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1. Frost BM, Forestier E, Gustafsson G, Nygren P, Hellebostad M, Jonsson OG, Kanerva J, Schmiegelow K, Larsson R, Lönnerholm G: Translocation t(12;21) is related to in vitro cellular drug sensitivity to doxorubicin and etoposide in childhood acute lymphoblastic leukemia. Blood; 2004 Oct 15;104(8):2452-7
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  • [Title] Translocation t(12;21) is related to in vitro cellular drug sensitivity to doxorubicin and etoposide in childhood acute lymphoblastic leukemia.
  • The t(12;21) (p13;q22) translocation resulting in ETV6/RUNX1 (previously named TEL/AML1) gene fusion is present in about 25% of children with precursor B-lineage acute lymphoblastic leukemia (B-ALL).
  • We successfully tested 275 precursor B-ALL samples from children aged 1 to 17 years to determine the relation between t(12;21) and in vitro cellular drug resistance, measured by the fluorometric microculture cytotoxicity assay (FMCA).
  • After matching for unevenly distributed patient characteristics, that is, excluding patients with high hyperdiploidy (> 51 chromosomes), t(9; 22), t(1;19), or 11q23 rearrangement, the ETV6/RUNX1(+) samples remained significantly more sensitive to doxorubicin (P = .001) and etoposide (P = .001).
  • For the other drugs tested (amsacrine, cytarabine, dexamethasone, prednisolone, vincristine, 6-thioguanine, and 4-hydroperoxy-cyclophosphamide), no significant difference in cellular drug sensitivity was found.
  • High throughput techniques should now be used to elucidate the cellular mechanisms by which ETV6/RUNX1 gene fusion is linked to increased sensitivity to these drugs.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 21 / genetics. Doxorubicin / pharmacology. Drug Resistance, Neoplasm / genetics. Etoposide / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Diploidy. Female. Gene Order. Humans. Infant. Male. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-ets. Repressor Proteins / genetics. Repressor Proteins / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 15217836.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin
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2. Brown P, Levis M, Shurtleff S, Campana D, Downing J, Small D: FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with high levels of FLT3 expression. Blood; 2005 Jan 15;105(2):812-20
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  • [Title] FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with high levels of FLT3 expression.
  • FMS-like tyrosine kinase 3 (FLT3) is almost universally expressed in B-precursor childhood acute lymphoblastic leukemia (ALL).
  • Cases of ALL with MLL gene rearrangements and those with high hyperdiploidy (> 50 chromosomes) express the highest levels of FLT3, and activating mutations of FLT3 occur in 18% of MLL-rearranged and 28% of hyperdiploid ALL cases.
  • Sensitivity to FLT3 inhibition was particularly high in samples with MLL gene rearrangements (82%, n = 11; P = .0005), high hyperdiploidy (100%, n = 5; P = .0007), and/or FLT3 mutations (100%, n = 4; P = .0021).
  • Clinical testing of CEP-701 as a novel molecularly targeted agent for the treatment of childhood ALL is warranted.
  • [MeSH-major] Carbazoles / pharmacology. Gene Expression Regulation, Leukemic. Indoles / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Age Factors. Apoptosis / drug effects. Child. DNA-Binding Proteins / genetics. Enzyme Inhibitors / pharmacology. Gene Rearrangement. Genotype. Histone-Lysine N-Methyltransferase. Humans. Infant. Myeloid-Lymphoid Leukemia Protein. Phenotype. Ploidies. Proto-Oncogenes / genetics. Transcription Factors / genetics. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3

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  • (PMID = 15374878.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA095600; United States / NCI NIH HHS / CA / CA60441; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCI NIH HHS / CA / CA91177
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbazoles; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; DO989GC5D1 / lestaurtinib; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; 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
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3. Appel IM, Kazemier KM, Boos J, Lanvers C, Huijmans J, Veerman AJ, van Wering E, den Boer ML, Pieters R: Pharmacokinetic, pharmacodynamic and intracellular effects of PEG-asparaginase in newly diagnosed childhood acute lymphoblastic leukemia: results from a single agent window study. Leukemia; 2008 Sep;22(9):1665-79
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  • [Title] Pharmacokinetic, pharmacodynamic and intracellular effects of PEG-asparaginase in newly diagnosed childhood acute lymphoblastic leukemia: results from a single agent window study.
  • L-asparaginase is an effective drug for treatment of children with acute lymphoblastic leukemia (ALL).
  • The in vivo window response was significantly related to immunophenotype and genotype: 26/38 common/pre B-ALL cases, especially those with hyperdiploidy and TELAML1 rearrangement, demonstrated a good clinical response compared to 8/17 T-ALL (P=0.01) and BCRABL-positive ALL (P=0.04).
  • After administration of one in vivo dose of PEG-asparaginase no changes in apoptotic parameters or in intracellular levels of twenty amino acids in leukemic cells could be measured, in contradiction to the changes found after in vitro exposure.
  • [MeSH-major] Asparaginase / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Amino Acids / analysis. Amino Acids / drug effects. Apoptosis / drug effects. Child. Genotype. Humans. Immunophenotyping. Polyethylene Glycols. Prognosis. Survival Analysis. Treatment Outcome


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4. Iwamoto S, Mihara K, Downing JR, Pui CH, Campana D: Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase. J Clin Invest; 2007 Apr;117(4):1049-57
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  • [Title] Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase.
  • Because of their low asparagine synthetase (ASNS) expression and asparagine biosynthesis, acute lymphoblastic leukemia (ALL) cells are exquisitely sensitive to asparagine depletion.
  • Consequently, asparaginase is a major component of ALL therapy, but the mechanisms regulating the susceptibility of leukemic cells to this agent are unclear.
  • In 288 children with ALL, cellular ASNS expression was more likely to be high in T-lineage ALL and low in B-lineage ALL with TEL-AML1 or hyperdiploidy.

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  • (PMID = 17380207.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA58297; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA058297; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7006-34-0 / Asparagine; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
  • [Other-IDs] NLM/ PMC1821067
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5. Chang P, Kang M, Xiao A, Chang J, Feusner J, Buffler P, Wiemels J: FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia. BMC Cancer; 2010 Sep 27;10:513
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  • [Title] FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia.
  • BACKGROUND: Mutations in FLT3 result in activated tyrosine kinase activity, cell growth stimulation, and a poor prognosis among various subtypes of leukemia.
  • We evaluated the prevalence and timing of origin of FLT3 mutations in a population series of childhood leukemia patients from Northern California.
  • METHODS: We screened and sequenced FLT3 mutations (point mutations and internal tandem duplications, ITDs) among 517 childhood leukemia patients, and assessed whether these mutations occurred before or after birth using sensitive "backtracking" methods.
  • Among AMLs, FLT3 mutations were more common in older patients, and among ALLs, FLT3 mutations were more common in patients with high hyperdiploidy (3.7%) than those without this cytogenetic feature (1.4%).

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  • (PMID = 20875128.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NIEHS NIH HHS / ES / P42ES0470; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / R01CA89032; United States / NIEHS NIH HHS / ES / R01ES09137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2955609
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6. Piloto O, Nguyen B, Huso D, Kim KT, Li Y, Witte L, Hicklin DJ, Brown P, Small D: IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples. Cancer Res; 2006 May 1;66(9):4843-51
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  • [Title] IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples.
  • The class III receptor tyrosine kinase FLT3 is expressed on the blasts of >90% of patients with B-lineage acute lymphoblastic leukemias (ALL).
  • In addition, it is expressed at extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy and is sometimes mutated in these same patients.
  • Through antibody-dependent, cell-mediated cytotoxicity, such an antibody could still prove efficacious against leukemia cells in vivo.
  • Therefore, such an antibody, either naked or conjugated to radioactive isotopes or cytotoxic agents, may prove useful in the therapy of infant ALL as well as childhood and adult ALL patients whose blasts typically express FLT3.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Child. Cytotoxicity, Immunologic. Female. Humans. Immunization, Passive / methods. Killer Cells, Natural / immunology. Male. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Signal Transduction / drug effects

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  • (PMID = 16651440.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCRR NIH HHS / RR / RR00171
  • [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 / Antibodies, Monoclonal; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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7. Usvasalo A, Räty R, Knuutila S, Vettenranta K, Harila-Saari A, Jantunen E, Kauppila M, Koistinen P, Parto K, Riikonen P, Salmi TT, Silvennoinen R, Elonen E, Saarinen-Pihkala UM: Acute lymphoblastic leukemia in adolescents and young adults in Finland. Haematologica; 2008 Aug;93(8):1161-8
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  • [Title] Acute lymphoblastic leukemia in adolescents and young adults in Finland.
  • BACKGROUND: Interest has recently been paid to adolescents and young adults with acute lymphoblastic leukemia, particularly because all reports so far published indicate that these patients have a better outcome when treated with pediatric rather than adult therapeutic protocols.
  • There are different biological subtypes of acute lymphoblastic leukemia with distinct features and prognoses; the distribution of these subtypes is not well known among adolescents.
  • We, therefore, studied acute lymphoblastic leukemia in adolescents and young adults aged 10 to 25 years in Finland.
  • DESIGN AND METHODS: This population-based study included 225 consecutive patients aged 10-25 years diagnosed with acute lymphoblastic leukemia during 1990-2004.
  • One hundred and twenty-eight patients (10-16 years) were treated with pediatric Nordic (NOPHO) protocols, and 97 patients (17-25 years) with Finnish Leukemia Group National protocols.
  • We characterized the biological subtypes, clinical features and outcome of these patients.
  • Good prognostic features were TEL-AML1, hyperdiploidy, and pediatric intermediate risk stratification.
  • CONCLUSIONS: Unlike all previous studies, we found that the outcome of adolescents and young adults with acute lymphoblastic leukemia treated with pediatric or adult therapeutic protocols was comparable.
  • The success of the adult acute lymphoblastic leukemia therapy emphasizes the benefit of central referral of patients to academic centers and adherence to research protocols.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Blast Crisis. Child. Disease-Free Survival. Female. Finland. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / mortality. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukocyte Count. Male. Phenotype. Philadelphia Chromosome. Survival Analysis

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  • [CommentIn] Haematologica. 2008 Aug;93(8):1124-8 [18669975.001]
  • (PMID = 18556413.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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8. Liang DC, Shih LY, Yang CP, Hung IJ, Liu HC, Jaing TH, Yeh TC, Liang ST, Chang CL, Lee EH, Lai CL, Chang WH: Frequencies of ETV6-RUNX1 fusion and hyperdiploidy in pediatric acute lymphoblastic leukemia are lower in far east than west. Pediatr Blood Cancer; 2010 Sep;55(3):430-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequencies of ETV6-RUNX1 fusion and hyperdiploidy in pediatric acute lymphoblastic leukemia are lower in far east than west.
  • BACKGROUND: Both ETV6-RUNX1 (TEL-AML1) fusion and hyperdiploidy (>50 chromosomes) in transformed lymphoblasts are favorable genetic features in childhood acute lymphoblastic leukemia (ALL).
  • PROCEDURE: Among 433 Taiwanese children with ALL diagnosed at our hospitals between 1997 and 2007, the ETV6-RUNX1 fusion was found in 15.8%, and hyperdiploidy (>50 chromosomes) in 14.1% of the patients.
  • These frequencies were lower than those reported in the West, leading us to conduct a meta-analysis of ETV6-RUNX1 fusion and hyperdiploidy frequencies in childhood ALL based on published reports.
  • Similarly, the frequency of hyperdiploidy in Japan and Taiwan was 14.3% (333/2,334, range: 12-20%, median 16%), significantly lower than the 25.2% in the West (5,173/20,510, range: 18-34%, median 23.5%; P < 0.001, odds ratio = 2.0, 95% CI: 1.8-2.3).
  • CONCLUSIONS: This meta-analysis demonstrates lower frequencies of ETV6-RUNX1 fusion and hyperdiploidy among leukemia patients in the Far East compared with the West.
  • The integral relationship of these genetic features with a favorable outcome in childhood ALL warrants further study of potentially important epidemiologic factors, including placental exposure to leukemogenic agents, and host pharmacogenetics.
  • [MeSH-major] Diploidy. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658612.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Meta-Analysis
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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9. Yang YL, Lin SR, Chen JS, Hsiao CC, Lin KH, Sheen JM, Cheng CN, Wu KH, Lin SW, Yu SL, Chen HY, Lu MY, Chang HH, Yen CT, Lin JF, Su YH, Li YP, Lin CY, Jou ST, Lin DT: Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Nov;32(8):e323-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia.
  • BACKGROUND: The classification of B-lineage acute lymphoblastic leukemia (ALL) by specific chromosomal translocations has prognostic implications for risk-directed therapy.
  • METHODS: Multiplex RT-PCR and nested-PCR assays were used to detect ALL-type BCR-ABL1 transcripts of the t(9;22), TCF-PBX1 transcripts of t(1;19), the MLL-AF4 transcripts of t(4;11), and 2 variants of ETV6-RUNX1 of the cryptic t(12;21) in 148 leukemic samples upon diagnosis.
  • The patients received risk-directed protocols of the Taiwan Pediatric Oncology Group-ALL-2002 that consisted of multiple chemotherapeutic agents of different intensities.
  • RESULTS: In this cohort of Taiwanese children, the relative frequencies of the 4 translocations of B-lineage ALL were 8% with ALL-type t(9;22)/BCR-ABL1, 4% with (1;19)/TCF-PBX1, 2% with t(4;11)/MLL-AF4, and 17.6% with t(12;21)/ETV6-RUNX1.
  • Patients with t(12;21)/ETV6-RUNX1 fusion, hyperdiploidy, and t(1;19)/TCF-PBX1 fusion had the most favorable outcomes, whereas those with the t(9;22)/BCR-ABL1 fusion or t(4;11) and other MLL gene rearrangement had poor prognosis (P<0.001 for EFS and OS).
  • CONCLUSIONS: The biological factors of leukemia cells are associated with treatment outcomes in childhood ALL.
  • Multiplex RT-PCR assay is an efficient and sensitive diagnostic tool that may improve the ability to accurately and rapidly risk-stratify children with ALL.
  • [MeSH-major] Genetic Testing / methods. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Cell Lineage / genetics. Child. Child, Preschool. Chimera. Core Binding Factor Alpha 2 Subunit. Female. Fusion Proteins, bcr-abl / genetics. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction / methods. Prognosis. Risk Factors. Sensitivity and Specificity. Taiwan / epidemiology

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  • (PMID = 20930648.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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10. Schmiegelow K, Al-Modhwahi I, Andersen MK, Behrendtz M, Forestier E, Hasle H, Heyman M, Kristinsson J, Nersting J, Nygaard R, Svendsen AL, Vettenranta K, Weinshilboum R, Nordic Society for Paediatric Haematology and Oncology: Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Blood; 2009 Jun 11;113(24):6077-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Among 1614 children with acute lymphoblastic leukemia (ALL) treated with the Nordic Society for Paediatric Haematology and Oncology (NOPHO) ALL-92 protocol, 20 patients developed a second malignant neoplasm (SMN) with a cumulative risk of 1.6% at 12 years from the diagnosis of ALL.
  • In Cox multivariate analysis, longer duration of oral 6-mercaptopurine (6MP)/methotrexate (MTX) maintenance therapy (P = .02; longest for standard-risk patients) and presence of high hyperdiploidy (P = .07) were related to increased risk of SMN.
  • Among 427 TPMT wild-type patients for whom the 6MP dose was registered, those who developed SMN received higher average 6MP doses than the remaining patients (69.7 vs 60.4 mg/m2; P = .03).

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  • (PMID = 19224761.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2699230
  • [Investigator] Schmiegelow K; Hejl M; Østergård M; Schrøder H; Pihkala U; Ilanmaa E; Antila K; Korpela K; Vuorinen O; Perkkiö M; Kojo N; Nyman R; Pere M; Lanning M; Niemi A; Vuoristo A; Niemi S; Isotalo J; Laapas H; Mäkipernaa A; Salmi T; Varsamäki T; Kristinsson J; Zeller B; Danielsen O; Madsen B; Nielsen B; Stensvold K; Lund JH; Danielsen K; Brekke P; Stamnes O; Glomstein A; Widing E; Hapnes C; Stokland T; Kolmannskog S; Halvorsen B; Spangen S; Carlsson G; Bergkvist M; Skanka N; Korlén B; Dimberg A; Adrian BA; Mellander L; Aronson S; Jensen D; Winiarski J; Lagerwall A; Jonsson NO; Cervin T; Samuelsson U; Berg A; Nilsson H; Behrendtz M; Wiebe T; Ljung R; Tessin I; Ljungren CG; Dohlwitz A; Christensen HO; Ronge E; Berglund M; Björk O; Fransson D; Eriksson M; Forestier E; Kreuger A; Blomgren M; Rönnblad B; Eriksson B; Berg T; Hedling L; Forsberg T; Lindquist B; Kriström B; Hjalmars U
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