[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 255
1. Styczynski J, Wysocki M, Dluzniewska A, Juraszewska E, Balwierz W, Czyzewski K, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M, Kowalczyk J, Stefaniak J, Badowska W, Sonta-Jakimczyk D, Szczepanski T, Matysiak M, Stanczak E, Malinowska I, Wachowiak J, Konatkowska B, Gil L, Balcerska A, Kapuscinska L, Szczepanek J, Kolodziej B, Rafinska B, Kubicka M: Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia. Anticancer Res; 2008 May-Jun;28(3B):1927-31
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia.
  • BACKGROUND: The role of cellular drug resistance in childhood acute myeloid leukemia (AML) has not yet been established.
  • The aim of the study was the analysis of the clinical value of ex vivo drug resistance in pediatric AML.
  • PATIENTS AND METHODS: A cohort of 90 children with de novo AML were assayed for drug resistance profile by the 3-4,5-dimethylthiazol-2-yl-2,5-difenyl tetrazolium bromide (MTT) assay and prognostic model of in vitro drug sensitivity was analyzed.
  • A combined in vitro drug resistance profile to fludarabine, treosulfan and mitoxantrone (FTM score) was defined and it had an independent prognostic significance for disease free survival in pediatric AML.
  • CONCLUSION: The combined fludarabine, treosulfan and mitoxantrone resistance profile to possibly may be used for better stratification of children with AML or indicate the necessity for additional therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Busulfan / administration & dosage. Busulfan / analogs & derivatives. Child. Child, Preschool. Cohort Studies. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Male. Mitoxantrone / administration & dosage. Prognosis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. TREOSULFAN .
  • 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 = 18630483.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] BZ114NVM5P / Mitoxantrone; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  •  go-up   go-down


2. Braoudaki M, Papathanassiou C, Katsibardi K, Tourkadoni N, Karamolegou K, Tzortzatou-Stathopoulou F: The frequency of NPM1 mutations in childhood acute myeloid leukemia. J Hematol Oncol; 2010;3:41
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The frequency of NPM1 mutations in childhood acute myeloid leukemia.
  • BACKGROUND: Mutations in the nucleophosmin (NPM1) gene have been solely associated with childhood acute myeloid leukemia (AML).
  • We evaluated the frequency of NPM1 mutations in childhood AML, their relation to clinical and cytogenetic features and the presence of common FLT3 and RAS mutations.
  • The role of different types of NPM1 mutations, either individually or in the presence of other common gene mutations may be essential for childhood AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Gene Frequency. Humans. Infant. Prognosis. Survival Analysis

  • 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
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Leuk Res. 2007 Jan;31(1):109-11 [16678898.001]
  • [Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]
  • [Cites] APMIS. 2007 Apr;115(4):341-6 [17504301.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Leuk Lymphoma. 2007 Nov;48(11):2141-4 [17990177.001]
  • [Cites] Leuk Res. 2008 Jul;32(7):1141-3 [18180033.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1565-9 [18641025.001]
  • [Cites] Ann Hematol. 2009 Feb;88(2):159-66 [18726096.001]
  • [Cites] Hematol Oncol. 2009 Jun;27(2):90-7 [19365794.001]
  • [Cites] Hematol Oncol. 2009 Dec;27(4):171-81 [19569254.001]
  • [Cites] Med Oncol. 2009 Dec;26(4):460-2 [19085113.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1909-12 [11877259.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • (PMID = 20979630.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC2988697
  •  go-up   go-down


3. Xie C, Edwards H, Xu X, Zhou H, Buck SA, Stout ML, Yu Q, Rubnitz JE, Matherly LH, Taub JW, Ge Y: Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia. Clin Cancer Res; 2010 Nov 15;16(22):5499-510
Hazardous Substances Data Bank. VALPROIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia.
  • PURPOSE: To determine the possibility of synergistic antileukemic activity and the underlying molecular mechanisms associated with cytarabine combined with valproic acid (VPA; a histone deacetylase inhibitor and a Food and Drug Administration-licensed drug for treating both children and adults with epilepsy) in pediatric acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: The type and extent of antileukemic interactions between cytarabine and VPA in clinically relevant pediatric AML cell lines and diagnostic blasts from children with AML were determined by MTT assays and standard isobologram analyses.
  • RESULTS: We showed synergistic antileukemic activities between cytarabine and VPA in four pediatric AML cell lines and nine diagnostic AML blast samples. t(8;21) AML blasts were significantly more sensitive to VPA and showed far greater sensitivities to combined cytarabine and VPA than non-t(8;21) AML cases.
  • CONCLUSIONS: Our results establish global synergistic antileukemic activity of combined VPA and cytarabine in pediatric AML and provide compelling evidence to support the use of VPA in the treatment of children with this deadly disease.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Blood. 2008 Mar 1;111(5):2505-15 [18299451.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):865-72 [11504778.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4500-10 [18628465.001]
  • [Cites] Blood. 2009 Sep 24;114(13):2744-52 [19638627.001]
  • [Cites] Mol Cell Biol. 2009 Dec;29(23):6149-69 [19805519.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):6969-78 [11742974.001]
  • [Cites] Leuk Res. 2002 May;26(5):495-502 [11916526.001]
  • [Cites] Leukemia. 2003 Jan;17(1):120-4 [12529668.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):425-9 [14706334.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1246-51 [15116123.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1266-9 [15155466.001]
  • [Cites] Br J Haematol. 2004 Nov;127(3):264-79 [15491285.001]
  • [Cites] Adv Cancer Res. 1998;72:197-233 [9338077.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1393-400 [10438727.001]
  • [Cites] Nat Med. 2005 Jan;11(1):71-6 [15619634.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):226-31 [15687366.001]
  • [Cites] Leuk Res. 2005 Jul;29(7):739-48 [15927669.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1335-42 [15936818.001]
  • [Cites] Trends Mol Med. 2005 Oct;11(10):442-4 [16150641.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):16090-5 [16243973.001]
  • [Cites] Blood. 2006 Jan 1;107(1):241-9 [16141349.001]
  • [Cites] Cancer. 2006 Jan 1;106(1):112-9 [16323176.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1174-82 [16675713.001]
  • [Cites] Mol Cancer Res. 2006 Aug;4(8):563-73 [16877702.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8903-11 [16951208.001]
  • [Cites] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068.001]
  • [Cites] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Seizure. 2006 Dec;15(8):630-2 [17070075.001]
  • [Cites] Leukemia. 2007 Feb;21(2):248-52 [17122863.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1979-85 [17513804.001]
  • [Cites] Blood. 2007 Jul 1;110(1):267-77 [17356134.001]
  • [Cites] Curr Drug Targets. 2007 Jun;8(6):727-37 [17584028.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):886-95 [10959836.001]
  • [Cites] Cancer Treat Rev. 2008 May;34(3):206-22 [18226465.001]
  • (PMID = 20889917.001).
  • [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 / CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NCI NIH HHS / CA / R01 CA120772-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ NIHMS238223; NLM/ PMC3018695
  •  go-up   go-down


Advertisement
4. Fleĭshman EV, Sokova OI, Kirichenko OP, Konstantinova LN, Metel'kova NF, Popa AV, Shneĭder MM: [Complex karyotype abnormalities in pediatric acute myeloid leukemia]. Vestn Ross Akad Med Nauk; 2008;(5):3-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Complex karyotype abnormalities in pediatric acute myeloid leukemia].
  • A majority of the data on the prognostic significance of distinct chromosome changes and combinations of them in pediatric acute myeloid leukemia (AML) has been derived from adult studies, with not numerous published data in pediatric patients.
  • We investigated characteristic features of complex karyotype in newly diagnosed pediatric AML de novo.
  • New data were obtained for complex karyotype differences of adult and pediatric AML.
  • In the great majority (76%) of complex karyotypes in our adult patients chromosome abnormalities associated with adverse risk were found but in pediatric patients their frequency was significantly less (30%).
  • Complex karyotype is considered to be characteristic of older AML patients and in the majority of the patients the karyotype contains markers of adverse risk.
  • Possibly, worse outcome in older AML patients is connected with the markers but not with multiple chromosome changes.
  • New data of frequency and the peculiarities of complex karyotype in pediatric AML are important for understanding of AML pathogenesis and for development a more effective AML treatment.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18589906.001).
  • [ISSN] 0869-6047
  • [Journal-full-title] Vestnik Rossiiskoi akademii meditsinskikh nauk
  • [ISO-abbreviation] Vestn. Akad. Med. Nauk SSSR
  • [Language] RUS
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


5. 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
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [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.
  • [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


6. Styczynski J, Toporski J, Wysocki M, Debski R, Chybicka A, Boruczkowski D, Wachowiak J, Wojcik B, Kowalczyk J, Gil L, Balwierz W, Matysiak M, Krawczuk-Rybak M, Balcerska A, Sonta-Jakimczyk D: Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia. Anticancer Res; 2007 May-Jun;27(3B):1547-51
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia.
  • BACKGROUND: The prognostic role of the ex vivo drug resistance profile has not yet been proved in childhood acute myeloid leukemia (AML).
  • The aim of the study was the analysis of the impact of the ex vivo drug resistance profile in a cohort of 44 children with AML undergoing hematopoietic stem cell transplantation (HSCT).
  • CONCLUSION: The combined drug resistance profile to fludarabine, treosulfan and etoposide may be useful for better stratification of children with AML undergoing stem cell transplantation or to indicate the necessity for additional post-transplant therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Granulocyte Precursor Cells / drug effects. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Busulfan / analogs & derivatives. Busulfan / pharmacology. Child. Child, Preschool. Etoposide / pharmacology. Female. Humans. Infant. Male. Prognosis. Recurrence. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. TREOSULFAN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17595774.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  •  go-up   go-down


7. 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

  • [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

  • [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


8. 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
COS Scholar Universe. author profiles.

  • [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.
  • [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


9. McGrath P, Paton MA, Huff N: Beginning treatment for pediatric acute myeloid leukemia: the family connection. Issues Compr Pediatr Nurs; 2005 Apr-Jun;28(2):97-114
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beginning treatment for pediatric acute myeloid leukemia: the family connection.
  • There is a loud silence on psycho-oncology research in relation to pediatric Acute Myeloid Leukemia (AML).
  • The present article documents the less obvious, often hidden, aspect of beginning treatment for pediatric AML--the "behind the scenes" experience of the home and family connection.
  • The findings are from the first stage of a five year longitudinal study that examines through qualitative research the experience of childhood leukemia from the perspective of the child, siblings and parents.
  • The findings emphasise the need for support for families coping with childhood AML.
  • [MeSH-major] Adaptation, Psychological. Attitude to Health. Child, Hospitalized / psychology. Family / psychology. Leukemia, Myeloid / psychology
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Family Health. Health Services Needs and Demand. Holistic Health. Hospitals, Pediatric. Humans. Infant. Longitudinal Studies. Models, Psychological. Nursing Methodology Research. Parent-Child Relations. Qualitative Research. Queensland. Sibling Relations. Social Support. Surveys and Questionnaires

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Children's Health.
  • MedlinePlus Health Information. consumer health - Family Issues.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16006383.001).
  • [ISSN] 0146-0862
  • [Journal-full-title] Issues in comprehensive pediatric nursing
  • [ISO-abbreviation] Issues Compr Pediatr Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


10. Castellino SM, Alonzo TA, Buxton A, Gold S, Lange BJ, Woods WG: Outcomes in childhood AML in the absence of transplantation in first remission--Children's Cancer Group (CCG) studies 2891 and CCG 213. Pediatr Blood Cancer; 2008 Jan;50(1):9-16
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes in childhood AML in the absence of transplantation in first remission--Children's Cancer Group (CCG) studies 2891 and CCG 213.
  • BACKGROUND: The majority of childhood acute myeloid leukemia (AML) patients lack a matched-related bone marrow transplant (BMT) donor in first remission.
  • PROCEDURE: Disease-free survival (DFS), overall survival (OS), relapse-free survival (RFS), and post-relapse outcome were evaluated for children with de novo AML on CCG 213 and the standard timing (ST) and intensive timing (IT) induction arms of CCG 2891 who were randomized to (intent-to-treat, ITT) or who received (as-treated, AT) only chemotherapy intensification.
  • Overall survival for childhood AML in the absence of BMT in CR1 is influenced by duration of CR1 and by race.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Child. Disease-Free Survival. Female. Humans. Male. Remission Induction. Survival Analysis. Survival Rate

  • Genetic Alliance. consumer health - Childhood Cancer.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17252564.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  •  go-up   go-down


11. Lapillonne H, Renneville A, Auvrignon A, Flamant C, Blaise A, Perot C, Lai JL, Ballerini P, Mazingue F, Fasola S, Dehée A, Bellman F, Adam M, Labopin M, Douay L, Leverger G, Preudhomme C, Landman-Parker J: High WT1 expression after induction therapy predicts high risk of relapse and death in pediatric acute myeloid leukemia. J Clin Oncol; 2006 Apr 1;24(10):1507-15
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High WT1 expression after induction therapy predicts high risk of relapse and death in pediatric acute myeloid leukemia.
  • PURPOSE: To determine whether minimal residual disease (MRD) measured by Wilms' tumor gene 1 (WT1) expression is a prognostic marker in pediatric acute myeloid leukemia (AML), we quantified WT1 transcript by real-time quantitative-polymerase chain reaction in 92 AML at diagnosis and during follow-up.
  • PATIENTS AND METHODS: Patients (median age, 6 years; cytogenetics, favorable 27%, intermediate 59%, poor 13%) were treated between 1995 and 2002 and enrolled in Leucémie aiguë Myéloblastique Enfant (LAME) 89/91, LAME 99 pilot study and Acute Promyelocytic Leukemia French collaborative protocols.
  • CONCLUSION: WT1 quantification is an informative molecular marker for MRD in pediatric AML and is now performed as prospective analysis in ELAM02 protocol.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Dosage. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Recurrence. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16575000.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  •  go-up   go-down


12. de Figueiredo AF, Mkrtchyan H, Liehr T, Soares Ventura EM, de Jesus Marques-Salles T, Santos N, Ribeiro RC, Abdelhay E, Macedo Silva ML: A case of childhood acute myeloid leukemia AML (M5) with a neocentric chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter) and tetrasomy of chromosomes 8 and 21. Cancer Genet Cytogenet; 2009 Sep;193(2):123-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of childhood acute myeloid leukemia AML (M5) with a neocentric chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter) and tetrasomy of chromosomes 8 and 21.
  • Hyperdiploidy is rarely observed in childhood acute myeloid leukemia (AML).
  • Described here is the case of a 2(1/2)-year-old girl with AML-M5 and 51 chromosomes characterized by double tetrasomy of chromosomes 8 and 21 and also a neocentric derivative chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter).
  • Little is known about the prognostic significance of these chromosomal abnormalities in childhood AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping


13. Queudeville M, Eckhoff SM, Debatin K, Meyer LH: Correlatoin of apoptosis signaling in primary pediatric BCP-ALL xenograft cells with the kinetics of engraftment in vivo in a NOD/SCID model and patient outcome. J Clin Oncol; 2009 May 20;27(15_suppl):10043

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlatoin of apoptosis signaling in primary pediatric BCP-ALL xenograft cells with the kinetics of engraftment in vivo in a NOD/SCID model and patient outcome.
  • : 10043 Background: We previously identified the importance of intact apoptosis signaling for treatment response in pediatric ALL and AML by analyzing two key apoptogenic events, caspase-3 activation and cytochrome c release.
  • Using a NOD/SCID mouse model for pediatric BCP-ALL we found that short time from transplant to overt leukemia in the recipient mice (short time to leukemia, TTLshort) determines poor patient outcome.
  • METHODS: In this study we investigated the importance of deficient apoptosis signaling for leukemia engraftment in this model.
  • CONCLUSIONS: Our finding in the NOD/SCID/huALL model matches our results in pediatric ALL and AML to conclude that the functional integrity of a downstream apoptotic checkpoint is an important feature regulating leukemia biology.
  • Thus, deficient apoptosis signaling appears to determine rapid engraftment of leukemia cells in the NOD/SCID model in vivo and consequently poor patient outcome.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962469.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • In contrast, none or a few of the CpG dinucleotides were methylated in the CD10-positive ALL, AML (M5) with MLL/AF9 or AML (M2) with AML1/ETO.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962471.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Rubnitz J, Inaba H, Ribeiro R, Pounds S, Pui C, Leung W: Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10034

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.
  • We hypothesized that the transplantation of purified haploidentical NK cells may be a safe and effective form of consolidation therapy that will reduce the risk of relapse among children with acute myeloid leukemia (AML) who are not treated with HSCT.
  • In this pilot study, we assessed the safety, feasibility, and engraftment of NK cell infusions in 10 patients with AML in first remission.
  • CONCLUSIONS: Haploidentical NK cells can be safely administered to AML patients who are in remission.
  • We have recently opened a new trial to evaluate the efficacy of NK cell therapy in children in first remission of AML.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962581.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. ter Bals E, Kaspers GJ: Treatment of childhood acute myeloid leukemia. Expert Rev Anticancer Ther; 2005 Oct;5(5):917-29
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood acute myeloid leukemia.
  • Childhood acute myeloid leukemia is rare, but accounts for a significant number of malignancy-related deaths in this age group.
  • Therefore, there is a need for further improved treatment of pediatric acute myeloid leukemia.
  • Subgroup-directed treatment has become a reality for acute myeloid leukemia in young children with Down's syndrome and in acute promyelocytic leukemia.
  • In addition to tailoring therapy according to biologic features and especially monitoring treatment by measurements of minimal residual disease, targeted therapy for subgroups with activating mutations in receptor tyrosine kinases will further optimize the treatment of pediatric acute myeloid leukemia.
  • Together with the development of many novel agents that have different mechanisms of action than the currently available anticancer agents, and improved supportive care, it is realistic that the prognosis of acute myeloid leukemia in children and adolescents will improve further in the next 5-10 years.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Child. Clinical Trials as Topic. Cranial Irradiation. Down Syndrome / complications. Humans. Neoplasm, Residual. Prognosis. Quality of Life. Remission Induction. Risk Assessment. Transplantation, Homologous

  • 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 = 16221060.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 90
  •  go-up   go-down


17. Xu XJ, Tang YM, Song H, Yang SL, Shi SW, Wei J: Long-term outcome of childhood acute myeloid leukemia in a developing country: experience from a children's hospital in China. Leuk Lymphoma; 2010 Dec;51(12):2262-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of childhood acute myeloid leukemia in a developing country: experience from a children's hospital in China.
  • Data on childhood acute myeloid leukemia (AML) in developing countries are limited.
  • Herein we report the outcome of childhood AML treated with modified NPCLC-AML97 in our institution from 1997 to 2005.
  • One hundred and eighty-five children with newly diagnosed AML were admitted.
  • Thirty-one patients (25.2%) relapsed, but no central nervous system leukemia was observed.
  • Although the cure rate of childhood AML in China was low, the treatment outcome for patients who could adhere to the treatment protocol was satisfactory.
  • [MeSH-major] Developing Countries. Hospitals, Pediatric / statistics & numerical data. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. China. Cohort Studies. Female. Humans. Infant. Male. Survival Analysis. Time Factors. Treatment Outcome


18. Tomizawa D, Tabuchi K, Kinoshita A, Hanada R, Kigasawa H, Tsukimoto I, Tsuchida M, Tokyo Children's Cancer Study Group: Repetitive cycles of high-dose cytarabine are effective for childhood acute myeloid leukemia: long-term outcome of the children with AML treated on two consecutive trials of Tokyo Children's Cancer Study Group. Pediatr Blood Cancer; 2007 Aug;49(2):127-32
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Repetitive cycles of high-dose cytarabine are effective for childhood acute myeloid leukemia: long-term outcome of the children with AML treated on two consecutive trials of Tokyo Children's Cancer Study Group.
  • BACKGROUND: Various methods of intensive chemotherapy have contributed to an improved survival in pediatric acute myeloid leukemia (AML).
  • PROCEDURE: A total of 216 eligible children with newly diagnosed AML were treated in the two consecutive multi-center trials of TCCSG, M91-13 and M96-14, from August 1991 to September 1998.
  • Among patients without Down syndrome (DS) or acute promyelocytic leukemia (APL), the presence of t(8;21) or inv(16) was a significant good prognostic factor both in the univariate and multivariate analyses.
  • CONCLUSIONS: These results suggest that repetitive use of HD-Ara-C was effective and safe for childhood AML.
  • However, further optimization of AML therapy is required.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Disease-Free Survival. Down Syndrome / complications. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Drug Administration Schedule. Etoposide / administration & dosage. Female. Hematopoietic Stem Cell Transplantation. Humans. Hydrocortisone / administration & dosage. Infant. Infection / etiology. Infection / mortality. Japan / epidemiology. Kaplan-Meier Estimate. Male. Methotrexate / administration & dosage. Mitoxantrone / administration & dosage. Remission Induction. Survival Analysis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome. Tretinoin / administration & dosage. Vincristine / administration & dosage


19. Abdelhaleem M, Shago M, Beimnet K, Sayeh E, Bartakke S, Weitzman S: Childhood acute myeloid leukemia with hemophagocytosis by the blasts and inv(8)(p11q13) with MOZ-TIF2 fusion transcripts. J Pediatr Hematol Oncol; 2007 Sep;29(9):643-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute myeloid leukemia with hemophagocytosis by the blasts and inv(8)(p11q13) with MOZ-TIF2 fusion transcripts.
  • We describe a unique case of de novo childhood acute myeloid leukemia in which the blasts showed evidence of hemophagocytosis and harbored inv(8) (p11q13) chromosomal abnormality.
  • To our knowledge, this is the eighth overall and the fourth childhood case of acute myeloid leukemia with inv(8) (p11q13) with MOZ-TIF2 fusion.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Child. Female. Humans. Transcription, Genetic

  • 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 = 17805042.001).
  • [ISSN] 1077-4114
  • [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 / MOZ-TIF2 protein, human; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


20. Armengol G, Canellas A, Alvarez Y, Bastida P, Toledo JS, Pérez-Iribarne Mdel M, Camós M, Tuset E, Estella J, Coll MD, Caballín MR, Knuutila S: Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia. Leuk Lymphoma; 2010 Jan;51(1):114-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.
  • We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).
  • Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Male. Polymerase Chain Reaction. Prognosis. Translocation, Genetic


21. Gu LJ, Tie LJ, Xue HL, Tang JY, Chen J, Pan C, Chen J, Ye H, Wang YP, Dong L: [Analysis of prognostic variables in childhood acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Jan;27(1):10-3
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of prognostic variables in childhood acute myeloid leukemia].
  • OBJECTIVE: To assess the prognostic value of the biological features and therapy-related factors in childhood acute myeloid leukemia (AML).
  • METHODS: From January 1998 to May 2003, 75 patients with newly diagnosed AML were enrolled on the protocol AML-XH-99.
  • Univariate analysis also demonstrated that the 5-year pEFS for patients with age < 1 year or > 10 years, platelet count < 20 x 10(9)/L, FAB M(5), hepatomegaly, BM blasts >or= 0.150 at 48 h after the first induction course and no response to the first induction course, central nervous system (CNS) leukemia was unfavorable, while the outcome of patients with cytogenetic abnormalities of t (8;.
  • 17) were better. (2) Multivariate analysis suggested that cytogenetic abnormality of t (15; 17), achieved CR after the first induction course and no CNS leukemia were independent favorable prognostic factors.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Karyotyping. Male. Prognosis. 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 = 16732931.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


22. Radhi M, Meshinchi S, Gamis A: Prognostic factors in pediatric acute myeloid leukemia. Curr Hematol Malig Rep; 2010 Oct;5(4):200-6
COS Scholar Universe. author profiles.

  • [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.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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


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
Hazardous Substances Data Bank. METHOTREXATE .

  • [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. Manola KN: Cytogenetics of pediatric acute myeloid leukemia. Eur J Haematol; 2009 Nov;83(5):391-405
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [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.
  • [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


25. Johnston DL, Alonzo TA, Gerbing RB, Lange BJ, Woods WG: Risk factors and therapy for isolated central nervous system relapse of pediatric acute myeloid leukemia. J Clin Oncol; 2005 Dec 20;23(36):9172-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors and therapy for isolated central nervous system relapse of pediatric acute myeloid leukemia.
  • PURPOSE: CNS relapse of pediatric acute myeloid leukemia (AML) is an infrequent occurrence.
  • PATIENTS AND METHODS: Records of 886 patients with de novo AML were reviewed, and patients who entered remission at the end of one course of therapy and developed an isolated CNS relapse as their first event were analyzed (n = 690).
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Prognosis. Recurrence. Retrospective Studies. Risk Factors. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16361619.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


26. Ribeiro RC, Razzouk BI, Pounds S, Hijiya N, Pui CH, Rubnitz JE: Successive clinical trials for childhood acute myeloid leukemia at St Jude Children's Research Hospital, from 1980 to 2000. Leukemia; 2005 Dec;19(12):2125-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successive clinical trials for childhood acute myeloid leukemia at St Jude Children's Research Hospital, from 1980 to 2000.
  • Despite substantial progress in the management of childhood acute myeloid leukemia (AML), only about 50% of patients are cured by intensive chemotherapy.
  • From 1980 to 2000, 251 patients <15 years of age with newly diagnosed AML were enrolled on one of the five consecutive St Jude AML studies.
  • With the exception of one protocol (AML-83), outcomes improved in general over the two decades.
  • The estimated 5-year event-free survival (+/-s.e.) was 30.8+/-5.6% for AML-80; 11.1+/-4.3% for AML-83; 35.9+/-7.4% for AML-87; 43.5+/-6.2% for AML-91; and 45.0+/-11.1% for AML-97.
  • Resistant or relapsed AML caused the great majority of treatment failures.
  • Increasing the intensity of chemotherapy (AML-87) did not improve outcome, partially because of toxicity, nor did prolonging postremission therapy by adding sequential myeloablative (AML-80) or nonmyeloablative (AML-83) chemotherapy cycles.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Survival Analysis. Treatment Failure. Treatment Outcome

  • 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
  • (PMID = 16281077.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


27. Bakhshi S, Singh P, Swaroop C: Outpatient consolidation chemotherapy in pediatric acute myeloid leukemia: a retrospective analysis. Hematology; 2009 Oct;14(5):255-60
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outpatient consolidation chemotherapy in pediatric acute myeloid leukemia: a retrospective analysis.
  • BACKGROUND: To assess the outcomes of outpatient high dose cytosine arabinoside consolidation cycles in pediatric acute myeloid leukemia (AML) patients in comparison to inpatient treatment.
  • METHODS: We retrospectively analyzed 90 cycles of AML consolidation given to 30 patients between July 2003 and July 2007.
  • CONCLUSIONS: Outpatient AML consolidation therapy is safe and feasible in children.
  • To our knowledge, this report is the first of its kind looking specifically at outpatient consolidation chemotherapy in AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Anti-Infective Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Child, Preschool. Female. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Humans. Infant. Leukocyte Count. Male. Neutropenia / blood. Neutropenia / drug therapy. Platelet Count. Recombinant Proteins. Retrospective Studies

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19843379.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Recombinant Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


28. MRD-AML-BFM Study Group, Langebrake C, Creutzig U, Dworzak M, Hrusak O, Mejstrikova E, Griesinger F, Zimmermann M, Reinhardt D: Residual disease monitoring in childhood acute myeloid leukemia by multiparameter flow cytometry: the MRD-AML-BFM Study Group. J Clin Oncol; 2006 Aug 1;24(22):3686-92
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Residual disease monitoring in childhood acute myeloid leukemia by multiparameter flow cytometry: the MRD-AML-BFM Study Group.
  • PURPOSE: Monitoring of residual disease (RD) by flow cytometry in childhood acute myeloid leukemia (AML) may predict outcome.
  • PATIENTS AND METHODS: Five hundred forty-two specimens of 150 children enrolled in the AML-Berlin-Frankfurt-Muenster (BFM) 98 study were analyzed by four-color immunophenotyping at up to four predefined time points during treatment.
  • For each of the 12 leukemia-associated immunophenotypes and time points, a threshold level based on a previous retrospective analysis of another cohort of children with AML and on control bone marrows was determined.
  • Compared with commonly defined risk factors in the AML-BFM studies, flow cytometry does not provide additional information for outcome prediction, but may be helpful to evaluate the remission status at day 28.
  • [MeSH-major] Flow Cytometry. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Adolescent. Adult. Analysis of Variance. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Predictive Value of Tests. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Factors. Survival Analysis. Treatment Outcome


29. Balgobind BV, Lugthart S, Hollink IH, Arentsen-Peters ST, van Wering ER, de Graaf SS, Reinhardt D, Creutzig U, Kaspers GJ, de Bont ES, Stary J, Trka J, Zimmermann M, Beverloo HB, Pieters R, Delwel R, Zwaan CM, van den Heuvel-Eibrink MM: EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia. Leukemia; 2010 May;24(5):942-9
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia.
  • Overexpression of the ecotropic virus integration-1 (EVI1) gene (EVI1+), localized at chromosome 3q26, is associated with adverse outcome in adult acute myeloid leukemia (AML).
  • In pediatric AML, 3q26 abnormalities are rare, and the role of EVI1 is unknown.
  • We studied 228 pediatric AML samples for EVI1+ using gene expression profiling and RQ-PCR.
  • EVI1+ was found in 20/213 (9%) of children with de novo AML, and in 4/8 with secondary AML.
  • It was predominantly found in MLL-rearranged AML (13/47), monosomy 7 (2/3), or FAB M6/7 (6/10), and mutually exclusive with core-binding factor AML, t(15;17), and NPM1 mutations.
  • Although significant differences in 4 years pEFS for EVI1+ and EVI1- pediatric AML were observed (28%+/-11 vs 44%+/-4, P=0.04), multivariate analysis did not identify EVI1+ as an independent prognostic factor.
  • We conclude that EVI1+ can be found in approximately 10% of pediatric AML.
  • Although EVI1+ was not an independent prognostic factor, it was predominantly found in subtypes of pediatric AML that are related with an intermediate to unfavorable prognosis.
  • Remarkably, no 3q26 abnormalities were identified in EVI1+ pediatric AML.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Child. Child, Preschool. Chromosome Aberrations. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20357826.001).
  • [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 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / RNA, Messenger; 0 / Transcription Factors
  •  go-up   go-down


30. Dłuzniewska A, Balwierz W, Balcerska A, Chybicka A, Kamieńska E, Karolczyk G, Karpińska-Derda I, Krawczuk-Rybak M, Kowalczyk JR, Lewandowska D, Maciejka-Kapuścińska L, Kołtano S, Malinowska I, Matysiak M, Mikołajczyk M, Mizia-Malarz A, Muszyńska-Rosłan K, Niedźwiedzki M, Pohorecka J, Sikorska-Fic B, Sobol G, Sońta-Jakimczyk D, Tomaszewska R, Urasiński T, Wachowiak J, Wieczorek M, Wójcik B, Wysocki M: [Treatment failure in children with acute myelocytic leukemia: over 25-year experience of Polish Pediatric Leukemia/Lymphoma Study Group with four consecutive unified treatment protocols for childhood acute myelocytic leukemia]. Przegl Lek; 2010;67(6):366-70
Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment failure in children with acute myelocytic leukemia: over 25-year experience of Polish Pediatric Leukemia/Lymphoma Study Group with four consecutive unified treatment protocols for childhood acute myelocytic leukemia].
  • Four consecutive intensive unified regimens (BFM-AML-83, PGP-AML 94, PGP-AML 98 AML-BFM 2004 Interim) for acute myelocytic leukemia (AML) have been conducted by the Polish Pediatric Leukemia/Lymphoma Study Group (PPLLSG) since 1983.
  • There were 726 children with AML diagnosed (226, 102, 247 and 151 in the I, II , III and IV periods, respectively), and 603 of them were eligible for evaluation (208, 83, 195 and 117, respectively).
  • Five-year overall survival (OS) and event-free survival (EFS) rates were: 33% and 32% for PGP-AML 83 regimen, 38% and 36% for PGP-AML 94 regimen, and 53% and 46% for PGP-AML 98 regimen, respectively.
  • For AML-BFM Interim 2004 the 3-year OS and EFS were 57% and 57%, respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Poland / epidemiology. Remission Induction. Survival Rate. Treatment Failure

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21344763.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


31. Styczynski J: Drug resistance in childhood acute myeloid leukemia. Curr Pharm Biotechnol; 2007 Apr;8(2):59-75
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug resistance in childhood acute myeloid leukemia.
  • Therapy results in childhood AML differ from those of ALL.
  • The development of drug resistance is the limiting factor in the therapy of AML.
  • Different problems of drug resistance in childhood AML, with emphasis to age and in comparison to adult AML are presented.
  • Taking into account both children and adults, it seems that age is adversely related to therapy outcome in AML, and the percentage of patients with favorable cytogenetics decreases with age; however, age is positively correlated with multi-drug resistance and the proportion of patients with unfavorable cytogenetics.
  • AML is considered a stem cell disease.
  • Cellular drug resistance in AML cells seems to be similar throughout all other age groups, however the higher the age, the worse the outcome.
  • In childhood AML, no drug is more effective in comparison to ALL, and cellular drug resistance is partially related to chromosomal abnormalities.
  • Pediatric AML is equally resistant as adult AML.
  • Pediatric and adult AML, respectively, are possibly equally drug resistant on initial diagnosis and at relapse.
  • In contrast to ALL, the prognostic value of in vitro drug resistance in childhood AML has not been well documented yet.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / epidemiology. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control

  • 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 = 17430154.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 165
  •  go-up   go-down


32. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.
  • Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Clone Cells. DNA Mutational Analysis / methods. Gene Frequency. Humans. Infant. Infant, Newborn. Polymerase Chain Reaction / methods

  • 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 = 15618961.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  •  go-up   go-down


33. Anak S, Saribeyoglu ET, Bilgen H, Unuvar A, Karakas Z, Devecioglu O, Agaoglu L, Gedikoglu G: Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience. Pediatr Blood Cancer; 2005 Jun 15;44(7):654-9
MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience.
  • BACKGROUND: Treatment of childhood acute myelocytic leukemia (AML) in first remission, is still evolving.
  • PROCEDURE: Out of 81 pediatric patients with AML in first CR, 67 were biologically randomized for allogeneic (n = 31), autologous (n = 20), or peripheral stem cell transplant (n = 16) after completing consolidation treatment, with the remaining (n = 11) dropping out or receiving chemotherapy.
  • CONCLUSION: In pediatric AML patients without a donor, autologous BMT or autologous PBSCT appears to be an effective treatment option with low transplant related mortality especially in less privileged countries where the chemotherapy only results are still low.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Transplantation, Autologous. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15700262.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


34. Krstovski N, Tosic N, Janic D, Dokmanovic L, Kuzmanovic M, Spasovski V, Pavlovic S: Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature. Med Oncol; 2010 Sep;27(3):640-5
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature.
  • Mutations in the fms-like tyrosine kinase 3 (FLT3) gene (internal tandem duplication (ITD) and point mutation in the tyrosine kinase domain, FLT3/D835) as well as the nucleophosmin (NPM1) gene are the most common abnormalities in adult acute myeloid leukemia (AML).
  • Their significance in pediatric AML is still unclear.
  • In this study we evaluated the frequency of FLT3 and NPM1 mutations in childhood AML.
  • FLT3 and NPM1 mutations were analysed in 42 and 37 childhood AML patients, respectively, using polymerase chain reaction (PCR) and direct sequencing.
  • Here we report the results of the study of FLT3 and NPM1 gene mutations in childhood AML patients in Serbia.
  • Comparative study of data on NPM1 mutations in childhood AML revealed that various NPM1 gene mutation types are associated with childhood AML.
  • Our findings as well as previously reported data, contributes to a hypothesis of different biology and etiology of adult and childhood AML.
  • More extensive studies of NPM1 and FLT3 mutations in childhood AML are needed to determine their biological and clinical importance.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Female. Humans. Male. Serbia

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19557552.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


35. Meshinchi S, Arceci RJ: Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia. Oncologist; 2007 Mar;12(3):341-55
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML) has posed significant therapeutic challenges to pediatric oncologists.
  • Despite intensive therapy, half of the children with AML relapse and die from their disease.
  • Efforts to identify risk factors in AML are directed toward defining populations who may benefit from alternative therapies.
  • Management of high-risk patients may prove more difficult, as the nearly myeloablative nature of AML therapy leaves little room for therapy escalation short of stem cell transplantation.
  • This review evaluates prognostic factors in pediatric AML and discusses the feasibility of using these factors in risk-adapted therapy regimens.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Humans. Neoplasm Recurrence, Local. Prognosis. Risk Assessment. Risk Factors. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17405900.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 133
  •  go-up   go-down


36. 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
COS Scholar Universe. author profiles.

  • [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.
  • [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


37. Roberson JR, Onciu M, Pounds S, Rubnitz JE, Pui CH, Razzouk BI: Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):542-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.
  • BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.
  • PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).
  • Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.
  • CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.
  • [MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

  • 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
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763467.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [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 / Biomarkers; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


38. van der Velden VH, van der Sluijs-Geling A, Gibson BE, te Marvelde JG, Hoogeveen PG, Hop WC, Wheatley K, Bierings MB, Schuurhuis GJ, de Graaf SS, van Wering ER, van Dongen JJ: Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol. Leukemia; 2010 Sep;24(9):1599-606
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol.
  • Analysis of minimal residual disease (MRD) in childhood acute myeloid leukemia (AML) may predict for clinical outcome.
  • MRD levels were assessed by flowcytometric immunophenotyping in 94 children with AML enrolled into a single trial (United Kingdom Medical Research Council AML12 and similar Dutch Childhood Oncology Group ANLL97).
  • In conclusion, flowcytometric MRD detection is possible in children with AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Child. Clinical Protocols. Flow Cytometry. Humans. Immunophenotyping. Probability. Prognosis. RNA, Messenger / genetics. Recurrence

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20668473.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300133
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger
  •  go-up   go-down


39. Meshinchi S, Alonzo TA, Stirewalt DL, Zwaan M, Zimmerman M, Reinhardt D, Kaspers GJ, Heerema NA, Gerbing R, Lange BJ, Radich JP: Clinical implications of FLT3 mutations in pediatric AML. Blood; 2006 Dec 1;108(12):3654-61
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical implications of FLT3 mutations in pediatric AML.
  • FLT3 mutation status of 630 children with de novo acute myeloid leukemia (AML) treated on CCG-2941 and -2961 was determined, and ITD-AR was calculated for patients with FLT3/ITD.
  • ITD-AR defines the prognostic significance in FLT3/ITD-positive AML, and ITD-AR greater than 0.4 is a significant and independent prognostic factor for relapse in pediatric AML.

  • 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 Mol Diagn. 2003 May;5(2):96-102 [12707374.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2646-54 [15251987.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1447-52 [9305596.001]
  • [Cites] Leukemia. 1999 Jan;13(1):38-43 [10049058.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4792-9 [15718420.001]
  • [Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1345-9 [15959528.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3658-65 [16076872.001]
  • [Cites] Blood. 2006 Jul 1;108(1):400; author reply 400-1 [16790584.001]
  • [Cites] Med Pediatr Oncol. 1999 Dec;33(6):525-9 [10573574.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):322-30 [10691863.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):983-8 [11442493.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]
  • [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]
  • (PMID = 16912228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R21 CA10262-01
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1895470
  •  go-up   go-down


40. Jain M, Bakhshi S, Shukla AA, Chauhan SS: Cathepsins B and L in peripheral blood mononuclear cells of pediatric acute myeloid leukemia: potential poor prognostic markers. Ann Hematol; 2010 Dec;89(12):1223-32
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cathepsins B and L in peripheral blood mononuclear cells of pediatric acute myeloid leukemia: potential poor prognostic markers.
  • However, their significance in acute leukemias is lacking.
  • This study was planned to investigate expression and significance of these proteases in peripheral blood mononuclear cells (PBMCs) of patients with pediatric acute myeloid leukemia (AML).
  • CTSL and CTSB activities were assayed in PBMCs of 24 children with AML and ten healthy controls by spectrofluorimetry.
  • CTSL and CTSB protease activity and their mRNA expression were significantly higher in AML patients compared to controls (p ≤ 0.001).
  • Cystatin expression though significantly high (p ≤ 0.001) in AML was negatively correlated with CTSL (r = -0.920; p ≤ 0.001) and CTSB (r = -0.580, p ≤ 0.001) expression.
  • AML patients with higher CTSL and CTSB activity exhibited an inferior EFS (CTSL: p = 0.045; CTSB: p = 0.002) and overall survival (OS; CTSL: p = 0.05; CTSB: p = 0.004) compared to patients with lower levels of these proteases.
  • This is the first report demonstrating increased expression of CTSL and CTSB in AML, mechanism of their increased expression in relation to VEGF, and their association with poor EFS and OS.
  • [MeSH-major] Cathepsin B / metabolism. Cathepsin L / metabolism. Leukemia, Myeloid / enzymology. Leukocytes, Mononuclear / enzymology
  • [MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Cystatin C / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor A / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20567828.001).
  • [ISSN] 1432-0584
  • [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 / Biomarkers, Tumor; 0 / Cystatin C; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / Cathepsin L
  •  go-up   go-down


41. Brown P, Smith FO: Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date. Paediatr Drugs; 2008;10(2):85-92
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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] New Zealand
  • [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


42. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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


43. Kaspers GJ, Zwaan CM: Pediatric acute myeloid leukemia: towards high-quality cure of all patients. Haematologica; 2007 Nov;92(11):1519-32
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric acute myeloid leukemia: towards high-quality cure of all patients.
  • Prognosis of childhood acute myeloid leukemia (AML) has improved significantly over the past decades, from nearly no child surviving to a present probability of cure of approximately 60%.
  • This review summarizes current and future classification of pediatric AML, ongoing phase III studies, and subgroup-directed treatment.
  • These include minimal residual disease monitoring, pharmacogenomics and the detection of AML-specific molecular abnormalities.
  • Finally, we discuss the opportunities for innovative therapy in pediatric AML, such as the use of novel analogues, monoclonal antibody-mediated drugs, and receptor tyrosine kinase inhibitors.
  • Given the enormous increase in our understanding of the underlying biology of AML, and the development of many new targeted drugs, it should be possible to achieve high-quality cure in nearly all children and adolescents with AML within the next few decades.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Humans. Neoplasm, Residual / diagnosis. Pharmacogenetics. 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 = 18024401.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 147
  •  go-up   go-down


44. Schultz KA, Chen L, Chen Z, Zeltzer LK, Nicholson HS, Neglia JP: Health and risk behaviors in survivors of childhood acute myeloid leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2010 Jul 15;55(1):157-64
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Health and risk behaviors in survivors of childhood acute myeloid leukemia: a report from the Children's Oncology Group.
  • BACKGROUND: Survivors of childhood acute myeloid leukemia (AML) face increased risks of chronic disease and secondary malignancies.
  • PROCEDURES: Participants were diagnosed with AML at <21 years of age and survived > or =5 years following diagnosis.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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] Oncol Nurs Forum. 1999 Oct;26(9):1475-86 [11064879.001]
  • [Cites] Drug Alcohol Depend. 2008 Nov 1;98(1-2):13-23 [18585871.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882.001]
  • [Cites] Med Pediatr Oncol. 2001 Jul;37(1):42-6 [11466722.001]
  • [Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):189-96 [12525509.001]
  • [Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]
  • [Cites] Ann Intern Med. 2004 Apr 6;140(7):557-68 [15068985.001]
  • [Cites] Semin Oncol. 1982 Mar;9(1):34-51 [6176027.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1448-57 [8336184.001]
  • [Cites] J Clin Oncol. 1994 Jan;12(1):127-35 [8270968.001]
  • [Cites] J Natl Cancer Inst. 1994 Jan 19;86(2):131-7 [8271296.001]
  • [Cites] J Clin Oncol. 1994 Nov;12(11):2367-77 [7964952.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] J Natl Cancer Inst. 1998 Feb 4;90(3):219-25 [9462679.001]
  • [Cites] Ann Epidemiol. 2005 Mar;15(3):202-6 [15723765.001]
  • [Cites] J Clin Oncol. 2005 Sep 20;23(27):6516-23 [16116148.001]
  • [Cites] Semin Hematol. 2006 Jan;43(1):42-52 [16412788.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):476-83 [16421424.001]
  • [Cites] Pediatr Blood Cancer. 2006 May 1;46(5):565-9 [16261562.001]
  • [Cites] Prev Med. 2006 Jun;42(6):435-42 [16626797.001]
  • [Cites] Cancer. 2006 Sep 15;107(6):1303-12 [16894525.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] MMWR Morb Mortal Wkly Rep. 2007 Nov 9;56(44):1157-61 [17989644.001]
  • [Cites] Cancer. 2008 May 1;112(9):2071-9 [18327823.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):618-29 [11309438.001]
  • (PMID = 20232426.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA055727; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / 5U10CA78960; United States / NCI NIH HHS / CA / U24 CA55727; United States / NCI NIH HHS / CA / U10 CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543-08; None / None / / U10 CA098543-08; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA078960-04; United States / NCI NIH HHS / CA / CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413-08; None / None / / U10 CA098413-08; United States / NCI NIH HHS / CA / U10 CA98543; United States / NCI NIH HHS / CA / 5U10 CA07306; United States / NCI NIH HHS / CA / R01 CA078960-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS166508; NLM/ PMC3152207
  •  go-up   go-down


45. Brown P, McIntyre E, Rau R, Meshinchi S, Lacayo N, Dahl G, Alonzo TA, Chang M, Arceci RJ, Small D: The incidence and clinical significance of nucleophosmin mutations in childhood AML. Blood; 2007 Aug 1;110(3):979-85
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The incidence and clinical significance of nucleophosmin mutations in childhood AML.
  • Frameshift mutations in exon 12 of the nucleophosmin gene (NPM1) result in aberrant cytoplasmic localization of the NPM protein (NPMc(+)) and occur in 25% to 35% of adult acute myeloid leukemia (AML).
  • In adults with AML, NPMc(+) has been associated with normal karyotype, FLT3/ITD mutations, high remission induction rates, and improved survival (particularly in patients lacking FLT3/ITD).
  • NPMc(+) has not been well characterized in childhood AML.
  • This study examines the incidence and clinical significance of NPMc(+) in 295 children with newly diagnosed AML treated on a large cooperative group clinical trial (POG-9421).
  • We find that NPMc(+) is relatively uncommon in childhood AML (23 of 295 patients, 8%); and is significantly associated with FLT3/ITD mutations (P = .046), female sex (P = .029), older age (P = .047), and normal cytogenetics (P < .001).
  • We conclude that NPMc(+) is relatively rare in childhood AML, particularly in younger children.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2000 Sep 29;103(1):127-40 [11051553.001]
  • [Cites] Mutat Res. 2002 Nov 30;509(1-2):79-91 [12427532.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Nat Cell Biol. 2002 Jul;4(7):529-33 [12080348.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Biosci Biotechnol Biochem. 2002 Oct;66(10):2239-42 [12450141.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9327-38 [15485902.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2646-54 [15251987.001]
  • [Cites] Biometrics. 1979 Mar;35(1):25-39 [497336.001]
  • [Cites] Biochemistry. 1986 Jan 28;25(2):484-91 [3955008.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Blood. 1999 Jan 15;93(2):632-42 [9885226.001]
  • [Cites] Protein Sci. 1999 Apr;8(4):905-12 [10211837.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • [Cites] Leukemia. 2006 Feb;20(2):368-71 [16341033.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]
  • [Cites] Mutat Res. 2006 Sep 28;608(2):136-56 [16829162.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]
  • [Cites] Leukemia. 2007 May;21(5):998-1004 [17361227.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • (PMID = 17440048.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / K23 CA 111728
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1924773
  •  go-up   go-down


46. Meyer LH, Queudeville M, Eckhoff SM, Creutzig U, Reinhardt D, Karawajew L, Ludwig WD, Stahnke K, Debatin KM: Intact apoptosis signaling in myeloid leukemia cells determines treatment outcome in childhood AML. Blood; 2008 Mar 1;111(5):2899-903
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intact apoptosis signaling in myeloid leukemia cells determines treatment outcome in childhood AML.
  • Recently we reported that intact apoptosis signaling is indicative of favorable outcome in childhood acute lymphoblastic leukemia.
  • Here we addressed this issue in 45 pediatric acute myeloid leukemia patients analyzing 2 core apoptogenic events: cytochrome c release and caspase-3 activation.
  • Thus, the propensity to undergo apoptosis of leukemia cells is an important feature for favorable treatment outcome and may serve as an additional stratification tool for pediatric AML patients.
  • [MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Signal Transduction
  • [MeSH-minor] Caspase 3 / metabolism. Child. Cytochromes c / metabolism. Disease-Free Survival. Enzyme Activation. Humans. Remission Induction. Risk Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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
  • (PMID = 18083847.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00111345
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


47. Rodrigues PC, Oliveira SN, Viana MB, Matsuda EI, Nowill AE, Brandalise SR, Yunes JA: Prognostic significance of WT1 gene expression in pediatric acute myeloid leukemia. Pediatr Blood Cancer; 2007 Aug;49(2):133-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of WT1 gene expression in pediatric acute myeloid leukemia.
  • High expression of WT1 at diagnosis has been associated with unfavorable prognosis in adult acute myeloid leukemia (AML).
  • The prognostic relevance of WT1 expression in pediatric AML was evaluated in only one study, including 47 patients, which showed that very low levels of WT1 at presentation were associated with an excellent outcome.
  • To test the validity of these findings we measured levels of WT1 in 41 newly diagnosed pediatric AML of the non-M3 FAB subtype.
  • PROCEDURE: Patients were treated according to an AML-BFM 83-based protocol in a single institution.
  • CONCLUSIONS: Higher WT1 expression was associated with favorable cytogenetics subtypes and accordingly with better outcome in children with AML in this study.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brazil / epidemiology. Child. Child, Preschool. Chromosome Inversion. Chromosomes, Human, Pair 16 / ultrastructure. Chromosomes, Human, Pair 21 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Etoposide / therapeutic use. Female. Follow-Up Studies. Gene Expression Regulation, Leukemic. Humans. Infant. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / mortality. Male. Neoplasm Proteins / biosynthesis. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Translocation, Genetic. WT1 Proteins / biosynthesis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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
  • (PMID = 16883592.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / WT1 Proteins; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin; DAV regimen
  •  go-up   go-down


48. 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
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [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.
  • [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


49. Niewerth D, Creutzig U, Bierings MB, Kaspers GJ: A review on allogeneic stem cell transplantation for newly diagnosed pediatric acute myeloid leukemia. Blood; 2010 Sep 30;116(13):2205-14
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A review on allogeneic stem cell transplantation for newly diagnosed pediatric acute myeloid leukemia.
  • Survival of pediatric acute myeloid leukemia (AML) has improved considerably over the past decades.
  • However, it remains controversial whether allo-SCT is superior to chemotherapy for children with newly diagnosed AML.
  • This review summarizes phase 3 clinical trials that compared allo-SCT with chemotherapy (including autologous SCT) in pediatric AML, excluding studies that did not use the intention-to-treat analysis or correct for time-to-transplantation.
  • Because allo-SCT also gives more severe side effects and results more often in secondary malignancies than chemotherapy, we do not recommend allo-SCT in first remission for pediatric AML in general.
  • Further research should focus on the possibility that subgroups might benefit from allo-SCT, aiming at further improvements in the prognosis of pediatric AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials, Phase III as Topic. Cost-Benefit Analysis. Disease-Free Survival. Humans. Remission Induction. Survival Analysis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


50. 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
MedlinePlus Health Information. consumer health - Organ Donation.

  • [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.
  • [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


51. Shimada A, Taki T, Tabuchi K, Taketani T, Hanada R, Tawa A, Tsuchida M, Horibe K, Tsukimoto I, Hayashi Y: Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group. Pediatr Blood Cancer; 2008 Feb;50(2):264-9
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.
  • BACKGROUND: Mixed-lineage leukemia (MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult acute myeloid leukemia (AML), but its relationship to pediatric AML is unknown.
  • PROCEDURE: One hundred fifty-eight newly diagnosed AML patients, including 13 FAB-M3 and 10 Down syndrome (DS) patients, who were treated on the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed for MLL-PTD, as well as internal tandem duplication (ITD) and the kinase domain mutation (D835Mt) in the FLT3 gene.
  • RESULTS: We found MLL-PTD in 21 (13.3%) of 158 AML patients, but not in FAB-M3 or DS patients.
  • The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018), disease-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.
  • CONCLUSION: AML patients with FLT3-ITD, but not D835Mt, showed a poor prognosis.
  • AML patients with MLL-PTD were also correlated with poor prognosis in this study.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. DNA Mutational Analysis. Down Syndrome / complications. Down Syndrome / genetics. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Mutation. Prognosis. Tandem Repeat Sequences. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763464.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


52. Langebrake C, Brinkmann I, Teigler-Schlegel A, Creutzig U, Griesinger F, Puhlmann U, Reinhardt D: Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring. Cytometry B Clin Cytom; 2005 Jan;63(1):1-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring.
  • BACKGROUND: Determination of antigen expression patterns is, in addition to morphologic analysis, essential to the diagnosis of acute myeloid leukemia (AML).
  • The present study was performed to determine (a) the degree of changes in immunophenotype and their consequences on the monitoring of minimal residual disease (MRD) in childhood AML and (b) whether certain clusters of changes in antigen expression patterns exist between diagnosis and relapse.
  • METHODS: Bone marrow specimens of 48 children enrolled in the German AML-BFM-93/98 (Acute Myeloid Leukemia-Berlin-Frankfurt-Munster) studies were analyzed immunologically, morphologically, and genetically at diagnosis and at first relapse.
  • We did not observe significant changes for lineage specific markers, with comparable occurrences of loss or gain of myeloid and lymphoid antigens in the sample pairs.
  • The antibody panels used for MRD monitoring in childhood AML should therefore not be restricted to the immunophenotype detected at presentation but should include in particular markers of lineage immaturity.
  • [MeSH-major] Antigens, Neoplasm / immunology. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Bone Marrow / immunology. Bone Marrow / pathology. Child. Child, Preschool. Clone Cells. Flow Cytometry. Humans. Infant. Karyotyping. Recurrence

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15624201.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
  •  go-up   go-down


53. Johnston DL, Alonzo TA, Gerbing RB, Lange BJ, Woods WG: The presence of central nervous system disease at diagnosis in pediatric acute myeloid leukemia does not affect survival: a Children's Oncology Group study. Pediatr Blood Cancer; 2010 Sep;55(3):414-20
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The presence of central nervous system disease at diagnosis in pediatric acute myeloid leukemia does not affect survival: a Children's Oncology Group study.
  • BACKGROUND: The presence of central nervous system (CNS) disease in pediatric acute myeloid leukemia (AML) is often thought to confer a worse prognosis.
  • This study examined the outcome of children with AML who had CNS disease at diagnosis.
  • METHODS: Patients enrolled on Children's Cancer Group protocols 2861, 2891, 2941, and 2961 being treated for de novo AML were classified for the presence of CNS disease at diagnosis as CNS1 (<5 WBC in the CSF without blasts), CNS2 (<5 WBC in the CSF with blasts), or CNS3 (> or =5 WBC in the CSF with blasts).

  • 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
  • [Copyright] 2010 Wiley-Liss, Inc.
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] Leukemia. 2000 Apr;14(4):684-7 [10764155.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1201-7 [10914543.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Leukemia. 2001 Jan;15(1):46-9 [11243398.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1714-20 [11535502.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):365-77 [12139720.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):378-84 [12139721.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Oct;25(10):760-8 [14528097.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2090-6 [14523477.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] Leuk Res. 2004 Oct;28(10):1007-11 [15289011.001]
  • [Cites] Blood. 1985 Nov;66(5):1062-7 [3840394.001]
  • [Cites] J Clin Oncol. 1987 Jul;5(7):1026-32 [3474356.001]
  • [Cites] J Clin Oncol. 1990 Jan;8(1):75-83 [2295913.001]
  • [Cites] J Clin Oncol. 1991 Apr;9(4):572-80 [2066754.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1448-57 [8336184.001]
  • [Cites] Blood. 1994 Jul 15;84(2):355-66 [8025264.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 Mar-Apr;21(2):91-102 [10206454.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1355-60 [15920490.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2030-42 [16304570.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9172-8 [16361619.001]
  • [Cites] Cancer. 2007 Jan 1;109(1):157-63 [17133407.001]
  • [Cites] Pediatr Blood Cancer. 2007 Apr;48(4):393-8 [16550530.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):17-22 [16856158.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [CommentIn] Pediatr Blood Cancer. 2010 Sep;55(3):399-400 [20658608.001]
  • (PMID = 20658610.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA098543-01; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS218661; NLM/ PMC2990693
  •  go-up   go-down


54. Rubnitz JE, Crews KR, Pounds S, Yang S, Campana D, Gandhi VV, Raimondi SC, Downing JR, Razzouk BI, Pui CH, Ribeiro RC: Combination of cladribine and cytarabine is effective for childhood acute myeloid leukemia: results of the St Jude AML97 trial. Leukemia; 2009 Aug;23(8):1410-6
Hazardous Substances Data Bank. CLADRIBINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of cladribine and cytarabine is effective for childhood acute myeloid leukemia: results of the St Jude AML97 trial.
  • Because cladribine can increase cytarabine triphosphate levels, we tested a cladribine-cytarabine combination in the St Jude AML97, trial in which this combination was administered before standard chemotherapy to 96 children with acute myeloid leukemia (AML) or myelodysplastic syndrome.
  • Our results suggest that cladribine in combination with continuous-infusion cytarabine is effective therapy for childhood AML.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • 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
  • [Cites] Blood. 1994 Aug 15;84(4):1237-42 [7914104.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] Leukemia. 1996 Oct;10(10):1563-9 [8847890.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Leuk Lymphoma. 2000 Sep;39(1-2):121-9 [10975390.001]
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]
  • [Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]
  • [Cites] Br J Haematol. 2003 Jul;122(2):217-25 [12846889.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]
  • [Cites] Leuk Res. 2004 Apr;28(4):349-52 [15109533.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4384-93 [15514380.001]
  • [Cites] J Clin Invest. 1990 Nov;86(5):1480-8 [1700795.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):416-22 [1671875.001]
  • [Cites] J Clin Oncol. 1992 Mar;10(3):364-70 [1346800.001]
  • [Cites] Blood. 1993 Jan 1;81(1):143-50 [8093345.001]
  • [Cites] Blood. 1996 Jan 1;87(1):256-64 [8547650.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3532-9 [17660380.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • (PMID = 19242495.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 47M74X9YT5 / Cladribine; 6PLQ3CP4P3 / Etoposide; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS90802; NLM/ PMC2726271
  •  go-up   go-down


55. Wang D, Tang YM, Xu XJ, Shen HQ, Qian BQ: [Determination of leukemia stem cells in childhood acute myeloid leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):952-8
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Determination of leukemia stem cells in childhood acute myeloid leukemia and its clinical significance].
  • The aim of this study was to detect the presence of human AML leukemia stem cells (LSC) in childhood patients with acute leukemia (AL) and analyze the correlation between LSC concentrations and minimal residual disease (MRD) levels in AML cases after remission.
  • The multi-parameter flow cytometry (FCM) and a panel of monoclonal antibody combination were used to detect the AML LSC or AML LSC immunophenotype-identical cell (AML LSC-IPIC) concentrations in childhood AML or ALL leukemia both at new diagnosis and at remission and correlated AML LSC to the MRD levels at different time points after remission.
  • The results indicated that the AML LSC or AML LSC-IPIC concentrations [in average 166 (range 14 - 1459)/100 000 mononuclear cells (MNCs)] in AML at initial diagnosis were significantly higher than those in ALL [7 (range 0 - 560)/100 000 MNCs, p < 0.017] and control [0 (range 0 - 6)/100 000 MNCs, p < 0.017], respectively.
  • The AML LSC concentrations in AML at non-CR were in average 36 (range 5 - 224)/100 000 MNCs.
  • No statistical difference (p > 0.05) was found between the AML LSC or AML LSC-IPIC concentrations in AML (in average 6 (range 0 - 41)/100, 000 MNCs) and ALL [10 (range 0 - 105)/100, 000 MNCs] after CR.
  • The significantly negative correlation was noticed between AML LSC concentrations and MRD levels.
  • It is concluded that the AML LSCs exist in newly diagnosed AML, which are significantly reduced when complete remission has achieved, but the low levels of these populations still remain.
  • The phenotypically similar (CD34(+)CD38⁻CD123(+)) AML LSC populations have also been found in the bone marrow from ALL patients, but their concentrations are not significantly different when CR has achieved.
  • The significantly negative correlation between AML LSC concentrations and MRD levels is observed in AML patients after remission.

  • 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 = 20723307.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


56. Goemans BF, Zwaan CM, Cloos J, de Lange D, Loonen AH, Reinhardt D, Hählen K, Gibson BE, Creutzig U, Kaspers GJ: FLT3 and KIT mutated pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to the tyrosine kinase inhibitor SU11657. Leuk Res; 2010 Oct;34(10):1302-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FLT3 and KIT mutated pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to the tyrosine kinase inhibitor SU11657.
  • New treatment strategies to improve the outcome of pediatric acute myeloid leukemia (AML) are required as 40% of children diagnosed with AML do not survive.
  • Around 30% of pediatric AML patients harbour a mutation in the tyrosine kinases FLT3 (+/-20%) or KIT (+/-10%).
  • In this study we investigated whether pediatric AML samples (N=61) were sensitive to the tyrosine kinase inhibitor SU11657 (similar to the clinically available drug sunitinib) in vitro, and whether sensitivity was related to expression of, and mutations in, FLT3 and KIT.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Mutation. Organic Chemicals / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Female. Humans. Male

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20435347.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organic Chemicals; 0 / SU 11657; 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


57. 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
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [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.
  • [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


58. Mizushima Y, Taki T, Shimada A, Yui Y, Hiraumi Y, Matsubara H, Watanabe M, Watanabe K, Kamitsuji Y, Hayashi Y, Tsukimoto I, Kobayashi R, Horibe K, Tawa A, Nakahata T, Adachi S: Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2010 Jun;91(5):831-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group.
  • High BAALC (brain and acute leukemia, cytoplasmic) gene expression may indicate an adverse prognosis for adults who have acute myeloid leukemia (AML) and a normal karyotype, but its prognostic significance for pediatric AML cases is unclear.
  • Newly diagnosed AML patients with normal karyotype who were treated by the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed in terms of their BAALC expression levels (n = 29), BAALC isoforms (n = 29), and CEBPA mutations (n = 49).
  • Thus, 1-5-6-8 isoform expression may be associated with an adverse prognosis in pediatric AML with normal karyotype.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. CCAAT-Enhancer-Binding Proteins. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Mutation. Neoplasm Proteins
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Prognosis. Protein Isoforms / genetics

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • 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 = 20495894.001).
  • [ISSN] 1865-3774
  • [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] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Neoplasm Proteins; 0 / Protein Isoforms
  •  go-up   go-down


59. 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
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [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


60. Morerio C, Acquila M, Rosanda C, Rapella A, Tassano E, Micalizzi C, Panarello C: t(9;11)(p22;p15) with NUP98-LEDGF fusion gene in pediatric acute myeloid leukemia. Leuk Res; 2005 Apr;29(4):467-70
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(9;11)(p22;p15) with NUP98-LEDGF fusion gene in pediatric acute myeloid leukemia.
  • The rare t(9;11)(p22;p15) translocation is associated with adult acute myeloid leukemia (AML) with immature forms.
  • We report a novel fusion of the NUP98 and LEDGF genes in a pediatric AML with intermediate characteristics between M2-M3 French-American-British (FAB) subtypes exhibiting the same chromosomal rearrangement.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 22. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Artificial Gene Fusion. Child, Preschool. Chromosome Mapping. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15725483.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / lens epithelium-derived growth factor
  •  go-up   go-down


61. Mehta PA, Alonzo TA, Gerbing RB, Elliott JS, Wilke TA, Kennedy RJ, Ross JA, Perentesis JP, Lange BJ, Davies SM, Children's Oncology Group: XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report. Blood; 2006 Jan 1;107(1):39-45
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report.
  • Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related acute myeloid leukemia (AML) and with poor outcome of AML in elderly patients.
  • We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of AML in children and, as shown in adults, may affect the outcome of childhood AML therapy.
  • Genotyping of 456 children treated for de novo AML was performed at XPD exon 23.
  • Gene frequencies in AML patients and healthy controls were similar.
  • There were no significant differences in overall survival (P = .82), event-free survival (P = .78), treatment-related mortality (P = .43), or relapse rate (RR) (P = .92) between patients with XPD751AA versus 751AC versus 751CC genotypes, in contrast to reports in adult AML.
  • These data, representing the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of childhood AML.
  • [MeSH-major] Leukemia, Myeloid / genetics. Polymorphism, Single Nucleotide. Xeroderma Pigmentosum Group D Protein / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Female. Gene Frequency. Genetic Testing. Genotype. Humans. Infant. Infant, Newborn. Male. Mutation, Missense. 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 = 16150943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
  •  go-up   go-down


62. Fisher BT, Aplenc R, Localio R, Leckerman KH, Zaoutis TE: Cefepime and mortality in pediatric acute myelogenous leukemia: a retrospective cohort study. Pediatr Infect Dis J; 2009 Nov;28(11):971-5
MedlinePlus Health Information. consumer health - Antibiotics.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cefepime and mortality in pediatric acute myelogenous leukemia: a retrospective cohort study.
  • Pediatric patients with acute myelogenous leukemia (AML) have frequent episodes of fever necessitating the use of antibiotics such as cefepime.
  • We evaluated the association of cefepime and other beta-lactam antibiotic exposures with all cause in-hospital mortality in pediatric AML patients.
  • METHODS: We performed a retrospective cohort study using the Pediatric Health Information System, an inpatient database.
  • Exposure to cefepime, ceftazidime, antipseudomonal penicillin, and carbapenems was evaluated for each 30-day period within the first year from AML diagnosis.
  • CONCLUSIONS: In this cohort of pediatric AML patients, cefepime exposure in the 30 days preceding death did not result in an increased mortality risk when compared with ceftazidime, antipseudomonal penicillins, or carbapenems.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Cephalosporins / therapeutic use. Leukemia, Myeloid, Acute / complications. Opportunistic Infections / drug therapy. Opportunistic Infections / mortality
  • [MeSH-minor] Adolescent. Animals. Child. Child, Preschool. Cohort Studies. Female. Humans. Immunocompromised Host. Infant. Infant, Newborn. Male. Retrospective Studies

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19859014.001).
  • [ISSN] 1532-0987
  • [Journal-full-title] The Pediatric infectious disease journal
  • [ISO-abbreviation] Pediatr. Infect. Dis. J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Cephalosporins; 807PW4VQE3 / cefepime
  •  go-up   go-down


63. Steinbach D, Gillet JP, Sauerbrey A, Gruhn B, Dawczynski K, Bertholet V, de Longueville F, Zintl F, Remacle J, Efferth T: ABCA3 as a possible cause of drug resistance in childhood acute myeloid leukemia. Clin Cancer Res; 2006 Jul 15;12(14 Pt 1):4357-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABCA3 as a possible cause of drug resistance in childhood acute myeloid leukemia.
  • BACKGROUND: A major issue in the treatment of acute myeloid leukemia (AML) is resistance to chemotherapeutic drugs.
  • EXPERIMENTAL DESIGN: A newly developed microarray for the simultaneous quantification of 38 ABC transporter genes and Taqman real-time PCR was used to analyze the expression of ABC transporters in pediatric AML and healthy bone marrow.
  • RESULTS: Using the microarray, we identified four new ABC transporters, which were overexpressed in many AML samples compared with healthy bone marrow: ABCA2, ABCA3, ABCB2, and ABCC10.
  • The overexpression of these four genes was verified by real-time PCR in 42 samples from children with AML and 18 samples of healthy bone marrow.
  • CONCLUSION: Our results show that ABCA2, ABCA3, ABCB2, and ABCC10 are overexpressed in childhood AML compared with healthy bone marrow.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / metabolism. Child. Child, Preschool. Cluster Analysis. Drug Resistance, Multiple. Female. Humans. Jurkat Cells. Male. Oligonucleotide Array Sequence Analysis. RNA, Small Interfering / metabolism

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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 = 16857811.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCA3 protein, human; 0 / RNA, Small Interfering
  •  go-up   go-down


64. Meyer S, Fergusson WD, Whetton AD, Moreira-Leite F, Pepper SD, Miller C, Saunders EK, White DJ, Will AM, Eden T, Ikeda H, Ullmann R, Tuerkmen S, Gerlach A, Klopocki E, Tönnies H: Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption. Genes Chromosomes Cancer; 2007 Apr;46(4):359-72
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption.
  • Fanconi anemia (FA) is an inherited disease with congenital abnormalities and an extreme risk of acute myeloid leukemia (AML).
  • Genetic events occurring during malignant transformation in FA and the biology of FA-associated AML are poorly understood, but are often preceded by the development of chromosomal aberrations involving 3q26-29 in bone marrow of FA patients.
  • We report here the molecular cytogenetic characterization of FA-derived AML cell lines SB1685CB and SB1690CB by conventional and array comparative genomic hybridization, fluorescence in situ hybridization, and SKY.
  • We identified gains of a 3.7 MB chromosomal region on 3q26.2-26.31, which preceded transformation to overt leukemia.
  • Rearrangements of 3q, which are rare in childhood AML, commonly result in overexpression of EVI1, which determines specific gene expression patterns and confers poor prognosis.
  • We detected overexpression of EVI1 in all three FA-derived AML.
  • We hypothesize that constitutional or acquired FA defects might be a common factor for the development of 3q abnormalities in AML.
  • In addition, cryptic imbalances as detected here might account for overexpression of EVI1 in AML without overt 3q26 rearrangements.
  • [MeSH-major] BRCA2 Protein / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Fanconi Anemia / genetics. Gene Amplification. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line. Child. Humans


65. Sander A, Zimmermann M, Dworzak M, Fleischhack G, von Neuhoff C, Reinhardt D, Kaspers GJ, Creutzig U: Consequent and intensified relapse therapy improved survival in pediatric AML: results of relapse treatment in 379 patients of three consecutive AML-BFM trials. Leukemia; 2010 Aug;24(8):1422-8
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Consequent and intensified relapse therapy improved survival in pediatric AML: results of relapse treatment in 379 patients of three consecutive AML-BFM trials.
  • Relapse remains the major cause of treatment failure in pediatric acute myeloid leukemia (AML).
  • We analyzed the clinical characteristics, treatment response to relapse treatment and overall survival (OS) of 379 children with AML relapse treated according to three consecutive frontline protocols of the AML-Berlin/Frankfurt/Muenster study group (AML-BFM-87/-93/-98).
  • Overall, one-third of children with relapsed AML can be cured today.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery
  • [MeSH-minor] Child. Child, Preschool. Cohort Studies. Female. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Prognosis. Recurrence. Remission Induction. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20535146.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


66. Lee DH, Kwon YJ, Lim J, Kim Y, Han K, Chung NG, Jeong DC, Cho B, Kim HK: Comparable outcomes of HLA-matched unrelated and HLA-identical sibling donor bone marrow transplantation for childhood acute myeloid leukemia in first remission. Pediatr Transplant; 2009 Mar;13(2):210-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparable outcomes of HLA-matched unrelated and HLA-identical sibling donor bone marrow transplantation for childhood acute myeloid leukemia in first remission.
  • We retrospectively investigated the outcomes of HLA-matched unrelated BMT (MU-BMT, n = 13) and HLA-identical sibling donor BMT (MS-BMT, n = 17) for childhood AML in CR1 between June 2002 and August 2005.
  • The cumulative incidence of grade II-IV acute GVHD and any chronic GVHD at three yr was not different between MS-BMT and MU-BMT.
  • The outcome of HLA-matched unrelated BMT is comparable to that of HLA-identical sibling BMT for childhood AML in CR1.
  • HLA-matched unrelated BMT may be recommended for patients who have AML in CR1 without an HLA-matched sibling donor.
  • [MeSH-major] Bone Marrow Transplantation / methods. HLA Antigens / metabolism. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Blood Platelets / metabolism. Child. Child, Preschool. Female. Humans. Living Donors. Male. Neutrophils / metabolism. Remission Induction. Retrospective Studies. Siblings. Treatment Outcome


67. 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
Hazardous Substances Data Bank. NOVANTRONE .

  • [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 .
  • [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


68. Hollink IH, van den Heuvel-Eibrink MM, Zimmermann M, Balgobind BV, Arentsen-Peters ST, Alders M, Willasch A, Kaspers GJ, Trka J, Baruchel A, de Graaf SS, Creutzig U, Pieters R, Reinhardt D, Zwaan CM: Clinical relevance of Wilms tumor 1 gene mutations in childhood acute myeloid leukemia. Blood; 2009 Jun 4;113(23):5951-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical relevance of Wilms tumor 1 gene mutations in childhood acute myeloid leukemia.
  • Wilms tumor 1 (WT1) mutations have recently been identified in approximately 10% of adult acute myeloid leukemia (AML) with normal cytogenetics (CN-AML) and are associated with poor outcome.
  • Using array-based comparative genome hybridization in pediatric CN-AML samples, we detected a WT1 deletion in one sample.
  • This prompted us to further investigate the role of WT1 aberrations in childhood AML.
  • Mutations were found in 35 of 298 (12%) diagnostic pediatric AML samples.
  • WT1 mutations clustered significantly in the CN-AML subgroup (22%; P < .001) and were associated with FLT3/ITD (43 vs 17%; P < .001).
  • WT1 mutations occur at a significant rate in childhood AML and are a novel independent poor prognostic marker.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Base Sequence. Child. Child, Preschool. Female. Humans. Male. Multivariate Analysis. Mutation / genetics. Prognosis. Recurrence. Survival Rate


69. Corbacioglu S, Kilic M, Westhoff MA, Reinhardt D, Fulda S, Debatin KM: Newly identified c-KIT receptor tyrosine kinase ITD in childhood AML induces ligand-independent growth and is responsive to a synergistic effect of imatinib and rapamycin. Blood; 2006 Nov 15;108(10):3504-13
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Newly identified c-KIT receptor tyrosine kinase ITD in childhood AML induces ligand-independent growth and is responsive to a synergistic effect of imatinib and rapamycin.
  • Internal tandem duplications (ITDs) of exon 11, which encodes the juxtamembrane domain (JMD), are constitutively activating mutations found in 7% of gastrointestinal stromal tumors (GISTs) but have not been described in childhood acute myeloid leukemia (AML).
  • DNA and cDNA from 60 children with AML were screened by polymerase chain reaction (PCR) for mutations of the JMD.
  • The findings presented may have immediate therapeutic impact for a subgroup of childhood AML-expressing c-KIT mutations.
  • [MeSH-major] Cell Proliferation / drug effects. DNA, Neoplasm / genetics. Leukemia, Myeloid / enzymology. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Sirolimus / pharmacology. Tandem Repeat Sequences
  • [MeSH-minor] Acute Disease. Adolescent. Animals. Benzamides. Cell Line. Child. Child, Preschool. Drug Synergism. Female. Humans. Imatinib Mesylate. Infant. Male. Mice. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Receptor Cross-Talk. STAT Transcription Factors / metabolism. Transfection

  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16840725.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / DNA, Neoplasm; 0 / Piperazines; 0 / Pyrimidines; 0 / STAT Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


70. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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] Antigens, CD34. Apoptosis / physiology. Leukemia, Myeloid, Acute. Lymphocyte Subsets / metabolism. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] 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.
  • [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 / Antigens, CD34; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
  •  go-up   go-down


71. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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 .
  • [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


72. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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


73. Mullighan CG, Kennedy A, Zhou X, Radtke I, Phillips LA, Shurtleff SA, Downing JR: Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias. Leukemia; 2007 Sep;21(9):2000-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias.
  • Somatic mutations in nucleophosmin (NPM1) occur in approximately 35% of adult acute myeloid leukemia (AML).
  • To assess the frequency of NPM1 mutations in pediatric AML, we sequenced NPM1 in the diagnostic blasts from 93 pediatric AML patients.
  • As dysregulated homeobox gene expression is also a feature of MLL-rearranged leukemia, the gene expression signatures of NPM1-mutated and MLL-rearranged leukemias were compared.
  • Significant differences were identified between these leukemia subtypes including the expression of different HOX genes, with NPM1-mutated AML showing higher levels of expression of HOXB2, B3, B6 and D4.
  • These results confirm recent reports of perturbed HOX expression in NPM1-mutated adult AML, and provide the first evidence that the NPM1-mutated signature is distinct from MLL-rearranged AML.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Cohort Studies. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Male. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leukemia. 2007 Sep;21(9):1849-50 [17712359.001]
  • (PMID = 17597811.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P01 CA71907-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXB2 protein, human; 0 / HOXB6 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 140441-81-2 / HOXA10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


74. Razzouk BI, Estey E, Pounds S, Lensing S, Pierce S, Brandt M, Rubnitz JE, Ribeiro RC, Rytting M, Pui CH, Kantarjian H, Jeha S: Impact of age on outcome of pediatric acute myeloid leukemia: a report from 2 institutions. Cancer; 2006 Jun 1;106(11):2495-502
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of age on outcome of pediatric acute myeloid leukemia: a report from 2 institutions.
  • BACKGROUND: The prognostic significance of age among pediatric patients with acute myeloid leukemia (AML) was investigated.
  • METHODS: The authors reviewed the outcome of 424 patients who were <or=21 years of age at the time of diagnosis of AML (excluding acute promyelocytic leukemia) between 1983 and 2002 at St. Jude Children's Research Hospital (n=288) or the M. D.
  • CONCLUSIONS: These results suggest that age is an independent prognostic factor in childhood AML and that children younger than 10 years benefit more than older children from newer intensive therapies.
  • [MeSH-major] Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Bone Marrow Transplantation. Child. Female. Humans. Male. Prognosis. Retrospective Studies

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2006 American Cancer Society.
  • (PMID = 16639734.001).
  • [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; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


75. Ho PA, Zeng R, Alonzo TA, Gerbing RB, Miller KL, Pollard JA, Stirewalt DL, Heerema NA, Raimondi SC, Hirsch B, Franklin JL, Lange B, Meshinchi S: Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group. Blood; 2010 Aug 05;116(5):702-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
  • Recent studies of WT1 mutations in acute myeloid leukemia (AML) mostly report an association with unfavorable clinical outcome.
  • We screened 842 patients treated on 3 consecutive pediatric AML trials for WT1 zinc-finger mutations.
  • In current risk stratification schemes incorporating cytogenetics and FLT3/ITD status, the presence of WT1 mutations has no independent prognostic significance in predicting outcome in pediatric AML.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Karyotyping. Male. Prevalence. Prognosis. Proportional Hazards Models. Retrospective Studies. Tandem Repeat Sequences / genetics. Treatment Outcome. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Leukemia. 2007 May;21(5):868-76 [17361230.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):590-600 [15147374.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4140-6 [15483024.001]
  • [Cites] Leukemia. 1992 May;6(5):405-9 [1317488.001]
  • [Cites] Hum Mol Genet. 1994 Sep;3(9):1633-7 [7833922.001]
  • [Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]
  • [Cites] Biochemistry. 1996 Sep 17;35(37):12070-6 [8810912.001]
  • [Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):106-14 [17255787.001]
  • [Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):346-55 [18692685.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]
  • [Cites] Blood. 2009 Jun 4;113(23):5951-60 [19171881.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]
  • [Cites] Cancer. 2009 Aug 15;115(16):3719-27 [19536888.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1472-9 [19322206.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]
  • [Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]
  • [Cites] Gene. 2001 Aug 8;273(2):141-61 [11595161.001]
  • (PMID = 20413658.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R21CA10262-01; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2918327
  •  go-up   go-down


76. Shah N, Leaker MT, Teshima I, Baruchel S, Abdelhaleem M, Ye CC: Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 May;50(5):1052-3
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia.
  • A 3-year-old female was diagnosed with acute myeloid leukemia (AML-M2).
  • The late occurrence of the Philadelphia chromosome in AML has been documented rarely in adults.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome
  • [MeSH-minor] Blast Crisis. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Fusion Proteins, bcr-abl / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Trisomy

  • 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
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18213712.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


77. Al-Adnani M, Williams S, Anderson J, Ashworth M, Malone M, Sebire NJ: Immunohistochemical nuclear positivity for WT1 in childhood acute myeloid leukemia. Fetal Pediatr Pathol; 2007 Jul-Aug;26(4):193-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical nuclear positivity for WT1 in childhood acute myeloid leukemia.
  • Several studies have reported previously that acute myeloid leukemia (AML) may express WT1 detected by RT-PCR and/or Northern blotting.
  • The diagnostic utility of WT1 expression in AML using immunohistochemistry has not been reported previously.
  • Paraffin-embedded tissue sections from 55 AML, 12 acute lymphoblastic leukemia (ALL), and 10 normal bone marrow specimens were immunostained for WT1 (anti-N terminus antibody).
  • 22/55 AML cases (40%) demonstrated nuclear immunopositivity for WT1, including 20/47 bone marrow trephines and 2/4 granulocytic sarcomas.
  • A significant proportion of AML expresses nuclear immunostaining for WT1, a finding that has only been described previously in Wilms' tumor and desmoplastic small round cell tumor.
  • This finding is important for the correct interpretation of immunohistochemical findings in the diagnosis of "small round cell" tumors of childhood, especially in cases of extramedullary deposits of AML, in which traditional myeloid markers may be negative.
  • [MeSH-major] Cell Nucleus / metabolism. Leukemia, Myeloid, Acute / metabolism. WT1 Proteins / metabolism


78. Radtke I, Mullighan CG, Ishii M, Su X, Cheng J, Ma J, Ganti R, Cai Z, Goorha S, Pounds SB, Cao X, Obert C, Armstrong J, Zhang J, Song G, Ribeiro RC, Rubnitz JE, Raimondi SC, Shurtleff SA, Downing JR: Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12944-9
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia.
  • Pediatric de novo acute myeloid leukemia (AML) is an aggressive malignancy with current therapy resulting in cure rates of only 60%.
  • To better understand the cause of the marked heterogeneity in therapeutic response and to identify new prognostic markers and therapeutic targets a comprehensive list of the genetic mutations that underlie the pathogenesis of AML is needed.
  • To approach this goal, we examined diagnostic leukemic samples from a cohort of 111 children with de novo AML using single-nucleotide-polymorphism microarrays and candidate gene resequencing.
  • Our data demonstrate that, in contrast to pediatric acute lymphoblastic leukemia (ALL), de novo AML is characterized by a very low burden of genomic alterations, with a mean of only 2.38 somatic copy-number alterations per leukemia, and less than 1 nonsynonymous point mutation per leukemia in the 25 genes analyzed.
  • The only exception to the presence of few mutations was acute megakaryocytic leukemias, with the majority of these leukemias being characterized by a high number of copy-number alterations but rare point mutations.
  • These data reflect a remarkably low burden of genomic alterations within pediatric de novo AML, which is in stark contrast to most other human malignancies.

  • 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] Mutat Res. 2008 Apr 2;640(1-2):97-106 [18243251.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Sep;47(9):729-39 [18506749.001]
  • [Cites] Leuk Lymphoma. 2008 Jun;49(6):1178-83 [18452069.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16224-9 [18852474.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] Nature. 2008 Nov 6;456(7218):66-72 [18987736.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Nature. 2009 Mar 12;458(7235):223-7 [19182780.001]
  • [Cites] Cancer. 2007 Jan 1;109(1):157-63 [17133407.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Genes Dev. 2000 Jul 15;14(14):1810-23 [10898795.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:179-98 [12194988.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Nat Rev Cancer. 2004 Mar;4(3):177-83 [14993899.001]
  • [Cites] Oncogene. 2004 Jun 17;23(28):4903-10 [15077163.001]
  • [Cites] Oncogene. 2004 Aug 26;23(39):6612-20 [15208665.001]
  • [Cites] Leukemia. 2004 Nov;18(11):1831-4 [15385933.001]
  • [Cites] Oncogene. 1996 Nov 21;13(10):2121-30 [8950979.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1361-6 [15902284.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]
  • [Cites] Blood. 2006 May 15;107(10):3847-53 [16434492.001]
  • [Cites] PLoS Comput Biol. 2006 May;2(5):e41 [16699594.001]
  • [Cites] Oncogene. 2006 Jun 22;25(26):3735-44 [16449964.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1282-97 [16893685.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Curr Oncol Rep. 2006 Nov;8(6):430-6 [17040621.001]
  • [Cites] Am J Hum Genet. 2007 Nov;81(5):906-12 [17924334.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] J Pharmacol Exp Ther. 2008 Jan;324(1):86-94 [17959747.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):123-32 [18173751.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • (PMID = 19651601.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 21765
  • [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 / CCDC26 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLLT4 protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; EC 3.6.1.- / Kinesin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2716382
  •  go-up   go-down


79. 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
The Lens. Cited by Patents in .

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

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • 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 = 15870172.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  •  go-up   go-down


80. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • Frequency of evolution of clonal chromosome abnormalities in AML constituted 42,3%.
  • Identity of abnormal chromosome structure at diagnosis and relapse of disease can be an evidence of the influence of chemical agent on establishment of some types of evolution of chromosome abnormalities in leukemic cells in AML in children.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosome Deletion. Clone Cells. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Monosomy. Translocation, Genetic. Trisomy

  • 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 = 20608159.001).
  • [ISSN] 0564-3783
  • [Journal-full-title] T︠S︡itologii︠a︡ i genetika
  • [ISO-abbreviation] Tsitol. Genet.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  •  go-up   go-down


81. Willasch AM, Gruhn B, Coliva T, Kalinova M, Schneider G, Kreyenberg H, Steinbach D, Weber G, Hollink IH, Zwaan CM, Biondi A, van der Velden VH, Reinhardt D, Cazzaniga G, Bader P, Trka J, European Study Group on WT1 Expression in Childhood AML: Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study. Leukemia; 2009 Aug;23(8):1472-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study.
  • A standardized, sensitive and universal method for minimal residual disease (MRD) detection in acute myeloid leukemia (AML) is still pending.
  • Although hyperexpression of Wilms' tumor (WT1) gene transcript has been frequently proposed as an MRD marker in AML, wide comparability of the various methods used for evaluating WT1 expression has not been given.
  • In a series of quality-control rounds, we analyzed 69 childhood AML samples and 47 normal bone marrow (BM) samples from 4 participating centers.
  • In AML samples, the median WT1/1E+04 Abelson (ABL) expression was 3.5E+03 compared with that of 2.3E+01 in healthy BM samples.
  • As 11.5% of childhood AML samples in this cohort harbored WT1 mutations in exon 7, the effect of mutations on WT1 expression has been investigated, showing that mutated cases expressed significantly higher WT1 levels than wild-type cases.
  • [MeSH-major] Bone Marrow Examination / standards. Genes, Wilms Tumor. Leukemia, Myeloid / pathology. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / standards
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Cohort Studies. DNA Primers. Exons / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm, Residual. Sensitivity and Specificity. WT1 Proteins / biosynthesis. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19322206.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
  •  go-up   go-down


82. Dawczynski K, Steinbach D, Wittig S, Pfaffendorf N, Kauf E, Zintl F: Expression of components of the IGF axis in childhood acute myelogenous leukemia. Pediatr Blood Cancer; 2008 Jan;50(1):24-8
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of components of the IGF axis in childhood acute myelogenous leukemia.
  • PROCEDURE: We analyzed the mRNA expression profile of IGF-I, -II, and IGFBP-2, -3 in 50 children with previously untreated AML (mean age 10.8 +/- 4.8 years; patients in CCR n = 20, patients with relapse during later course of disease n = 15).
  • RESULTS: IGFBP-2 expression was significantly higher in AML cells than in healthy cells of peripheral MNC (P < 0.001) and of bone marrow cells (P < 0.01).
  • Conversely, AML cells showed significantly lower IGFBP-3 and IGF-I gene expression compared to controls (P = 0.02; P < 0.001).
  • CONCLUSIONS: Results identified different expressions of IGF components between normal and AML cells.
  • [MeSH-major] Insulin-Like Growth Factor Binding Protein 2 / metabolism. Insulin-Like Growth Factor Binding Protein 3 / metabolism. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor II / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Child. Disease-Free Survival. Gene Expression. Humans. RNA, Messenger / metabolism

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17635002.001).
  • [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 / Insulin-Like Growth Factor Binding Protein 2; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / RNA, Messenger; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II
  •  go-up   go-down


83. Absalon MJ, Smith FO: Treatment strategies for pediatric acute myeloid leukemia. Expert Opin Pharmacother; 2009 Jan;10(1):57-79
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment strategies for pediatric acute myeloid leukemia.
  • Therapeutic strategies utilized in recently completed Phase III clinical trials in children with de novo acute myeloid leukemia have led to long-term disease-free survival in 50 - 60% of children.
  • Future improvements in the treatment of children with acute myeloid leukemia will depend on a better understanding of the biology of the disease, targeted therapeutic approaches directed to specific biologic targets, selective use of allogeneic transplantation and innovative clinical trial designs that will allow for the testing of an increasing number of new agents in increasingly small numbers of patients in defined risk groups.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation
  • [MeSH-minor] Animals. Child. Disease-Free Survival. Humans


84. Majeed F, Jadko S, Freedman MH, Dror Y: Mutation analysis of SBDS in pediatric acute myeloblastic leukemia. Pediatr Blood Cancer; 2005 Dec;45(7):920-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation analysis of SBDS in pediatric acute myeloblastic leukemia.
  • BACKGROUND: Shwachman-Diamond syndrome (SDS) is associated with a high risk of myelodysplasia, acute myeloid leukemia (AML), and chromosome 7 abnormalities.
  • Herein, we studied the role of genetic alterations in SBDS in AML.
  • PROCEDURE: DNA was extracted from marrows of SDS patients with AML, as well as from children with de novo AML.
  • To study whether SBDS heterozygosity confers a risk for MDS/AML, data on family members of SDS patients on the Canadian Inherited Marrow Failure Registry (CIMFR) was analyzed.
  • RESULTS: Of two SDS patients with SDS/AML one was homozygous 258 + 2T > C, and one was compound heterozygous 183-184TA > CT/258 + 2T > C.
  • To determine whether a subset of patients with SDS can present with AML, we analyzed 48 AML samples at remission, but no mutations were identified.
  • To address whether acquired mutated SBDS gene is associated with leukemic transformation in de novo AML, we analyzed 77 AML samples at diagnosis or relapse (4 with -7 and 7q-) for SBDS mutations; no alterations were detected.
  • Also, among the relatives of an SDS patient cohort on the registry no cases of MDS/AML were reported.
  • CONCLUSIONS: Common mutations occurred in our SDS patients who develop AML, and thus, AML is not confined to a rare genetic subgroup of SDS.
  • Newly diagnosed patients with AML are unlikely to have an underlying undiagnosed SDS.
  • Acquired SBDS gene mutations also would appear unlikely to play a mechanistic role in de novo AML, and might not be involved in the pathogenesis of chromosome 7 abnormalities as well.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Exons. Leukemia, Myeloid, Acute / genetics. Point Mutation. Proteins / genetics
  • [MeSH-minor] Bone Marrow Diseases / complications. Bone Marrow Diseases / genetics. Case-Control Studies. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Exocrine Pancreatic Insufficiency / complications. Exocrine Pancreatic Insufficiency / genetics. Heterozygote. Humans. Male. Osteochondrodysplasias / complications. Osteochondrodysplasias / genetics. Syndrome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16007594.001).
  • [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 / Proteins; 0 / SBDS protein, human
  •  go-up   go-down


85. Zhang JH, Zheng YC, Wang YX, Zhang JY, Liu ZG: Laboratory study on near-tetraploid acute myelogenous leukemia of childhood. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):263-6
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laboratory study on near-tetraploid acute myelogenous leukemia of childhood.
  • Near-tetraploidy is a rare cytogenetic abnormality in myelocytic malignancies in children, and its significance is unknown.
  • To investigate the characteristics of near-tetraploidy in a child with acute myelogenous leukemia (AML-M4), bone marrow smears were prepared for morphological analysis.
  • Combined with morphological and immunophenotypic results, AML-M4 was confirmed.
  • However, the duration achieving the remission in the child was longer than AML children with normal karyotype.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Polyploidy
  • [MeSH-minor] Bone Marrow Cells / pathology. Child. DNA, Neoplasm / analysis. Female. Humans. Immunophenotyping. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19374808.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


86. Liang DC, Chan TT, Lin KH, Lin DT, Lu MY, Chen SH, Liu HC, Lin MT, Lee MT, Shu SG, Chang TK, Chen JS, Hsiao CC, Hung IJ, Hsieh YL, Chen RL, Cheng SN, Chang WH, Lee CH, Lin KS: Improved treatment results for childhood acute myeloid leukemia in Taiwan. Leukemia; 2006 Jan;20(1):136-41
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved treatment results for childhood acute myeloid leukemia in Taiwan.
  • To improve treatment results for children with de novo acute myeloid leukemia (AML), we introduced a novel protocol, Taiwan Pediatric Oncology Group-AML-97A, for AML other than acute promyelocytic leukemia (APL), for which modified conventional protocols were used.
  • From January 1, 1997, to December 31, 2002, 141 children younger than 17 years old with de novo AML were enrolled.
  • In total, 117 patients with non-APL AML were treated with induction therapy of idarubicin and cytarabine (Ara-C), postremission therapy with high-dose Ara-C - containing regimens for four monthly courses, and moderate-dose therapy with idarubicin and Ara-C for four monthly courses.
  • The remission rate in the AML-97A study was 90%, the 5-year survival 51 +/- 5.3% (s.e.) and the 5-year event-free survival 50 +/- 4.8%; for APL, these were 100%, 86 +/- 7.0, and 75 +/- 9.8%.
  • The AML-97A regimen was well tolerated.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Leukemia, Promyelocytic, Acute / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Remission Induction. Taiwan. 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 = 16281075.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


87. Walter RB, Alonzo TA, Gerbing RB, Ho PA, Smith FO, Raimondi SC, Hirsch BA, Gamis AS, Franklin JL, Hurwitz CA, Loken MR, Meshinchi S: High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group. J Clin Oncol; 2010 Jun 10;28(17):2831-8
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group.
  • PURPOSE: To evaluate the prognostic significance of the integrin cell adhesion molecule very late antigen-4 (VLA-4) in acute myeloid leukemia (AML).
  • Subgroup analyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with standard-risk AML, in whom low VLA-4 expression was associated with inferior DFS (34% +/- 16% v 69% +/- 14% for high expression; P = .011) and higher RR (61% +/- 16% v 26% +/- 14% for high expression; P = .009).
  • CONCLUSION: High VLA-4 expression is associated with better clinical outcome in pediatric AML and is an independent predictor of relapse that may refine our abilities to stratify patients without identifiable cytogenetic or molecular risk 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. 2001 Apr 1;97(7):2121-9 [11264180.001]
  • [Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):579-89 [12899713.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3125-32 [7693037.001]
  • [Cites] Leukemia. 1996 Apr;10(4):682-6 [8618447.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3008-17 [19636064.001]
  • [Cites] Nat Rev Immunol. 2007 Sep;7(9):678-89 [17717539.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]
  • [Cites] Blood. 2009 Jan 22;113(4):866-74 [18927435.001]
  • [Cites] Annu Rev Immunol. 2009;27:339-62 [19302044.001]
  • [Cites] Leuk Res. 2009 Jun;33(6):764-8 [19042019.001]
  • [Cites] Genome Biol. 2007;8(5):215 [17543136.001]
  • (PMID = 20421533.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha4beta1
  • [Other-IDs] NLM/ PMC2903318
  •  go-up   go-down


88. Nilsson B, Andersson A, Johansson M, Fioretos T: Cross-platform classification in microarray-based leukemia diagnostics. Haematologica; 2006 Jun;91(6):821-4
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-platform classification in microarray-based leukemia diagnostics.
  • As proof-of-principle, we performed cross-platform classification of acute myeloid leukemia and childhood acute lymphoblastic leukemia using expression data from four different facilities.
  • [MeSH-major] Leukemia / classification. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16769585.001).
  • [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
  •  go-up   go-down


89. Tsukimoto I, Tawa A, Horibe K, Tabuchi K, Kigasawa H, Tsuchida M, Yabe H, Nakayama H, Kudo K, Kobayashi R, Hamamoto K, Imaizumi M, Morimoto A, Tsuchiya S, Hanada R: Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia: the AML99 trial from the Japanese Childhood AML Cooperative Study Group. J Clin Oncol; 2009 Aug 20;27(24):4007-13
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia: the AML99 trial from the Japanese Childhood AML Cooperative Study Group.
  • PURPOSE: To improve the prognosis in children with newly diagnosed acute myeloid leukemia (AML) by introducing a dose-dense intensive chemotherapy regimen and an appropriate risk stratification system.
  • PATIENTS AND METHODS: Two hundred forty children with de novo AML were treated with continuous cytarabine-based induction therapy and stratified to three risk groups based on the initial treatment response, age, and WBC at diagnosis and cytogenetics.
  • CONCLUSION: A high survival rate, 75.6% at 5 years, was achieved for childhood with de novo AML in the AML99 trial.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Transplantation, Homologous


90. Kurt B, Flynn P, Shenep JL, Pounds S, Lensing S, Ribeiro RC, Pui CH, Razzouk BI, Rubnitz JE: Prophylactic antibiotics reduce morbidity due to septicemia during intensive treatment for pediatric acute myeloid leukemia. Cancer; 2008 Jul 15;113(2):376-82
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prophylactic antibiotics reduce morbidity due to septicemia during intensive treatment for pediatric acute myeloid leukemia.
  • METHODS: The authors reviewed outcomes of 78 evaluable patients who were consecutively treated for acute myeloid leukemia (AML) from October 2002 through January 2007.
  • CONCLUSIONS: Prophylaxis with intravenous cefepime or a vancomycin regimen, and voriconazole, reduced morbidity in children with AML, and resulted in dramatic decreases in the incidence of septicemia and hospitalization days.
  • [MeSH-major] Antibiotic Prophylaxis. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Sepsis / drug therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Sepsis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18459178.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; 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
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


91. de Jonge HJ, Weidenaar AC, Ter Elst A, Boezen HM, Scherpen FJ, Bouma-Ter Steege JC, Kaspers GJ, Goemans BF, Creutzig U, Zimmermann M, Kamps WA, de Bont ES: Endogenous vascular endothelial growth factor-C expression is associated with decreased drug responsiveness in childhood acute myeloid leukemia. Clin Cancer Res; 2008 Feb 1;14(3):924-30
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endogenous vascular endothelial growth factor-C expression is associated with decreased drug responsiveness in childhood acute myeloid leukemia.
  • PURPOSE: We hypothesized that downstream effects of endogenous vascular endothelial growth factor (VEGF)/VEGF receptor signaling on acute myelogenous leukemia (AML) cell survival resulted in increased in vitro cellular drug resistance and a longer time to kill most leukemic cells in vivo upon drug exposure.
  • EXPERIMENTAL DESIGN: In primary AML cells from pediatric patients, VEGFA and VEGFC mRNA expression and in vitro cellular resistance to nine cytotoxic drugs were studied.
  • As in vivo equivalents for in vitro drug resistance, in vivo AML blast reduction upon drug exposure, measured as blast cell reduction on day 15 in the bone marrow and as time in days from diagnosis to complete remission (CR) were used.
  • RESULTS: Increased endogenous VEGFC levels significantly correlated with increased in vitro resistance for six typical AML drugs in primary AML cells from pediatric patients.
  • CONCLUSIONS: These results suggest for the first time that higher endogenous VEGFC levels of AML cells are related to decreased in vitro and in vivo drug responsiveness.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Vascular Endothelial Growth Factor C / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Female. Humans. Infant. Karyotyping. Male. RNA, Messenger / genetics. Risk Assessment. Treatment Outcome. Vascular Endothelial Growth Factor A / genetics

  • 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 = 18245556.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
  •  go-up   go-down


92. Tajeddine N, Louis M, Vermylen C, Gala JL, Tombal B, Gailly P: Tumor associated antigen PRAME is a marker of favorable prognosis in childhood acute myeloid leukemia patients and modifies the expression of S100A4, Hsp 27, p21, IL-8 and IGFBP-2 in vitro and in vivo. Leuk Lymphoma; 2008 Jun;49(6):1123-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor associated antigen PRAME is a marker of favorable prognosis in childhood acute myeloid leukemia patients and modifies the expression of S100A4, Hsp 27, p21, IL-8 and IGFBP-2 in vitro and in vivo.
  • We also demonstrated that PRAME overexpression induced the repression of three genes (Hsp27, S100A4 and p21) associated with an unfavorable prognosis in leukemia.
  • In a series of 28 acute myeloid leukemia pediatric patients, we observed that PRAME expression was associated with an increased leukemia-free survival.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Heat-Shock Proteins / metabolism. Insulin-Like Growth Factor Binding Protein 2 / metabolism. Interleukin-8 / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. S100 Proteins / metabolism
  • [MeSH-minor] Child. Gene Expression Profiling. HSP27 Heat-Shock Proteins. Humans. In Vitro Techniques. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Small Interfering / pharmacology

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 18452107.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Interleukin-8; 0 / Neoplasm Proteins; 0 / PRAME protein, human; 0 / RNA, Small Interfering; 0 / S100 Proteins; 142662-27-9 / S100A4 protein, human
  •  go-up   go-down


93. Children's Oncology Group, Aplenc R, Alonzo TA, Gerbing RB, Smith FO, Meshinchi S, Ross JA, Perentesis J, Woods WG, Lange BJ, Davies SM: Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group. Blood; 2006 Jul 1;108(1):74-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group.
  • We evaluated differences in outcome by ethnicity among children with acute myeloid leukemia (AML).
  • In conclusion, Hispanic and black children with AML have worse survival than white children.
  • Access to chemotherapy, differences in supportive care or leukemia phenotype, and reduced compliance are unlikely explanations for this difference because therapy was given intravenously according to CCG protocols.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Transplant Proc. 1991 Oct;23(5):2531-2 [1926465.001]
  • [Cites] Blood. 1984 Mar;63(3):694-700 [6696996.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2644-51 [9215836.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Biol Blood Marrow Transplant. 2001;7(1):45-8 [11215698.001]
  • [Cites] J Clin Oncol. 2001 May 15;19(10):2705-13 [11352963.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1957-64 [12200352.001]
  • [Cites] Arch Intern Med. 2002 Sep 23;162(17):1985-93 [12230422.001]
  • [Cites] Am J Hematol. 2003 Feb;72(2):127-34 [12555217.001]
  • [Cites] N Engl J Med. 2003 Mar 20;348(12):1166-70 [12646675.001]
  • [Cites] N Engl J Med. 2003 Mar 20;348(12):1170-5 [12646676.001]
  • [Cites] N Engl J Med. 2003 Jun 19;348(25):2581-2; author reply 2581-2 [12815151.001]
  • [Cites] N Engl J Med. 2003 Jun 19;348(25):2581-2; author reply 2581-2 [12816115.001]
  • [Cites] Curr Oncol Rep. 2003 Nov;5(6):489-97 [14521808.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2008-14 [14559954.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4036-42 [14976037.001]
  • [Cites] JAMA. 1995 Feb 22;273(8):633-7 [7844873.001]
  • (PMID = 16537811.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1 U10 CA98413-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1895824
  •  go-up   go-down


94. Dluzniewska A, Balwierz W, Armata J, Balcerska A, Chybicka A, Kowalczyk J, Matysiak M, Ochocka M, Radwanska U, Rokicka-Milewska R, Sonta-Jakimczyk D, Wachowiak J, Wysocki M: Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia. Leukemia; 2005 Dec;19(12):2117-24
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia.
  • Until 1983, results of treatment of acute myelogenous leukemia (AML) in Poland with different regimens were very poor.
  • In 1983, the Polish Pediatric Leukemia/Lymphoma Study Group introduced a unified treatment protocol--a modified version of BFM-83 protocol.
  • This led to an increase in the curability of AML from 15% to approximately 32%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Transplantation. Cause of Death. Child. Child, Preschool. Cytarabine / administration & dosage. Female. Follow-Up Studies. Humans. Idarubicin / therapeutic use. Infant. Infant, Newborn. Male. Poland. Remission Induction / methods. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107894.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


95. Lehrnbecher T, Zimmermann M, Reinhardt D, Dworzak M, Stary J, Creutzig U: Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia. Blood; 2007 Feb 1;109(3):936-43
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia.
  • Children with acute myelogenous leukemia (AML) have a high risk of infectious complications that might be reduced by prophylactic granulocyte colony-stimulating factor (G-CSF).
  • However, G-CSF could induce AML blast proliferation.
  • The prospective randomized trial AML-BFM 98 investigated the impact of G-CSF on hematopoetic recovery and infectious complications (primary endpoints) and on outcome (secondary endpoint) in children (aged 0-18 years) with de novo AML.
  • Between 1998 and 2003, 161 children with AML were randomized to receive G-CSF after inductions 1 and 2, whereas 156 patients were assigned to the control group.
  • Since G-CSF does not influence the risk of infectious complications or outcome in children undergoing therapy for AML, one cannot advocate the routine use of G-CSF in this patient group.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Cell Proliferation / drug effects. Child. Child, Preschool. Disease-Free Survival. Hematopoiesis / drug effects. Humans. Infant. Infection / drug therapy. Infection / mortality. Infection Control. Neutropenia. Premedication. Remission Induction. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17008536.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


96. 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
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [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.
  • [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


97. Balgobind BV, Zwaan CM, Reinhardt D, Arentsen-Peters TJ, Hollink IH, de Haas V, Kaspers GJ, de Bont ES, Baruchel A, Stary J, Meyer C, Marschalek R, Creutzig U, den Boer ML, Pieters R, van den Heuvel-Eibrink MM: High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome. Leukemia; 2010 Dec;24(12):2048-55
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome.
  • Translocations involving the mixed lineage leukemia (MLL) gene, localized at 11q23, frequently occur in pediatric acute myeloid leukemia (AML).
  • To unravel the latter, we used microarrays to generate gene expression profiles of 245 pediatric AML cases, including 53 MLL-rearranged cases.
  • Patients with high BRE expression showed a significantly better 3-year relapse-free survival (pRFS) (80±13 vs 30±10%, P=0.02) within MLL-rearranged AML cases.
  • Moreover, multivariate analysis identified high BRE expression as an independent favorable prognostic factor within pediatric AML for RFS (HR=0.2, P=0.04).
  • In conclusion, overexpression of the BRE gene is predominantly found in MLL-rearranged AML with t(9;11)(p22;q23).
  • Although further investigation for the role of BRE in leukemogenesis and outcome is warranted, high BRE expression is an independent prognostic factor for pRFS in pediatric AML.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20861917.001).
  • [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 / BRE protein, human; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


98. Balgobind BV, Raimondi SC, Harbott J, Zimmermann M, Alonzo TA, Auvrignon A, Beverloo HB, Chang M, Creutzig U, Dworzak MN, Forestier E, Gibson B, Hasle H, Harrison CJ, Heerema NA, Kaspers GJ, Leszl A, Litvinko N, Nigro LL, Morimoto A, Perot C, Pieters R, Reinhardt D, Rubnitz JE, Smith FO, Stary J, Stasevich I, Strehl S, Taga T, Tomizawa D, Webb D, Zemanova Z, Zwaan CM, van den Heuvel-Eibrink MM: Novel prognostic subgroups in childhood 11q23/MLL-rearranged acute myeloid leukemia: results of an international retrospective study. Blood; 2009 Sep 17;114(12):2489-96
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel prognostic subgroups in childhood 11q23/MLL-rearranged acute myeloid leukemia: results of an international retrospective study.
  • Translocations involving chromosome 11q23 frequently occur in pediatric acute myeloid leukemia (AML) and are associated with poor prognosis.
  • We retrospectively collected outcome data of 756 children with 11q23- or MLL-rearranged AML from 11 collaborative groups to identify differences in outcome based on translocation partners.
  • The event-free survival of 11q23/MLL-rearranged pediatric AML at 5 years from diagnosis was 44% (+/- 5%), with large differences across subgroups (11% +/- 5% to 92% +/- 5%).
  • We identified large differences in outcome within 11q23/MLL-rearranged pediatric AML and novel subgroups based on translocation partners that independently predict clinical outcome.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):14-22 [10738298.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2302-9 [11981001.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3352-60 [12384437.001]
  • [Cites] Br J Haematol. 2003 Jul;122(2):217-25 [12846889.001]
  • [Cites] J Clin Oncol. 2004 Aug 15;22(16):3432-3 [15310791.001]
  • [Cites] Cancer. 2004 Sep 15;101(6):1420-7 [15368330.001]
  • [Cites] Cancer Res. 1995 Oct 1;55(19):4220-4 [7671224.001]
  • [Cites] Int J Hematol. 1997 Jul;66(1):103-10 [9220666.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4532-8 [9373264.001]
  • [Cites] Leukemia. 1998 May;12(5):792-800 [9593283.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3058-63 [15217837.001]
  • [Cites] Br J Haematol. 2005 Apr;129(2):189-98 [15813846.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2043-53 [16107897.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2082-9 [16121218.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2054-62 [16136168.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2030-42 [16304570.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Mol Cancer Ther. 2008 Oct;7(10):3160-8 [18852119.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1490-9 [19262598.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jan;48(1):10-5 [16642489.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4641-7 [17299091.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [CommentIn] Blood. 2009 Sep 17;114(12):2365-6 [19762500.001]
  • (PMID = 19528532.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [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
  • [Other-IDs] NLM/ PMC2927031
  •  go-up   go-down


99. Yeh TC, Liu HC, Wang LY, Chen SH, Lin WY, Liang DC: The development of a novel protocol for the treatment of de novo childhood acute myeloid leukemia in a single institution in Taiwan. J Pediatr Hematol Oncol; 2007 Dec;29(12):826-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The development of a novel protocol for the treatment of de novo childhood acute myeloid leukemia in a single institution in Taiwan.
  • From November 1, 1995 to July 31, 2004, 49 children with de novo acute myeloid leukemia (AML) were treated at our institution.
  • In total, 48 patients with de novo AML were enrolled in this study.
  • Forty-two patients with AML other than acute promyelocytic leukemia (non-APL) were treated consecutively with 2 novel protocols: Mackay Memorial Hospital (MMH)-AML-96, designed as a pilot phase, and Taiwan Pediatric Oncology Group (TPOG)-AML-97A, on the basis of MMH-AML-96 with minor modifications.
  • The 5-year overall survival was 64%+/-6.9% (SE), and the 5-year event-free survival was 60%+/-7.1%; for non-APL AML, the rates were 62%+/-7.5% and 59%+/-7.6%; for APL, 83+/-15.2 and 67+/-19.3%.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Child. Child, Preschool. Drug Administration Schedule. Female. Humans. Infant. Male. Survival Rate. Survivors. Taiwan


100. Simmons HM, Ruis BL, Kapoor M, Hudacek AW, Conklin KF: Identification of NOM1, a nucleolar, eIF4A binding protein encoded within the chromosome 7q36 breakpoint region targeted in cases of pediatric acute myeloid leukemia. Gene; 2005 Feb 28;347(1):137-45
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of NOM1, a nucleolar, eIF4A binding protein encoded within the chromosome 7q36 breakpoint region targeted in cases of pediatric acute myeloid leukemia.
  • In this report, we describe the characterization of a novel MIF4G/MA3 family member called NOM1 (nucleolar protein with MIF4G domain 1) that was identified at the chromosome 7q36 breakpoint involved in 7;12 translocations associated with certain acute leukemias of childhood.
  • [MeSH-major] Chromosomes, Human, Pair 7 / genetics. Eukaryotic Initiation Factor-4A / metabolism. Exons / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. RNA-Binding Proteins / genetics






Advertisement