintensive therapy for myelodysplastic syndromes and acute myeloid leukemia (AML), differ in structure and metabolism, suggesting that they may have differential molecular activity.
  • We investigated cellular and molecular effects of the three substances relative to cytarabine in Kasumi-1 AML blasts.
  • Under in vitro conditions mimicking those used in clinical trials, the DNMT inhibitors inhibited proliferation and triggered apoptosis but did not induce myeloid differentiation.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytidine / analogs & derivatives. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19194470.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 5CSZ8459RP / Cytidine; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  •  go-up   go-down


5. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Child. Chromosome Banding. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Pediatric T-cell leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


6. Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D: Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol; 2010 Jun;11(6):543-52
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] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
  • BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
  • METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
  • Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.
  • INTERPRETATION: Our findings suggest that the use of targeted chemotherapy and HSCT, in the context of a comprehensive risk-stratification strategy based on genetic features and MRD findings, can improve outcome in patients with childhood AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] J Clin Oncol. 2010 Feb 20;28(6):955-9 [20085940.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2302-9 [11981001.001]
  • [Cites] Lancet. 2002 May 11;359(9318):1686-9 [12020548.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]
  • [Cites] J Chronic Dis. 1974 Sep;27(7-8):365-75 [4612056.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Biometrics. 1979 Sep;35(3):549-56 [497341.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2090-100 [16304571.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2495-502 [16639734.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] Cancer. 2006 Jul 1;107(1):116-24 [16721819.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]
  • [Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]
  • [Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1410-6 [19242495.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4007-13 [19620491.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]
  • [CommentIn] Lancet Oncol. 2010 Jun;11(6):502-3 [20522371.001]
  • (PMID = 20451454.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
  • [Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799
  •  go-up   go-down


7. Choi HW, Shin MG, Sawyer JR, Cho D, Kee SJ, Baek HJ, Kook H, Kim HJ, Shin JH, Suh SP, Hwang TJ, Ryang DW: Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22). Cancer Genet Cytogenet; 2006 Jun;167(2):172-6
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] Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22).
  • We report on a case of pediatric acute myelocytic leukemia showing 47,XX,+10,t(16;21)(p11;q22) that resulted in an unusual TLS/FUS-ERG chimeric transcript.
  • The leukemic cells showed erythrophagocytosis, positive reactions for myeloperoxidase and Sudan black B stains, and negative reactions for periodic acid-Schiff and alpha-naphtyl butyrate esterase stains as well as expression of myeloid antigens.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Marrow Cells / cytology. Child, Preschool. Chromosomes, Human, Pair 10. Female. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Trisomy

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16737920.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
  •  go-up   go-down


8. Bellezza I, Tucci A, Minelli A: 2-Chloroadenosine and human prostate cancer cells. Anticancer Agents Med Chem; 2008 Oct;8(7):783-9
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.
  • Cladribine, i.e.2-deoxy-Chloroadenosine is currently in use as chemotherapeutic agent in chronic lymphoid malignancies and pediatric acute myelogenous leukemia whereas the structurally related counterpart, 2-Chloroadenosine, has been less studied.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18855579.001).
  • [ISSN] 1871-5206
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-23; 0 / Receptor, PAR-1; 146-77-0 / 2-Chloroadenosine
  • [Number-of-references] 137
  •  go-up   go-down


9. Zwaan CM, den Boer ML, Kazemier KM, Hählen K, Loonen AH, Reinhardt D, Creutzig U, Kaspers GJ, Pieters R: Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia? Blood; 2006 Jun 15;107(12):4975-6; author reply 4976-7
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] Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia?
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Antibodies, Monoclonal / chemistry. Child. Child, Preschool. Cyclosporine / pharmacology. Female. Flow Cytometry. Humans. Male. Randomized Controlled Trials as Topic. Remission Induction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • (PMID = 16754781.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / P-Glycoprotein; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


10. Manola KN: Cytogenetics of pediatric acute myeloid leukemia. Eur J Haematol; 2009 Nov;83(5):391-405
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] Cytogenetics of pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a clinically and genetically heterogeneous disease accounting for 15-20% of all childhood acute leukemias, while it is responsible for more than half of the leukemic deaths in these patients.
  • This article focuses on the significance of cytogenetic analysis in pediatric AML supporting the importance of cytogenetic analysis in the pathogenesis, diagnosis, prognosis, follow-up and treatment selection in childhood AML.
  • Furthermore, it discusses the association of specific chromosome rearrangements with prenatal exposure to carcinogenic agents or therapeutic agents and highlights the ongoing and future research on pediatric AML in the evolving field of Cytogenetics.
  • [MeSH-major] Cytogenetics / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

  • 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 = 19563518.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens, Environmental
  • [Number-of-references] 123
  •  go-up   go-down


11. Harrison CJ, Hills RK, Moorman AV, Grimwade DJ, Hann I, Webb DK, Wheatley K, de Graaf SS, van den Berg E, Burnett AK, Gibson BE: Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12. J Clin Oncol; 2010 Jun 01;28(16):2674-81
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] Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.
  • PURPOSE: Karyotype is an independent indicator of prognosis in acute myeloid leukemia (AML) that is widely applied to risk-adapted therapy.
  • Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
  • PATIENTS AND METHODS: This cytogenetic study of 729 childhood patients classified them into 22 subgroups and evaluated their incidence and risk.
  • Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this childhood series.
  • CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Confidence Intervals. Cytogenetic Analysis. Disease-Free Survival. Female. Fluorescence. Genetic Predisposition to Disease / epidemiology. Humans. In Situ Hybridization. Infant. Kaplan-Meier Estimate. Karyotyping. Logistic Models. Male. Multivariate Analysis. Odds Ratio. Probability. Prognosis. Proportional Hazards Models. Registries. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome. United Kingdom


12. Karabacak BH, Erbey F, Bayram I, Yilmaz S, Acipayam C, Kilinç Y, Tanyeli A: Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis. Asian Pac J Cancer Prev; 2010;11(4):923-7
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] Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis.
  • OBJECTIVE: In this study, the presence of FLT3 mutations in childhood acute leukemias patients and their association with prognosis were investigated.
  • MATERIALS AND METHODS: A total of 120 patients, 80 with acute lymphoblastic leukemia (ALL) and 40 with acute myeloblastic leukemia (AML), were included.
  • RESULTS: FLT3/ITD (internal tandem duplication) mutations were found in 6 (7.5%) of the patients with ALL and in 9 (22.5%) of those with AML, whereas no FLT3/TKD (trans kinase domain) mutation was evident in any case.
  • However, in FLT3/ITD positive and negative AML patients, there was a statistically significant difference in OS (p=0.0041), but not EFS and DFS (p=0.09, p=0.095, respectively).
  • CONCLUSION: We found that FLT3/ITD positivity increased with age and that it was associated with decrease in OS in AML patients, providing further evidence that it is an independent factor negatively influencing prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease-Free Survival. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. Recurrence

  • 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 = 21133602.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


13. Hollink IH, Zwaan CM, Zimmermann M, Arentsen-Peters TC, Pieters R, Cloos J, Kaspers GJ, de Graaf SS, Harbott J, Creutzig U, Reinhardt D, van den Heuvel-Eibrink MM, Thiede C: Favorable prognostic impact of NPM1 gene mutations in childhood acute myeloid leukemia, with emphasis on cytogenetically normal AML. Leukemia; 2009 Feb;23(2):262-70
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] Favorable prognostic impact of NPM1 gene mutations in childhood acute myeloid leukemia, with emphasis on cytogenetically normal AML.
  • Nucleophosmin (NPM1) mutations occur frequently in adult cytogenetically normal acute myeloid leukemia (CN-AML) and confer favorable outcome.
  • We investigated the frequency and prognostic significance of NPM1 mutations in childhood AML (n=298), specifically focusing on the CN-AML subgroup (n=100).
  • Mutations were found in 8.4%, and clustered significantly in the CN-AML subgroup (22%).
  • No mutations were found in patients below the age of 3 years; in CN-AML, there was an increasing incidence above this age.
  • In the CN-AML cohort, NPM1 mutations were an independent prognostic factor on pEFS (80 vs 39%; P=0.01), and pOS (85 vs 60%; P=0.06), which was not influenced by FLT3/ITD.
  • However, in NPM1 wild-type CN-AML, FLT3/ITD-positive patients had a significantly worse outcome (pEFS 48 vs 18%; P<0.001).
  • We conclude that NPM1 mutations confer a favorable prognosis in childhood AML and in CN-AML in particular.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. Infant. Male. Predictive Value of Tests. Prognosis. Retrospective Studies. Survival Analysis


14. Lin CH, Wu KH, Lin WC, Tsai JD, Peng CT, Chen AC: Granulocytic sarcoma of the colon in a child with acute myeloid leukemia presenting as hematochezia. J Pediatr Hematol Oncol; 2008 Dec;30(12):981-3
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] Granulocytic sarcoma of the colon in a child with acute myeloid leukemia presenting as hematochezia.
  • Granulocytic sarcoma (GS), an extramedullary myeloid tumor composed of immature cells of the granulocytic series, can occur in patients with acute myeloid leukemia (AML), myelodysplastic syndrome, or chronic myelogenous leukemia.
  • We report here an extremely rare case of GS in the colon of a 10-year-old boy with AML presenting with hematochezia.
  • In conclusion, hematochezia may be due to colonic involvement of GS, which should be considered in the differentials in addition to thrombocytopenia, as it is usually encountered in AML patients.
  • [MeSH-major] Colonic Neoplasms / complications. Gastrointestinal Hemorrhage / complications. Gastrointestinal Hemorrhage / diagnosis. Leukemia, Myeloid, Acute / complications. Neoplasms, Multiple Primary / pathology. Sarcoma, Myeloid / complications
  • [MeSH-minor] Child. Colonoscopy. Diagnosis, Differential. Humans. Male


15. Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS: Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
  • PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.
  • Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with AML.
  • Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.
  • Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+ AML.
  • EXPERIMENTAL DESIGN: Eight patients with CD33+ AML received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.
  • CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk AML is feasible and well tolerated with minimal toxicity.
  • The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+ AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Humanized. Busulfan / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Female. Graft vs Host Disease / prevention & control. Histocompatibility Testing. Humans. Infant. Male. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3. Time Factors. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16203817.001).
  • [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 / NHLBI NIH HHS / HL / T32 HL07968
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  •  go-up   go-down


16. Zhang Y, Zhang M, Yang L, Xiao Z: NPM1 mutations in myelodysplastic syndromes and acute myeloid leukemia with normal karyotype. Leuk Res; 2007 Jan;31(1):109-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 mutations in myelodysplastic syndromes and acute myeloid leukemia with normal karyotype.
  • Mutations at exon 12 of the nucleophosmin (NPM1) gene are the most frequent acquired molecular abnormalities in adult and pediatric acute myeloid leukaemia (AML) with normal karyotype.
  • We screened 28 patients with new diagnosed primary AML with normal karyotype, 38 patients with myelodysplastic symdromes (MDS) and 19 healthy volunteer for mutations at exon 12 of NPM1 gene.
  • NPM1 mutations were identified in four AML patients and two MDS patients, including one novel sequence variant.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics


17. Stasevich I, Utskevich R, Kustanovich A, Litvinko N, Savitskaya T, Chernyavskaya S, Saharova O, Aleinikova O: Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism. Cancer Genet Cytogenet; 2006 Sep;169(2):114-20
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] Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism.
  • This translocation represented 28% of all cases of childhood AML treated at our center in 2004, and 63% of AML with rearrangements of 11q23.
  • The median event-free survival of patients was 8.1 months, and we conclude that the t(10;11)(p12;q23) is associated with unfavorable prognosis in childhood acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16938568.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


18. Ashfaq K, Yahaya I, Hyde C, Andronis L, Barton P, Bayliss S, Chen YF: Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review. Health Technol Assess; 2010 Dec;14(54):iii-iv, ix-xi, 1-141
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 effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review.
  • BACKGROUND: Acute leukaemia is a group of rapidly progressing cancers of bone marrow and blood classified as either acute myeloid leukaemia (AML) or acute lymphoblastic leukaemia (ALL).
  • OBJECTIVES: A systematic overview of the best available evidence on the clinical effectiveness and cost-effectiveness of SCT in the treatment of acute leukaemia.
  • Included randomised controlled trials (RCTs) and donor versus no donor (DvND) studies were mapped to the evidence covered in existing systematic reviews and meta-analyses according to a framework of 12 decision problems (DPs): DP1 related to SCT in adults with AML in first complete remission (CR1); DP2 to adults with AML in second or subsequent remission or with refractory disease (CR2+); DP3 to children with AML in CR1; DP4 to children with AML in CR2+; DP5 to adults with ALL in CR1; DP6 to adults with ALL in CR2+; DP7 to children with ALL in CR1; DP8 to children with ALL in CR2+; DP9 to comparison of different sources of stem cells in transplantation; DP10 to different conditioning regimens; DP11 to the use of purging in autologous SCT; and DP12 to the use of T-cell depletion in allogeneic SCT.
  • Although there is a wealth of information on costs and some information on cost-effectiveness of allogeneic SCT in adults with AML (DPs 1 and 2), there is very limited evidence on relative costs and cost-effectiveness for other DPs.
  • CONCLUSIONS: Bearing in mind the limitations, existing evidence suggests that sibling donor allogeneic SCT may be more effective than chemotherapy in adult AML (except in good-risk patients) in CR1, childhood AML in CR1 and adult ALL in CR1, and that autologous SCT is equal to or less effective than chemotherapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery
  • [MeSH-minor] Adult. Child. Cost-Benefit Analysis. Humans


19. Unal S, Cetin M, Tuncer AM, Gümrük F, Yetgin S: The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients. Turk J Pediatr; 2008 Nov-Dec;50(6):533-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients.
  • The incidence of mixed-lineage leukemias in the pediatric age group was previously reported as 13.8% for myeloid antigen-positive ALL and 11.1% for lymphoid antigen-positive acute myeloid leukemia (AML).
  • Recent studies showed that extensive chemotherapy protocols overcome the risk of myeloid lineage.
  • Our study also supports most of the previous data and we postulate that myeloid antigen expression in pediatric ALL cases has insignificant effect on clinical presentation, relapse rates and survival.
  • Importantly, 54% of myeloid antigen-expressing ALL patients received high-risk treatment protocols for some other reasons and this may also have contributed to similar outcome in these patients to that observed in myeloid antigen-negative ALL patients.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunophenotyping. Male. Prognosis. Retrospective Studies. Survival Rate

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19227415.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm
  •  go-up   go-down


20. Klingebiel T, Reinhardt D, Bader P, EBMT Paediatric Diseases Working Party: Place of HSCT in treatment of childhood AML. Bone Marrow Transplant; 2008 Oct;42 Suppl 2:S7-9
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] Place of HSCT in treatment of childhood AML.
  • This short review focuses on the role of hematopoietic SCT (HSCT) in childhood AML.
  • Data on haploidentical HSCT and on cord blood HSCT are still lacking in the case of AML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Living Donors
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Clinical Trials as Topic. Disease-Free Survival. Humans. Infant. Remission Induction. Siblings. Survival Rate. Transplantation, Autologous. Transplantation, Homologous

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Organ Donation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18978749.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 15
  •  go-up   go-down


21. 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


22. Garderet L, Labopin M, Gorin NC, Polge E, Baruchel A, Meloni G, Ortega J, Vossen J, Bunjes D, Leverger G, Blaise D, Ferrant A, Brune M, Dore E, Gadner H, Zintl F, Yaniv I, Dini G, Frassoni F, Acute Leukemia Working Party and Pediatric Working Party of the European Group for Blood and Marrow Transplantation: Hematopoietic stem cell transplantation for de novo acute megakaryocytic leukemia in first complete remission: a retrospective study of the European Group for Blood and Marrow Transplantation (EBMT). Blood; 2005 Jan 1;105(1):405-9
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] Hematopoietic stem cell transplantation for de novo acute megakaryocytic leukemia in first complete remission: a retrospective study of the European Group for Blood and Marrow Transplantation (EBMT).
  • Acute megakaryoblastic leukemia (M7 AML) is a highly aggressive disease.
  • We evaluated outcomes in 57 children (11 with Down syndrome) and 69 adults with M7 AML after first complete remission (CR1) following autologous or HLA-identical allogeneic transplantation.
  • Results for autologous transplantation were (children and adults, respectively): engraftment, 90% and 100%; 3-year treatment-related mortality (TRM) rate, 3% and 8%; relapse rate, 45% and 64%; leukemia-free survival (LFS) rate, 52% and 27%; overall survival (OS) rate, 61% and 30%.
  • We conclude that M7 AML patients in CR1 (except children with Down syndrome, who already have better outcomes) can benefit from transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Megakaryoblastic, Acute / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Disease-Free Survival. Down Syndrome / complications. Europe. Female. Graft vs Host Disease / immunology. Humans. Infant. Male. Middle Aged. Prognosis. Recurrence. Retrospective Studies. Survival Rate. Transplantation, Autologous / adverse effects. Transplantation, Homologous / adverse effects

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15191953.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


23. Kaspers GJ, Reinhardt D, Fleischhack G, Armendariz H, Stark B, Zwaan CM, Zimmermann M, Creutzig U: Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML. Pediatr Blood Cancer; 2006 Oct 15;47(5):539-42
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] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.
  • BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.
  • PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.
  • By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.
  • CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.
  • However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Humans. Infant. Infusions, Intravenous. Male. Maximum Tolerated Dose. Recurrence. Treatment Outcome


24. Chatterjee T, Mahapatra M, Dixit A, Naithani R, Tyagi S, Mishra P, Bhattacharya J, Dutta P, Pati HP, Choudhary DR, Kumar R, Choudhry VP, Saxena R: Primary myelodysplastic syndrome in children--clinical, hematological and histomorphological profile from a tertiary care centre in India. Hematology; 2005 Dec;10(6):495-9
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.
  • Twenty-one patients of primary MDS aged 17 year or less were classified using the latest proposed WHO classification for Pediatric MDS.
  • A complete analysis of clinical features in conjunction with the bone marrow profile revealed 8 cases of refractory cytopenia (RC), 3 cases of refractory anemia with excess blasts (RAEB), 5 cases of refractory anemia with excess blasts in transformation (RAEB-T), 4 cases of Juvenile myelomonocytic leukemia (JMML) and a solitary cases of acute myeloid leukemia (AML) in Downs syndrome.
  • Three patients of RAEB-T progressed to AML within 3-4 months.
  • The solitary case of AML of Downs syndrome died 1.5 months after initial diagnosis.
  • Three cases of RAEB-T died (all had progressed to AML); the remaining 2 cases were lost to follow up.
  • We conclude that the latest proposed WHO classification for Pediatric MDS can be successfully applied to all cases of primary MDS.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Hematologic Tests. Humans. Immunohistochemistry. India. Infant. Male. Retrospective Studies


25. Altinkaynak S, Selimoglu MA, Turgut A, Kilicaslan B, Ertekin V: Breast-feeding duration and childhood acute leukemia and lymphomas in a sample of Turkish children. J Pediatr Gastroenterol Nutr; 2006 May;42(5):568-72
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] Breast-feeding duration and childhood acute leukemia and lymphomas in a sample of Turkish children.
  • We evaluated childhood acute leukemia and lymphoma in relation to duration of breast-feeding.
  • METHODS: We investigated this issue in a case-control study comprising 137 patients, aged 1 to 16 years, with acute lymphocytic leukemia (ALL), acute myeloid leukemia (AML), Hodgkin or non-Hodgkin lymphoma, in addition to 146 controls matched for age and sex.
  • Patients with ALL and AML had shorter mean breast-feeding duration compared with healthy children (P = 0.001 and P < 0.001, respectively).
  • The shortest mean breast-feeding duration was noted in the children with AML.
  • Breast-feeding for a duration of 0 to 6 months, when compared with feeding of longer than 6 months, was associated with increased odds ratios (ORs) for ALL [OR = 2.44, 95% confidence interval (CI) = 1.17-5.10], AML (OR = 6.67, 95% CI = 1.32-33.69), Hodgkin lymphoma (OR = 3.33, 95% CI = 0.60-18.54), non-Hodgkin lymphoma (OR = 1.90, 95% CI = 0.68-5.34) and overall (OR = 2.54, 95% CI = 1.51-4.26).
  • CONCLUSIONS: Our findings suggest that breast-feeding of more than 6 months is protective against childhood lymphoid malignancies, especially for AML and ALL.
  • [MeSH-major] Breast Feeding. Leukemia / prevention & control. Lymphoma / prevention & control
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male. Risk Factors. Time Factors. Turkey

  • MedlinePlus Health Information. consumer health - Breastfeeding.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16707982.001).
  • [ISSN] 1536-4801
  • [Journal-full-title] Journal of pediatric gastroenterology and nutrition
  • [ISO-abbreviation] J. Pediatr. Gastroenterol. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


26. Elgendi HM, Mekawy MA, Abdel Wahab SE, Tawfik LM, Ismail EA, Adly AA: AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome. J Pediatr Hematol Oncol; 2010 May;32(4):286-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome.
  • Hence, it is expected to be a valuable prognostic marker in acute leukemia.
  • Sixty Egyptian children with acute leukemia were enrolled into this prospective study divided into 2 groups: 30 acute myeloblastic leukemia (AML) and 30 acute lymphoblastic leukemia (ALL) patients.
  • AC133 was expressed in 66.7% and 40% of AML and ALL patients, respectively.
  • In AML, 80% of patients with poor clinical outcome (relapse or death) were positive for AC133 expression, whereas, all ALL patients who developed resistance as well as those who displayed poor clinical outcome had AC133-positive expression (P<0.05).
  • Patients with positive AC133 expression had significantly shorter overall and disease-free survival times compared with AC133-negative patients in both ALL (P<0.001) and AML (P<0.05) groups.
  • AC133-positive expression is an independent poor prognostic factor in childhood acute leukemia and could characterize a group of patients with resistance to standard chemotherapy, as well as high incidence of relapse and death.
  • [MeSH-major] Antigens, CD / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glycoproteins / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Peptides / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Immunophenotyping. Infant. Karyotyping. Male. Prospective Studies. Survival Rate. 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 = 20224439.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
  •  go-up   go-down


27. Mehta PA, Gerbing RB, Alonzo TA, Elliott JS, Zamzow TA, Combs M, Stover E, Ross JA, Perentesis JP, Meschinchi S, Lange BJ, Davies SM: FAS promoter polymorphism: outcome of childhood acute myeloid leukemia. A children's oncology group report. Clin Cancer Res; 2008 Dec 1;14(23):7896-9
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] FAS promoter polymorphism: outcome of childhood acute myeloid leukemia. A children's oncology group report.
  • Previous work has shown increased risk of developing acute myeloid leukemia (AML) in adult patients with a variant allele at this site.
  • The same authors have shown that the presence of an adenine residue rather than a guanine residue at -1,377 bp significantly attenuates transcription factor stimulatory protein 1 binding and may contribute to a reduction in FAS expression and ultimately to the enrichment of apoptosis-resistant clones in AML.
  • We hypothesized that FAS genotype by altering susceptibility to apoptosis might affect outcome of childhood AML therapy.
  • EXPERIMENTAL DESIGN: Four hundred forty-four children treated for de novo AML on a uniform protocol were genotyped for FAS 1377.
  • CONCLUSIONS: FAS 1377 genotype does not alter outcome of de novo AML in children.

  • 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.
  • 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] J Mol Med (Berl). 2000;78(6):312-25 [11001528.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] J Exp Med. 1989 May 1;169(5):1747-56 [2469768.001]
  • [Cites] Cell. 1991 Jul 26;66(2):233-43 [1713127.001]
  • [Cites] Blood. 1992 Mar 1;79(5):1291-8 [1536952.001]
  • [Cites] J Biol Chem. 1992 May 25;267(15):10709-15 [1375228.001]
  • [Cites] J Biol Chem. 1993 May 25;268(15):10932-7 [7684370.001]
  • [Cites] Cell. 1994 Mar 25;76(6):969-76 [7511063.001]
  • [Cites] Science. 1995 Jun 2;268(5215):1347-9 [7539157.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3848-60 [7579353.001]
  • [Cites] J Exp Med. 1998 Jun 1;187(11):1825-38 [9607923.001]
  • [Cites] Immunity. 1998 Jul;9(1):47-57 [9697835.001]
  • [Cites] Exp Hematol. 1999 May;27(5):868-74 [10340403.001]
  • [Cites] Cancer Res. 1999 Jul 1;59(13):3068-72 [10397246.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):8101-8 [15520222.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4327-30 [12907599.001]
  • (PMID = 19047119.001).
  • [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 / U10 CA098543-06; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA 76326-01; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA093552-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95
  • [Other-IDs] NLM/ NIHMS103099; NLM/ PMC2787450
  •  go-up   go-down


28. Shimada A, Ichikawa H, Taki T, Kubota C, Hongo T, Sako M, Morimoto A, Tawa A, Tsukimoto I, Hayashi Y: Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2007 Oct;86(3):289-90
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] Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group.
  • [MeSH-major] Chromosome Inversion. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Survival Rate


29. Zelezníková T, Babusíková O: The value of dot plot patterns and leukemia-associated phenotypes in AML diagnosis by multiparameter flow cytometry. Neoplasma; 2005;52(6):517-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The value of dot plot patterns and leukemia-associated phenotypes in AML diagnosis by multiparameter flow cytometry.
  • The immunophenotypic features in patients with acute myeloid leukemia (AML) were investigated at diagnosis using a wide antibody panel including progenitor-associated, myeloid and lymphoid markers in quadruple combinations.
  • Analyzed were bone marrow samples from 37 adult and pediatric patients for exact identification of AML blasts according their localization on CD45/SSC dot plots and aberrant immunophenotypes in various subtype of AML.
  • We found the localization of AML blasts on CD45/SSC dot plots, which in combination with immunophenotype profile of blasts allow discrimination of several AML subtypes (M0-M2, M3, M4/M5 and other types).
  • In 27/37 AML patients (73%) at least one leukemia-associated phenotype (LAP) was found, two or more aberrancies coexisted in more than a half of them (78%).
  • Presented study showed that leukemic cells of each AML patient had a unique antigenic profile and could be discriminated from their normal counterparts based on typical light scatter profiles and aberrant antigen expression that could further be used for detection of minimal residual disease.
  • [MeSH-major] Flow Cytometry. Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / analysis. Blast Crisis / diagnosis. Blast Crisis / immunology. Child. Child, Preschool. Female. HLA-DR Antigens / analysis. Humans. Male. Middle Aged. Neoplasm, Residual / diagnosis. Neoplasm, Residual / immunology. Phenotype

  • 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 = 16284699.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA-DR Antigens
  •  go-up   go-down


30. Hattori H, Matsuzaki A, Suminoe A, Koga Y, Tashiro K, Hara T: Identification of novel genes with prognostic value in childhood leukemia using cDNA microarray and quantitative RT-PCR. Pediatr Hematol Oncol; 2006 Mar;23(2):115-27
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] Identification of novel genes with prognostic value in childhood leukemia using cDNA microarray and quantitative RT-PCR.
  • The aim of this study was to identify genes distinctively expressed or suppressed in childhood leukemia with different prognoses, using cDNA microarray and quantitative reverse transcription-polymerase chain reaction (RT-PCR).
  • The expression levels of the selected genes by cDNA microarray were quantified in primary leukemic blasts from 44 patients (acute lymphoblastic leukemia, 28; acute myelogenous leukemia (AML), 13; transient myeloproliferative disorder, 3).
  • The expression levels of CDKN2C, CRADD, and IGFBP-2 genes were significantly associated with the event-free survival of the patients in AML.
  • The present results suggest that a combination of cDNA microarray and quantitative RT-PCR may be useful to identify novel genes with prognostic value in childhood AML.
  • [MeSH-major] Genes, Neoplasm. Leukemia / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adolescent. CRADD Signaling Adaptor Protein. Caspase 2. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p18 / genetics. Cysteine Endopeptidases / genetics. Female. Gene Expression Profiling. Humans. Infant. Infant, Newborn. Insulin-Like Growth Factor Binding Protein 2 / genetics. Male. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Prognosis. Protein-Serine-Threonine Kinases / genetics. Receptor-Interacting Protein Serine-Threonine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / genetics

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - 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 = 16651240.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CDKN2C protein, human; 0 / CRADD Signaling Adaptor Protein; 0 / CRADD protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p18; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Neoplasm Proteins; 0 / Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / RIPK1 protein, human; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinases; EC 3.4.22.- / CASP2 protein, human; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Cysteine Endopeptidases
  •  go-up   go-down


31. Celkan T, Berrak S, Kazanci E, Ozyürek E, Unal S, Uçar C, Yilmaz S, Gürgey A: Malignancy-associated hemophagocytic lymphohistiocytosis in pediatric cases: a multicenter study from Turkey. Turk J Pediatr; 2009 May-Jun;51(3):207-13
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] Malignancy-associated hemophagocytic lymphohistiocytosis in pediatric cases: a multicenter study from Turkey.
  • Twenty cases (18 ALL and 2 AML) with acute leukemia (10 girls/10 boys, median age: 8 years [3-14 years]) were found to have sHLH.
  • Five patients with acute leukemia had HLH at the time of diagnosis (Group 1a), and 15 patients with acute leukemia were diagnosed as having sHLH during therapy (Group 1b), namely reactive sHLH associated with the chemotherapy.
  • Pediatric malignancy-associated HLH patients have been commonly described as case presentations or in a review of the literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Child. Child, Preschool. Female. Humans. Male. Retrospective Studies. Turkey


32. Quezada G, Kopp L, Estey E, Wells RJ: All-trans-retinoic acid and arsenic trioxide as initial therapy for acute promyelocytic leukemia. Pediatr Blood Cancer; 2008 Jul;51(1):133-5
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] All-trans-retinoic acid and arsenic trioxide as initial therapy for acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (APL) is a rare subtype of acute myeloid leukemia (AML).
  • Treatment of pediatric APL is based on the combination of all-trans-retinoic acid (ATRA), an anthracycline and cytosine arabinoside.
  • There is little data on combination therapy with ATRA and ATO in pediatric APL.
  • [MeSH-major] Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18293388.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


33. Zhang LJ, Wang PP, Lu XL, He J, Li Y, Zhai M: [Identification of chromosome 21 anomalies in patients with acute myeloid leukemia by fluorescence in situ hybridization]. Zhonghua Yi Xue Za Zhi; 2006 Dec 26;86(48):3393-6
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] [Identification of chromosome 21 anomalies in patients with acute myeloid leukemia by fluorescence in situ hybridization].
  • OBJECTIVE: To investigate the possible complex anomalies of chromosome 21 in patients with acute myeloid leukemia (AML).
  • METHODS: Fluorescence in situ hybridization (FISH) was performed by using commercially available DNA probes, including whole chromosome painting probes, locus specific probes, and specific and dual color translocation fusion probes, on 50 AML patients, 37 adults and 13 children.
  • Four of the 13 pediatric patients were found to have trisomy of chromosome 21, among which one had an additional chromosome rearrangement: 47-49,XX,der(1)t(1;17)(p36.1;q23), +4, +10, der(11)t(11;17)(q23;q23), -17, -18, +20, +21.
  • CONCLUSION: Rearrangement of chromosome 21 is common in both childhood and adult patients with AML.
  • However, childhood patients tend to have numerical change of chromosome 21, whereas the adult patients are likely to have structural changes of chromosome 21.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. 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 = 17313849.001).
  • [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
  •  go-up   go-down


34. Kardos G, Zwaan CM, Kaspers GJ, de-Graaf SS, de Bont ES, Postma A, Bökkerink JP, Weening RS, van der Does-van den Berg A, van Wering ER, Korbijn C, Hählen K: Treatment strategy and results in children treated on three Dutch Childhood Oncology Group acute myeloid leukemia trials. Leukemia; 2005 Dec;19(12):2063-71
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] Treatment strategy and results in children treated on three Dutch Childhood Oncology Group acute myeloid leukemia trials.
  • This report describes the long-term follow-up data of three consecutive Dutch Childhood Oncology Group acute myeloid leukemia (AML) protocols.
  • A total of 303 children were diagnosed with AML, of whom 209 were eligible for this report.
  • The first study was the AML-82 protocol.
  • Study AML-87 was based on the BFM-87 protocol, with prophylactic cranial irradiation in high-risk patients only, and without maintenance therapy.
  • The subsequent study AML-92/94 consisted of a modified BFM-93 protocol, that is, without maintenance therapy and prophylactic cranial irradiation.
  • Our results demonstrate that outcome in childhood AML is still unsatisfactory, and that further intensification of therapy carries the risk of enhanced toxicity.
  • Our patients are currently included in the MRC AML studies, based on the results of their AML 10 trial.
  • [MeSH-major] Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cranial Irradiation. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Male. Recurrence. Risk Assessment. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107896.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  •  go-up   go-down


35. Phillips CL, Gerbing R, Alonzo T, Perentesis JP, Harley IT, Meshinchi S, Bhatla D, Radloff G, Davies SM: MDM2 polymorphism increases susceptibility to childhood acute myeloid leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2010 Aug;55(2):248-53
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] MDM2 polymorphism increases susceptibility to childhood acute myeloid leukemia: a report from the Children's Oncology Group.
  • PROCEDURE: We genotyped children (n = 575) with de novo acute myeloid leukemia (AML) treated on three Children's Oncology Group protocols (CCG 2941/2961/AAML 03P1) for the presence of SNP309.
  • RESULTS: The variant G/G genotype was associated with an increased susceptibility to AML (OR 1.5; P = 0.049).
  • CONCLUSIONS: The variant SNP 309 influences susceptibility to pediatric AML, but does not impact overall response to therapy.

  • 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.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • 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) 2010 Wiley-Liss, Inc.
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5831-9 [17575151.001]
  • [Cites] J Clin Oncol. 2007 Jun 1;25(16):2243-7 [17538168.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] J Clin Oncol. 2008 May 10;26(14):2252-7 [18467716.001]
  • [Cites] Radiother Oncol. 2008 May;87(2):243-52 [18423915.001]
  • [Cites] Clin Cancer Res. 2008 Jun 1;14(11):3248-53 [18519749.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):4010-5 [18559624.001]
  • [Cites] Cancer. 2008 Aug 15;113(4):799-807 [18618574.001]
  • [Cites] Leuk Res. 2009 Nov;33(11):1454-8 [19423162.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] Cell. 2004 Nov 24;119(5):591-602 [15550242.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Feb;5(1):27-41 [15720187.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):651-5 [15767345.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26776-87 [15908423.001]
  • [Cites] Hum Mutat. 2006 Jan;27(1):110-7 [16287156.001]
  • [Cites] Mod Pathol. 2006 Jan;19(1):69-74 [16258514.001]
  • [Cites] J Natl Cancer Inst. 2006 Feb 15;98(4):285-8 [16478747.001]
  • [Cites] Int J Cancer. 2006 Aug 1;119(3):718-21 [16496380.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5104-10 [16707433.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 5;98(13):911-9 [16818855.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4434-40 [16983111.001]
  • [Cites] Clin Cancer Res. 2007 Jul 15;13(14):4123-9 [17634539.001]
  • (PMID = 20582981.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM063483-08S2; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NINR NIH HHS / NR / R21 NR010262-01; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / CA098543-05; United States / NIGMS NIH HHS / GM / T32 GM063483; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / U10 CA098543-05; United States / NINR NIH HHS / NR / R21 NR010262; United States / NIGMS NIH HHS / GM / T32 GM063483-08S2; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA093552-01; United States / NCI NIH HHS / CA / R01 CA93552-01; United States / NINR NIH HHS / NR / NR010262-01; United States / NCI NIH HHS / CA / CA114563-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS217002; NLM/ PMC2915901
  •  go-up   go-down


36. Babicz M, Kowalczyk JR, Winnicka D, Gaworczyk A, Lejman M, Dmowski R, Kaczanowska K: The effectiveness of high-resolution-comparative genomic hybridization in detecting the most common chromosomal abnormalities in pediatric myelodysplastic syndromes. Cancer Genet Cytogenet; 2005 Apr 1;158(1):49-54
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] The effectiveness of high-resolution-comparative genomic hybridization in detecting the most common chromosomal abnormalities in pediatric myelodysplastic syndromes.
  • In our study, we present 5 cases of MDS and 4 cases of acute myelogenous leukemia (AML).
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male


37. Radhi M, Meshinchi S, Gamis A: Prognostic factors in pediatric acute myeloid leukemia. Curr Hematol Malig Rep; 2010 Oct;5(4):200-6
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] Prognostic factors in pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML), a heterogeneous group of diseases with variable responses to the same therapy, comprises nearly a quarter of childhood acute leukemias.
  • Although historically very few prognostic markers have been incorporated into therapeutic decision making in AML, recent advances in technology have enabled identification of numerous factors associated with disease outcome.
  • This review provides a detailed analysis of most clinically relevant factors associated with disease outcome in childhood AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis
  • [MeSH-minor] Age Factors. Biomarkers, Tumor. Body Mass Index. Child. Cytogenetics. Humans. Polymorphism, Genetic. Prognosis. Risk Factors. Sex Factors

  • 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
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):62-7 [15604893.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]
  • [Cites] Leukemia. 2002 May;16(5):776-84 [11986937.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S108-12 [15124698.001]
  • [Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1279-87 [11230469.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Best Pract Res Clin Haematol. 2008 Dec;21(4):621-8 [19041601.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4641-7 [17299091.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]
  • [Cites] Blood. 1985 Feb;65(2):298-304 [3881140.001]
  • [Cites] Cancer. 2008 Jan 15;112(2):407-15 [18058809.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] Br J Haematol. 1999 Oct;107(1):69-79 [10520026.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jan;48(1):10-5 [16642489.001]
  • [Cites] Blood. 2009 Sep 17;114(12):2489-96 [19528532.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4172-4 [17909077.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):578-85 [20038731.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4791-7 [18695255.001]
  • [Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Leukemia. 2002 Apr;16(4):601-7 [11960339.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]
  • [Cites] Best Pract Res Clin Haematol. 2009 Dec;22(4):523-8 [19959103.001]
  • [Cites] J Clin Oncol. 2004 Apr 15;22(8):1404-12 [15084614.001]
  • (PMID = 20652454.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


38. Fazlina N, Maha A, Jamal R, Zarina AL, Cheong SK, Hamidah H, Ainoon O, Zulkifli SZ, Hamidah NH: Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias. Hematology; 2007 Feb;12(1):33-7
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] Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias.
  • The expression of the multidrug resistance (MDR) proteins may influence the outcome of treatment in patients with acute leukemia.
  • A total of 82 newly diagnosed acute leukemia cases (43 adult myeloid leukaemia, AML cases and 39 acute lymphoblastic leukaemia, ALL cases) and 16 relapsed cases (8 AML cases and 8 ALL cases) were studied.
  • In newly diagnosed cases, we found that childhood ALL samples showed higher IC50 values of dnr (0.040 +/- 2.320) compared to adult AML samples (0.021 +/- 0.158).
  • In contrast, newly diagnosed adult AML samples showed higher IC50 values of ara-C (0.157 +/- 0.529) compared to childhood ALL samples (0.100 +/- 2.350).
  • In relapsed cases, two samples of childhood ALL showed IC50 values of dnr (0.910 +/- 1.760) and ara-C (1.310 +/- 2.390), which was higher compared to childhood AML samples (0.129 +/- 0.214 and 0.210 +/- 0.003, respectively).
  • In conclusion, we found that MTS assay is an easy, rapid and non laborious method to study in vitro drug resistance in acute leukaemia cases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia / metabolism. Neoplasm Proteins / metabolism. P-Glycoproteins / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cell Survival. Child. Child, Preschool. Coloring Agents / analysis. Cytarabine / pharmacology. Daunorubicin / pharmacology. Female. Humans. Infant. Inhibitory Concentration 50. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Methylphenazonium Methosulfate / pharmacology. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recurrence. Staining and Labeling / methods. Tetrazolium Salts / analysis. Thiazoles / analysis. Treatment Outcome. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / ultrastructure

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17364990.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Neoplasm Proteins; 0 / P-Glycoproteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 138169-43-4 / 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; 299-11-6 / Methylphenazonium Methosulfate; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


39. Faaij CM, Willemze AJ, Révész T, Balzarolo M, Tensen CP, Hoogeboom M, Vermeer MH, van Wering E, Zwaan CM, Kaspers GJ, Story C, van Halteren AG, Vossen JM, Egeler RM, van Tol MJ, Annels NE: Chemokine/chemokine receptor interactions in extramedullary leukaemia of the skin in childhood AML: differential roles for CCR2, CCR5, CXCR4 and CXCR7. Pediatr Blood Cancer; 2010 Aug;55(2):344-8
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] Chemokine/chemokine receptor interactions in extramedullary leukaemia of the skin in childhood AML: differential roles for CCR2, CCR5, CXCR4 and CXCR7.
  • We analysed chemokine receptor expression by acute myeloid leukaemic (AML) cells present in peripheral blood (n = 7), bone marrow (n = 6), or skin (n = 11) obtained from 15 paediatric AML patients with skin involvement and in 10 AML patients without skin involvement.
  • High percentages of circulating CCR2(pos) AML cells were only detected in patients with extramedullary disease.
  • Skin-residing AML cells displayed a different set of receptors in situ, namely: CCR5, CXCR4, CXCR7 and CX3CR1.
  • These results suggest the involvement of different chemokine/chemokine receptor interactions in homing and retention of AML blasts in the skin.
  • [MeSH-major] Chemokines / analysis. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Receptors, Chemokine / analysis. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Receptors, CCR2 / analysis. Receptors, CCR5 / analysis. Receptors, CXCR / analysis. Receptors, CXCR4 / analysis. Skin / chemistry. Skin / pathology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2010 Aug;55(2):218-9 [20582958.001]
  • (PMID = 20582977.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR2 protein, human; 0 / CX3CR1 protein, human; 0 / CXCR7 protein, human; 0 / Chemokines; 0 / Receptors, CCR2; 0 / Receptors, CCR5; 0 / Receptors, CXCR; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine
  •  go-up   go-down


40. Meshinchi S, Stirewalt DL, Alonzo TA, Boggon TJ, Gerbing RB, Rocnik JL, Lange BJ, Gilliland DG, Radich JP: Structural and numerical variation of FLT3/ITD in pediatric AML. Blood; 2008 May 15;111(10):4930-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural and numerical variation of FLT3/ITD in pediatric AML.
  • FLT3 internal tandem duplication (FLT3/ITD) is a common somatic mutation in acute myeloid leukemia (AML) with significant variation in the position, length, and number of duplications of the FLT3 gene.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1474-9 [12702504.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Mol Cell. 2004 Jan 30;13(2):169-78 [14759363.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Acta Crystallogr A. 1991 Mar 1;47 ( Pt 2):110-9 [2025413.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Blood. 2006 May 1;107(9):3724-6 [16368883.001]
  • [Cites] Blood. 2006 May 1;107(9):3700-7 [16410449.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1339-45 [16627759.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Blood. 2007 Jul 15;110(2):686-94 [17387224.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • (PMID = 18305215.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / K23 CA92405; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / CA114563; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / R21 CA102624
  • [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 / STAT5 Transcription Factor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2384125
  •  go-up   go-down


41. Goemans BF, Zwaan CM, Miller M, Zimmermann M, Harlow A, Meshinchi S, Loonen AH, Hählen K, Reinhardt D, Creutzig U, Kaspers GJ, Heinrich MC: Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia. Leukemia; 2005 Sep;19(9):1536-42
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] Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia.
  • Activating mutations in RAS and receptor tyrosine kinases such as KIT and FLT3 are hypothesized to cooperate with chimeric transcription factors in the pathogenesis of acute myeloid leukemia (AML).
  • To test this hypothesis, we genotyped 150 pediatric AML samples for mutations in KIT (exons 8, 17), NRAS and KRAS (exons 1, 2) and FLT3/ITD.
  • This is the largest cohort of pediatric AML patients reported thus far screened for all four mutations.
  • Of the children with AML, 40% had a mutation in KIT (11.3%), RAS (18%) or FLT3/ITD (11.1%), and 70% of cases of core-binding factor (CBF) leukemia were associated with a mutation of KIT or RAS.
  • Our results demonstrate that abnormalities of signal transduction pathways are frequent in pediatric AML.
  • [MeSH-major] Genes, ras / genetics. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins c-kit / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. CHO Cells. Child. Child, Preschool. Core Binding Factors. Cricetinae. Cytogenetic Analysis. Exons. Follow-Up Studies. Humans. Imatinib Mesylate. Infant. Infant, Newborn. Mutation. Neoplasm Proteins / biosynthesis. Piperazines / pharmacology. Proto-Oncogene Proteins / genetics. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / genetics. Retrospective Studies. Survival Analysis. Treatment Outcome. fms-Like Tyrosine Kinase 3

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16015387.001).
  • [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 / Benzamides; 0 / Core Binding Factors; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


42. Kawamura M, Kaku H, Ito T, Funata N, Taki T, Shimada A, Hayashi Y: FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):292-6
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] FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia.
  • Patients diagnosed with t(8;21)-acute myeloid leukemia (AML) are currently considered to have good prognoses, but about half of these patients relapse.
  • FLT3-internal tandem duplication (ITD) is generally thought to be strongly associated with poor prognosis in AML, but is rarely reported in patients with t(8;21)-AML.
  • Expression of the neural cell-adhesion molecule (CD56) is also associated with a significantly shorter complete remission duration and survival in patients with t(8;21)-AML.
  • Patients with t(8;21)-AML expressing CD56 have been reported to exhibit a higher incidence of granulocytic sarcoma (GS), and t(8;21)-AML with GS results in a less favorable prognosis than AML with this translocation alone.
  • Here, we report on a 15-year-old girl with t(8;21)-AML having both CD56 expression and FLT3-ITD.
  • For earlier detection of relapse, we suggest that it would be useful to examine existence of GS in CD56-positive t(8;21)-AML patients at diagnosis and hematologic remission.
  • Even though t(8;21)-AML is less likely to co-occur with FLT3-ITD in pediatric patients, this report suggests that prognostic factors, including FLT3 and KIT genes and the surface marker CD56, should be analyzed in these patients.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • 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
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156247.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


43. Imashuku S: Etoposide-related secondary acute myeloid leukemia (t-AML) in hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2007 Feb;48(2):121-3
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] Etoposide-related secondary acute myeloid leukemia (t-AML) in hemophagocytic lymphohistiocytosis.
  • [MeSH-major] Etoposide / adverse effects. Leukemia, Myeloid / chemically induced. Lymphohistiocytosis, Hemophagocytic / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Male


44. Ghosh JB, Roy M, Halder A: Granulocytic sarcoma. Indian J Pediatr; 2009 May;76(5):558-9
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] Granulocytic sarcoma.
  • We present two cases where GS was sole presentations, months before the diagnosis of AML.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Neoplasm Invasiveness / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy, Fine-Needle. Child. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. Male. Risk Assessment. Tomography, X-Ray Computed. Treatment Refusal

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] AJR Am J Roentgenol. 1995 Sep;165(3):525-34 [7645463.001]
  • [Cites] Radiology. 1994 Mar;190(3):698-702 [8115614.001]
  • [Cites] Blut. 1989 Jan;58(1):45-6 [2917202.001]
  • [Cites] Cancer. 1979 Sep;44(3):1017-21 [383264.001]
  • [Cites] Br J Haematol. 2000 Sep;110(4):863-6 [11054069.001]
  • [Cites] J Laryngol Otol. 1980 Dec;94(12):1423-7 [6934247.001]
  • [Cites] J Clin Oncol. 1995 Jul;13(7):1800-16 [7602369.001]
  • (PMID = 19390807.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  •  go-up   go-down


45. Markaki EA, Stiakaki E, Zafiropoulos A, Arvanitis DA, Katzilakis N, Dimitriou H, Spandidos DA, Kalmanti M: Mutational analysis of the cell cycle inhibitor Kip1/p27 in childhood leukemia. Pediatr Blood Cancer; 2006 Jul;47(1):14-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutational analysis of the cell cycle inhibitor Kip1/p27 in childhood leukemia.
  • METHODS: Bone marrow blasts from 49 children with leukemia, 37 acute lymphoblastic leukemia (ALL), and 12 acute myeloid leukemia (AML) were studied.
  • RESULTS: Mutations in Kip1/p27 gene were detected in 2 out of 3 T-ALL, 6 out of 12 AML patients, and only 1 out of 34 B lineage ALL cases.
  • Although the patient groups are small, a highly significant relation of the mutation status with the type of leukemia (P = 0.0037) and the risk group according to treatment protocols (P = 0.00021) was estimated.
  • CONCLUSIONS: Based upon these results, the Kip1/p27 mutations should be considered for further prospective testing as an additional parameter for risk stratification and treatment of childhood leukemia.
  • [MeSH-major] Biomarkers, Tumor / genetics. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Leukemia, Myeloid / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow / pathology. Cell Cycle / drug effects. Child. Child, Preschool. DNA Mutational Analysis. Female. Humans. Infant. Male. Prognosis

  • 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
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16526056.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  •  go-up   go-down


46. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • As the proportion of leukemic blast cells is critical for exact cytochemical analysis, study was restricted to the evaluation of 48 adult and pediatric patients with newly diagnosed AMLs with 80% or more blasts in analyzed samples.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
  •  go-up   go-down


47. Lin CH, Hung GY, Chang CY, Chien JC: Subdural hemorrhage in a child with acute promyelocytic leukemia presenting as subtle headache. J Chin Med Assoc; 2005 Sep;68(9):437-40
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] Subdural hemorrhage in a child with acute promyelocytic leukemia presenting as subtle headache.
  • Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia (AML) and is rare in children (< 10% of childhood AML).
  • We report a 12-year-old child with APL who suffered a subdural hemorrhage and initially presented with a subtle headache mistaken as the side effect of all-trans-retinoic acid (ATRA).
  • Blood component therapy and a pediatric dosage of ATRA (25 mg/m2/day) combined with idarubicin as induction chemotherapy were administered in the first week, but the bleeding diathesis persisted and DIC profiles showed no improvement.
  • This case suggests that the ATRA dosage for pediatric APL patients must be modified according to clinical condition.
  • [MeSH-major] Headache / etiology. Hematoma, Subdural / etiology. Leukemia, Promyelocytic, Acute / complications
  • [MeSH-minor] Child. Disseminated Intravascular Coagulation / complications. Humans. Male. Partial Thromboplastin Time. Prothrombin Time. Tretinoin / adverse effects

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Headache.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16187602.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  •  go-up   go-down


48. Lamba JK, Pounds S, Cao X, Downing JR, Campana D, Ribeiro RC, Pui CH, Rubnitz JE: Coding polymorphisms in CD33 and response to gemtuzumab ozogamicin in pediatric patients with AML: a pilot study. Leukemia; 2009 Feb;23(2):402-4
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.
  • [Title] Coding polymorphisms in CD33 and response to gemtuzumab ozogamicin in pediatric patients with AML: a pilot study.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Aug 1;96(3):870-7 [10910899.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1490-6 [11410481.001]
  • [Cites] J Clin Pharmacol. 2001 Nov;41(11):1206-14 [11697753.001]
  • [Cites] Expert Opin Biol Ther. 2001 Sep;1(5):893-901 [11728223.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Dec;323(3):935-45 [17855478.001]
  • [Cites] J Clin Pharmacol. 2004 Aug;44(8):873-80 [15286091.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10506-10 [7479829.001]
  • [Cites] Blood. 2007 May 15;109(10):4168-70 [17227830.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • (PMID = 18615103.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393-09; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NIGMS NIH HHS / GM / GM061374-07; United States / NIGMS NIH HHS / GM / U01GM61374; United States / NIGMS NIH HHS / GM / U01 GM061374-07; United States / NCI NIH HHS / CA / CA-21765; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061374; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / P30 CA021765-30
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Other-IDs] NLM/ NIHMS93698; NLM/ PMC2659556
  •  go-up   go-down


49. Kang HJ, Lee JW, Kho SH, Kim MJ, Seo YJ, Kim H, Shin HY, Ahn HS: High transcript level of FLT3 associated with high risk of relapse in pediatric acute myeloid leukemia. J Korean Med Sci; 2010 Jun;25(6):841-5
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] High transcript level of FLT3 associated with high risk of relapse in pediatric acute myeloid leukemia.
  • Identification of prognostic factors and risk-based post-remission therapy was proposed to improve the outcomes of acute myeloid leukemia (AML) and a mutation of FLT3 has been reported to be a risk factor, especially for pediatric patients.
  • Recently, FLT3 expression level was implicated to have prognostic significance in adults, but little is known for childhood AML.
  • To define the prognostic significance, transcript level of FLT3 was analyzed in 52 pediatric AML patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Gene Frequency. Humans. Infant. Male. Multivariate Analysis. Mutation. Peripheral Blood Stem Cell Transplantation. Prognosis. Recurrence. Risk Factors

  • 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
  • [Cites] Med Pediatr Oncol. 1999 Dec;33(6):525-9 [10573574.001]
  • [Cites] N Engl J Med. 1996 May 30;334(22):1428-34 [8618581.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Pediatr Clin North Am. 1997 Aug;44(4):847-62 [9286288.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2121-6 [9310463.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1999 Jan;13(1):38-43 [10049058.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):155-62 [10233379.001]
  • [Cites] Leuk Res. 2005 Jun;29(6):617-23 [15863200.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3658-65 [16076872.001]
  • [Cites] Haematologica. 2005 Dec;90(12):1617-25 [16330434.001]
  • [Cites] Blood. 2006 Jul 1;108(1):400; author reply 400-1 [16790584.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3292-8 [12115363.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2264-5; author reply 2265 [17312001.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Sep;63(3):215-30 [17658267.001]
  • [Cites] Br J Haematol. 2007 Sep;138(6):687-99 [17655729.001]
  • [Cites] Bone Marrow Transplant. 2008 Jan;41(2):141-8 [18176616.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Curr Oncol Rep. 2003 Nov;5(6):489-97 [14521808.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:82-101 [14633778.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1901-8 [14604973.001]
  • [Cites] Bone Marrow Transplant. 2004 Mar;33(5):471-6 [14716339.001]
  • [Cites] Blood. 1992 Nov 15;80(10):2584-93 [1384791.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1046-54 [8501490.001]
  • [Cites] Leukemia. 1996 Apr;10(4):588-99 [8618433.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • (PMID = 20514303.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2877222
  • [Keywords] NOTNLM ; FLT3 / Leukemia, Myeloid, Acute / Pediatric Age / Transcript Level
  •  go-up   go-down


50. Parikh SH, Mendizabal A, Martin PL, Prasad VK, Szabolcs P, Driscoll TA, Kurtzberg J: Unrelated donor umbilical cord blood transplantation in pediatric myelodysplastic syndrome: a single-center experience. Biol Blood Marrow Transplant; 2009 Aug;15(8):948-55
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] Unrelated donor umbilical cord blood transplantation in pediatric myelodysplastic syndrome: a single-center experience.
  • Between 1995 and 2006, 23 pediatric patients with MDS were transplanted with unrelated donor umbilical cord blood (UUCB) at our center.
  • Patients with acute myelogenous leukemia (AML) were excluded.
  • Three patients developed acute GVHD (aGVHD) grades II-IV with a cumulative incidence at 100 days of 13% (95% CI 0.0%-27.1.0%).
  • UUCB should be actively considered for pediatric MDS patients lacking matched related or unrelated adult donors.
  • [MeSH-minor] Adolescent. Adult. Anemia, Refractory, with Excess of Blasts. Chemoprevention / methods. Child. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Tissue Donors. Treatment Outcome. Whole-Body Irradiation. Young Adult


51. de Jonge HJ, Valk PJ, Veeger NJ, ter Elst A, den Boer ML, Cloos J, de Haas V, van den Heuvel-Eibrink MM, Kaspers GJ, Zwaan CM, Kamps WA, Löwenberg B, de Bont ES: High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia. Blood; 2010 Sep 9;116(10):1747-54
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] High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia.
  • High VEGFC mRNA expression of acute myeloid leukemia (AML) blasts is related to increased in vitro and in vivo drug resistance.
  • We studied effect of VEGFC on treatment outcome and investigated gene expression profiles associated with VEGFC using microarray data of 525 adult and 100 pediatric patients with AML.
  • High VEGFC expression appeared strongly associated with reduced complete remission rate (P = .004), reduced overall and event-free survival (OS and EFS) in adult AML (P = .002 and P < .001, respectively).
  • Also, in pediatric AML high VEGFC was related to reduced OS (P = .041).
  • A unique series of differentially expressed genes was identified that distinguished AML with high VEGFC from AML with low VEGFC, that is, 331 up-regulated genes (representative of proliferation, vascular endothelial growth factor receptor activity, signal transduction) and 44 down-regulated genes (eg, related to apoptosis) consistent with a role in enhanced chemoresistance.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Vascular Endothelial Growth Factor C / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Child. Child, Preschool. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Leukocyte Count. Middle Aged. Multivariate Analysis. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prognosis. Risk Factors. Young Adult


52. Hiçsönmez G: A novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells. Turk J Haematol; 2010 Mar 5;27(1):1-7
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 novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells.
  • [Transliterated title] Çocukluk yaşı akut myeloblastik lösemi ve myelodisplastik sendromunda myeloid lösemik hücrelerde farklılaşma ve apoptosisi sağlayan yüksek doz metilprednizolon ile yeni bir tedavi yaklaşımı.
  • Differentiation-inducing therapy with all-trans retinoic acid significantly improved the outcome in children with acute promyelocytic leukemia (APL).
  • Based on the experimental studies in mice, we have shown that short-course high-dose methylprednisolone (HDMP) treatment can induce terminal differentiation of leukemic cells in children with various subtypes of acute myeloblastic leukemia (AML-M1,-M2,-M3,-M4,-M7).
  • It has also been shown to induce apoptosis of myeloid leukemic cells with or without differentiation.
  • Administration of HDMP as a single agent resulted in a rapid clinical improvement, a marked decrease in blast cells in both peripheral blood and bone marrow and dramatic decreases in the size of extramedullary leukemic mass in children with AML and myelodysplastic syndrome (MDS).

  • 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 = 27265790.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  •  go-up   go-down


53. Lehrnbecher T, Bernig T, Hanisch M, Koehl U, Behl M, Reinhardt D, Creutzig U, Klingebiel T, Chanock SJ, Schwabe D: Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia. Leukemia; 2005 Oct;19(10):1745-50
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] Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia.
  • Infectious complications represent a substantial cause of morbidity and mortality in children undergoing therapy for acute myeloid leukemia (AML).
  • Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes (TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for pediatric AML.
  • The study population consisted of 168 North European Caucasian children enrolled on the clinical trial AML-BFM 93.
  • Our data suggest that variant alleles of both IL6 and CHIT could influence susceptibility to infection with Gram-negative bacteria in children undergoing therapy for AML.
  • [MeSH-major] Gram-Negative Bacterial Infections / etiology. Hexosaminidases / genetics. Interleukin-6 / genetics. Leukemia, Myeloid / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Alleles. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Female. Genetic Variation. Genotype. Gram-Negative Bacteria / isolation & purification. Humans. Infant. Infant, Newborn. Male

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 16107886.001).
  • [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 / Interleukin-6; EC 3.2.1.- / Hexosaminidases; EC 3.2.1.- / chitotriosidase
  •  go-up   go-down


54. Hubeek I, Stam RW, Peters GJ, Broekhuizen R, Meijerink JP, van Wering ER, Gibson BE, Creutzig U, Zwaan CM, Cloos J, Kuik DJ, Pieters R, Kaspers GJ: The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia. Br J Cancer; 2005 Dec 12;93(12):1388-94
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 human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia.
  • Cytarabine (ara-C) is the most effective agent for the treatment of acute myeloid leukaemia (AML).
  • We determined mRNA expression of these factors using quantitative-real-time-PCR in leukemic blasts from children diagnosed with de novo AML.
  • In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytarabine / pharmacology. Equilibrative Nucleoside Transporter 1 / physiology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Cell Membrane. Child. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. CYTARABINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1999 Mar;104(3):630-9 [10086807.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1270-6 [12406912.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):78-85 [10444166.001]
  • [Cites] Klin Padiatr. 1999 Jul-Aug;211(4):239-44 [10472557.001]
  • [Cites] Leukemia. 2005 Apr;19(4):537-44 [15690069.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2879-86 [11023525.001]
  • [Cites] J Mol Diagn. 2001 May;3(2):55-61 [11333300.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2914-27 [11032837.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7217-24 [11585758.001]
  • [Cites] Eur J Cancer. 2003 Mar;39(5):691-7 [12628850.001]
  • [Cites] Leuk Res. 2003 Dec;27(12):1075-6 [12921942.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7524-36 [14576856.001]
  • [Cites] Curr Opin Investig Drugs. 2003 Dec;4(12):1442-50 [14763130.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S108-12 [15124698.001]
  • [Cites] Cancer Res. 1978 Mar;38(3):579-85 [203385.001]
  • [Cites] J Clin Invest. 1982 Feb;69(2):479-89 [6948829.001]
  • [Cites] Mol Pharmacol. 1983 Jan;23(1):159-64 [6306421.001]
  • [Cites] Science. 1983 Aug 5;221(4610):514-9 [6306767.001]
  • [Cites] Semin Oncol. 1985 Jun;12(2 Suppl 3):65-74 [3892704.001]
  • [Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]
  • [Cites] Cancer Res. 1985 Nov;45(11 Pt 2):5952-7 [4053067.001]
  • [Cites] Cancer Res. 1986 Mar;46(3):1079-83 [3484676.001]
  • [Cites] Pharmacol Ther. 1985;30(3):287-99 [2433703.001]
  • [Cites] Semin Oncol. 1987 Jun;14(2 Suppl 1):159-66 [3589690.001]
  • [Cites] Leukemia. 1988 May;2(5):253-60 [3287015.001]
  • [Cites] Blood. 1990 Dec 1;76(11):2327-36 [2257305.001]
  • [Cites] Cancer Res. 1991 May 15;51(10):2559-65 [2021937.001]
  • [Cites] Br J Cancer. 1991 Sep;64(3):469-74 [1911186.001]
  • [Cites] Cancer Res. 1992 May 1;52(9):2389-93 [1568208.001]
  • [Cites] Leukemia. 1993 Jul;7(7):1005-11 [7686601.001]
  • [Cites] Cancer Surv. 1993;17:123-56 [8137339.001]
  • [Cites] Leukemia. 1994 Jul;8(7):1224-9 [8035616.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5401-7 [7923172.001]
  • [Cites] Br J Cancer. 1994 Dec;70(6):1047-52 [7981053.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1864-9 [7475276.001]
  • [Cites] Leuk Res. 1996 Aug;20(8):677-82 [8913321.001]
  • [Cites] Adv Cancer Res. 1998;72:197-233 [9338077.001]
  • [Cites] FEBS Lett. 1997 Dec 15;419(2-3):263-7 [9428647.001]
  • [Cites] Adv Exp Med Biol. 1998;431:667-71 [9598149.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Trends Pharmacol Sci. 1998 Oct;19(10):424-30 [9803833.001]
  • [Cites] Leuk Lymphoma. 1998 Oct;31(3-4):405-9 [9869205.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45270-5 [11584005.001]
  • [Cites] Hematol Oncol. 2001 Dec;19(4):151-7 [11754391.001]
  • [Cites] Curr Opin Oncol. 2002 Jan;14(1):3-9 [11790973.001]
  • [Cites] Leuk Res. 2002 Jul;26(7):621-9 [12008078.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):860-8 [12060121.001]
  • [Cites] Lancet Oncol. 2002 Jul;3(7):415-24 [12142171.001]
  • [Cites] Mol Cancer Ther. 2002 Apr;1(6):371-6 [12477049.001]
  • [Cites] Cancer Treat Res. 2002;112:27-47 [12481710.001]
  • [Cites] Biochem Cell Biol. 1998;76(5):761-70 [10353709.001]
  • (PMID = 16333246.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ PMC2361532
  •  go-up   go-down


55. Castagnola E, Rossi MR, Cesaro S, Livadiotti S, Giacchino M, Zanazzo G, Fioredda F, Beretta C, Ciocchello F, Carli M, Putti MC, Pansini V, Berger M, Licciardello M, Farina S, Caviglia I, Haupt R: Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study. Pediatr Blood Cancer; 2010 Dec 1;55(6):1103-7
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] Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study.
  • BACKGROUND: Data on the epidemiology of bacteremias and invasive fungal diseases (IFD) in children with acute myeloid leukemia (AML) are scarce.
  • DESIGN AND METHODS: In a multi-center, retrospective study, we analyzed proportion, rate per 1,000 person-days at risk, and cumulative risk of bacteremias and IFD in children with AML.
  • RESULTS: Between January 1998 and December 2005, 240 children were treated for AML at 8 Italian Centers, for a total of 521 treatment courses and 63,232 person-days at risk.
  • The epidemiology of bacteremias and IFD was different during front-line therapy for M3 as compared to other types of AML, but the differences were not statistically significant.
  • CONCLUSIONS: Severe infectious complications are frequent during the treatment of pediatric AML, especially during relapse treatment, and bacteremias are more frequent than IFD.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bacteremia / etiology. Leukemia, Myeloid, Acute / microbiology. Mycoses / etiology
  • [MeSH-minor] Child. Female. Follow-Up Studies. Humans. Incidence. Italy. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / microbiology. Retrospective Studies


56. Vettenranta K, EBMT Paediatric Working Party: Current European practice in pediatric myeloablative conditioning. Bone Marrow Transplant; 2008 Jun;41 Suppl 2:S14-7
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] Current European practice in pediatric myeloablative conditioning.
  • Myeloablative conditioning continues to be employed in hematopoietic stem cell transplantation among patients with pediatric transplant indications.
  • Fractionated TBI (fTBI) remains, with its considerable anti-leukemic potential, the cornerstone of conditioning in the most common of pediatric indications, ALL in its first, second or subsequent remission despite its well-established long-term sequelae.
  • The feasibility of chemotherapy-only regimens has been established and these regimens widely employed in other pediatric indications, for example, in ALL below the age of 2 years, AML, myelodysplasias or severe aplastic anemia.
  • Conditioning regimens are being modified with data accumulating on the role of, for example, pre-transplant residual disease, advanced HLA-typing or haploidentical transplantations in the pediatric setting.
  • [MeSH-minor] Child. Child, Preschool. Humans. Infant. Leukemia / therapy. Myelodysplastic Syndromes / therapy. Practice Guidelines as Topic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18545236.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  •  go-up   go-down


57. Noronha SA, Farrar JE, Alonzo TA, Gerbing RB, Lacayo NJ, Dahl GV, Ravindranath Y, Arceci RJ, Loeb DM: WT1 expression at diagnosis does not predict survival in pediatric AML: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2009 Dec;53(6):1136-9
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] WT1 expression at diagnosis does not predict survival in pediatric AML: a report from the Children's Oncology Group.
  • WT1 is a transcription factor that is aberrantly overexpressed in acute and chronic leukemias.
  • Overexpression of WT1 in pediatric acute myeloid leukemia has been reported, but the prognostic significance is unclear because sample sizes in these studies have been relatively small.
  • WT1 expression was measured by quantitative RT-PCR in samples obtained at diagnosis from 155 pediatric AML patients treated on a cooperative group protocol.

  • 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
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):414-20 [18202418.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Blood. 2009 Jun 4;113(23):5951-60 [19171881.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1381-9 [12094264.001]
  • [Cites] Leukemia. 2003 May;17(5):965-71 [12750711.001]
  • [Cites] Haematologica. 2004 Aug;89(8):926-33 [15339675.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3071-9 [7949179.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1405-12 [9028964.001]
  • [Cites] Leukemia. 1997 May;11(5):639-43 [9180285.001]
  • [Cites] Blood. 1997 Aug 1;90(3):1217-25 [9242555.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2969-76 [9531608.001]
  • [Cites] Leukemia. 1998 Dec;12(12):1886-94 [9844919.001]
  • [Cites] Ann Hematol. 2004 Dec;83(12):745-50 [15340762.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]
  • [Cites] Leukemia. 2006 Feb;20(2):254-63 [16341043.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1507-15 [16575000.001]
  • [Cites] Leuk Res. 2007 Apr;31(4):570-2 [16876863.001]
  • [Cites] Pediatr Blood Cancer. 2007 Aug;49(2):133-8 [16883592.001]
  • (PMID = 19618455.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5T32CA060441-15; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / CA060441-15; United States / NCI NIH HHS / CA / L40 CA117542; United States / NCI NIH HHS / CA / CA120535; United States / NCI NIH HHS / CA / T32 CA060441-15; United States / NCI NIH HHS / CA / R01 CA120535
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins
  • [Other-IDs] NLM/ NIHMS123739; NLM/ PMC2926132
  •  go-up   go-down


58. Yuan J, McDonough C, Kulharya A, Ramalingam P, Manaloor E: Isolated trisomy 10 in an infant with acute myeloid leukemia: a case report and review of literature. Int J Clin Exp Pathol; 2010;3(7):718-22
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] Isolated trisomy 10 in an infant with acute myeloid leukemia: a case report and review of literature.
  • Trisomy 10 as the sole cytogenetic abnormality in AML is rare, with an incidence rate of < 0.5%.
  • It tends to affect the elderly and is extremely rare in pediatric patients.
  • Compared to the two other reported pediatric cases, our patient has some unique features such as much younger age and additional findings such as bilineage dysplasia and bone marrow fibrosis.
  • Both reported cases and our case were classified as AML-M2 indicating that this may be a common subtype in pediatric patients.
  • These findings suggest that isolated trisomy 10 may be associated with distinct clinicopathologic features in pediatric AML.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Trisomy / genetics. Trisomy / pathology

  • 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
  • [Cites] Cancer Genet Cytogenet. 1999 Nov;115(1):47-51 [10565299.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jul 15;89(2):114-7 [8697414.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jul 15;89(2):173-4 [8697428.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Jan 1;100(1):84-7 [9406587.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Feb;101(1):68-71 [9460504.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Jun;103(2):130-2 [9614911.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Jan 15;108(2):175 [9973950.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Feb;109(1):88-9 [9973969.001]
  • [Cites] Ann Genet. 1999;42(1):5-10 [10214501.001]
  • [Cites] Int J Hematol. 2008 Jul;88(1):123-4 [18566741.001]
  • [Cites] Clin Pediatr (Phila). 2009 May;48(4):444-8 [19224868.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jul 15;120(2):141-3 [10942805.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Apr 1;134(1):81-3 [11996802.001]
  • [Cites] Leuk Res. 1990;14(6):515-23 [1695699.001]
  • [Cites] Leuk Res. 1992 Aug;16(8):789-96 [1528067.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1167-72 [7630192.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Apr 15;118(2):148-50 [10748296.001]
  • (PMID = 20830243.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2933392
  • [Keywords] NOTNLM ; CD13 / CD33 / CD34 / CD7 / Trisomy 10 / acute myeloid leukemia / infant / review
  •  go-up   go-down


59. MacMillan ML, Davies SM, Nelson GO, Chitphakdithai P, Confer DL, King RJ, Kernan NA: Twenty years of unrelated donor bone marrow transplantation for pediatric acute leukemia facilitated by the National Marrow Donor Program. Biol Blood Marrow Transplant; 2008 Sep;14(9 Suppl):16-22
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 unrelated donor bone marrow transplantation for pediatric acute leukemia facilitated by the National Marrow Donor Program.
  • Availability of banked unrelated donor cord blood (incorporated into the NMDP registry in 2000) as a source of stem cells has become an important option for children with leukemia, offering the advantages of immediate availability for children with high-risk disease, the need for a lesser degree of HLA match, and expanding access for those with infrequent HLA haplotypes.
  • Overall survival (OS) in children with acute leukemia transplanted with unrelated donor bone marrow (BM) is markedly better in more recent years, largely attributable to less treatment-related mortality (TRM).
  • Within this cohort, 2-year survival was markedly better for patients with acute lymphoblastic leukemia (ALL) in first complete response (CR1) (74%) versus second complete response (CR2) (62%) or more advanced disease (33%).
  • Similar findings are observed with patients with AML, suggesting earlier referral to bone marrow transplant (BMT) is optimal for survival.
  • [MeSH-minor] Child. Hematologic Neoplasms / therapy. History, 20th Century. History, 21st Century. Humans. Registries. Survival Rate. Tissue Donors. Transplantation, Homologous. United States

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18721776.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
  •  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. Pais A, Amare Kadam P, Raje G, Sawant M, Kabre S, Jain H, Advani S, Banavali S: Identification of various MLL gene aberrations that lead to MLL gene mutation in patients with acute lymphoblastic leukemia (ALL) and infants with acute leukemia. Leuk Res; 2005 May;29(5):517-26
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of various MLL gene aberrations that lead to MLL gene mutation in patients with acute lymphoblastic leukemia (ALL) and infants with acute leukemia.
  • Studies were done to investigate MLL gene aberrations using Conventional Cytogenetics, Southern blotting as well as FISH using a panel of probes on 218 cases which included 206 cases of pediatric/young adult ALL and 12 cases of infantile acute leukemias from Tata Memorial Hospital, India.
  • The incidence of MLL gene rearrangements in acute lymphoblastic leukemia (ALL) was 9.4% which included infants as well as pediatric/young adults.
  • In infantile group which included ALL as well as AML cases, MLL gene rearrangement was very common (75% frequency).
  • [MeSH-major] Chromosome Aberrations. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. India. Infant. Karyotyping. Male. Mutation. Myeloid-Lymphoid Leukemia Protein. Prognosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15755504.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [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


62. Balamurugan S, Sugapriya D, Shanthi P, Thilaka V, Venkatadesilalu S, Pushpa V, Madhavan M: Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):73-8
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] Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias.
  • We have studied MDR1 expression and AgNORS in 41 cases of acute leukemia in children.
  • In this study, AgNOR counts in patients with acute lymphoblastic leukemia (ALL) L2 subtype (FAB classification) were significantly higher as compared to the ALL L1 subtype.
  • Similarly, mean AgNOR count in the acute myeloid Leukemia (AML) M2 subtype was significantly higher as compared to the ALL L1 subtype.
  • However, there was no correlation between AgNOR and treatment outcome or between AgNOR counts and MDR1 expression in any of the subtypes of acute leukemia included in this series.
  • In AML, MDR1 gene expression was found to be related to reduced remission induction rates and hence poorer prognosis.
  • This would suggest that factors other than MDR1 may be of relevance in Pediatric ALL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Blood. 1992 Jan 15;79(2):295-8 [1346094.001]
  • [Cites] Blood. 1992 Jan 15;79(2):473-6 [1370388.001]
  • [Cites] Br J Haematol. 1991 Jan;77(1):50-3 [1671821.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1202-10 [12663440.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] J Pathol. 1989 Jul;158(3):185-8 [2475599.001]
  • [Cites] Br J Haematol. 1981 Apr;47(4):553-61 [6938236.001]
  • [Cites] Blood. 1993 May 1;81(9):2394-8 [8097634.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3480-1 [8507883.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):135-40 [8574159.001]
  • [Cites] Cancer Lett. 1996 Nov 12;108(1):87-91 [8950214.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1673-80 [9324288.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1512-8 [9552060.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):149-52 [10367797.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):309-14 [11999562.001]
  • [Cites] Mol Cancer Res. 2004 Jun;2(6):339-47 [15235109.001]
  • [Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):641-51 [15494300.001]
  • (PMID = 23100919.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453125
  • [Keywords] NOTNLM ; Acute leukemia / AgNOR / Multidrug Resistance 1 / P-glycoprotein
  •  go-up   go-down


63. Belson M, Kingsley B, Holmes A: Risk factors for acute leukemia in children: a review. Environ Health Perspect; 2007 Jan;115(1):138-45
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] Risk factors for acute leukemia in children: a review.
  • Although overall incidence is rare, leukemia is the most common type of childhood cancer.
  • Within this population, acute lymphocytic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses.
  • Epidemiologic studies of acute leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.
  • Only one environmental risk factor (ionizing radiation) has been significantly linked to ALL or AML.
  • Most environmental risk factors have been found to be weakly and inconsistently associated with either form of acute childhood leukemia.
  • Our review focuses on the demographics of childhood leukemia and the risk factors that have been associated with the development of childhood ALL or AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1989 Jul 15;49(14):4030-7 [2736544.001]
  • [Cites] BMJ. 1990 Feb 17;300(6722):423-9 [2107892.001]
  • [Cites] Am J Hum Genet. 1990 Jun;46(6):1041-52 [2160192.001]
  • [Cites] Pediatr Hematol Oncol. 1987;4(1):63-72 [3152913.001]
  • [Cites] Br J Cancer. 1990 Dec;62(6):1008-14 [2257204.001]
  • [Cites] Environ Health Perspect. 1990 Aug;88:325-37 [2272330.001]
  • [Cites] Med J Aust. 1991 Apr 1;154(7):483-7 [2005848.001]
  • [Cites] BMJ. 1991 Mar 23;302(6778):681-7 [2021741.001]
  • [Cites] BMJ. 1991 Mar 23;302(6778):687-92 [2021742.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1351-5 [1873786.001]
  • [Cites] Br J Cancer. 1991 Sep;64(3):549-54 [1911197.001]
  • [Cites] Br J Cancer. 2001 Feb 2;84(3):406-12 [11161408.001]
  • [Cites] Int J Epidemiol. 2001 Feb;30(1):125-9 [11171872.001]
  • [Cites] Am J Epidemiol. 2001 Mar 15;153(6):615-7 [11257071.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2542-6 [11289128.001]
  • [Cites] Am J Public Health. 2001 Apr;91(4):564-7 [11291366.001]
  • [Cites] Cancer Causes Control. 2001 Aug;12(6):483-90 [11519756.001]
  • [Cites] Paediatr Perinat Epidemiol. 2001 Oct;15(4):338-45 [11703681.001]
  • [Cites] Radiat Res. 2001 Dec;156(6):718-23 [11741495.001]
  • [Cites] Environ Health Perspect. 1991 Aug;94:5-7 [1954939.001]
  • [Cites] Eur J Cancer. 1992;29A(1):87-95 [1445751.001]
  • [Cites] BMJ. 1993 Jan 9;306(6870):89-94 [8435648.001]
  • [Cites] Leukemia. 1993 Mar;7(3):349-60 [8445941.001]
  • [Cites] BMJ. 1993 Mar 6;306(6878):615-21 [8461811.001]
  • [Cites] BMJ. 1993 May 1;306(6886):1153-8 [8499814.001]
  • [Cites] Leukemia. 1993 Aug;7 Suppl 2:S146-7 [8361221.001]
  • [Cites] BMJ. 1993 Oct 16;307(6910):959-66 [8241906.001]
  • [Cites] Med Pediatr Oncol. 1994;22(2):78-83 [8259105.001]
  • [Cites] Nature. 1994 Feb 24;367(6465):678-80 [8107860.001]
  • [Cites] BMJ. 1994 Jul 16;309(6948):154-7 [8044093.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Sep;3(6):457-60 [8000294.001]
  • [Cites] Br J Cancer. 1995 Jan;71(1):1-5 [7819022.001]
  • [Cites] Am J Public Health. 1995 Feb;85(2):249-52 [7856787.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):645-53 [7881337.001]
  • [Cites] Cancer. 1995 Apr 15;75(8):2186-95 [7697611.001]
  • [Cites] Epidemiol Rev. 1994;16(2):243-72 [7713179.001]
  • [Cites] Environ Health Perspect. 1995 Jun;103(6):550-4 [7556005.001]
  • [Cites] Eur J Cancer Prev. 1995 Sep;4 Suppl 1:3-107 [7496333.001]
  • [Cites] J Natl Cancer Inst. 1996 Jan 3;88(1):24-31 [8847721.001]
  • [Cites] Ann Epidemiol. 1995 Sep;5(5):354-9 [8653207.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:177-84 [8549470.001]
  • [Cites] Epidemiology. 1999 Sep;10(5):481-7 [10468419.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • [Cites] Curr Opin Pediatr. 2004 Feb;16(1):9-14 [14758108.001]
  • [Cites] Environ Mol Mutagen. 2004;43(2):100-9 [14991750.001]
  • [Cites] Cancer Detect Prev. 2004;28(2):83-7 [15068830.001]
  • [Cites] Cancer Res. 1967 Dec;27(12):2420-3 [4230121.001]
  • [Cites] J Natl Cancer Inst. 1968 May;40(5):1079-85 [5648133.001]
  • [Cites] Nature. 1971 Apr 9;230(5293):370-3 [4927726.001]
  • [Cites] Lancet. 1971 Apr 3;1(7701):699-701 [4101637.001]
  • [Cites] Science. 1973 Dec 28;182(4119):1355-6 [4586464.001]
  • [Cites] J Med Genet. 1977 Apr;14(2):81-90 [856959.001]
  • [Cites] Cancer Res. 1978 Mar;38(3):485-93 [203382.001]
  • [Cites] Cancer. 1980 Apr 1;45(7):1675-8 [6929216.001]
  • [Cites] J Pediatr. 1981 Sep;99(3):425-8 [7264801.001]
  • [Cites] Am J Ind Med. 1981;2(3):217-45 [7345926.001]
  • [Cites] J Occup Med. 1984 Sep;26(9):679-82 [6207280.001]
  • [Cites] Leuk Res. 1985;9(6):817-23 [3159943.001]
  • [Cites] Am J Epidemiol. 1985 Feb;121(2):216-24 [3860001.001]
  • [Cites] Nature. 1987 Jan 22-28;325(6102):355-7 [3808031.001]
  • [Cites] Br J Cancer. 1987 Feb;55(2):179-90 [3814487.001]
  • [Cites] J Natl Cancer Inst. 1987 Jul;79(1):39-46 [3474448.001]
  • [Cites] Prog Clin Biol Res. 1987;246:19-32 [2958880.001]
  • [Cites] Am J Epidemiol. 1988 Apr;127(4):713-25 [3354538.001]
  • [Cites] Int J Epidemiol. 2001 Dec;30(6):1428-37 [11821358.001]
  • [Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]
  • [Cites] Lancet. 2002 Feb 2;359(9304):431-4 [11844534.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Feb;11(2):177-85 [11867505.001]
  • [Cites] Environ Health Perspect. 2002 Mar;110(3):319-24 [11882484.001]
  • [Cites] Rev Environ Health. 2001 Jul-Sep;16(4):263-79 [12041882.001]
  • [Cites] Lancet Oncol. 2002 May;3(5):269-79 [12067803.001]
  • [Cites] Environ Health Perspect. 2002 Sep;110(9):955-60 [12204832.001]
  • [Cites] Br J Cancer. 2002 Sep 23;87(7):740-5 [12232757.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6 [12415113.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):655-8 [12439226.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]
  • [Cites] Br J Cancer. 1998 Mar;77(5):842-9 [9514068.001]
  • [Cites] Epidemiology. 1998 May;9(3):234-45 [9583414.001]
  • [Cites] Leukemia. 1998 May;12(5):645-51 [9593260.001]
  • [Cites] Environ Health Perspect. 1998 Jun;106 Suppl 3:893-908 [9646054.001]
  • [Cites] Br J Cancer. 1998 Jul;78(1):119-24 [9662261.001]
  • [Cites] Radiat Environ Biophys. 1998 Jul;37(2):87-93 [9728740.001]
  • [Cites] Radiat Res. 1998 Nov;150(5 Suppl):S30-41 [9806607.001]
  • [Cites] Cancer. 1999 Mar 15;85(6):1380-8 [10189146.001]
  • [Cites] Teratology. 1999 Apr;59(4):227-33 [10331524.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 16;91(12):1051-8 [10379968.001]
  • [Cites] Int J Radiat Biol. 1999 Jul;75(7):801-10 [10489891.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):783-91 [10498397.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):793-9 [10498398.001]
  • [Cites] Br J Cancer. 1999 Oct;81(3):549-53 [10507784.001]
  • [Cites] N Engl J Med. 1955 Jul 21;253(3):88-90 [14394332.001]
  • [Cites] Lancet. 1956 Sep 1;271(6940):447 [13358242.001]
  • [Cites] Arch Intern Med. 1961 Jul;108:86-90 [13720079.001]
  • [Cites] N Engl J Med. 1965 Apr 29;272:882-7 [14274439.001]
  • [Cites] N Engl J Med. 1959 Sep 17;261:585-9 [14425443.001]
  • [Cites] J Epidemiol Community Health. 2005 Feb;59(2):101-5 [15650139.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):651-5 [15767345.001]
  • [Cites] Environ Health. 2004;3(1):12 [15533260.001]
  • [Cites] Occup Environ Med. 2006 Feb;63(2):131-4 [16421392.001]
  • [Cites] Environ Health Perspect. 2003 Apr;111(4):663-8 [12676632.001]
  • [Cites] Hematol Oncol. 2003 Jun;21(2):51-5 [12802809.001]
  • [Cites] Environ Health Perspect. 2003 Jun;111(7):962-70 [12782499.001]
  • [Cites] Epidemiology. 2003 Jul;14(4):437-41 [12843769.001]
  • [Cites] Epidemiology. 2003 Sep;14(5):569-77 [14501272.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Lancet. 1988 Sep 17;2(8612):665-9 [2901525.001]
  • [Cites] Lancet. 1988 Dec 10;2(8624):1323-7 [2904050.001]
  • [Cites] Cancer. 1989 May 15;63(10):1904-11 [2649219.001]
  • [Cites] Radiat Res. 1996 May;145(5):595-601 [8619025.001]
  • [Cites] Br J Cancer. 1996 Apr;73(8):1006-12 [8611419.001]
  • [Cites] Med Pediatr Oncol Suppl. 1996;1:29-34 [8643045.001]
  • [Cites] Nature. 1996 Jul 25;382(6589):352-3 [8684463.001]
  • [Cites] Int J Cancer. 1996 Jul 29;67(3):343-52 [8707407.001]
  • [Cites] Cancer. 1995 Apr 1;75(7):1718-27 [8826933.001]
  • [Cites] Cancer Causes Control. 1996 Nov;7(6):581-90 [8932918.001]
  • [Cites] J Natl Cancer Inst. 1997 Feb 5;89(3):238-44 [9017004.001]
  • [Cites] Br J Cancer. 1997;75(3):457-63 [9020498.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):3-16 [9045302.001]
  • [Cites] Occup Environ Med. 1996 Nov;53(11):773-81 [9038803.001]
  • [Cites] Br J Radiol. 1997 Feb;70:130-9 [9135438.001]
  • [Cites] Ann Epidemiol. 1997 Apr;7(3):172-9 [9141639.001]
  • [Cites] Cancer. 1997 May 15;79(10):2045-51 [9149034.001]
  • [Cites] Nature. 1997 May 15;387(6630):246 [9153387.001]
  • [Cites] Occup Environ Med. 1997 Mar;54(3):152-66 [9155776.001]
  • [Cites] N Engl J Med. 1997 Jul 3;337(1):1-7 [9203424.001]
  • [Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673.001]
  • [Cites] Pediatr Clin North Am. 1997 Aug;44(4):831-46 [9286287.001]
  • [Cites] Environ Health Perspect. 1997 Oct;105(10):1068-77 [9349828.001]
  • [Cites] J Natl Cancer Inst. 1999 Oct 20;91(20):1765-72 [10528028.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(4):813-23 [10673523.001]
  • [Cites] Curr Opin Oncol. 2000 Jan;12(1):3-12 [10687723.001]
  • [Cites] Am J Epidemiol. 2000 Mar 1;151(5):512-5 [10707920.001]
  • [Cites] CA Cancer J Clin. 2000 Jan-Feb;50(1):7-33 [10735013.001]
  • [Cites] Br J Cancer. 2000 Sep;83(5):692-8 [10944614.001]
  • [Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]
  • [Cites] Epidemiology. 2000 Nov;11(6):624-34 [11055621.001]
  • [CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395-6 [17687418.001]
  • [CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395 [17687419.001]
  • [ErratumIn] Environ Health Perspect. 2010 Sep;118(9):A380
  • (PMID = 17366834.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 145
  • [Other-IDs] NLM/ PMC1817663
  •  go-up   go-down


64. Lim N, Ahn H, Moon H, Chen JJ: Classification of high-dimensional data with ensemble of logistic regression models. J Biopharm Stat; 2010 Jan;20(1):160-71
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.
  • The proposed classification method is applied to gene expression data on pediatric acute myeloid leukemia (AML) patients to predict each patient's risk for treatment failure or relapse at the time of diagnosis.
  • Hence, specific prognostic biomarkers can be used to predict outcomes in pediatric AML and formulate individual risk-adjusted treatment.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / classification. Models, Statistical

  • 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 = 20077255.001).
  • [ISSN] 1520-5711
  • [Journal-full-title] Journal of biopharmaceutical statistics
  • [ISO-abbreviation] J Biopharm Stat
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  •  go-up   go-down


65. Sharma P, Dhingra KK, Roy S, Singh T: An acute myeloid leukemia M6b blast crisis with giant proerythroblasts in chronic myeloid leukemia. J Pediatr Hematol Oncol; 2009 Mar;31(3):220-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An acute myeloid leukemia M6b blast crisis with giant proerythroblasts in chronic myeloid leukemia.
  • The case of a 12 yr old female with bcr-abl positive chronic myeloid leukemia who subsequently developed a fatal AML-M6b (pure erythroleukemia) blast crisis is presented.
  • The case is unique for its rarity of occurrence and for the striking resemblance that the circulating proerythroblasts showed to the giant cells characteristically seen in Parvovirus B19-induced acute pure red cell aplasia.
  • This is, to the best of our knowledge, the first description of such cells in a blast crisis of chronic myeloid leukemia.
  • [MeSH-major] Blast Crisis / pathology. Erythroblasts / pathology. Leukemia, Erythroblastic, Acute / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Blood Transfusion. Child. Female. Humans. Hydroxyurea / therapeutic use. Immunohistochemistry

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19262253.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


66. Tan PL, Wagner JE, Auerbach AD, Defor TE, Slungaard A, Macmillan ML: Successful engraftment without radiation after fludarabine-based regimen in Fanconi anemia patients undergoing genotypically identical donor hematopoietic cell transplantation. Pediatr Blood Cancer; 2006 May 1;46(5):630-6
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.
  • The patient with MDS relapsed with AML and a maternal donor recipient experienced secondary graft failure.
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / immunology. Bone Marrow / pathology. Child. Child, Preschool. Chronic Disease. Cyclophosphamide / administration & dosage. Cyclosporine / therapeutic use. Female. Fetal Blood / cytology. Fetal Blood / immunology. Graft vs Host Disease. Histocompatibility Testing. Humans. Immunosuppressive Agents / therapeutic use. Male. Methylprednisolone / therapeutic use. Myelodysplastic Syndromes / immunology. Myelodysplastic Syndromes / therapy. Neoplasm Recurrence, Local. Survival Rate. T-Lymphocytes / immunology. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Fanconi Anemia.
  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • Hazardous Substances Data Bank. METHYLPREDNISOLONE .
  • 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 = 16078221.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R37 HL32987
  • [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 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


67. Takeda M, Yamaguchi S, Eguchi K, Kajiume T, Nishimura S, Kobayashi M, Kurisu K: Spinal epidural granulocytic sarcoma in a child precedent to clinical manifestation of acute myeloid lymphoma: case report. Neurol Med Chir (Tokyo); 2009 May;49(5):221-4
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.
  • [Title] Spinal epidural granulocytic sarcoma in a child precedent to clinical manifestation of acute myeloid lymphoma: case report.
  • A 13-year-old boy presented with an epidural thoracic granulocytic sarcoma manifesting as rapidly progressive paraplegia preceding clinical manifestation of acute myeloid leukemia (AML).
  • The correct diagnosis of epidural granulocytic sarcoma and AML was established based on cell-surface markers and a chromosomal study of the bone marrow cells.
  • A combination of chemotherapy and bone marrow transfusion achieved complete remission of leukemia.
  • No evidence of AML has emerged over the 18-month follow-up period.
  • Granulocytic sarcoma should be considered in the differential diagnosis of an epidural mass in pediatric patients with or without acute leukemia.
  • [MeSH-major] Epidural Neoplasms / surgery. Leukemia, Myeloid, Acute / diagnosis. Sarcoma, Myeloid / surgery. Spinal Neoplasms / surgery

  • Genetic Alliance. consumer health - Myeloid sarcoma.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. METHYLPREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19465795.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


68. Gray TL, Ooi CY, Tran D, Traubici J, Gerstle JT, Sung L: Gastrointestinal complications in children with acute myeloid leukemia. Leuk Lymphoma; 2010 May;51(5):768-77
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] Gastrointestinal complications in children with acute myeloid leukemia.
  • Gastrointestinal complications in pediatric acute myeloid leukemia (AML) have not been systematically described in the literature.
  • Our objective was to describe complications related to the small and large bowel in children with AML.
  • We included any study design that described gastrointestinal complications in children and/or adults with AML.
  • Both leukemia infiltration and intensive chemotherapy likely play a role in the etiology of these conditions.
  • Gastrointestinal complications are relatively common in children with AML.
  • Randomized trials are required to develop evidence-based guidelines for the management of gastrointestinal complications in pediatric AML.
  • [MeSH-major] Gastrointestinal Diseases / etiology. Leukemia, Myeloid, Acute / complications
  • [MeSH-minor] Child. Humans. Prognosis

  • 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 = 20350277.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 73
  •  go-up   go-down


69. Yang Y, Tian Y, Yan C, Jin X, Tang J, Shen X: Determinants of urinary 8-hydroxy-2'-deoxyguanosine in Chinese children with acute leukemia. Environ Toxicol; 2009 Oct;24(5):446-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determinants of urinary 8-hydroxy-2'-deoxyguanosine in Chinese children with acute leukemia.
  • In the present study, the level of urinary 8-OHdG was examined in 116 Chinese children with acute leukemia (94 acute lymphoid leukemia, ALL, 22 acute myeloid leukemia, AML), and its correlation with urinary metal elements was investigated.
  • Our result showed that the level of urinary 8-OHdG in children with acute leukemia before treatment was significantly elevated compared with that in normal controls (11.92 +/- 15.42 vs. 4.03 +/- 4.70 ng/mg creatinine, P < 0.05).
  • In particular, urinary 8-OHdG was higher in children with acute leukemia aged under 3 years (20.86 +/- 21.75 ng/mg creatinine) than in those aged 3-15 years (8.09 +/- 9.65 ng/mg creatinine), whereas no differences were shown in terms of gender, parental smoking and education, household income, place of residence, and use of paracetamol.
  • In addition, urinary 8-OHdG levels were similar among different subtypes of acute lymphoid leukemia (ALL) patients.
  • Furthermore, linear regression analysis revealed a significant correlation between urinary 8-OHdG and urinary Cr, but not Fe or As, in group aged <3 years compared with group aged 3-15 years (P = 0.041), indicating that the metal elements may be involved in increasing urinary 8-OHdG level in younger children with acute leukemia.
  • Our results suggest that children with acute leukemia undergo an increased risk of oxidative DNA damage, which may be correlated with high level of Cr exposure in Chinese children with acute leukemia.
  • [MeSH-major] Carcinogens / metabolism. Deoxyguanosine / analogs & derivatives. Leukemia, Myeloid, Acute / urine. Precursor Cell Lymphoblastic Leukemia-Lymphoma / urine
  • [MeSH-minor] Adolescent. Asian Continental Ancestry Group. Child. Child, Preschool. China / epidemiology. DNA Damage. Enzyme-Linked Immunosorbent Assay. Female. Humans. Infant. Infant, Newborn. Male. Metals / urine. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18979530.001).
  • [ISSN] 1522-7278
  • [Journal-full-title] Environmental toxicology
  • [ISO-abbreviation] Environ. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Metals; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
  •  go-up   go-down


70. Kaspers GJ, Creutzig U: Pediatric acute myeloid leukemia: international progress and future directions. Leukemia; 2005 Dec;19(12):2025-9
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] Pediatric acute myeloid leukemia: international progress and future directions.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Child. Forecasting. Humans. Prognosis. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16304569.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Number-of-references] 30
  •  go-up   go-down


71. Mantadakis E, Samonis G, Kalmanti M: A comprehensive review of acute promyelocytic leukemia in children. Acta Haematol; 2008;119(2):73-82
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] A comprehensive review of acute promyelocytic leukemia in children.
  • The outcome of patients with acute promyelocytic leukemia (APL) has substantially improved since the successful introduction of tretinoin, and nowadays combining tretinoin with chemotherapy is potentially curative for at least 70-75% of patients with newly diagnosed APL.
  • In most pediatric series, APL represents < or = 10% of childhood acute myelogenous leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Child. Humans. Prognosis. Risk Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2008 S. Karger AG, Basel
  • (PMID = 18285695.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 70
  •  go-up   go-down


72. Liu CF, Liu GL, Zhang LP, Cheng YF, Lu AD, Tian KG, Liu YR, Qin YZ: [Clinical significance of detection of AML1/ETO fusion transcripts in childhood AML using real-time quantitative reverse transcription polymerase chain reaction]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Feb;13(1):76-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical significance of detection of AML1/ETO fusion transcripts in childhood AML using real-time quantitative reverse transcription polymerase chain reaction].
  • Fourteen AML1/ETO positive children out of 52 AML children were selected.
  • It is concluded that real-time RT-PCR is a suitable approach for quantifying AML1/ETO transcripts in monitoring of AML patients with t(8;21) during/after chemotherapy and provides data of diagnostic relevance.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15748440.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


73. Sharma A, Gupta D, Mohanti BK, Thulkar S, Dwary A, Goyal S, Muzumder S, Das P: Non-Hodgkin lymphoma following temozolomide. Pediatr Blood Cancer; 2009 Oct;53(4):661-2
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 MDS/AML or non-Hodgkin lymphoma attributed to TMZ exposure has been reported.


74. Tabuchi K: [Acute myeloid leukemia]. Gan To Kagaku Ryoho; 2007 Feb;34(2):156-61
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] [Acute myeloid leukemia].
  • The annual incident rate of pediatric acute myeloid leukemia (AML) is now 10 per million in Japan, against 5 to 9 per million in the USA and Europe.
  • Overall long-term survival has now been achieved for more than 50% of pediatric patients with AML in the USA and in Europe.
  • The prognostic factors of pediatric AML were analyzed,and patients with AML were classified according to prognostic factors.
  • The t(15;17), inv(16) and t(8;21) have emerged as predictors of good prognosis in children with AML.
  • In addition to chromosomal deletions, FLT 3/ITD identifies pediatric patients with a particularly poor prognosis.
  • Clinical trials of AML feature intensive chemotherapy with or without subsequent stem cell transplantation.
  • Risk group stratification is becoming increasingly important in planning AML therapy.
  • APL can be distinguished from other subtypes of AML by virtue of its excellent response and overall outcome as a result of differentiation therapy with ATRA.
  • Children with Down syndrome and AML have been shown to have a superior prognosis to AML therapy compared to other children with AML.
  • With the consideration of quality of life (QOL), risk-adapted therapy was introduced in the AML 99 trial conducted by the Japanese Childhood AML Cooperative Study Group.
  • A high survival rate of 79% at 3 years was achieved for childhood de novo AML in the AML 99 trial.
  • To evaluate the efficacy and safety of the treatment strategy according to risk stratification based on leukemia cell biology and response to the initial induction therapy in children with AML, the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) has organized multi-center phase II trials in children with newly diagnosed AML.
  • [MeSH-major] Antineoplastic Protocols. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Child. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Survival Rate. Transplantation, Homologous

  • 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 = 17301520.001).
  • [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
  •  go-up   go-down


75. Mercher T, Raffel GD, Moore SA, Cornejo MG, Baudry-Bluteau D, Cagnard N, Jesneck JL, Pikman Y, Cullen D, Williams IR, Akashi K, Shigematsu H, Bourquin JP, Giovannini M, Vainchenker W, Levine RL, Lee BH, Bernard OA, Gilliland DG: The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model. J Clin Invest; 2009 Apr;119(4):852-64
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 OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.
  • Acute megakaryoblastic leukemia (AMKL) is a form of acute myeloid leukemia (AML) associated with a poor prognosis.
  • We generated a knockin mouse model of the one twenty-two-megakaryocytic acute leukemia (OTT-MAL) fusion oncogene that results from the t(1;22)(p13;q13) translocation specifically associated with a subtype of pediatric AMKL.
  • Furthermore, cooperation between OTT-MAL and an activating mutation of the thrombopoietin receptor myeloproliferative leukemia virus oncogene (MPL) efficiently induced a short-latency AMKL that recapitulated all the features of human AMKL, including megakaryoblast hyperproliferation and maturation block, thrombocytopenia, organomegaly, and extensive fibrosis.

  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 2005 Oct 1;19(19):2331-42 [16166372.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4220-6 [18755984.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]
  • [Cites] Cell. 2006 Mar 10;124(5):973-83 [16530044.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] FEBS Lett. 2006 May 22;580(12):2860-8 [16574107.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):678-89 [16921404.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2770-9 [16804112.001]
  • [Cites] Br J Haematol. 2006 Sep;134(5):453-66 [16856888.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1967-77 [16990763.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3472-6 [16868251.001]
  • [Cites] Cell Mol Life Sci. 2006 Nov;63(21):2460-76 [16909203.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1633-41 [10688818.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2023-30 [11264167.001]
  • [Cites] Mol Cell Biol. 2001 Apr;21(8):2659-70 [11283246.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5776-9 [11344311.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] Nat Genet. 2001 Jul;28(3):220-1 [11431691.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jan;33(1):22-8 [11746984.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3359-67 [12032774.001]
  • [Cites] J Clin Invest. 2002 Jun;109(12):1579-85 [12070305.001]
  • [Cites] Blood. 2002 Jul 15;100(2):618-26 [12091356.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5417-26 [12374742.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jan 7;100(1):205-10 [12490656.001]
  • [Cites] Immunity. 2003 Feb;18(2):301-12 [12594956.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):930-8 [12648061.001]
  • [Cites] Cell. 2003 May 2;113(3):329-42 [12732141.001]
  • [Cites] Am J Hematol. 2003 Jun;73(2):71-80 [12749007.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1909-20 [12897056.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):387-96 [15288264.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Blood. 1992 Jun 15;79(12):3325-30 [1596573.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1273-82 [10438715.001]
  • [Cites] Growth Factors. 2004 Sep;22(3):151-5 [15518238.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):613-9 [15895080.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1610-5 [17242367.001]
  • [Cites] Mol Cell Biol. 2007 Apr;27(8):3056-64 [17283045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):6001-6 [17376872.001]
  • [Cites] Immunity. 2007 Jul;27(1):100-10 [17658278.001]
  • [Cites] Immunity. 2007 Jul;27(1):89-99 [17658279.001]
  • [Cites] Stem Cells. 2008 Mar;26(3):621-9 [18055448.001]
  • [Cites] Cell Stem Cell. 2008 Sep 11;3(3):314-26 [18786418.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6302-13 [18694962.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6171-81 [18710951.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):541-54 [18345353.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • (PMID = 19287095.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / U01 CA105423; United States / NIDDK NIH HHS / DK / DK50654; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / K08 CA111399; United States / NIDDK NIH HHS / DK / P01 DK050654
  • [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 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Mpl protein, mouse; 0 / OTT-MAL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Rbpj protein, mouse; 0 / Receptors, Notch; 0 / Receptors, Thrombopoietin
  • [Other-IDs] NLM/ PMC2662544
  •  go-up   go-down


76. Cazzaniga G, Dell'Oro MG, Mecucci C, Giarin E, Masetti R, Rossi V, Locatelli F, Martelli MF, Basso G, Pession A, Biondi A, Falini B: Nucleophosmin mutations in childhood acute myelogenous leukemia with normal karyotype. Blood; 2005 Aug 15;106(4):1419-22
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 mutations in childhood acute myelogenous leukemia with normal karyotype.
  • Nucleophosmin (NPM) is a nucleocytoplasmic shuttling protein involved in leukemia-associated chromosomal translocations, and it regulates the alternate reading frame (ARF)-p53 tumor-suppressor pathway.
  • Cytoplasmic NPM was detected in 35% of adult patients with primary non-French-American-British (FAB) classification M3 acute myeloid leukemia (AML), associated mainly with normal karyotype.
  • We evaluated the prevalence of the NPM1 gene mutation in non-M3 childhood AML patients enrolled in the ongoing Associazione Italiana di Ematologia e Oncologia Pediatrica (AIEOP-AML02) protocol in Italy.
  • Thus, the NPM1 mutation is a frequent abnormality in AML patients without known genetic marker; the mutation may represent a new target to monitor minimal residual disease in AML and a potential candidate for alternative and targeted treatments.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Age Factors. Base Sequence. Child. Child, Preschool. Cytoplasm / chemistry. DNA Mutational Analysis. Exons. Female. Humans. Karyotyping. Male. Molecular Sequence Data


77. Zidan H, Lo S, Wiebe D, Talano J, Alemzadeh R: Severe hypercholesterolemia mediated by lipoprotein X in a pediatric patient with chronic graft-versus-host disease of the liver. Pediatr Blood Cancer; 2008 Jun;50(6):1280-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Severe hypercholesterolemia mediated by lipoprotein X in a pediatric patient with chronic graft-versus-host disease of the liver.
  • We describe a case of extreme hypercholesterolemia, mediated by lipoprotein X, in a 12-year-old Caucasian female who underwent an unrelated allogenic bone marrow transplant for relapsed acute myelocytic leukemia (AML).
  • [MeSH-minor] Bile Reflux / etiology. Child. Chronic Disease. Female. Humans


78. Neudorf S, Sanders J, Kobrinsky N, Alonzo TA, Buxton A, Buckley JD, Howells W, Gold S, Barnard DR, DeSwarte J, Kalousek D, Lange BJ, Woods WG: Autologous bone marrow transplantation for children with AML in first remission. Bone Marrow Transplant; 2007 Aug;40(4):313-8
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] Autologous bone marrow transplantation for children with AML in first remission.
  • In Children's cancer group (CCG) 2891, newly diagnosed patients with AML were randomized between standard and intensive timing induction therapies.
  • Myeloid and platelet engraftment occurred at a median of 44 and 42 days, respectively.
  • The results confirm previous studies that ABMT is effective post remission therapy for pediatric patients with AML in first remission.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Remission Induction / methods
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Graft Survival. Humans. Infant. Male. Prospective Studies. Transplantation Conditioning / methods. Transplantation, Autologous


79. Nebral K, König M, Schmidt HH, Lutz D, Sperr WR, Kalwak K, Brugger S, Dworzak MN, Haas OA, Strehl S: Screening for NUP98 rearrangements in hematopoietic malignancies by fluorescence in situ hybridization. Haematologica; 2005 Jun;90(6):746-52
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.
  • BACKGROUND AND OBJECTIVES: The aim of this study was to determine the incidence of rearrangements of NUP98 (the gene coding for nucleoporin 98kDa protein) in childhood acute myeloid leukemia (AML) and selected patients with 11p13-15 rearrangements.
  • DESIGN AND METHODS: Screening of 59 consecutive patients enrolled in the Austrian AML-BFM93 clinical trial was performed by dual-color FISH.
  • RESULTS: Among the 59 AML patients, one NUP98-NSD1 positive case (1.7%) was detected.
  • INTERPRETATION AND CONCLUSIONS: The observed frequency of 1.7% confirmed the low incidence of NUP98 rearrangements in childhood AML.
  • [MeSH-major] Chromosome Aberrations. Hematologic Neoplasms / diagnosis. Hematologic Neoplasms / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Chromosome Inversion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Molecular Sequence Data. Translocation, Genetic

  • 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 = 15951287.001).
  • [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 / Nuclear Pore Complex Proteins; 0 / nuclear pore complex protein 98
  •  go-up   go-down


80. Tebbi CK, London WB, Friedman D, Villaluna D, De Alarcon PA, Constine LS, Mendenhall NP, Sposto R, Chauvenet A, Schwartz CL: Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease. J Clin Oncol; 2007 Feb 10;25(5):493-500
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] Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease.
  • PURPOSE: Pediatric Oncology Group (POG) studies 9426 and 9425 evaluated dexrazoxane (DRZ) as a cardiopulmonary protectant during treatment for Hodgkin's disease (HD).
  • We evaluated incidence and risk factors of acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and second malignant neoplasms (SMNs).
  • Six of eight patients developed AML/MDS, and both solid tumors (osteosarcoma and papillary thyroid carcinoma) occurred in recipients of DRZ.
  • With median 58 months' follow-up, 4-year cumulative incidence rate (CIR) for AML/MDS was 2.55% +/- 1.0% with DRZ versus 0.85% +/- 0.6% in the non-DRZ group (P = .160).
  • Among patients receiving DRZ, the standardized incidence rate (SIR) for AML/MDS was 613.6 compared with 202.4 for those not receiving DRZ (P = .0990).
  • Adding DRZ to ABVE and ABVE-PC may have increased the incidence of SMN and AML/MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chelating Agents / adverse effects. Hodgkin Disease / drug therapy. Leukemia, Myeloid / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Razoxane / adverse effects
  • [MeSH-minor] Acute Disease. Adolescent. Cohort Studies. Enzyme Inhibitors / adverse effects. Female. Follow-Up Studies. Heart Diseases / chemically induced. Heart Diseases / prevention & control. Humans. Incidence. Lung Diseases / chemically induced. Lung Diseases / prevention & control. Male. Neoplasm Staging. Osteosarcoma / chemically induced. Risk Assessment. Risk Factors. Thyroid Neoplasms / chemically induced. Time Factors. Topoisomerase II Inhibitors


81. Su YC, Chen CB, Chang YT, Tung YT, Li DK: hSNF5 /INI1 mutation analysis in acute myeloid leukemia. Int J Hematol; 2008 Mar;87(2):172-5
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] hSNF5 /INI1 mutation analysis in acute myeloid leukemia.
  • Previous studies indicated that region 11.2 of the long arm of chromosome 22 (22q11.2) might be a locus encoding a tumor suppressor gene, since its deletion is a recurrent genetic characteristic of aggressive pediatric cancer.
  • To investigate whether the hSNF5/INI1 gene is involved in leukemogenesis, mutation analysis of the hSNF5/INI1 gene was performed in the present study using 5 hematopoietic cell lines, acute myeloid leukemia (AML) specimen and normal control.
  • The results of this study suggest that the hSNF5/INI1 gene does not play an important role in the leukemogenesis of AML.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide / genetics. Transcription Factors / 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
  • [Cites] Genes Chromosomes Cancer. 1996 Jan;15(1):10-7 [8824720.001]
  • [Cites] Nature. 1998 Jul 9;394(6689):203-6 [9671307.001]
  • [Cites] Hum Mol Genet. 1999 Dec;8(13):2359-68 [10556283.001]
  • [Cites] Nucleic Acids Res. 1995 Apr 11;23 (7):1127-32 [7739891.001]
  • [Cites] Genes Chromosomes Cancer. 1994 Nov;11(3):146-52 [7530483.001]
  • [Cites] Science. 1987 Jan 16;235(4786):305-11 [3541204.001]
  • [Cites] Trends Biochem Sci. 1995 Apr;20(4):143-6 [7770913.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3870-4 [10463572.001]
  • [Cites] Genes Chromosomes Cancer. 1994 May;10(1):49-54 [7519873.001]
  • [Cites] Am J Hum Genet. 1999 Nov;65(5):1342-8 [10521299.001]
  • [Cites] Nature. 1994 Aug 11;370(6489):477-81 [8047169.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2759-63 [10914721.001]
  • [Cites] Genes Chromosomes Cancer. 1996 Jun;16(2):94-105 [8818656.001]
  • [Cites] Curr Opin Cell Biol. 1994 Jun;6(3):396-402 [7917331.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4152-7 [9539705.001]
  • [Cites] Oncogene. 1999 Dec 9;18(52):7559-65 [10602515.001]
  • [Cites] Genes Chromosomes Cancer. 1998 Feb;21(2):82-9 [9491318.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1993;58:257-63 [7956037.001]
  • [Cites] Cancer Lett. 2000 May 29;153(1-2):57-61 [10779630.001]
  • [Cites] Science. 1994 Jul 1;265(5168):53-60 [8016655.001]
  • [Cites] Am J Hum Genet. 2000 Apr;66(4):1403-6 [10739763.001]
  • [Cites] N Engl J Med. 1994 Feb 3;330(5):328-36 [8277954.001]
  • [Cites] Genes Dev. 1996 Sep 1;10(17):2117-30 [8804307.001]
  • [Cites] Science. 1994 Dec 23;266(5193):2002-6 [7801128.001]
  • [Cites] Curr Opin Genet Dev. 1996 Apr;6(2):171-5 [8722173.001]
  • [Cites] Genes Chromosomes Cancer. 1990 Sep;2(3):210-6 [1964081.001]
  • [Cites] Genes Dev. 1992 Dec;6(12A):2288-98 [1459453.001]
  • [Cites] J Hum Genet. 1999;44(5):354-5 [10496084.001]
  • (PMID = 18266055.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 Protein; 0 / SMARCB1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


82. Shman TV, Fedasenka UU, Savitski VP, Aleinikova OV: CD34+ leukemic subpopulation predominantly displays lower spontaneous apoptosis and has higher expression levels of Bcl-2 and MDR1 genes than CD34- cells in childhood AML. Ann Hematol; 2008 May;87(5):353-60
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] CD34+ leukemic subpopulation predominantly displays lower spontaneous apoptosis and has higher expression levels of Bcl-2 and MDR1 genes than CD34- cells in childhood AML.
  • In view of obscure clinical and biological significance of leukemic cells heterogeneity, we studied the efficacy of apoptosis, proliferation, and expression levels of the Bcl-2, MDR1, LRP, and BCRP genes in sorted CD34+ and CD34- subpopulations of childhood AML leukemic samples.
  • [MeSH-major] ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Antigens, CD34. Apoptosis / physiology. Leukemia, Myeloid, Acute. Lymphocyte Subsets / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. Child. Child, Preschool. Cohort Studies. Gene Expression Profiling. Humans. Neoplasm Proteins / metabolism. Neoplasm, Residual / metabolism. Neoplasm, Residual / physiopathology. Recurrence. Vault Ribonucleoprotein Particles / metabolism

  • 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] Ann Hematol. 2008 Dec;87(12):1017-8 [18629500.001]
  • (PMID = 18228020.001).
  • [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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antigens, CD34; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
  •  go-up   go-down


83. Burjanivova T, Madzo J, Muzikova K, Meyer C, Schneider B, Votava F, Marschalek R, Stary J, Trka J, Zuna J: Prenatal origin of childhood AML occurs less frequently than in childhood ALL. BMC Cancer; 2006;6:100
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] Prenatal origin of childhood AML occurs less frequently than in childhood ALL.
  • BACKGROUND: While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive.
  • Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant childhood AML and ALL patients for the presence of their respective leukemic markers.
  • In AML patients (n = 13, age 1-14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers.
  • We did not find patient-specific molecular markers in any patient with AML.
  • CONCLUSION: In the largest cohort examined so far we used identical approach for the backtracking of non-infant childhood ALL and AML.
  • Our data suggest that either the prenatal origin of AML is less frequent or the load of pre-leukemic cells is significantly lower at birth in AML compared to ALL cases.
  • [MeSH-major] Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Fetal Blood / chemistry. Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte. Leukemia, Myeloid / embryology. Oncogene Proteins, Fusion / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / embryology
  • [MeSH-minor] Bone Marrow Cells / chemistry. Child. Child, Preschool. Clone Cells / chemistry. Cohort Studies. Core Binding Factor Alpha 2 Subunit / blood. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / blood. Myeloid-Lymphoid Leukemia Protein / genetics. Neonatal Screening. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / blood. fms-Like Tyrosine Kinase 3 / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2003 Jul;122(1):24-9 [12823342.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):449-54 [15626757.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2000 Jul 1;96(1):264-8 [10891460.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Blood. 2001 Jul 15;98(2):478-82 [11435320.001]
  • [Cites] Blood. 2001 Oct 1;98(7):2272-4 [11568017.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2992-6 [11929791.001]
  • [Cites] Blood. 2002 May 15;99(10):3801-5 [11986239.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6 [12415113.001]
  • [Cites] Br J Cancer. 2002 Oct 21;87(9):994-9 [12434291.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):36-43 [12661004.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4640-1 [12756163.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):406-11 [12800152.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2202-6 [12931229.001]
  • [Cites] Leuk Lymphoma. 2003 Dec;44(12):2099-102 [14959854.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Apr;39(4):335-40 [14978794.001]
  • [Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]
  • [Cites] Nucleic Acids Res. 1995 Sep 25;23(18):3788-9 [7479012.001]
  • [Cites] Blood. 1997 Jan 1;89(1):281-5 [8978302.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 May-Jun;20(3):264-7 [9628441.001]
  • [Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4079-85 [10361104.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1057-62 [10419898.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1667-9 [12886258.001]
  • (PMID = 16630339.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF6 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1463004
  •  go-up   go-down


84. Adachi S, Manabe A, Imaizumi M, Taga T, Tawa A, Tsurusawa M, Kikuchi A, Masunaga A, Tsuchida M, Nakahata T, MDS Committee of the Japanese Society of Pediatric Hematology: Acute myeloid leukemia with multilineage dysplasia in children. Int J Hematol; 2007 Nov;86(4):358-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia with multilineage dysplasia in children.
  • We retrospectively surveyed pediatric acute myeloid leukemia (AML) patients with multilineage dysplasia treated with the AML 99 and the Children's Cancer and Leukemia Study Group (CCLSG) AML 9805 protocols.
  • We found only 9 AML patients (2.6%) with multilineage dysplasia among the 341 patients with newly diagnosed de novo AML.
  • Eight of the 9 patients obtained complete remission (CR) following the intensive AML-oriented treatments.
  • No reports have described AML with multilineage dysplasia in children, and the incidence of the disease is expected to be very low.
  • We plan to conduct a prospective pathologic review to select cases with this disease entity in the next Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) AML-05 protocol.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Male

  • 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
  • [Cites] Leukemia. 1996 Jun;10(6):946-51 [8667650.001]
  • [Cites] Leukemia. 2000 Nov;14(11):1861-6 [11069020.001]
  • [Cites] Leukemia. 2001 Nov;15(11):1713-20 [11681412.001]
  • [Cites] Ann Hematol. 1997 Sep;75(3):91-4 [9368477.001]
  • [Cites] Br J Haematol. 2003 Jan;120(1):56-62 [12492577.001]
  • [Cites] Br J Haematol. 1987 Aug;66(4):445-50 [3478074.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):256-65 [12525517.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1992 Jun;6(6):520-5 [1318461.001]
  • [Cites] Cancer. 1994 Jan 15;73(2):314-21 [8293394.001]
  • [Cites] Leuk Lymphoma. 1998 May;29(5-6):523-31 [9643566.001]
  • [Cites] Pediatr Blood Cancer. 2007 Aug;49(2):127-32 [16807916.001]
  • [Cites] Int J Hematol. 2001 Jan;73(1):93-9 [11372762.001]
  • [Cites] Clin Lab Haematol. 1990;12(1):57-65 [2344717.001]
  • [Cites] Br J Haematol. 1994 Apr;86(4):767-73 [7918070.001]
  • (PMID = 18055345.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


85. 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


86. Chen YM, Liu TF, Ruan M, Zou Y, Chen XJ, Guo Y, Wang SC, Zhu XF: [Prognosis and chromosomal abnormalities in 79 children with t (8;21) acute myeloid leukemia]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2009 Oct;31(5):542-6
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] [Prognosis and chromosomal abnormalities in 79 children with t (8;21) acute myeloid leukemia].
  • OBJECTIVE: To investigate the chromosomal abnormalities and evaluate the prognostic value of post-remission chemotherapy in children with t (8;21) acute myeloid leukemia (AML).
  • METHODS: The diagnosis of AML and its subtyping were performed using morphological, immunological, and cytogenetic methodologies in 79 children.
  • CONCLUSION: Most children with t (8;21) AML have additional chromosomal abnormalities, although they do not affect the prognosis and long-term survival.
  • Childhood t (8;21) AML usually has high CR rate with relatively good prognosis, and post-remission consolidation by HDAC can improve the survival.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Female. Humans. Karyotype. Male. Prognosis

  • 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 = 19968066.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


87. Tan RM, Quah TC, Aung L, Liang S, Kirk RC, Yeoh AE: Improved outcome in childhood acute myeloid leukemia in Singapore with the MRC AML 10 protocol. Pediatr Blood Cancer; 2007 Mar;48(3):262-7
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] Improved outcome in childhood acute myeloid leukemia in Singapore with the MRC AML 10 protocol.
  • BACKGROUND: The introduction of the United Kingdom Medical Research Council's 10th AML trial (MRC AML 10) protocol incorporating high-dose anthracycline therapy has improved outcome of children with acute myeloid leukemia (AML).
  • In this study, we review the results of childhood AML therapy in a Singapore university hospital over the last 17 years emphasizing toxicity and outcome.
  • PROCEDURE: Retrospective analysis revealed 34 children with AML between 1988 and 2003.
  • From September 1996, all but one of 15 children received MRC AML 10 treatment.
  • MRC AML 10-treated patients (n = 14) had significantly better 3-year overall, event-free, and disease-free survival (74% vs. 35%, 77% vs. 20%, 83% vs. 31%; P = 0.019, P = 0.002, and P = 0.010, respectively) and were likelier to achieve complete remission (CR) than non-MRC AML 10 patients (P = 0.102).
  • Among patients who achieved CR, MRC AML 10-treated patients were significantly more likely to achieve CR after only one cycle of chemotherapy (P = 0.016).
  • CONCLUSIONS: These findings suggest that MRC AML 10 treatment results in significantly superior survival, without excess toxicity.
  • Future studies should attempt to elucidate the relative importance of individual MRC AML 10 components and reduce the high cumulative anthracycline dose without compromising outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects. Acute Disease. Amsacrine / administration & dosage. Amsacrine / adverse effects. Azacitidine / administration & dosage. Azacitidine / adverse effects. Child. Child, Preschool. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Developing Countries. Disease-Free Survival. Drug Evaluation. Drug-Induced Liver Injury / etiology. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Gastrointestinal Diseases / chemically induced. Heart Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Infant. Infection / etiology. Kaplan-Meier Estimate. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prednisone / administration & dosage. Prednisone / adverse effects. Remission Induction. Retrospective Studies. Singapore / epidemiology. Survival Analysis. Thioguanine / administration & dosage. Thioguanine / adverse effects. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. AMSACRINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16602120.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 00DPD30SOY / Amsacrine; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; M801H13NRU / Azacitidine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; MRC AML 10 protocol; POG-8498 protocol
  •  go-up   go-down


88. Evrard AS, Hémon D, Billon S, Laurier D, Jougla E, Tirmarche M, Clavel J: Childhood leukemia incidence and exposure to indoor radon, terrestrial and cosmic gamma radiation. Health Phys; 2006 Jun;90(6):569-79
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] Childhood leukemia incidence and exposure to indoor radon, terrestrial and cosmic gamma radiation.
  • This study was undertaken to evaluate the ecological association between terrestrial and cosmic gamma radiation, indoor radon, and acute leukemia incidence among children under 15 y of age.
  • From 1990 to 2001, 5,330 cases of acute leukemia were registered by the French National Registry of Childhood Leukemia and Lymphoma.
  • There was no evidence of an ecological association between terrestrial gamma dose (range: 0.22-0.90 mSv y) or total gamma dose (range: 0.49-1.28 mSv y) and childhood acute leukemia incidence, for acute myeloid leukemia (AML) or for acute lymphoblastic leukemia (ALL), in univariate or multivariate regression analyses including indoor radon.
  • A significant positive association between indoor radon (range: 22-262 Bq m) and AML incidence among children was observed and remained significant in multivariate regression analyses including either terrestrial gamma dose [SIR per 100 Bq m = 1.29 (1.09-1.53)] or total gamma dose [SIR per 100 Bq m = 1.29 (1.09-1.53)].
  • The study showed no ecological association between terrestrial gamma radiation and childhood leukemia for the range of variation in gamma dose rates observed in France.
  • The moderate ecological association between childhood AML incidence and indoor radon does not appear to be confounded by terrestrial gamma dose.
  • [MeSH-major] Air Pollution, Indoor / analysis. Cosmic Radiation. Environmental Exposure / statistics & numerical data. Gamma Rays. Leukemia, Radiation-Induced / epidemiology. Radon / analysis. Risk Assessment / methods
  • [MeSH-minor] Body Burden. Child. Child, Preschool. Confounding Factors (Epidemiology). Female. France / epidemiology. Humans. Incidence. Male. Radiation Dosage. Registries. Relative Biological Effectiveness. Risk Factors

  • MedlinePlus Health Information. consumer health - Indoor Air Pollution.
  • MedlinePlus Health Information. consumer health - Radon.
  • Hazardous Substances Data Bank. RADON, RADIOACTIVE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16691105.001).
  • [ISSN] 0017-9078
  • [Journal-full-title] Health physics
  • [ISO-abbreviation] Health Phys
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] Q74S4N8N1G / Radon
  •  go-up   go-down


89. Rubnitz JE, Razzouk BI, Lensing S, Pounds S, Pui CH, Ribeiro RC: Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia. Cancer; 2007 Jan 1;109(1):157-63
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] Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia.
  • BACKGROUND: Outcome after recurrence of childhood acute myeloid leukemia (AML) is poor.
  • We performed this study to identify prognostic factors for recurrence and for survival after recurrence of AML.
  • METHODS: The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo AML who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied.
  • CONCLUSIONS: Survival after recurrence was poor in children with AML.
  • Novel therapies are urgently needed to prevent or to treat recurring AML.
  • [MeSH-major] Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Prognosis. Recurrence. Sex Factors. Stem Cell Transplantation. Survival Rate. Time Factors. Transplantation, Autologous

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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
  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17133407.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


90. Brown P, Smith FO: Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date. Paediatr Drugs; 2008;10(2):85-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date.
  • While acute myeloid leukemia (AML) is significantly less common than acute lymphoblastic leukemia (ALL) in childhood, it is significantly more deadly with only half as many children likely to be cured with standard therapy.
  • In addition, the typical treatment for AML is among the most toxic of treatments for pediatric cancer; it includes intensive multiagent chemotherapy and, often, hematopoietic stem cell transplantation.
  • Given the poor prognosis of pediatric AML and the significant toxicity of standard AML therapy, novel therapies are needed.
  • Improved understanding of the molecular and cellular biology of leukemia has facilitated the development of molecularly targeted therapies.
  • In this article, we review progress to date with agents that are showing promise in the treatment of pediatric AML including targeted immunoconjugates, inhibitors of signaling molecules (e.g.
  • For the specific agents in each of these classes, we summarize the published preclinical data and the clinical trials that have been completed, are in progress, or are being planned for children with AML.
  • Finally, we discuss potential challenges to the success of molecularly targeted therapy including demonstrating adequate targeting of leukemia stem cells, developing synergistic and tolerable combinations of agents, and designing adequately powered clinical trials to test efficacy in molecularly defined subsets of patients.
  • [MeSH-major] Leukemia, Myeloid, Acute

  • 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 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] Blood. 2006 Oct 15;108(8):2764-9 [16809615.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Pediatr Blood Cancer. 2006 May 1;46(5):565-9 [16261562.001]
  • [Cites] Leukemia. 2003 May;17 (5):995-7 [12750723.001]
  • [Cites] Blood. 1992 Apr 1;79(7):1811-6 [1373089.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1277-84 [15735013.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]
  • [Cites] Leuk Lymphoma. 2006 Feb;47(2):207-22 [16321850.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3262-70 [16857985.001]
  • [Cites] Blood. 2007 Feb 15;109 (4):1387-94 [17082323.001]
  • [Cites] Blood. 2001 Oct 15;98 (8):2301-7 [11588023.001]
  • [Cites] Leukemia. 1999 Jan;13(1):38-43 [10049058.001]
  • [Cites] Int J Hematol. 2005 Aug;82(2):100-7 [16146839.001]
  • [Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]
  • [Cites] Blood. 1999 Mar 15;93(6):2043-56 [10068678.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1183-8 [15886328.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Blood. 2007 May 15;109 (10 ):4168-70 [17227830.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2005-12 [7718872.001]
  • [Cites] Curr Hematol Rep. 2004 May;3(3):203-9 [15087069.001]
  • [Cites] Med Pediatr Oncol. 1999 Dec;33(6):525-9 [10573574.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1841-9 [15166029.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4222-4 [12010830.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):837-41 [9041182.001]
  • [Cites] Blood. 1999 May 15;93(10):3302-8 [10233882.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1516-22 [17332297.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3058-65 [15626743.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4276-84 [14962898.001]
  • [Cites] Blood. 1997 Jul 15;90(2):489-519 [9226149.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Leukemia. 2003 Feb;17(2):350-8 [12592335.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jun;321(3):953-60 [17389244.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23 ):4816-22 [15570084.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1267-70 [15988530.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] Eur J Clin Invest. 2007 Jan;37(1):73-82 [17181570.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Leukemia. 1998 Sep;12(9):1333-7 [9737679.001]
  • [Cites] Leukemia. 2003 Jan;17 (1):83-8 [12529664.001]
  • [Cites] Blood. 2005 Jul 15;106(2):673-80 [15797998.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2325-31 [14644997.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):811-4 [9486654.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1466-73 [12689934.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16220-5 [12451177.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2000 Jan 15;95(2):639-45 [10627474.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1995-9 [15187030.001]
  • [Cites] Cell Growth Differ. 1992 Jul;3(7):461-9 [1419908.001]
  • [Cites] Leukemia. 2002 May;16(5):813-9 [11986941.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]
  • [Cites] Blood. 2004 Aug 15;104(4):1145-50 [15126317.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1079-82 [11834837.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S30-5 [16341238.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Clin Cancer Res. 2004 May 15;10(10):3371-6 [15161691.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] Adv Exp Med Biol. 2003;532:121-40 [12908554.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3361-9 [11369625.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Br J Haematol. 1991 Mar;77(3):323-7 [2012756.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1932-42 [10602413.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]
  • [Cites] Leukemia. 1987 Oct;1(10):697-705 [3312833.001]
  • [Cites] Blood. 2001 Aug 15;98 (4):988-94 [11493443.001]
  • [Cites] Eur J Cancer. 2004 Mar;40(5):707-21, discussion 722-4 [15010072.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2707-16 [16981007.001]
  • [Cites] Cell Cycle. 2006 Feb;5(3):271-3 [16397415.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] Semin Hematol. 2004 Apr;41(2 Suppl 4):27-32 [15190513.001]
  • [Cites] Leukemia. 2004 Mar;18(3):375-84 [14737069.001]
  • [Cites] Blood. 2007 Jun 15;109 (12 ):5151-6 [17351110.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1089-96 [8562934.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] Blood. 1993 Aug 1;82(3):792-9 [8338945.001]
  • [Cites] Lancet. 2007 Jul 28;370(9584):342-50 [17662883.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]
  • (PMID = 18345718.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA111728
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Proteasome Inhibitors; 0 / Protein Kinase Inhibitors; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 92
  •  go-up   go-down


91. Blair CK, Roesler M, Xie Y, Gamis AS, Olshan AF, Heerema NA, Robison LL, Ross JA, Children's Oncology Group (COG): Vitamin supplement use among children with Down's syndrome and risk of leukaemia: a Children's Oncology Group (COG) study. Paediatr Perinat Epidemiol; 2008 May;22(3):288-95
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.
  • Because children with DS have a 50-fold increased risk of developing acute leukaemia during the first 5 years of life, we explored the relation between child vitamin and herbal supplement use and the risk of leukaemia in a case-control study.
  • During the period 1997-2002, we enrolled 158 children with DS aged 0-18 years that were diagnosed with acute lymphoblastic leukaemia (ALL) (n = 97) or acute myeloid leukaemia (AML) (n = 61) at participating Children's Oncology Group institutions.
  • Data were collected via telephone interviews with mothers of the index child regarding use of multivitamins, zinc, vitamin C, iron and herbal supplements, including age at first use, frequency and duration.
  • Among controls, 57% reported regular multivitamin use (>/=3 times/week for >/=3 months) compared with 48% of ALL cases and 61% of AML cases.
  • We found no evidence of an association between children's regular multivitamin use and ALL or AML (adjusted odds ratios [OR] = 0.94 [95% CI 0.52, 1.70] and 1.90 [0.73, 4.91] respectively).
  • There was a suggestion of an increased risk for AML associated with regular multivitamin use during the first year of life or for an extended duration (ORs = 2.38 [0.94, 5.76] and 2.59 [1.02, 6.59] respectively).
  • Future research should include larger sample sizes as well as a full assessment of diet including vitamin supplementation to adequately examine the relation between nutritional status and childhood leukaemia.

  • MedlinePlus Health Information. consumer health - Dietary Supplements.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pediatrics. 1997 Nov;100(5):E4 [9346998.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1866-72 [15520821.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):40-4 [15390312.001]
  • [Cites] Adv Data. 2004 Nov 9;(349):1-7 [15586828.001]
  • [Cites] J Am Diet Assoc. 2005 May;105(5):763-72; quiz 773-4 [15883554.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):405-10 [15952191.001]
  • [Cites] Proc Nutr Soc. 2005 Nov;64(4):543-53 [16313697.001]
  • [Cites] J Am Diet Assoc. 2006 Jan;106(1 Suppl 1):S52-65 [16376630.001]
  • [Cites] J Pediatr Health Care. 2006 Jan-Feb;20(1):47-54 [16399479.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Mutat Res. 2001 Apr 18;475(1-2):7-20 [11295149.001]
  • [Cites] Ann N Y Acad Sci. 1999;889:87-106 [10668486.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • [Cites] J Am Diet Assoc. 2000 Mar;100(3):371-5 [10719417.001]
  • [Cites] Arch Fam Med. 2000 Mar;9(3):258-62 [10728113.001]
  • [Cites] Dev Med Child Neurol. 2000 Mar;42(3):207-13 [10755461.001]
  • [Cites] Lancet. 2001 Dec 8;358(9297):1935-40 [11747917.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1786-94 [12365028.001]
  • [Cites] Br J Nutr. 2002 Nov;88 Suppl 2:S165-77 [12495459.001]
  • [Cites] Cancer. 2003 Mar 1;97(5):1339-45 [12599243.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):930-8 [12648061.001]
  • [Cites] Lancet. 2003 Apr 12;361(9365):1281-9 [12699967.001]
  • [Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]
  • [Cites] Int J Vitam Nutr Res. 1978;48(2):188-216 [151083.001]
  • [Cites] Endocrinologie. 1988 Apr-Jun;26(2):113-7 [2970667.001]
  • [Cites] Clin Immunol Immunopathol. 1991 Feb;58(2):207-16 [1824686.001]
  • [Cites] Int J Neurosci. 1992 Jul-Aug;65(1-4):259-68 [1341688.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Cancer Causes Control. 1994 Mar;5(2):141-8 [8167261.001]
  • [Cites] Cancer Causes Control. 1994 Mar;5(2):195-202 [8167267.001]
  • [Cites] N Engl J Med. 1996 May 2;334(18):1150-5 [8602180.001]
  • [Cites] Cancer. 1996 Jan 1;77(1):201-7 [8630931.001]
  • [Cites] Cancer Causes Control. 1997 Sep;8(5):786-802 [9328202.001]
  • [Cites] Am J Epidemiol. 2004 Dec 1;160(11):1098-107 [15561989.001]
  • (PMID = 18426524.001).
  • [ISSN] 1365-3016
  • [Journal-full-title] Paediatric and perinatal epidemiology
  • [ISO-abbreviation] Paediatr Perinat Epidemiol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169; United States / NCI NIH HHS / CA / U10 CA098543; United States / NIEHS NIH HHS / ES / P30ES10126
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Vitamins
  • [Other-IDs] NLM/ NIHMS378452; NLM/ PMC3365502
  •  go-up   go-down


92. Jain D, Singh T, Arora P: Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report. J Med Case Rep; 2007;1:147
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] Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report.
  • BACKGROUND: Acute promyelocytic leukemia (APL) accounts for less than 10% of pediatric AML.
  • CASE PRESENTATION: We present a case of a five-year-old female with Down syndrome diagnosed with acute promyelocytic leukemia (APL).
  • CONCLUSION: This case report emphasizes the importance of a high index of suspicion in the diagnosis of acute promyelocytic leukemia microgranular variant in Down syndrome.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Tumori. 1987 Aug 31;73(4):403-6 [2958963.001]
  • [Cites] Leukemia. 1994 Aug;8(8):1264-8 [8057659.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Mar;165(2):176-9 [16527614.001]
  • [Cites] Am J Hematol. 1997 Nov;56(3):131-42 [9371524.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jan 1;132(1):74-6 [11801315.001]
  • (PMID = 18036234.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2211491
  •  go-up   go-down


93. Urbanová D, Bubanská E, Hrebík M, Mladosievicová B: [Severe heart failure in consequence of late anthracycline-induced cardiotoxicity--case report]. Klin Onkol; 2009;22(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.
  • The patient was treated for childhood acute myeloid leukemia by chemotherapy containing anthracyclines.
  • [MeSH-minor] Adolescent. Heart Transplantation. Humans. Leukemia, Myeloid, Acute / drug therapy. Male

  • MedlinePlus Health Information. consumer health - Heart Failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19534438.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] slo
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic
  •  go-up   go-down


94. Pigazzi M, Ricotti E, Germano G, Faggian D, Aricò M, Basso G: cAMP response element binding protein (CREB) overexpression CREB has been described as critical for leukemia progression. Haematologica; 2007 Oct;92(10):1435-7
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] cAMP response element binding protein (CREB) overexpression CREB has been described as critical for leukemia progression.
  • CREB has been described as critical for leukemia progress.
  • We investigated CREB expression in ALL and AML pediatric patients.
  • This study underlines the role of CREB in leukemia and suggests new insights into the transformation process.
  • [MeSH-major] Cyclic AMP Response Element-Binding Protein / metabolism. Leukemia / metabolism. Leukemia / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human / genetics. Disease Progression. Humans. Infant. 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 = 18024382.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein
  •  go-up   go-down


95. Trobaugh-Lotrario AD, Kletzel M, Quinones RR, McGavran L, Proytcheva MA, Hunger SP, Malcolm J, Schissel D, Hild E, Giller RH: Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT). Bone Marrow Transplant; 2005 Jan;35(2):143-9
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] Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT).
  • Pediatric acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) with monosomy 7 is associated with poor disease-free survival when treated by conventional chemotherapy, immunosuppression or supportive measures.
  • To better understand the curative potential of HSCT in these patients, all cases of AML and MDS with monosomy 7 treated by two transplant programs (1992 to present) were reviewed.
  • Primary diagnoses were MDS (N = 5), therapy-related MDS (N = 3), AML (N = 5) and therapy-related AML (N = 3).
  • Toxicity caused deaths of the five nonsurviving patients, four of whom were transplanted with active leukemia.
  • Allogeneic HSCT is effective therapy for childhood AML and MDS associated with monosomy 7, particularly for patients with AML in complete remission and MDS.
  • [MeSH-major] Chromosomes, Human, Pair 7. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Monosomy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Cause of Death. Child. Child, Preschool. Disease Management. Female. Humans. Male. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous. Treatment Outcome


96. Meyer C, Kowarz E, Hofmann J, Renneville A, Zuna J, Trka J, Ben Abdelali R, Macintyre E, De Braekeleer E, De Braekeleer M, Delabesse E, de Oliveira MP, Cavé H, Clappier E, van Dongen JJ, Balgobind BV, van den Heuvel-Eibrink MM, Beverloo HB, Panzer-Grümayer R, Teigler-Schlegel A, Harbott J, Kjeldsen E, Schnittger S, Koehl U, Gruhn B, Heidenreich O, Chan LC, Yip SF, Krzywinski M, Eckert C, Möricke A, Schrappe M, Alonso CN, Schäfer BW, Krauter J, Lee DA, Zur Stadt U, Te Kronnie G, Sutton R, Izraeli S, Trakhtenbrot L, Lo Nigro L, Tsaur G, Fechina L, Szczepanski T, Strehl S, Ilencikova D, Molkentin M, Burmeister T, Dingermann T, Klingebiel T, Marschalek R: New insights to the MLL recombinome of acute leukemias. Leukemia; 2009 Aug;23(8):1490-9
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] New insights to the MLL recombinome of acute leukemias.
  • Chromosomal rearrangements of the human MLL gene are associated with high-risk pediatric, adult and therapy-associated acute leukemias.
  • Genomic DNA was isolated from individual acute leukemia patients to identify and characterize chromosomal rearrangements involving the human MLL gene.
  • A total of 760 MLL-rearranged biopsy samples obtained from 384 pediatric and 376 adult leukemia patients were characterized at the molecular level.
  • The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes.
  • [MeSH-major] Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Recombination, Genetic. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Biopsy. Bone Marrow / chemistry. Bone Marrow / pathology. Child. Chromosome Breakage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Computational Biology. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19262598.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


97. Mittal R, Ramaswamy NV, Pandita R, Al Bahar S, Khalifa N, Omar S: Secondary acute myeloid leukemia after successful treatment for osteosarcoma. Indian J Med Paediatr Oncol; 2010 Jan;31(1):33-5
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] Secondary acute myeloid leukemia after successful treatment for osteosarcoma.
  • Secondary acute myeloid leukemia (sAML) is a rare complication following chemotherapy for osteogenic sarcoma.
  • Eight months after completion of therapy, while on follow-up, he presented with leukocytosis and thrombocytopenia and confirmed to have AML.

  • 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 = 20931020.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2941602
  • [Keywords] NOTNLM ; Acute myeloid leukemia / chemotherapy / osteosarcoma / secondary malignancy
  •  go-up   go-down


98. Riedt T, Ebinger M, Salih HR, Tomiuk J, Handgretinger R, Kanz L, Grünebach F, Lengerke C: Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia. Blood; 2009 Apr 23;113(17):4049-51
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] Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia.
  • Consistent with the notion that embryonic pathways can reactivate during adult oncogenesis, recent studies suggest involvement of CDX2 in human acute myeloid leukemia (AML).
  • Analysis of a cohort of 37 childhood acute lymphoblastic leukemia (ALL) patients treated in our hospital reveals that high CDX2 expression levels at diagnosis correlate with persistence of minimal residual disease (MRD) during the course of treatment.
  • Thus, CDX2 expression levels may serve as a marker for adverse prognosis in pediatric ALL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Homeodomain Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Case-Control Studies. Child. Humans. Transcription, Genetic / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19218548.001).
  • [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 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
  •  go-up   go-down


99. Ghosh I, Thulkar S, Arora R, Bakhshi S: Multifocal osteomyelitis as a presenting manifestation of childhood acute myeloid leukemia. J Pediatr Hematol Oncol; 2009 Jan;31(1):75-6
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] Multifocal osteomyelitis as a presenting manifestation of childhood acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Osteomyelitis / diagnosis


100. Stam RW, den Boer ML, Schneider P, Nollau P, Horstmann M, Beverloo HB, van der Voort E, Valsecchi MG, de Lorenzo P, Sallan SE, Armstrong SA, Pieters R: Targeting FLT3 in primary MLL-gene-rearranged infant acute lymphoblastic leukemia. Blood; 2005 Oct 1;106(7):2484-90
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] Targeting FLT3 in primary MLL-gene-rearranged infant acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) in infants is characterized by rearrangements of the mixed lineage leukemia (MLL) gene, drug resistance, and a poor treatment outcome.
  • Furthermore, leukemic cells from infants with MLL were significantly more sensitive to the Fms-like tyrosine kinase 3 (FLT3) inhibitor PKC412 (N-benzoyl staurosporine) than noninfant ALL cells, and at least as sensitive as internal tandem duplication-positive (ITD+) AML cells.
  • [MeSH-major] Gene Rearrangement. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • 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 = 15956279.001).
  • [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 / Antineoplastic Agents; 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / Ligands; 0 / Tetrazolium Salts; 0 / Thiazoles; 120685-11-2 / 4'-N-benzoylstaurosporine; 298-93-1 / thiazolyl blue; 63231-63-0 / RNA; 9007-49-2 / DNA; H88EPA0A3N / Staurosporine
  •  go-up   go-down






Advertisement