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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
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  • [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

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  • (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
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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
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  • [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

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  • (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
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3. 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
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  • [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.

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  • (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
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4. 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
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  • [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

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  • (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
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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
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  • [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

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  • (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
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6. Kaspers GJ, Zwaan CM: Pediatric acute myeloid leukemia: towards high-quality cure of all patients. Haematologica; 2007 Nov;92(11):1519-32
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  • [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

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  • (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
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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

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  • (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
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8. 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
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  • [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

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  • (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
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9. Radhi M, Meshinchi S, Gamis A: Prognostic factors in pediatric acute myeloid leukemia. Curr Hematol Malig Rep; 2010 Oct;5(4):200-6
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  • [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

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

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  • (PMID = 17301520.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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11. Manola KN: Cytogenetics of pediatric acute myeloid leukemia. Eur J Haematol; 2009 Nov;83(5):391-405
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  • [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

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  • (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
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12. 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
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  • [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

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  • (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
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13. 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
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  • [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

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  • [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
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14. 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
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  • [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


15. 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.

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  • (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
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16. 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.

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  • (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
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17. 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.

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  • (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
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18. Ayan I, Kebudi R, Ozger H, Yaman Agaoglu F, Gorgun O, Bilgic B, Eralp L, Dizdar Y, Darendeliler E: Childhood osteosarcoma: Evaluation of 94 cases. A single institution study. J Clin Oncol; 2009 May 20;27(15_suppl):10040

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood osteosarcoma: Evaluation of 94 cases. A single institution study.
  • 26 patients died; 20 of disease, 5 of toxicity, and 1 of second malignancy (acute myeloid leukemia).
  • Our results demonstrate that the combination of epirubicin, cisplatin, and ifosfamide is an active and reasonably well-tolerated regimen for childhood osteosarcoma.

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  • (PMID = 27962466.001).
  • [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
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19. 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
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  • [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

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  • (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
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20. 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
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  • [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.

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  • (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
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21. Styczynski J: Drug resistance in childhood acute myeloid leukemia. Curr Pharm Biotechnol; 2007 Apr;8(2):59-75
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  • [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

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  • (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
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22. 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
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  • [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


23. 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--&gt;q23 approximately 24::q23 approximately 24--&gt;q43--&gt;neo--&gt;q43--&gt;qter) and tetrasomy of chromosomes 8 and 21. Cancer Genet Cytogenet; 2009 Sep;193(2):123-6
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  • [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


24. Brown P, Smith FO: Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date. Paediatr Drugs; 2008;10(2):85-92
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  • [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

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  • (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
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25. 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
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  • [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


26. 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
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  • [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


27. 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
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  • [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

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  • [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
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28. 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
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  • [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

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  • [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
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29. 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
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  • [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

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  • (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
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30. 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
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  • [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


31. 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
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  • [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

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  • (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
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32. 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
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  • [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

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  • [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
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33. 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
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  • [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.

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  • (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
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34. 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
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  • [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


35. 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
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  • [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

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  • (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
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36. 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
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  • [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.

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  • (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
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37. 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
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  • [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.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (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
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38. 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
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  • [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


39. ter Bals E, Kaspers GJ: Treatment of childhood acute myeloid leukemia. Expert Rev Anticancer Ther; 2005 Oct;5(5):917-29
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  • [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

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  • (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
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40. Sung KW, Choi J, Hwang YK, Lee SJ, Kim HJ, Kim JY, Cho EJ, Yoo KH, Koo HH: Overexpression of X-linked inhibitor of apoptosis protein (XIAP) is an independent unfavorable prognostic factor in childhood de novo acute myeloid leukemia. J Korean Med Sci; 2009 Aug;24(4):605-13
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  • [Title] Overexpression of X-linked inhibitor of apoptosis protein (XIAP) is an independent unfavorable prognostic factor in childhood de novo acute myeloid leukemia.
  • This study was performed to investigate the prognostic relevance of XIAP expression in childhood acute myeloid leukemia (AML).
  • In 53 children with de novo AML, the level of XIAP expression was determined by using quantitative reverse transcriptase-polymerase chain reaction and was analyzed with respect to the clinical characteristics at diagnosis and treatment outcomes.
  • Collectively, XIAP overexpression may be used as an unfavorable prognostic marker in childhood AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. X-Linked Inhibitor of Apoptosis Protein / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Male. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 19654940.001).
  • [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] 0 / X-Linked Inhibitor of Apoptosis Protein
  • [Other-IDs] NLM/ PMC2719207
  • [Keywords] NOTNLM ; Apoptosis / Inhibitor of Apoptosis Protein / Leukemia, Myeloid, Acute / X-Linked Inhibitor of Apoptosis Protein
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41. Zou Y, Wang H, Chen XJ, Wang SC, Zhang L, Chen YM, Zhu XF: [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Sep;27(9):621-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia].
  • OBJECTIVE: To analyse the clinical outcome and the prognostic factor of childhood acute myeloid leukemia (AML).
  • METHODS: Disease-free survival (DFS), event-free survival (EFS) and overall survival (OS) rates were estimated by Kaplan-Meier method and prognostic factors were evaluated by Cox regression with SPSS in 141 childhood AML in our hospital from August 1995 to July 2004.
  • The patients were divided into 2 groups: acute promyelocytic leukemia (APL) as group A and AML other than APL as group B.
  • The cumulative 5 year DFS and OS rate for group B patients were (28.4 +/- 9.0)% and (35.5 +/- 6.3)%, the 51 group A patients were (94.3 +/- 4.0)% and (81.4 +/- 5.7)%, and for total 141 AML patients were (56.9 +/- 6.3)% and (53.3 +/- 4.8)% respectively.
  • Multivariate analysis demonstrated that higher bone marrow blast cell percentage at diagnosis, CR after more than one course of chemotherapy and less than six courses of consolidation chemotherapy were risk prognostic factors in childhood AML other than APL (P < 0.05).
  • CONCLUSION: The prognosis of childhood APL is better, while of childhood t(8;21) AML is no better than other FAB subtypes.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Prognosis. Regression Analysis. Retrospective Studies. Treatment Outcome

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  • (PMID = 17278430.001).
  • [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] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
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42. 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
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  • [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

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  • [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
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43. 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
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  • [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

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  • (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
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44. 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
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  • [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

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  • [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
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45. 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
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  • [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

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  • (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
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46. 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
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  • [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


47. 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
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  • [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

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  • (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
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48. Hasle H, Alonzo TA, Auvrignon A, Behar C, Chang M, Creutzig U, Fischer A, Forestier E, Fynn A, Haas OA, Harbott J, Harrison CJ, Heerema NA, van den Heuvel-Eibrink MM, Kaspers GJ, Locatelli F, Noellke P, Polychronopoulou S, Ravindranath Y, Razzouk B, Reinhardt D, Savva NN, Stark B, Suciu S, Tsukimoto I, Webb DK, Wojcik D, Woods WG, Zimmermann M, Niemeyer CM, Raimondi SC: Monosomy 7 and deletion 7q in children and adolescents with acute myeloid leukemia: an international retrospective study. Blood; 2007 Jun 1;109(11):4641-7
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  • [Title] Monosomy 7 and deletion 7q in children and adolescents with acute myeloid leukemia: an international retrospective study.
  • Monosomy 7 (-7) and deletion 7q del(7q)] are rare in childhood acute myeloid leukemia (AML).
  • We retrospectively collected data on 258 children with AML or refractory anemia with excess blasts in transformation (RAEB-T) and -7 or del(7q) with or without other cytogenetic aberrations +/- other].
  • Cytogenetic aberrations considered favorable in AML (8;21)(q22;q22), inv(16)(p13q22), t(15;17)(q22;q21), t(9;11)(p22;q23)] (n = 24) were strongly associated with del(7q) and a higher 5-year survival rate compared with del(7q) without favorable cytogenetics (75% versus 46%, P = .03).
  • Childhood AML with chromosome 7 aberrations represents a heterogeneous group of disorders with additional cytogenetic aberrations having a major prognostic impact which should be reflected in future risk-group stratification.
  • [MeSH-major] Chromosomes, Human, Pair 7. Gene Deletion. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Monosomy
  • [MeSH-minor] Adolescent. Child. Chromosome Aberrations. Female. Humans. International Cooperation. Male. Remission Induction. Retrospective Studies. Stem Cell Transplantation. Translocation, Genetic

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  • (PMID = 17299091.001).
  • [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
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49. 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
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  • [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.

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  • [Copyright] ©2010 AACR.
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  • (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
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50. Lee DH, Chung NG, Cho B, Kim HK, Kang HJ, Shin HY, Ahn HS, Yoo KH, Sung KW, Koo HH, Kook H, Hwang TJ, Im HJ, Seo JJ, Park HJ: Idarubicin plus behenoyl cytarabine and 6-thioguanine compares favorably with idarubicin plus cytarabine-based regimen for children with previously untreated acute myeloid leukemia: 10-year retrospective, multicenter study in Korea. J Korean Med Sci; 2010 Jan;25(1):9-15
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  • [Title] Idarubicin plus behenoyl cytarabine and 6-thioguanine compares favorably with idarubicin plus cytarabine-based regimen for children with previously untreated acute myeloid leukemia: 10-year retrospective, multicenter study in Korea.
  • We investigated the outcome of idarubicin plus N(4)-behenoyl-1-beta-D-arabinofuranosyl cytosine (BHAC)-based chemotherapy (BHAC group, n=149) compared to idarubicin plus cytarabine-based chemotherapy (cytarabine group, n=191) for childhood acute myeloid leukemia (AML).
  • Between January 1996 and December 2005, 340 children with AML from 5 university hospitals in Korea received the BHAC-based or cytarabine-based chemotherapy, with or without hematopoietic stem cell transplantation.
  • In the present study, the clinical outcomes of the BHAC-based chemotherapy, consisting of BHAC, idarubicin, and 6-TG, are comparable to that of the cytarabine-based chemotherapy for childhood AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / analogs & derivatives. Cytarabine / therapeutic use. Idarubicin / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Thioguanine / therapeutic use
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Cytogenetics. Female. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Male. Republic of Korea. Retrospective Studies. Survival Analysis. Young Adult

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  • (PMID = 20052341.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 9YVR68W306 / enocitabine; FTK8U1GZNX / Thioguanine; ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ PMC2800026
  • [Keywords] NOTNLM ; Childhood / Enocitabine / Leukemia, Myeloid, Acute
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51. 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
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  • [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.

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  • (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)
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52. 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
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  • [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


53. von Neuhoff C, Reinhardt D, Sander A, Zimmermann M, Bradtke J, Betts DR, Zemanova Z, Stary J, Bourquin JP, Haas OA, Dworzak MN, Creutzig U: Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98. J Clin Oncol; 2010 Jun 1;28(16):2682-9
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  • [Title] Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98.
  • PURPOSE: Because cytogenetic data are essential for risk stratification of childhood acute myeloid leukemia (AML), the impact of chromosomal aberrations is crucial.
  • PATIENTS AND METHODS: Data of a large group of patients younger than 18 years treated according to study AML-Berlin-Frankfurt-Münster (BFM) 98 (n = 454), including their cytogenetics, were analyzed.
  • CONCLUSION: Because the prognostic value of rare recurrent chromosomal aberrations still has to be elucidated, these data will contribute to future risk stratification for the treatment of pediatric AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Combined Modality Therapy. Confidence Intervals. Cytarabine / administration & dosage. Cytogenetic Analysis. Disease-Free Survival. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Idarubicin / administration & dosage. In Situ Hybridization, Fluorescence. Male. Probability. Proportional Hazards Models. Radiotherapy, Adjuvant. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Severity of Illness Index. Statistics, Nonparametric. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 20439630.001).
  • [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] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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54. 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
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  • [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

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  • (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
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55. 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
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  • [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

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  • (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
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56. 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
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  • [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


57. Latino-Martel P, Chan DS, Druesne-Pecollo N, Barrandon E, Hercberg S, Norat T: Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis. Cancer Epidemiol Biomarkers Prev; 2010 May;19(5):1238-60
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  • [Title] Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis.
  • BACKGROUND: Leukemia is the most frequently occurring cancer in children.
  • Although its etiology is largely unknown, leukemia is believed to result from an interaction between genetic and environmental factors.
  • METHODS: To assess the association between maternal alcohol consumption during pregnancy and childhood leukemia, a systematic review and meta-analysis of published studies was done.
  • Analyses were conducted by type of leukemia, children's age at diagnosis, and type of alcoholic beverage and trimester of pregnancy at alcohol use.
  • Alcohol intake during pregnancy (yes versus no) was statistically significantly associated with childhood acute myeloid leukemia (AML) [odds ratio (OR), 1.56; 95% confidence interval (CI), 1.13-2.15] but not with acute lymphoblastic leukemia (OR, 1.10; 95% CI, 0.93-1.29).
  • The OR of AML for an increase of a drink per week was 1.24 (95% CI, 0.94-1.64).
  • The association of alcohol intake during pregnancy with AML was observed for cancers diagnosed at age 0 to 4 years (OR, 2.68; 95% CI, 1.85-3.89) in five studies without heterogeneity (I2<or=0.1%).
  • CONCLUSIONS: The results of case-control studies indicate that maternal alcohol consumption during pregnancy is associated with a significantly increased risk of AML in young children.
  • IMPACT: Avoidance of maternal alcohol drinking during pregnancy might contribute to a decrease in the risk of childhood AML.
  • [MeSH-major] Alcohol Drinking / adverse effects. Leukemia / chemically induced. Prenatal Exposure Delayed Effects
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Mothers. Pregnancy. Risk Factors. Young Adult

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  • [Copyright] Copyright (c) 2010 AACR
  • (PMID = 20447918.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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58. 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
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  • [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


59. Woods WG: Curing childhood acute myeloid leukemia (AML) at the half-way point: promises to keep and miles to go before we sleep. Pediatr Blood Cancer; 2006 May 1;46(5):565-9
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  • [Title] Curing childhood acute myeloid leukemia (AML) at the half-way point: promises to keep and miles to go before we sleep.
  • Childhood and adolescent acute myeloid leukemia (AML) is traditionally one of the hardest childhood cancers to successfully treat and had an overall survival well under 10% in the 1960s.
  • Some of the challenges that will lead to ongoing reduction of population-based mortality for AML through young adulthood include:.
  • (1) improving access of adolescents to pediatric AML therapy;.
  • (3) individualized therapy based on individual genetics and leukemia cell biology;.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Disease-Free Survival. Enzyme Inhibitors / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Remission Induction. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


60. 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
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  • [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

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  • (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
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61. 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
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  • [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.

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  • (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
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62. 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
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  • [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

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  • (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
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63. 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
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  • [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

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  • (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
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64. 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
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  • [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


65. 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
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  • [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

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  • (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
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66. Haltrich I, Kost-Alimova M, Kovács G, Kriván G, Dobos M, Imreh S, Fekete G: [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia]. Magy Onkol; 2005;49(2):141-7
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  • [Title] [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia].
  • [Transliterated title] A "3q21q26-szindróma" azonosítása sokpontos interfázis-FISH vizsgálattal gyermekkori myeloid leukaemiában.
  • Cytogenetic syndrome involving bands 3q21 and 3q26, known as "3q21q26 syndrome" has been observed in adult patients with acute myelogenous leukemia (0.5-2%), chronic myelogenous leukemia in blast crisis (20%), myelodysplastic syndromes and myeloproliferative disorders.
  • In the present study bone marrow samples from two boys (12 and 16 years), diagnosed with CML and AML respectively, were investigated using conventional cytogenetic methods, interphase "multipoint" fluorescence in situ hybridization (FISH), dual color-FISH and multiplex FISH.
  • The "multipoint" FISH analysis identified in de novo childhood AML case an inv(3)(q21q26) and a complex 3q rearrangement including inversion and duplication in the CML case.
  • This syndrome is very rare in de novo childhood AML, and simultaneous presence of 3q inversion and duplication, to our knowledge, has not yet been identified in hematological malignancies.
  • [MeSH-major] Chromosomes, Human, Pair 3. Gene Rearrangement. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Bone Marrow. Child. Gene Duplication. Humans. Male. Syndrome

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  • (PMID = 16249810.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
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67. 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
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  • [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

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  • [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
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68. 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
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  • [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

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  • (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
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69. 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
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  • [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

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  • (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
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70. 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
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  • [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.

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  • (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
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71. 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

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  • [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
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72. Shimada A, Taki T, Tabuchi K, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y: KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group. Blood; 2006 Mar 1;107(5):1806-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group.
  • Patients with t(8;21) acute myeloid leukemia (AML) are considered to have a good prognosis; however, approximately 50% of them relapse.
  • The genetic alterations associated with a poor outcome in t(8;21) AML remain unknown.
  • Recently, aberrations of receptor tyrosine kinases (RTKs) were frequently found in patients with AML.
  • However, the prevalence and prognostic impact of RTK aberrations in pediatric t(8;21) AML remains undetermined.
  • Here, we found the kinase domain mutations of the KIT gene in 8 (17.4%) of 46 patients with t(8;21) AML among newly diagnosed pediatric patients with AML treated on the AML99 protocol in Japan.
  • These results suggested that KIT mutations are strongly associated with a poor prognosis in pediatric t(8;21) AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Child. DNA Mutational Analysis / methods. Disease-Free Survival. Female. Humans. Infant. Male. Prevalence. Prognosis


73. 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
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  • [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

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  • (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
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74. 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
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  • [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

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  • (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
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75. Nilsson B, Andersson A, Johansson M, Fioretos T: Cross-platform classification in microarray-based leukemia diagnostics. Haematologica; 2006 Jun;91(6):821-4
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  • [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

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  • (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
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76. 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
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  • [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

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  • (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
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77. 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
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  • [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

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  • (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
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78. Bakhshi S, Singh P, Swaroop C: Outpatient consolidation chemotherapy in pediatric acute myeloid leukemia: a retrospective analysis. Hematology; 2009 Oct;14(5):255-60
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  • [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

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  • (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
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79. 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
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  • [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

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  • [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
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80. 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
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  • [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.

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  • (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
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81. 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
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  • [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.

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  • (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
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82. Meshinchi S, Arceci RJ: Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia. Oncologist; 2007 Mar;12(3):341-55
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  • [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

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  • (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
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83. 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.

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  • (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
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84. 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
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  • [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

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  • (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
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85. 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
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  • [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

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  • [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
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86. 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
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  • [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


87. 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
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  • [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

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  • (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
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88. Harrison CJ, Hills RK, Moorman AV, Grimwade DJ, Hann I, Webb DK, Wheatley K, de Graaf SS, van den Berg E, Burnett AK, Gibson BE: Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12. J Clin Oncol; 2010 Jun 1;28(16):2674-81
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  • [Title] Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.
  • PURPOSE: Karyotype is an independent indicator of prognosis in acute myeloid leukemia (AML) that is widely applied to risk-adapted therapy.
  • Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
  • PATIENTS AND METHODS: This cytogenetic study of 729 childhood patients classified them into 22 subgroups and evaluated their incidence and risk.
  • Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this childhood series.
  • CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Confidence Intervals. Cytogenetic Analysis. Disease-Free Survival. Female. Fluorescence. Genetic Predisposition to Disease / epidemiology. Great Britain. Humans. In Situ Hybridization. Infant. Kaplan-Meier Estimate. Karyotyping. Logistic Models. Male. Multivariate Analysis. Odds Ratio. Probability. Prognosis. Proportional Hazards Models. Registries. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome


89. 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
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  • [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

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  • [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
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90. Rubnitz JE, Inaba H, Ribeiro RC, Pounds S, Rooney B, Bell T, Pui CH, Leung W: NKAML: a pilot study to determine the safety and feasibility of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia. J Clin Oncol; 2010 Feb 20;28(6):955-9
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  • [Title] NKAML: a pilot study to determine the safety and feasibility of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.
  • PURPOSE To conduct a pilot study to determine the safety, feasibility, and engraftment of haploidentical natural killer (NK) cell infusions after an immunosuppressive regimen in children with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS Ten patients (0.7 to 21 years old) who had completed chemotherapy and were in first complete remission of AML were enrolled on the Pilot Study of Haploidentical Natural Killer Cell Transplantation for Acute Myeloid Leukemia (NKAML) study.
  • We propose to further investigate the efficacy of KIR-mismatched NK cells in a phase II trial as consolidation therapy to decrease relapse without increasing mortality in children with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotherapy. Killer Cells, Natural / transplantation. Leukemia, Myeloid, Acute / therapy. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Feasibility Studies. Female. Haplotypes. Humans. Infant. Interleukin-2 / administration & dosage. Male. Neoplasm Staging. Pilot Projects. Prognosis. Survival Rate. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult


91. Tosi S, Ballabio E, Teigler-Schlegel A, Boultwood J, Bruch J, Harbott J: Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia. Genes Chromosomes Cancer; 2005 Nov;44(3):225-32
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  • [Title] Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia.
  • Chromosome abnormalities of 6q are not frequently observed in myeloid disorders.
  • In this article, we report the incidence of these chromosome changes in childhood myeloid leukemia as 2%-4% based on the cytogenetic database of a single institution.
  • We applied fluorescence in situ hybridization (FISH) to characterize precisely the types of 6q abnormalities in seven patients (six with acute myeloid leukemia and one with myelodysplastic syndrome).
  • Among these, we identified a novel translocation, t(6;11)(q24.1;p15.5), in a patient with acute megakaryoblastic leukemia.
  • Further studies will aim to fully characterize C6orf80 and will elucidate the role of this new NUP98 fusion in myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Artificial, Bacterial. Cytogenetic Analysis. DNA, Neoplasm / analysis. Humans. In Situ Hybridization, Fluorescence. Infant. Molecular Sequence Data. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16028218.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / nuclear pore complex protein 98
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92. 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
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  • [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

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  • (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
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93. 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
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  • [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

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  • (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
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94. 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
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  • [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


95. 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
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  • [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

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  • (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
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96. Sung KW, Choi J, Hwang YK, Lee SJ, Kim HJ, Lee SH, Yoo KH, Jung HL, Koo HH: Overexpression of Apollon, an antiapoptotic protein, is associated with poor prognosis in childhood de novo acute myeloid leukemia. Clin Cancer Res; 2007 Sep 1;13(17):5109-14
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  • [Title] Overexpression of Apollon, an antiapoptotic protein, is associated with poor prognosis in childhood de novo acute myeloid leukemia.
  • This study was done to investigate the clinical relevance of the expression of Apollon in childhood de novo acute myeloid leukemia.
  • EXPERIMENTAL DESIGN: In 55 pediatric patients with de novo acute myeloid leukemia, the level of Apollon expression was determined by using quantitative reverse transcriptase-PCR and was analyzed with respect to the patients' clinical features and treatment outcomes.
  • CONCLUSION: This is the first study demonstrating the prognostic implication of the Apollon expression in human cancers, indicating that Apollon overexpression may be used as a poor prognostic marker in childhood acute myeloid leukemia through validation by further studies.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adolescent. Apoptosis. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Treatment Outcome

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  • (PMID = 17785565.001).
  • [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 / BIRC6 protein, human; 0 / Inhibitor of Apoptosis Proteins
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97. 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
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  • [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).

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  • [Copyright] 2010 Wiley-Liss, Inc.
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  • (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
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98. Tartaglia M, Martinelli S, Iavarone I, Cazzaniga G, Spinelli M, Giarin E, Petrangeli V, Carta C, Masetti R, Aricò M, Locatelli F, Basso G, Sorcini M, Pession A, Biondi A: Somatic PTPN11 mutations in childhood acute myeloid leukaemia. Br J Haematol; 2005 May;129(3):333-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic PTPN11 mutations in childhood acute myeloid leukaemia.
  • In a recent study of 69 children and adolescents with de novo acute myeloid leukaemia (AML), we documented a non-random distribution of PTPN11 mutations among French-American-British (FAB) subtypes.
  • Here, we report on the results of a molecular screening performed on 181 additional unselected patients, enrolled in participating institutions of the Associazione Italiana Ematologia Oncologia Pediatrica-AML Study Group, to provide a more accurate picture of the prevalence, spectrum and distribution of PTPN11 mutations in childhood AML and to investigate their clinical relevance.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Neoplasm Proteins / genetics. Protein Tyrosine Phosphatases / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Genes, ras / genetics. Humans. Infant. Intracellular Signaling Peptides and Proteins. Leukemia, Monocytic, Acute / blood. Leukemia, Monocytic, Acute / genetics. Leukocyte Count. Male. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. fms-Like Tyrosine Kinase 3. ras Proteins

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  • (PMID = 15842656.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP04172
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / KRAS protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.6.5.2 / ras Proteins
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99. Haltrich I, Kost-Alimova M, Kovács G, Klein G, Fekete G, Imreh S: Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28 childhood AML patients. Eur J Haematol; 2006 Feb;76(2):124-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28 childhood AML patients.
  • To examine chromosome 3 abnormalities, in 28 childhood acute myeloid leukemia bone marrow samples, we performed interphase multipoint-fluorescence in situ hybridization using 84 chromosome 3-specific probes and detected clonal chromosome 3 aberrations in nine cases, which is of a higher frequency than the previously reported one.
  • We identified rare structural rearrangements in childhood acute myeloblastic leukemia, involving 3q21 and 3q26 loci around RPN1 and MDS1/EVI1 respectively.
  • The poor outcome in pediatric patients with 3q rearrangements appears to be quite uniform.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3. In Situ Hybridization, Fluorescence / methods. Interphase. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 16405433.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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100. 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

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  • (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
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