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1. Cheok MH, Pottier N, Kager L, Evans WE: Pharmacogenetics in acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):39-51
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  • [Title] Pharmacogenetics in acute lymphoblastic leukemia.
  • Progress in the treatment of acute lymphoblastic leukemia (ALL) in children has been remarkable, from a disease being lethal four decades ago to current cure rates exceeding 80%.
  • However, despite these high cure rates, the annual number of children whose leukemia relapses after their initial therapy remains greater than that of new cases of most types of childhood cancers.
  • In this review, we summarize recent pharmacogenomic studies related to the treatment of pediatric ALL.
  • These studies illustrate the promise of pharmacogenomics to further advance the treatment of human cancers, with childhood leukemia serving as a paradigm.

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  • (PMID = 19100367.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA036401-25; United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA21765; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA036401-25; United States / NCI NIH HHS / CA / R01 CA78224
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 120
  • [Other-IDs] NLM/ NIHMS89418; NLM/ PMC2665795
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2. Okamoto R, Ogawa S, Nowak D, Kawamata N, Akagi T, Kato M, Sanada M, Weiss T, Haferlach C, Dugas M, Ruckert C, Haferlach T, Koeffler HP: Genomic profiling of adult acute lymphoblastic leukemia by single nucleotide polymorphism oligonucleotide microarray and comparison to pediatric acute lymphoblastic leukemia. Haematologica; 2010 Sep;95(9):1481-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic profiling of adult acute lymphoblastic leukemia by single nucleotide polymorphism oligonucleotide microarray and comparison to pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Differences in survival have been reported between pediatric and adult acute lymphoblastic leukemia.
  • The inferior prognosis in adult acute lymphoblastic leukemia is not fully understood but could be attributed, in part, to differences in genomic alterations found in adult as compared to in pediatric acute lymphoblastic leukemia.
  • DESIGN AND METHODS: We compared two different sets of high-density single nucleotide polymorphism array genotyping data from 75 new diagnostic adult and 399 previously published diagnostic pediatric acute lymphoblastic leukemia samples.
  • RESULTS: The high density single nucleotide polymorphism array analysis of 75 samples of adult acute lymphoblastic leukemia led to the identification of numerous cryptic and submicroscopic genomic lesions with a mean of 7.6 genomic alterations per sample.
  • The patterns and frequencies of lesions detected in the adult samples largely reproduced known genomic hallmarks detected in previous single nucleotide polymorphism-array studies of pediatric acute lymphoblastic leukemia, such as common deletions of 3p14.2 (FHIT), 5q33.3 (EBF), 6q, 9p21.3 (CDKN2A/B), 9p13.2 (PAX5), 13q14.2 (RB1) and 17q11.2 (NF1).
  • Some differences between adult and pediatric acute lymphoblastic leukemia were identified when the pediatric data set was partitioned into hyperdiploid and non-hyperdiploid cases and then compared to the nearly exclusively non-hyperdiploid adult samples.
  • CONCLUSIONS: Our analysis of adult acute lymphoblastic leukemia cases led to the identification of new potential target lesions relevant for the pathogenesis of acute lymphoblastic leukemia.
  • However, no unequivocal pattern of submicroscopic genomic alterations was found to separate adult acute lymphoblastic leukemia from pediatric acute lymphoblastic leukemia.
  • Therefore, apart from different therapy regimen, differences of prognosis between adult and pediatric acute lymphoblastic leukemia are probably based on genetic subgroups according to cytogenetically detectable lesions but not focal genomic copy number microlesions.

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  • (PMID = 20435627.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2930948
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3. Aplenc R, Thompson J, Han P, La M, Zhao H, Lange B, Rebbeck T: Methylenetetrahydrofolate reductase polymorphisms and therapy response in pediatric acute lymphoblastic leukemia. Cancer Res; 2005 Mar 15;65(6):2482-7
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  • [Title] Methylenetetrahydrofolate reductase polymorphisms and therapy response in pediatric acute lymphoblastic leukemia.
  • A significant portion of patients treated for pediatric acute lymphoblastic leukemia (ALL) relapse.
  • Methotrexate (MTX), which interrupts folate metabolism, is a mainstay of pediatric ALL therapy.
  • This association remained significant (hazard ratio = 1.82, P = 0.008), controlling for important covariates, and was more predictive of relapse than other predictors, including day 7 bone marrow response.
  • These data provide evidence that the MTHFR C677T polymorphism is a common genetic variant conferring a moderate relative risk and a high attributable risk for relapse in pediatric ALL patients.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Methotrexate / therapeutic use. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology


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4. Costea I, Moghrabi A, Laverdiere C, Graziani A, Krajinovic M: Folate cycle gene variants and chemotherapy toxicity in pediatric patients with acute lymphoblastic leukemia. Haematologica; 2006 Aug;91(8):1113-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Folate cycle gene variants and chemotherapy toxicity in pediatric patients with acute lymphoblastic leukemia.
  • The gene polymorphisms of the methotrexate (MTX) action pathway influence event-free survival (EFS) in children with acute lymphoblastic leukemia (ALL).
  • Homozygous individuals for cyclin D1 (CCND1) A870 allele and carriers of at least one methylenetetrahydrofolate reductase (MTHFR) T677 variant had a significantly lower frequency of weeks with high-grade hematologic and liver toxicity during consolidation and maintenance treatment, as based on the analysis of 186 pediatric ALL patients.
  • [MeSH-major] Folic Acid / metabolism. Folic Acid Antagonists / therapeutic use. Methotrexate / therapeutic use. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


5. Curran MP, Perry CM: Clofarabine: in pediatric patients with acute lymphoblastic leukemia. Paediatr Drugs; 2005;7(4):259-64; discussion 265-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clofarabine: in pediatric patients with acute lymphoblastic leukemia.
  • In 61 pediatric patients with relapsed or refractory acute lymphoblastic leukemia treated with clofarabine 52 mg/m2 infused intravenously over 2 hours once daily for 5 days every 2-6 weeks, rates of complete remission, complete remission without platelet recovery, and partial remission were 12%, 8%, and 10%, respectively.
  • Data are from two non-comparative, multicenter, phase II studies.
  • The most common adverse events associated with clofarabine 52 mg/m2 once daily for 5 days every 2-6 weeks in 96 patients with acute myelogenous or lymphoblastic leukemia (combined analysis of phase I/II trials) were hematologic events (including anemia, leukopenia, thrombocytopenia, neutropenia, and febrile neutro-penia), gastrointestinal events (including vomiting, nausea, and diarrhea), infections, and transient elevations in liver enzymes.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16117562.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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6. Faderl S, O'Brien S, Pui CH, Stock W, Wetzler M, Hoelzer D, Kantarjian HM: Adult acute lymphoblastic leukemia: concepts and strategies. Cancer; 2010 Mar 01;116(5):1165-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult acute lymphoblastic leukemia: concepts and strategies.
  • Acute lymphoblastic leukemia (ALL), a clonal expansion of hematopoietic blasts, is a highly heterogeneous disease comprising many entities for which distinct treatment strategies are pursued.
  • Although ALL is a success story in pediatric oncology, results in adults lag behind those in children.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 20101737.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 103
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7. Hinds PS, Hockenberry MJ, Gattuso JS, Srivastava DK, Tong X, Jones H, West N, McCarthy KS, Sadeh A, Ash M, Fernandez C, Pui CH: Dexamethasone alters sleep and fatigue in pediatric patients with acute lymphoblastic leukemia. Cancer; 2007 Nov 15;110(10):2321-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dexamethasone alters sleep and fatigue in pediatric patients with acute lymphoblastic leukemia.
  • BACKGROUND: Dexamethasone improves the cure rate of childhood acute lymphoblastic leukemia (ALL) but causes physical and behavioral adverse events.
  • The objective of the current study was to determine the effect of dexamethasone exposure on sleep and fatigue in pediatric patients with ALL.
  • METHODS: One hundred pediatric patients with low-risk or standard-risk ALL were enrolled on 1 of 3 protocols (St. Jude Total XV, Children's Oncology Group [COG] 9904, or COG 9905) at 3 institutions.
  • CONCLUSIONS: Dexamethasone treatment during continuation therapy for childhood ALL significantly and adversely altered sleep and fatigue, confirming that sleep and fatigue are behavioral responses to dexamethasone.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Dexamethasone / adverse effects. Fatigue / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sleep / drug effects

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17926333.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765; United States / NINR NIH HHS / NR / R01NR007610
  • [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; 7S5I7G3JQL / Dexamethasone
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8. Styczynski J, Kurylak A, Wysocki M: Cytotoxicity of cortivazol in childhood acute lymphoblastic leukemia. Anticancer Res; 2005 May-Jun;25(3B):2253-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxicity of cortivazol in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Glucocorticoids are the most important group of drugs used in the treatment of childhood acute lymphoblastic leukemia (ALL), however, resistance to this group remains the main obstacle in curing the disease.
  • AIM: Analysis of ex vivo sensitivity to cortivazol and other glucocorticoids in childhood acute lymphoblastic leukemia, as well as the relationship to anticancer therapy outcome.
  • CVZ showed relatively better cytotoxicity than other glucocorticoids in prednisolone-poor-responders.
  • CVZ, like other glucocorticoids, caused cell cycle arrest in the GI-phase, and increased the percentage of apoptotic cells to a greater extent than other glucocorticoids.
  • CONCLUSION: Cortivazol has potent antileukemic activity in childhood ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pregnatrienes / pharmacology

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  • (PMID = 16158972.001).
  • [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 / Glucocorticoids; 0 / Pregnatrienes; 9PHQ9Y1OLM / Prednisolone; YM183K0H63 / cortivazol
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9. Al-Lamki Z, Wali YA, Wasifuddin SM, Zachariah M, Al-Mjeni R, Li C, Muralitharan S, Al-Kharusi K, Gunaratne P, Peterson L, Gibbs R, Gingras MC, Margolin JF: Identification of prognosis markers in pediatric high-risk acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2005 Oct-Nov;22(7):629-43
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  • [Title] Identification of prognosis markers in pediatric high-risk acute lymphoblastic leukemia.
  • Gene expression profiling may improve the understanding of the biology behind relapse in pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16166056.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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10. Sahu GR, Das BR: Alteration of p73 in pediatric de novo acute lymphoblastic leukemia. Biochem Biophys Res Commun; 2005 Feb 18;327(3):750-5
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  • [Title] Alteration of p73 in pediatric de novo acute lymphoblastic leukemia.
  • The frequency of p73 mutation is low in hematologic malignancies as well as solid tumors.
  • Aberrant DNA methylation of multiple promoter associated CpG islands is a frequent phenomenon in acute lymphoblastic leukemia (ALL).
  • One pediatric patient showed mutation in exon 4, two showed mutation in exon 5, and none of the patients showed mutation in exons 6 and 7.
  • However, p73 overexpression was observed in 58% of pediatric patients as demonstrated by immunocytochemistry and Western blot analysis.
  • Methylation of p73 does not play a role in pediatric ALL patients of our population.
  • This report is the first demonstrating the presence of p73 gene mutations in exons 4 and 5 with overexpression of p73 protein and absence of p73 methylation in pediatric ALL patients of eastern Indian population.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15649410.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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11. Ponce-Torres E, Ruíz-Rodríguez Mdel S, Alejo-González F, Hernández-Sierra JF, Pozos-Guillén Ade J: Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia. J Clin Pediatr Dent; 2010;34(3):275-9
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  • [Title] Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia.
  • The purpose of this study was to determine the prevalence of oral manifestations in pediatric patients with acute lymphoblastic leukemia (ALL) receiving chemotherapy, and to evaluate the significance of independent risk factors (oral health, gender, age, time and type of treatment, and phase of chemotherapy).
  • Other oral manifestations were: dry lips, mucosal pallor, mucosal petechiae, ecchymoses, and induced ulcers.
  • The type of leukemia, gender and phase of chemotherapy were apparently associated with the presence of candidiasis, gingivitis, and periodontitis, and they could be considered risk factors for the development of oral manifestations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Mouth Diseases / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20578668.001).
  • [ISSN] 1053-4628
  • [Journal-full-title] The Journal of clinical pediatric dentistry
  • [ISO-abbreviation] J Clin Pediatr Dent
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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12. Lowas SR, Marks D, Malempati S: Prevalence of transient hyperglycemia during induction chemotherapy for pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Jul;52(7):814-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of transient hyperglycemia during induction chemotherapy for pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Transient hyperglycemia (TH) is a recognized side effect of the corticosteroids and asparaginase given during induction chemotherapy for pediatric acute lymphoblastic leukemia (ALL).
  • This study examined the prevalence of TH in a cohort of pediatric ALL patients and the impact on TH of type of steroid or asparaginase used and of risk factors such as age, gender, and overweight.
  • There was a non-significant trend toward more TH in patients who received prednisone, but this disappeared in multivariate analysis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hyperglycemia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19260096.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone
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13. Maecker B, Mougiakakos D, Zimmermann M, Behrens M, Hollander S, Schrauder A, Schrappe M, Welte K, Klein C: Dendritic cell deficiencies in pediatric acute lymphoblastic leukemia patients. Leukemia; 2006 Apr;20(4):645-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dendritic cell deficiencies in pediatric acute lymphoblastic leukemia patients.
  • Acute lymphoblastic leukemia (ALL) cells are particularly poor at generating anti-leukemia immunity, despite residing in lymphoid organs.
  • To assess a potential role of dendritic cells (DC) in poor anti-leukemia immunity, we analyzed peripheral blood DC in 55 pediatric ALL patients at the time of initial diagnosis and 19 age-matched healthy controls.
  • Dendritic cells were identified by their expression of HLA-DR, lack of B, T, NK, and monocyte markers, and expression of CD11c (myeloid DC(mDC)) or BDCA-2 (plasmacytoid DC(pDC)) using flow cytometry.
  • However, aberrant expression of myeloid surface markers on leukemic blasts was frequent in patients lacking myeloid DC indicating a potential block of DC differentiation.
  • Thus, depletion of DC in B-lineage ALL patients may contribute to poor anti-leukemia immune responses.
  • [MeSH-major] Antigens, CD11c / biosynthesis. Dendritic Cells / immunology. Lectins, C-Type / biosynthesis. Membrane Glycoproteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Receptors, Immunologic / biosynthesis

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  • (PMID = 16498391.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11c; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CLEC4C protein, human; 0 / Lectins, C-Type; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 1.11.1.7 / Peroxidase; EC 3.4.11.2 / Antigens, CD13
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14. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Mean length of survivors 4 year (range 4-140 month) and mean length for non-survivors 1 year (range 0.1-40 months).

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  • (PMID = 27962474.001).
  • [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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15. Tai E, Richardson L, Townsend J, Steele B: Differences in length of stay among hospitalized children with acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10044

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in length of stay among hospitalized children with acute lymphoblastic leukemia.
  • : 10044 Background: Acute lymphoblastic leukemia (ALL) is the most common malignancy among children in the United States.
  • METHODS: We used 2000, 2003, and 2006 data from the Healthcare Cost and Utilization Project (HCUP) Kids' Inpatient Database (KID) which contains pediatric discharges from community, non-rehabilitation hospitals.
  • RESULTS: We found the following factors related to greater LOS among hospitalized children with ALL: Non-Hispanic blacks vs. non-Hispanic whites (Rate Ratio (RR) = 1.06, CI:1.03-1.10), Hispanics vs. non-Hispanic whites (RR = 1.07, CI:1.04-1.10), age < 1 year vs. age 1-5 years (RR = 1.93, CI:1.83-2.04), female vs. male (RR = 1.05, CI:1.03-1.07), lowest quartile of household income in patient's zip code vs. highest quartile (RR = 1.09, CI:1.06-1.12), Medicaid vs. private insurance (RR = 1.11, CI:1.09-1.14), children's hospital vs. non-children's (RR = 1.11, CI:1.08-1.14), Western region of United States vs. Northeast region (RR = 1.14, CI:1.11-1.17), emergency room admission vs. routine admission (RR = 1.23, CI:1.20-1.26), blood transfusion (RR = 1.64, CI:1.61-1.67), bone marrow transplant (RR = 7.64, CI:7.11-8.20), and neutropenia (RR = 1.22, CI:1.19-1.24).

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  • (PMID = 27962470.001).
  • [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. Gill HK, Keoh TS, Dhaliwal JS, Moore S, Kim TS, Hassan R, Karim FA, Zakaria Z, Murad S, Mohamed M, Li Ho CM, Ibrahim H, Rahman EJ: TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2005 Jan 15;156(2):129-33
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  • [Title] TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia.
  • Eighty-eight multi-ethnic Malaysian pediatric acute lymphoblastic leukemia (ALL) patients were screened for the TEL-AML1 rearrangement by reverse transcription-polymerase chain reaction (RT-PCR).
  • This study shows that in Malaysia, TEL-AML1 is found in the same distinct ALL subset and at a similar frequency as in other diverse childhood ALL cohorts.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15642392.001).
  • [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
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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17. da Costa Moraes CA, Trompieri NM, Cavalcante Felix FH: Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital. J Pediatr Hematol Oncol; 2008 May;30(5):387-90
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  • [Title] Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital.
  • Acute promyelocytic leukemia (APL) is an uncommon form of pediatric acute nonlymphocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Brazil. Female. Hospitals, Pediatric. Humans. Male. Retrospective Studies

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  • (PMID = 18458575.001).
  • [ISSN] 1077-4114
  • [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 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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18. Crazzolara R, Bendall L: Emerging treatments in acute lymphoblastic leukemia. Curr Cancer Drug Targets; 2009 Feb;9(1):19-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emerging treatments in acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a clonal proliferation of early B- and T-lymphocyte progenitors and results in the accumulation of leukemic blasts in the bone marrow and various extramedullary sites.
  • Despite current treatment protocols achieving rapid cytoreduction in the vast majority of patients, serious acute and late complications are frequent and resistance to chemotherapy often develops.
  • In contrast to the successes obtained with pediatric patients, treatment outcomes for adults remain poor with only 40% of patients being long-term survivors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19200049.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 136
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19. Jeha S, Pui CH: Risk-adapted treatment of pediatric acute lymphoblastic leukemia. Hematol Oncol Clin North Am; 2009 Oct;23(5):973-90, v
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk-adapted treatment of pediatric acute lymphoblastic leukemia.
  • Optimal use of antileukemic agents and stringent application of risk-directed therapy in clinical trials have resulted in steady improvement in the outcome of children with acute lymphoblastic leukemia, with current cure rates exceeding 80% in developed countries.
  • The intensity of treatment varies substantially among subsets of patients, as therapy is designed to reduce acute and long-term toxicity in low-risk groups while improving outcomes in poor risk groups by treatment intensification.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19825448.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 105
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20. Brentjens RJ: Cellular therapies in acute lymphoblastic leukemia. Curr Opin Mol Ther; 2009 Aug;11(4):375-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cellular therapies in acute lymphoblastic leukemia.
  • The majority of adult patients with acute lymphoblastic leukemia (ALL) will die from the disease.
  • Although the prognosis for pediatric patients is significantly better than for adult patients with ALL, the prognosis for patients with relapsed or refractory disease is poor in all cases.
  • Allogeneic hematopoietic stem cell transplantation (allo-HSCT) from a related donor offers a significant therapeutic benefit for pediatric patients, although the benefit of this therapy to adults with ALL is less established.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19649982.001).
  • [ISSN] 2040-3445
  • [Journal-full-title] Current opinion in molecular therapeutics
  • [ISO-abbreviation] Curr. Opin. Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA095152; United States / NCI NIH HHS / CA / R01 CA138738; United States / NCI NIH HHS / CA / CA95152; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA138738; United States / NCI NIH HHS / CA / P01 CA059350; United States / NCI NIH HHS / CA / CA59350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 65
  • [Other-IDs] NLM/ NIHMS746468; NLM/ PMC4694559
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21. Akiyama M, Yamada O, Agawa M, Yuza Y, Yanagisawa T, Eto Y, Yamada H: Effects of prednisolone on specifically expressed genes in pediatric acute B-lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Apr;30(4):313-6
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of prednisolone on specifically expressed genes in pediatric acute B-lymphoblastic leukemia.
  • Although glucocorticoid is essential in the treatment of pediatric acute lymphoblastic leukemia (ALL), their precise mechanisms of action remain unclear.
  • We used DNA microarray to evaluate prednisolone-regulated genes in pre-B-ALL cells from 2 pediatric patients.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. Lymphoma, B-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use

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  • (PMID = 18391702.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] VB0R961HZT / Prednisone
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22. Thompson PA, Murry DJ, Rosner GL, Lunagomez S, Blaney SM, Berg SL, Camitta BM, Dreyer ZE, Bomgaars LR: Methotrexate pharmacokinetics in infants with acute lymphoblastic leukemia. Cancer Chemother Pharmacol; 2007 May;59(6):847-53
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methotrexate pharmacokinetics in infants with acute lymphoblastic leukemia.
  • PURPOSE: We performed a pharmacokinetic evaluation of methotrexate (MTX) in infants with acute lymphoblastic leukemia enrolled on the Pediatric Oncology Group (POG) 9407 Infant Leukemia Study to evaluate the effects of age on MTX pharmacokinetics and pharmacodynamics.
  • METHODS: A pharmacokinetic database of 61 patients was developed by combining MTX data obtained from 16 patients in a pharmacokinetic sub-study with data obtained for clinical care in other patients enrolled on the POG 9407 protocol.
  • Steady-state clearance for the older infants is similar to values reported for children in other studies.
  • [MeSH-major] Methotrexate / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17136402.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30969
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate
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23. Gauffin F, Diffner E, Gustafsson B, Nordgren A, Wingren AG, Sander B, Persson JL, Gustafsson B: Expression of PTEN and SHP1, investigated from tissue microarrays in pediatric acute lymphoblastic, leukemia. Pediatr Hematol Oncol; 2009 Jan;26(1):48-56
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] Expression of PTEN and SHP1, investigated from tissue microarrays in pediatric acute lymphoblastic, leukemia.
  • The authors investigated the protein expression of PTEN and SHP1, by immunohistochemistry in tissue microarrays from bone marrow samples in children, diagnosed with acute lymphoblastic leukaemia and nonmalignant controls.
  • The roles of PTEN and SHP1 are not well investigated in pediatric leukemia and could in the future play a role as prognostic factors.
  • [MeSH-major] PTEN Phosphohydrolase / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / analysis

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  • (PMID = 19206008.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.67 / PTEN Phosphohydrolase
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24. Al-Khabori M, Minden MD, Yee KW, Gupta V, Schimmer AD, Schuh AC, Xu W, Brandwein JM: Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2010 Jan;51(1):61-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia.
  • All patients with newly diagnosed T-cell acute lymphoblastic leukemia (T-ALL) and treated over a 17-year period at a single institution were retrospectively analyzed.
  • From 2000 to 2007, a pediatric-based protocol, DFCI (Dana Farber Cancer Institute), was used as the standard regimen for all patients (n = 32).
  • The two groups (DFCI and non-DFCI) had comparable baseline characteristics.
  • Complete response rates were not significantly different between the DFCI- and non-DFCI-treated groups.
  • On multivariate analysis, the treatment group (DFCI vs. non-DFCI) was the major prognostic factor influencing both RFS and OS.
  • The results provide evidence supporting the superior efficacy of asparaginase-intensive pediatric-based regimens for adults with T-ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality


25. Henderson MJ, Choi S, Beesley AH, Sutton R, Venn NC, Marshall GM, Kees UR, Haber M, Norris MD: Mechanism of relapse in pediatric acute lymphoblastic leukemia. Cell Cycle; 2008 May 15;7(10):1315-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of relapse in pediatric acute lymphoblastic leukemia.
  • Relapse following initial chemotherapy remains a barrier to survival in approximately 20% of children suffering from acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Rearrangement / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control

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  • (PMID = 18418081.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Receptors, Antigen
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26. Riedt T, Ebinger M, Salih HR, Tomiuk J, Handgretinger R, Kanz L, Grünebach F, Lengerke C: Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia. Blood; 2009 Apr 23;113(17):4049-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia.
  • Consistent with the notion that embryonic pathways can reactivate during adult oncogenesis, recent studies suggest involvement of CDX2 in human acute myeloid leukemia (AML).
  • Analysis of a cohort of 37 childhood acute lymphoblastic leukemia (ALL) patients treated in our hospital reveals that high CDX2 expression levels at diagnosis correlate with persistence of minimal residual disease (MRD) during the course of treatment.
  • Thus, CDX2 expression levels may serve as a marker for adverse prognosis in pediatric ALL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Homeodomain Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19218548.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
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27. Wiemels JL, Zhang Y, Chang J, Zheng S, Metayer C, Zhang L, Smith MT, Ma X, Selvin S, Buffler PA, Wiencke JK: RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia. Leukemia; 2005 Mar;19(3):415-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia.
  • We explored the relationship of RAS gene mutations with epidemiologic and cytogenetic factors in a case series of children with leukemia.
  • Diagnostic bone marrow samples from 191 incident leukemia cases from the Northern California Childhood Leukemia Study were typed for NRAS and KRAS codon 12 and 13 mutations.
  • Among the 142 B-cell acute lymphoblastic leukemia (ALL) cases, RAS mutations were more common among Hispanic children (P=0.11) or children born to mothers <30 years (P=0.007).
  • Interestingly, smoking of the father in the 3 months prior to pregnancy was reported less frequently among hyperdiploid leukemia patients than among those without hyperdiploidy (P=0.02).
  • The data suggest that RAS and high hyperdiploidy may be cooperative genetic events to produce the leukemia subtype; and furthermore, that maternal age and paternal preconception smoking or other factors associated with these parameters are critical in the etiology of subtypes of childhood leukemia.
  • [MeSH-major] Genes, ras / genetics. Mutation. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15674422.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCHHSTP CDC HHS / PS / PS42 ES04705; United States / NCI NIH HHS / CA / R01 CA89032; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
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28. Roberson JR, Raju S, Shelso J, Pui CH, Howard SC: Diabetic ketoacidosis during therapy for pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Jun;50(6):1207-12
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diabetic ketoacidosis during therapy for pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Hyperglycemia is common during therapy for acute lymphoblastic leukemia (ALL), but diabetic ketoacidosis (DKA) occurs rarely.
  • Four of six patients with DKA as compared to 232 of the other 791 patients were older than 10 years (P = 0.03).
  • Race, sex, body mass index, leukemia immunophenotype, ALL risk category, white blood cell count at diagnosis, and treatment protocol were not associated with DKA.
  • [MeSH-major] Diabetic Ketoacidosis / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18266226.001).
  • [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; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / GM-61393
  • [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; 0 / Glucocorticoids; EC 3.5.1.1 / Asparaginase
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29. Bachmann PS, Gorman R, Papa RA, Bardell JE, Ford J, Kees UR, Marshall GM, Lock RB: Divergent mechanisms of glucocorticoid resistance in experimental models of pediatric acute lymphoblastic leukemia. Cancer Res; 2007 May 1;67(9):4482-90
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Divergent mechanisms of glucocorticoid resistance in experimental models of pediatric acute lymphoblastic leukemia.
  • Cell line models of glucocorticoid resistance in childhood acute lymphoblastic leukemia (ALL) almost invariably exhibit altered glucocorticoid receptor (GR) function.
  • However, these findings are incongruous with those using specimens derived directly from leukemia patients, in which GR alterations are rarely found.
  • We present a novel paradigm of glucocorticoid resistance in childhood ALL, in which patient biopsies have been directly established as continuous xenografts in immune-deficient mice, without prior in vitro culture.
  • This finding contrasts with five commonly used leukemia cell lines, all of which exhibited defective GRE binding.
  • Furthermore, the receptor tyrosine kinase inhibitor, SU11657, completely reversed dexamethasone resistance in a xenograft expressing functional GR, indicating that pharmacologic reversal of glucocorticoid resistance in childhood ALL is achievable.
  • [MeSH-major] Dexamethasone / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Receptors, Glucocorticoid / metabolism

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  • (PMID = 17483364.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Organic Chemicals; 0 / Proto-Oncogene Proteins; 0 / Receptors, Glucocorticoid; 0 / SU 11657; 0 / TSC22D3 protein, human; 0 / Transcription Factors; 7S5I7G3JQL / Dexamethasone; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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30. Li Z, Zhang W, Wu M, Zhu S, Gao C, Sun L, Zhang R, Qiao N, Xue H, Hu Y, Bao S, Zheng H, Han JD: Gene expression-based classification and regulatory networks of pediatric acute lymphoblastic leukemia. Blood; 2009 Nov 12;114(20):4486-93
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression-based classification and regulatory networks of pediatric acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) contains cytogenetically distinct subtypes that respond differently to cytotoxic drugs.
  • [MeSH-major] Gene Expression Profiling / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19755675.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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31. Zen PR, Capra ME, Silla LM, Loss JF, Fernandes MS, Jacques SM, Paskulin GA: ETV6/RUNX1 fusion lacking prognostic effect in pediatric patients with acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Jan 15;188(2):112-7
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6/RUNX1 fusion lacking prognostic effect in pediatric patients with acute lymphoblastic leukemia.
  • A Brazilian sample of 58 patients with acute lymphoblastic leukemia has been prospectively followed up with the objective of evaluating evolution of disease.
  • No significant difference was observed between overall survival and event-free survival, nor in any of the other data comparatively analyzed.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 19100516.001).
  • [ISSN] 1873-4456
  • [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
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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32. Davidsson J, Lilljebjörn H, Andersson A, Veerla S, Heldrup J, Behrendtz M, Fioretos T, Johansson B: The DNA methylome of pediatric acute lymphoblastic leukemia. Hum Mol Genet; 2009 Nov 1;18(21):4054-65
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The DNA methylome of pediatric acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy, with high hyperdiploidy [51-67 chromosomes] and the t(12;21)(p13;q22) [ETV6/RUNX1 fusion] representing the most frequent abnormalities.
  • Decreased methylation of gained chromosomes is a previously unknown phenomenon that may have ramifications not only for the pathogenesis of high hyperdiploid ALL but also for other disorders with acquired or constitutional numerical chromosome anomalies.
  • [MeSH-major] CpG Islands / genetics. DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19679565.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BBC3 protein, human; 0 / CAV1 protein, human; 0 / CDK2AP1 protein, human; 0 / Caveolin 1; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / PRKCDBP protein, human; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / Tumor Suppressor Proteins; 0 / bcl-Associated Death Protein; 117896-08-9 / nucleophosmin; EC 3.1.2.- / THEM4 protein, human; EC 3.1.2.- / Thiolester Hydrolases
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33. Van Vlierberghe P, Palomero T, Khiabanian H, Van der Meulen J, Castillo M, Van Roy N, De Moerloose B, Philippé J, González-García S, Toribio ML, Taghon T, Zuurbier L, Cauwelier B, Harrison CJ, Schwab C, Pisecker M, Strehl S, Langerak AW, Gecz J, Sonneveld E, Pieters R, Paietta E, Rowe JM, Wiernik PH, Benoit Y, Soulier J, Poppe B, Yao X, Cordon-Cardo C, Meijerink J, Rabadan R, Speleman F, Ferrando A: PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Apr;42(4):338-42
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PHF6 mutations in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males.
  • In this study, we report the identification of inactivating mutations and deletions in the X-linked plant homeodomain finger 6 (PHF6) gene in 16% of pediatric and 38% of adult primary T-ALL samples.

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  • (PMID = 20228800.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743
  • [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 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364
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34. Gutierrez A, Sanda T, Ma W, Zhang J, Grebliunaite R, Dahlberg S, Neuberg D, Protopopov A, Winter SS, Larson RS, Borowitz MJ, Silverman LB, Chin L, Hunger SP, Jamieson C, Sallan SE, Look AT: Inactivation of LEF1 in T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 08;115(14):2845-51
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] Inactivation of LEF1 in T-cell acute lymphoblastic leukemia.
  • To further unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performed high-resolution array comparative genomic hybridization on diagnostic specimens from 47 children with T-ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary samples.
  • [MeSH-major] Codon, Terminator. Lymphoid Enhancer-Binding Factor 1 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

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  • (PMID = 20124220.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / 5P01CA68484
  • [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 / Antigens, CD; 0 / Codon, Terminator; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2854430
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35. Kawamata N, Ogawa S, Seeger K, Kirschner-Schwabe R, Huynh T, Chen J, Megrabian N, Harbott J, Zimmermann M, Henze G, Schrappe M, Bartram CR, Koeffler HP: Molecular allelokaryotyping of relapsed pediatric acute lymphoblastic leukemia. Int J Oncol; 2009 Jun;34(6):1603-12
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular allelokaryotyping of relapsed pediatric acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) cells at relapse are frequently more resistant to treatment than primary clones and this may be caused by further genetic changes in the ALL cells at relapse.
  • [MeSH-major] Chromosome Aberrations. Gene Expression Regulation, Leukemic. Neoplasm Recurrence, Local / genetics. Polymorphism, Single Nucleotide / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19424578.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; EC 3.1.3.48 / PTPRD protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 2; EC 3.6.5.2 / ADP-Ribosylation Factor 1
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36. Mullighan CG, Downing JR: Global genomic characterization of acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):3-15
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global genomic characterization of acute lymphoblastic leukemia.
  • Leading this effort are studies of the molecular lesions that underlie pediatric acute lymphoblastic leukemia (ALL).
  • The recent application of microarray-based analyses of DNA copy number abnormalities (CNAs) in pediatric ALL, complemented by transcriptional profiling, resequencing and epigenetic approaches, has identified a high frequency of common genetic alterations in both B-progenitor and T-lineage ALL.

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  • (PMID = 19100363.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / P30 CA021765-30
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS168528; NLM/ PMC2834786
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37. Maiguma T, Hayashi Y, Ueshima S, Kaji H, Egawa T, Chayama K, Morishima T, Kitamura Y, Sendo T, Gomita Y, Teshima D: Relationship between oral mucositis and high-dose methotrexate therapy in pediatric acute lymphoblastic leukemia. Int J Clin Pharmacol Ther; 2008 Nov;46(11):584-90
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between oral mucositis and high-dose methotrexate therapy in pediatric acute lymphoblastic leukemia.
  • OBJECTIVE: Oral mucositis is a major toxicity in the high-dose methotrexate (HD-MTX) treatment for children with acute lymphoblastic leukemia (ALL).
  • The first aim of this study was to evaluate the relationship between the MTX serum concentration and occurrence of oral mucositis in pediatric ALL patients.
  • METHODS: 49 patients were treated according to the Japan Association of Childhood Leukemia Study (JACLS) ALL-HR02 protocol.
  • In the group with oral mucositis, the clearance decreased significantly (p = 0.042), and the t1/2b (p = 0.025) and AUC48h- yen (p = 0.025) increased significantly compared with the non-symptom group.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antimetabolites, Antineoplastic / therapeutic use. Keratinocytes / drug effects. Methotrexate / adverse effects. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Stomatitis / chemically induced

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  • (PMID = 19000557.001).
  • [ISSN] 0946-1965
  • [Journal-full-title] International journal of clinical pharmacology and therapeutics
  • [ISO-abbreviation] Int J Clin Pharmacol Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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38. Graham DK, Salzberg DB, Kurtzberg J, Sather S, Matsushima GK, Keating AK, Liang X, Lovell MA, Williams SA, Dawson TL, Schell MJ, Anwar AA, Snodgrass HR, Earp HS: Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 May 1;12(9):2662-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia.
  • To determine if Mer expression is ectopic in T-cell acute lymphoblastic leukemia (ALL) and potentially important in leukemogenesis, we analyzed Mer expression in normal human thymocytes and lymphocytes and in pediatric ALL patient samples.
  • CONCLUSIONS: Transforming Mer signals may contribute to T-cell leukemogenesis, and abnormal Mer expression may be a novel therapeutic target in pediatric ALL therapy.

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  • (PMID = 16675557.001).
  • [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 / T32 CA082086; United States / NCI NIH HHS / CA / CA 68346; United States / NCI NIH HHS / CA / P30 CA46934; United States / NCI NIH HHS / CA / T32CA8608604
  • [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 / Proto-Oncogene Proteins; 0 / RNA, Neoplasm; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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39. Rau T, Erney B, Göres R, Eschenhagen T, Beck J, Langer T: High-dose methotrexate in pediatric acute lymphoblastic leukemia: impact of ABCC2 polymorphisms on plasma concentrations. Clin Pharmacol Ther; 2006 Nov;80(5):468-76
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose methotrexate in pediatric acute lymphoblastic leukemia: impact of ABCC2 polymorphisms on plasma concentrations.
  • Subsequently, we assessed the association of polymorphisms with the methotrexate plasma concentrations in 44 pediatric patients with acute lymphoblastic leukemia (ALL) (29 male and 15 female patients; mean age, 6.8+/-4.8 years).
  • The mean plasma methotrexate area under the curve from 36 to 48 hours after the start of the infusion was significantly 2-fold higher in female patients carrying at least 1 -24T allele as compared with all other patients (14.2+/-12.8 h.micromol/L versus 6.9+/-4.2 h.micromol/L, P<.001).
  • [MeSH-major] Membrane Transport Proteins / genetics. Methotrexate / pharmacokinetics. Methotrexate / therapeutic use. Multidrug Resistance-Associated Proteins / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


40. Roberson JR, Spraker HL, Shelso J, Zhou Y, Inaba H, Metzger ML, Rubnitz JE, Ribeiro RC, Sandlund JT, Jeha S, Pui CH, Howard SC: Clinical consequences of hyperglycemia during remission induction therapy for pediatric acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):245-50
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  • [Title] Clinical consequences of hyperglycemia during remission induction therapy for pediatric acute lymphoblastic leukemia.
  • Hyperglycemia adversely affects outcome in adult patients with acute lymphoblastic leukemia (ALL), but its impact on children with this disease is unknown.
  • We evaluated the relationship between hyperglycemia during remission induction therapy and clinical outcomes among pediatric patients with ALL.
  • Patients with hyperglycemia were significantly older than the other patients (P<0.0001).
  • Pediatric patients with or without hyperglycemia during remission induction for ALL have similar clinical outcome.

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  • (PMID = 18923438.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393-09; United States / NCI NIH HHS / CA / CA-78224; United States / NCI NIH HHS / CA / R01 CA078224-09; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / R37 CA036401-21; United States / NCI NIH HHS / CA / R01 CA060419-13; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; None / None / / R01 CA051001-15; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / R01 CA051001-15; United States / NCI NIH HHS / CA / P30 CA021765; None / None / / R01 CA078224-09; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; None / None / / R01 CA060419-13; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NIGMS NIH HHS / GM / GM-61393; United States / NCI NIH HHS / CA / U01 CA060419; United States / NCI NIH HHS / CA / CA036401-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS104861; NLM/ PMC2706830
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41. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • Overexpression of survivin was found to correlate with poor prognosis in a variety of cancers including hematologic malignancies.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • RESULTS: Survivin overexpression, with an up to ten-fold increase of the normal level, was detected in 65% of the leukemic samples in contrast to negligible expression in non-malignant hematopoietic cells.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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42. Raetz EA, Salzer WL: Tolerability and efficacy of L-asparaginase therapy in pediatric patients with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Oct;32(7):554-63
Hazardous Substances Data Bank. ASPARAGINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tolerability and efficacy of L-asparaginase therapy in pediatric patients with acute lymphoblastic leukemia.
  • L-asparaginase (L-ASNase) has been an essential component of multiagent chemotherapy for acute lymphoblastic leukemia in childhood for over 3 decades.
  • There are currently 2 Food and Drug Administration (FDA)-approved formulations of L-ASNase derived from Escherichia coli and 1 non-FDA approved formulation derived from Erwinia chrysanthemi.
  • Other significant toxicities relate to a reduction in protein synthesis and include pancreatitis, thrombosis, central nervous system complications, and liver dysfunction.
  • [MeSH-major] Asparagine / administration & dosage. Asparagine / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20724951.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 7006-34-0 / Asparagine
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43. Schraders M, van Reijmersdal SV, Kamping EJ, van Krieken JH, van Kessel AG, Groenen PJ, Hoogerbrugge PM, Kuiper RP: High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage. Cancer Genet Cytogenet; 2009 May;191(1):27-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage.
  • Lymphoblastic lymphoma (LBL) is one of the most frequent occurring pediatric non-Hodgkin lymphomas.
  • In the WHO classification scheme, pediatric LBL is considered to be the same disease entity as pediatric acute lymphoblastic leukemia (ALL).
  • However, it is unclear whether the genetic basis of pediatric LBL development is similar to that of pediatric ALL.
  • We performed genome-wide analyses of copy number aberrations in 12 T-LBL and 7 precursor B-cell LBL pediatric cases using high-resolution SNP-based array CGH.
  • Taken together, our data suggest that pediatric LBL and ALL exhibit similar genomic abnormalities within confined immunophenotypic and cytogenetic subgroups, but that the representations of these subgroups differs between the two entities.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Gene Expression Profiling. Genome, Human / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Cell Cycle. Child. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 9 / genetics. Gene Duplication. Gene Expression Regulation, Leukemic. Humans. Polyploidy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes / pathology

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  • (PMID = 19389505.001).
  • [ISSN] 1873-4456
  • [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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44. Gokhale CD, Udipi SA, Ambaye RY, Pai SK, Advani SH: Post-therapy profile of serum total cholesterol, retinol and zinc in pediatric acute lymphoblastic leukemia and non-Hodgkin's lymphoma. J Am Coll Nutr; 2007 Feb;26(1):49-56
Hazardous Substances Data Bank. ZINC, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Post-therapy profile of serum total cholesterol, retinol and zinc in pediatric acute lymphoblastic leukemia and non-Hodgkin's lymphoma.
  • OBJECTIVE: To assess serum albumin, total cholesterol, retinol, zinc and hemoglobin in children who had completed treatment for acute lymphoblastic leukemia (ALL) and Non-Hodgkin's lymphoma (NHL).
  • [MeSH-major] Lymphoma, Non-Hodgkin / blood. Nutritional Status. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Trace Elements / blood. Vitamin A / blood. Vitamins / blood


45. Treepongkaruna S, Thongpak N, Pakakasama S, Pienvichit P, Sirachainan N, Hongeng S: Acute pancreatitis in children with acute lymphoblastic leukemia after chemotherapy. J Pediatr Hematol Oncol; 2009 Nov;31(11):812-5
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  • [Title] Acute pancreatitis in children with acute lymphoblastic leukemia after chemotherapy.
  • BACKGROUND: Acute pancreatitis (AP) is a complication in children with acute lymphoblastic leukemia (ALL) receiving chemotherapy and has often been reported associated with L-asparaginase (L-asp) therapy.
  • METHODS: Retrospective cohort study was conducted by reviewing the data of total 192 pediatric ALL patients from Pediatric Oncology Registry at Ramathibodi Hospital from 2000 to 2006 to assess incidence, clinical data, outcome, and mortality of AP.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Pancreatitis / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Registries
  • [MeSH-minor] Acute Disease. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Child, Preschool. Cohort Studies. Female. Humans. Incidence. Male. Retrospective Studies. Risk Factors. Survival Rate

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  • (PMID = 19801948.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.5.1.1 / Asparaginase
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46. Jiang H, Gu LJ, Xue HL, Tang JY, Chen J, Pan C, Chen J: [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Aug;8(4):272-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia].
  • OBJECTIVE: To study the cellular activity of asparagine synthetase in different types of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Aspartate-Ammonia Ligase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 16923354.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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47. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The 5-year event-free survival was 67% for the pediatric treatment group and 60% for the adult treatment group (p=n.s.).
  • 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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48. Schotte D, Chau JC, Sylvester G, Liu G, Chen C, van der Velden VH, Broekhuis MJ, Peters TC, Pieters R, den Boer ML: Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):313-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia.
  • To identify miRNAs relevant to pediatric acute lymphoblastic leukemia (ALL), we cloned 105 known and 8 new miRNA genes expressed in patients' leukemia cells.
  • Eight miRNAs were differentially expressed between MLL and non-MLL precursor B-ALL cases (P<0.05).
  • Most remarkably, miR-708 was 250- up to 6500-fold higher expressed in 57 TEL-AML1, BCR-ABL, E2A-PBX1, hyperdiploid and B-other cases than in 20 MLL-rearranged and 15 T-ALL cases (0.0001<P<0.01), whereas the expression of miR-196b was 500-fold higher in MLL-rearranged and 800-fold higher in 5 of 15 T-ALL cases as compared with the expression level in the remaining precursor B-ALL cases (P<0.001).
  • The expression did not correlate with the maturation status of leukemia cells based on immunoglobulin and T-cell receptor rearrangements, immunophenotype or MLL-fusion partner.
  • [MeSH-major] MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Cloning, Molecular. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 18923441.001).
  • [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 / MicroRNAs; 0 / RNA, Neoplasm; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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49. Huguet F, Leguay T, Raffoux E, Thomas X, Beldjord K, Delabesse E, Chevallier P, Buzyn A, Delannoy A, Chalandon Y, Vernant JP, Lafage-Pochitaloff M, Chassevent A, Lhéritier V, Macintyre E, Béné MC, Ifrah N, Dombret H: Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study. J Clin Oncol; 2009 Feb 20;27(6):911-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study.
  • PURPOSE: Retrospective comparisons have suggested that adolescents or teenagers with acute lymphoblastic leukemia (ALL) benefit from pediatric rather than adult chemotherapy regimens.
  • Thus, the aim of the present phase II study was to test a pediatric-inspired treatment, including intensified doses of nonmyelotoxic drugs, such as prednisone, vincristine, or L-asparaginase, in adult patients with ALL up to the age of 60 years.
  • PATIENTS AND METHODS: Between 2003 and 2005, 225 adult patients (median age, 31 years; range, 15 to 60 years) with Philadelphia chromosome-negative ALL were enrolled onto the Group for Research on Adult Acute Lymphoblastic Leukemia 2003 protocol, which included several pediatric options.
  • RESULTS: were retrospectively compared with the historical France-Belgium Group for Lymphoblastic Acute Leukemia in Adults 94 (LALA-94) trial experience in 712 patients age 15 to 55 years.
  • CONCLUSION: These results suggest that pediatric-inspired therapy markedly improves the outcome of adult patients with ALL, at least until the age of 45 years.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [ErratumIn] J Clin Oncol. 2009 May 20;27(15):2574. Dosage error in article text
  • (PMID = 19124805.001).
  • [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] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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50. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19526524.001).
  • [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
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51. Stanulla M, Schrappe M: Treatment of childhood acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):52-63
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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 lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood.
  • Studies in ALL have been a model for clinical and basic research beyond pediatric hemato-oncology.
  • As a result of sustained and well-organized research efforts since the early 1960s, childhood ALL now can be successfully treated in about 80% of patients by the application of intensive combination chemotherapy regimens, which in specific patient subgroups may need to be supplemented with radiation therapy and/or hematopoietic stem cell transplantation.
  • Thus, future research must extend our molecular understanding of leukemia and host factors in order to even more specifically identify the mechanisms underlying the differences in treatment response and outcome, and to finally address the therapeutic needs of the individual child.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19100368.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 101
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52. Litzow MR: Evolving paradigms in the therapy of Philadelphia-chromosome-negative acute lymphoblastic leukemia in adults. Hematology Am Soc Hematol Educ Program; 2009;:362-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving paradigms in the therapy of Philadelphia-chromosome-negative acute lymphoblastic leukemia in adults.
  • Important studies challenging previous approaches to the treatment of adults with Philadelphia chromosome-negative acute lymphoblastic leukemia (ALL) have emerged in the past decade.
  • Donor versus no donor comparisons of allogeneic transplant highlight a potent graft-versus-leukemia effect in ALL, and the application of reduced-intensity conditioning transplants may exploit this effect while reducing non-relapse mortality.
  • The adoption of the use of pediatric intensity-type regimens in adolescents and young adults shows promise to improve outcomes in this population.

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  • (PMID = 20008222.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 70
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53. van Vlierberghe P, Meijerink JP, Lee C, Ferrando AA, Look AT, van Wering ER, Beverloo HB, Aster JC, Pieters R: A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1245-53
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  • [Title] A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia.
  • Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities.
  • In this study, we used array-comparative genome hybridization (array-CGH) and identified a novel recurrent 9q34 amplification in 33% (12/36) of pediatric T-ALL samples, which is therefore one of the most frequent cytogenetic abnormalities observed in T-ALL thus far.
  • Episomal NUP214-ABL1 amplification and activating mutations in NOTCH1, two other recently identified 9q34 abnormalities in T-ALL, were also detected in our patient cohort.
  • [MeSH-major] Chromosomes, Human, Pair 9. Gene Duplication. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16673019.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1
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54. Airoldi I, Cocco C, Di Carlo E, Disarò S, Ognio E, Basso G, Pistoia V: Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells. Cancer Res; 2006 Apr 15;66(8):3978-80
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  • [Title] Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells.
  • The aim of this study was to investigate (i) whether the IL-12Rbeta2 gene is silenced in B-cell acute lymphoblastic leukemia (B-ALL) cells, and (ii) what the functional implications of such silencing for tumor growth are.
  • Similarly, primary tumor cells from pediatric pro-B, early pre-B, and pre-B ALL (30 cases) did not express the IL-12Rbeta2 chain.

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  • (PMID = 16618714.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / IL12RB2 protein, human; 0 / Il12rb2 protein, mouse; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-12
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55. Ribera JM, Oriol A: Acute lymphoblastic leukemia in adolescents and young adults. Hematol Oncol Clin North Am; 2009 Oct;23(5):1033-42, vi
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia in adolescents and young adults.
  • Today, long-term survival is achieved in more than 80% of children 1 to 10 years old with acute lymphoblastic leukemia (ALL).
  • Within childhood ALL populations, older children have shown inferior outcomes, whereas younger adults have shown superior outcomes among adult ALL patients.
  • The type of treatment (pediatric-based versus adult-based) for AYA has recently been a matter of debate.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19825451.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 43
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56. Ou-Yang LW, Chang PC, Tsai AI, Jaing TH, Lin SY: Salivary microbial counts and buffer capacity in children with acute lymphoblastic leukemia. Pediatr Dent; 2010 May-Jun;32(3):218-22
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  • [Title] Salivary microbial counts and buffer capacity in children with acute lymphoblastic leukemia.
  • METHODS: Forty-six children with acute lymphoblastic leukemia (ALL) were examined, the age ranged from 3 to 12 years with a mean age of 7(1/2) years.
  • They were under maintenance stage chemotherapy at the Department of Pediatric Hematology of Chang-Gung Memorial Hospital, Taoyuan, Taiwan.
  • [MeSH-major] Dental Caries / prevention & control. Oral Hygiene. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Saliva / physiology

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  • (PMID = 20557705.001).
  • [ISSN] 0164-1263
  • [Journal-full-title] Pediatric dentistry
  • [ISO-abbreviation] Pediatr Dent
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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57. Shalapour S, Eckert C, Seeger K, Pfau M, Prada J, Henze G, Blankenstein T, Kammertoens T: Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia. J Mol Med (Berl); 2010 Mar;88(3):249-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.
  • Even though childhood ALL can be cured in a large number of patients, around 20% of the patients suffer a relapse after chemotherapy.
  • Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.
  • MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).
  • Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.
  • The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.
  • [MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [CommentIn] J Mol Med (Berl). 2010 Mar;88(3):219-22 [20135087.001]
  • (PMID = 20155409.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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58. Davidsen ML, Dalhoff K, Schmiegelow K: Pharmacogenetics influence treatment efficacy in childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Nov;30(11):831-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacogenetics influence treatment efficacy in childhood acute lymphoblastic leukemia.
  • As most childhood acute lymphoblastic leukemia treatment protocols include up to 13 different chemotherapeutic agents, the impact of individual SNPs has been difficult to evaluate.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasm Proteins / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


59. Bachmann PS, Piazza RG, Janes ME, Wong NC, Davies C, Mogavero A, Bhadri VA, Szymanska B, Geninson G, Magistroni V, Cazzaniga G, Biondi A, Miranda-Saavedra D, Göttgens B, Saffery R, Craig JM, Marshall GM, Gambacorti-Passerini C, Pimanda JE, Lock RB: Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition. Blood; 2010 Oct 21;116(16):3013-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition.
  • Glucocorticoids play a critical role in the therapy of lymphoid malignancies, including pediatric acute lymphoblastic leukemia (ALL), although the mechanisms underlying cellular resistance remain unclear.
  • We report glucocorticoid resistance attributable to epigenetic silencing of the BIM gene in pediatric ALL biopsies and xenografts established in immune-deficient mice from direct patient explants as well as a therapeutic approach to reverse resistance in vivo.
  • These findings provide a novel therapeutic strategy to reverse glucocorticoid resistance and improve outcome for high-risk pediatric ALL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis Regulatory Proteins / genetics. Drug Resistance, Neoplasm. Gene Silencing. Glucocorticoids / therapeutic use. Histone Deacetylase Inhibitors / therapeutic use. Membrane Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 20647567.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0800784; United Kingdom / National Centre for the Replacement, Refinement and Reduction of Animals in Research / / G0900729/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 58IFB293JI / vorinostat; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.98 / Histone Deacetylases
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60. Campana D: Role of minimal residual disease monitoring in adult and pediatric acute lymphoblastic leukemia. Hematol Oncol Clin North Am; 2009 Oct;23(5):1083-98, vii
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of minimal residual disease monitoring in adult and pediatric acute lymphoblastic leukemia.
  • Assays that measure minimal residual disease (MRD) can determine the response to treatment in patients with acute lymphoblastic leukemia (ALL) much more precisely than morphologic screening of bone marrow smears.
  • The clinical significance of MRD, detected by flow cytometry or polymerase chain reaction-based methods in childhood ALL, has been established.

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  • (PMID = 19825454.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA060419-13; 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 / P30 CA021765; None / None / / R01 CA060419-13; 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; Review
  • [Publication-country] United States
  • [Number-of-references] 95
  • [Other-IDs] NLM/ NIHMS132490; NLM/ PMC2762949
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61. Harila MJ, Winqvist S, Lanning M, Bloigu R, Harila-Saari AH: Progressive neurocognitive impairment in young adult survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Aug;53(2):156-61
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  • [Title] Progressive neurocognitive impairment in young adult survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Despite the extensive literature on neuropsychological sequelae after treatment of childhood acute lymphoblastic leukemia (ALL), the very-long-term neurocognitive outcome of the survivors is poorly studied.
  • We assessed neuropsychological functioning in a population-based cohort of young adult childhood ALL survivors.
  • The mean VIQ test scores were 91, 100, and 109 (P < 0.001), and the mean PIQ test scores 100, 111, and 118 (P < 0.001) for the irradiated survivors, non-irradiated survivors and controls, respectively.
  • A significant decline in PIQ and VIQ test scores was observed in the irradiated survivor group during the follow-up period, but only in VIQ in the non-irradiated group.
  • CONCLUSIONS: Survivors of childhood ALL suffer from long-lasting progressive neuropsychological impairment, especially when treatment includes cranial irradiation.
  • [MeSH-major] Brain Neoplasms / complications. Cognition Disorders / epidemiology. Cognition Disorders / etiology. Cranial Irradiation / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


62. Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T: Infant acute bilineal leukemia. Leuk Res; 2009 Jul;33(7):1005-8
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  • [Title] Infant acute bilineal leukemia.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).
  • Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.
  • This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19286255.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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63. Liang DC, Yang CP, Lin DT, Hung IJ, Lin KH, Chen JS, Hsiao CC, Chang TT, Peng CT, Lin MT, Chang TK, Jaing TH, Liu HC, Wang LY, Yeh TC, Jou ST, Lu MY, Cheng CN, Sheen JM, Chiou SS, Wu KH, Hung GY, Chen RL, Chen SH, Cheng SN, Chang YH, Chen BW, Ho WL, Wang JL, Lin ST, Hsieh YL, Wang SC, Chang HH, Yang YL, Huang FL, Chang CY, Chang WH, Lin KS: Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia. Leukemia; 2010 Feb;24(2):397-405
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  • [Title] Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia.
  • The long-term outcome of 1390 children with acute lymphoblastic leukemia (ALL), treated in two successive clinical trials (Taiwan Pediatric Oncology Group (TPOG)-ALL-97 and TPOG-ALL-2002) between 1997 and 2007, is reported.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


64. Ladha AB, Courneya KS, Bell GJ, Field CJ, Grundy P: Effects of acute exercise on neutrophils in pediatric acute lymphoblastic leukemia survivors: a pilot study. J Pediatr Hematol Oncol; 2006 Oct;28(10):671-7
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  • [Title] Effects of acute exercise on neutrophils in pediatric acute lymphoblastic leukemia survivors: a pilot study.
  • PURPOSE: This nonrandomized controlled trial was designed to investigate the effects of acute exercise on neutrophil count and function in children and adolescents receiving maintenance treatment for acute lymphoblastic leukemia (ALL) compared to matched controls.
  • [MeSH-major] Exercise. Neutrophils / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Survivors
  • [MeSH-minor] Acute Disease. Adolescent. Child. Exercise Test. Humans. Leukocyte Count. Male. Pilot Projects. Time Factors


65. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
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  • [Title] CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
  • Acute lymphoblastic leukemia (ALL) is the most frequent malignancy of childhood.
  • We investigated CD1d expression in 80 pediatric B-cell precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
  • CD1d+ ALLs were significantly associated with infant leukemia, pro-B phenotype and mixed-lineage leukemia (MLL)/AF4 gene rearrangement.
  • [MeSH-major] Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15744356.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
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66. Jeha S: New therapeutic strategies in acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):76-88
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  • [Title] New therapeutic strategies in acute lymphoblastic leukemia.
  • While cure rates of over 80% are achieved in contemporary pediatric acute lymphoblastic leukemia (ALL) protocols, most adults with ALL succumb to their disease, and little progress has been made in the treatment of refractory and relapsed ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19100370.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Nucleosides; 0 / Protein Kinase Inhibitors; 935E97BOY8 / Folic Acid
  • [Number-of-references] 167
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67. Mantadakis E, Cole PD, Kamen BA: High-dose methotrexate in acute lymphoblastic leukemia: where is the evidence for its continued use? Pharmacotherapy; 2005 May;25(5):748-55
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  • [Title] High-dose methotrexate in acute lymphoblastic leukemia: where is the evidence for its continued use?
  • High-dose intravenous methotrexate is an important component of many effective chemotherapeutic regimens for childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Folic Acid Antagonists / administration & dosage. Methotrexate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15899736.001).
  • [ISSN] 0277-0008
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Folic Acid Antagonists; Q573I9DVLP / Leucovorin; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 58
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68. Heerema NA, Raimondi SC, Anderson JR, Biegel J, Camitta BM, Cooley LD, Gaynon PS, Hirsch B, Magenis RE, McGavran L, Patil S, Pettenati MJ, Pullen J, Rao K, Roulston D, Schneider NR, Shuster JJ, Sanger W, Sutcliffe MJ, van Tuinen P, Watson MS, Carroll AJ: Specific extra chromosomes occur in a modal number dependent pattern in pediatric acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2007 Jul;46(7):684-93
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  • [Title] Specific extra chromosomes occur in a modal number dependent pattern in pediatric acute lymphoblastic leukemia.
  • Children with acute lymphoblastic leukemia (ALL) and high hyperdiploidy (>50 chromosomes) are considered to have a relatively good prognosis.
  • High hyperdiploid pediatric ALL results from a single abnormal mitotic division.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17431878.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
  • [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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69. Zhu N, Gu L, Findley HW, Chen C, Dong JT, Yang L, Zhou M: KLF5 Interacts with p53 in regulating survivin expression in acute lymphoblastic leukemia. J Biol Chem; 2006 May 26;281(21):14711-8
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  • [Title] KLF5 Interacts with p53 in regulating survivin expression in acute lymphoblastic leukemia.
  • Transfection of KLF5 into a KLF5-negative acute lymphoblastic leukemia cell line EU-8 enhanced survivin expression, and conversely, silencing of KLF5 by small interfering RNA in a KLF5-overexpressing acute lymphoblastic leukemia cell line EU-4 down-regulated survivin expression.
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Microtubule-Associated Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16595680.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 82323
  • [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 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / KLF5 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin
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70. Lowe EJ, Pui CH, Hancock ML, Geiger TL, Khan RB, Sandlund JT: Early complications in children with acute lymphoblastic leukemia presenting with hyperleukocytosis. Pediatr Blood Cancer; 2005 Jul;45(1):10-5
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  • [Title] Early complications in children with acute lymphoblastic leukemia presenting with hyperleukocytosis.
  • BACKGROUND: The optimal management of childhood acute lymphoblastic leukemia (ALL) with hyperleukocytosis is unclear, largely because the risk of leukostasis-related complications is poorly characterized.
  • CONCLUSIONS: Serious leukostasis-related complications are relatively uncommon in childhood ALL and most occur at presentation.
  • [MeSH-major] Leukocytosis / complications. Leukostasis / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Acute Kidney Injury / epidemiology. Acute Kidney Injury / etiology. Acute Kidney Injury / mortality. Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Leukocyte Reduction Procedures. Logistic Models. Lung Diseases / epidemiology. Lung Diseases / etiology. Lung Diseases / mortality. Male. Multivariate Analysis. Nervous System Diseases / epidemiology. Nervous System Diseases / etiology. Nervous System Diseases / mortality. Tennessee / epidemiology

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  • (PMID = 15547931.001).
  • [ISSN] 1545-5009
  • [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; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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71. Brozek J, Bryl E, Płoszyńska A, Balcerska A, Witkowski JM: P-glycoprotein activity predicts outcome in childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Jul;31(7):493-9
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  • [Title] P-glycoprotein activity predicts outcome in childhood acute lymphoblastic leukemia.
  • Treatment of children with acute lymphoblastic leukemia (ALL) is based on P-glycoprotein (P-gp)-dependent cytostatics.
  • [MeSH-major] P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19564743.001).
  • [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 / Antineoplastic Agents; 0 / P-Glycoprotein
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72. Glass JO, Reddick WE, Li CS, Laningham FH, Helton KJ, Pui CH: Computer-aided detection of therapy-induced leukoencephalopathy in pediatric acute lymphoblastic leukemia patients treated with intravenous high-dose methotrexate. Magn Reson Imaging; 2006 Jul;24(6):785-91
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  • [Title] Computer-aided detection of therapy-induced leukoencephalopathy in pediatric acute lymphoblastic leukemia patients treated with intravenous high-dose methotrexate.
  • The purpose of this study was to use objective quantitative magnetic resonance imaging (MRI) methods to develop a computer-aided detection (CAD) tool to differentiate white matter (WM) hyperintensities into either leukoencephalopathy (LE) induced by chemotherapy or normal maturational processes in children treated for acute lymphoblastic leukemia without irradiation.

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  • (PMID = 16824973.001).
  • [ISSN] 0730-725X
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090246-05; United States / NCI NIH HHS / CA / R01 CA090246; United States / NCI NIH HHS / CA / P30CA21765; United States / NCI NIH HHS / CA / R01CA90246; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA090246-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS49117; NLM/ PMC2396783
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73. Jeha S, Gaynon PS, Razzouk BI, Franklin J, Kadota R, Shen V, Luchtman-Jones L, Rytting M, Bomgaars LR, Rheingold S, Ritchey K, Albano E, Arceci RJ, Goldman S, Griffin T, Altman A, Gordon B, Steinherz L, Weitman S, Steinherz P: Phase II study of clofarabine in pediatric patients with refractory or relapsed acute lymphoblastic leukemia. J Clin Oncol; 2006 Apr 20;24(12):1917-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of clofarabine in pediatric patients with refractory or relapsed acute lymphoblastic leukemia.
  • PURPOSE: To evaluate the efficacy and safety of clofarabine, a novel deoxyadenosine analog, in pediatric patients with refractory or relapsed acute lymphoblastic leukemia (ALL).
  • PATIENTS AND METHODS: In a phase II, open-label, multicenter study, 61 pediatric patients with refractory or relapsed ALL received clofarabine 52 mg/m2 intravenously over 2 hours daily for 5 days, every 2 to 6 weeks.
  • CONCLUSION: Clofarabine is active as a single agent in pediatric patients with multiple relapsed or refractory ALL.
  • Studies exploring rational combinations of clofarabine with other agents are ongoing in an effort to maximize clinical benefit.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


74. Graubner UB, Porzig S, Jorch N, Kolb R, Wessalowski R, Escherich G, Janka GE: Impact of reduction of therapy on infectious complications in childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Feb;50(2):259-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of reduction of therapy on infectious complications in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Infections are a major cause of morbidity and mortality in childhood acute lymphoblastic leukemia (ALL) and only limited information is available on infectious complications.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Infection / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / microbiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17635005.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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75. Jackman KM, Frye CB, Hunger SP: Flavopiridol displays preclinical activity in acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Apr;50(4):772-8
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  • [Title] Flavopiridol displays preclinical activity in acute lymphoblastic leukemia.
  • BACKGROUND: New agents are needed for treatment of children with relapsed acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Piperidines / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / drug effects. Neoplasm Recurrence, Local / drug therapy. Proto-Oncogene Proteins c-bcl-2 / drug effects. RNA Polymerase II / drug effects. Retinoblastoma Protein / drug effects

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18000861.001).
  • [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 / Antineoplastic Agents; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 45AD6X575G / alvocidib; EC 2.7.7.- / RNA Polymerase II
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76. te Winkel ML, van Beek RD, de Muinck Keizer-Schrama SM, Uitterlinden AG, Hop WC, Pieters R, van den Heuvel-Eibrink MM: Pharmacogenetic risk factors for altered bone mineral density and body composition in pediatric acute lymphoblastic leukemia. Haematologica; 2010 May;95(5):752-9
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  • [Title] Pharmacogenetic risk factors for altered bone mineral density and body composition in pediatric acute lymphoblastic leukemia.
  • BACKGROUND: This study investigates pharmacogenetic risk factors for bone mineral (apparent) density (BM(A)D) and body composition in pediatric acute lymphoblastic leukemia DESIGN AND METHODS: We determined the influence of SNPs in 4 genes (vitamin-D receptor (VDR: BsmI/ApaI/TaqI and Cdx-2/GATA), collagen type I alpha 1 (SpI), estrogen receptor 1 (ESR1: PvuII/XbaI), glucocorticoid receptor (BclI)) on body composition, BM(A)D and fracture risk during dexamethasone-based pediatric acute lymphoblastic leukemia treatment.
  • RESULTS: Non-carriers of VDR 5'-end (Cdx-2/GATA) haplotype 3 revealed a significant larger fat gain than carriers (Delta%fat: non-carriers: +1.76SDS, carriers: +0.77SDS, P<0.001).
  • At diagnosis and during therapy, lumbar spine BMD was significantly higher in non-carriers of VDR 5'-end (Cdx-2/GATA) haplotype 3 than in carriers.
  • The other SNPs did not influence BMD or fracture risk during/after treatment.
  • The year after treatment completion, lean body mass increased in non-carriers of ESR1 (PvuII/XbaI) haplotype 3 and decreased in carriers (Delta lean body mass: non-carriers:+0.28SDS, carriers: -0.55SDS, P<0.01).
  • Carrying ESR1 (PvuII/XbaI) haplotype 3 negatively influenced recovery of lean body mass after pediatric acute lymphoblastic leukemia treatment.
  • [MeSH-major] Body Composition / genetics. Bone Density / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


77. Pakakasama S, Sirirat T, Kanchanachumpol S, Udomsubpayakul U, Mahasirimongkol S, Kitpoka P, Thithapandha A, Hongeng S: Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Jan;48(1):16-20
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  • [Title] Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia.
  • This study was performed to evaluate the effect of the polymorphisms of DNA repair genes on risk of childhood acute lymphoblastic leukemia (ALL).
  • CONCLUSION: The XRCC1 194Trp allele and haplotype B showed a protective effect against development of childhood ALL.
  • [MeSH-major] Alleles. DNA Repair. DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16435384.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
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78. van Galen JC, Kuiper RP, van Emst L, Levers M, Tijchon E, Scheijen B, Waanders E, van Reijmersdal SV, Gilissen C, van Kessel AG, Hoogerbrugge PM, van Leeuwen FN: BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia. Blood; 2010 Jun 10;115(23):4810-9
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  • [Title] BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia.
  • Resistance to glucocorticoids (GCs) is a major clinical problem in the treatment of acute lymphoblastic leukemia (ALL), but the underlying mechanisms are not well understood.
  • Here we report that the protein encoded by the BTG1 gene, which is frequently deleted in (pediatric) ALL, is a key determinant of GC responsiveness.
  • Further characterization of this complex as part of the GR regulatory circuitry could offer novel opportunities for improving the efficacy of GC-based therapies in ALL and other hematologic malignancies.
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Glucocorticoid / biosynthesis

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  • (PMID = 20354172.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Multiprotein Complexes; 0 / Neoplasm Proteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 146835-72-5 / BTG1 protein, human; EC 2.1.1.- / PRMT1 protein, human; EC 2.1.1.- / Protein-Arginine N-Methyltransferases
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79. Spraker HL, Spyridis GP, Pui CH, Howard SC: Conservative management of pancreatic pseudocysts in children with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Dec;31(12):957-9
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  • [Title] Conservative management of pancreatic pseudocysts in children with acute lymphoblastic leukemia.
  • Treatment with asparaginase for acute lymphoblastic leukemia can cause acute pancreatitis.
  • We report 5 children with acute lymphoblastic leukemia who developed acute pancreatitis complicated by pancreatic pseudocysts.
  • In addition, these patients demonstrate that oral feeding can be initiated after the acute episode of pancreatitis resolves even if a pseudocyst is present.

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  • (PMID = 19956023.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / P30 CA021765-28; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA021765-28; United States / NIGMS NIH HHS / GM / GM-61393; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.5.1.1 / Asparaginase
  • [Other-IDs] NLM/ NIHMS149448; NLM/ PMC2811578
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80. Ceppi F, Brown A, Betts DR, Niggli F, Popovic MB: Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua. Pediatr Blood Cancer; 2009 Dec 15;53(7):1238-41
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  • [Title] Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua.
  • BACKGROUND: Within the frame of a twinning programme with Nicaragua, The La Mascota project, we evaluated in our study the contribution of cytogenetic characterization of acute lymphoblastic leukemia (ALL) as prognostic factor compared to clinical, morphological, and immunohistochemical parameters.
  • METHODS: All patients with ALL treated at the only cancer pediatric hospital in Nicaragua during 2006 were studied prospectively.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Aneuploidy. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Hepatomegaly / epidemiology. Hepatomegaly / etiology. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Nicaragua / epidemiology. Oncogene Proteins, Fusion / genetics. Prognosis. Prospective Studies. Risk. Splenomegaly / epidemiology. Splenomegaly / etiology

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19672974.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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81. Tissing WJ, den Boer ML, Meijerink JP, Menezes RX, Swagemakers S, van der Spek PJ, Sallan SE, Armstrong SA, Pieters R: Genomewide identification of prednisolone-responsive genes in acute lymphoblastic leukemia cells. Blood; 2007 May 1;109(9):3929-35
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  • [Title] Genomewide identification of prednisolone-responsive genes in acute lymphoblastic leukemia cells.
  • Glucocorticoids are keystone drugs in the treatment of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Gene Expression Regulation, Leukemic / drug effects. Genome, Human. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Prednisolone / pharmacology


82. Stam RW, den Boer ML, Schneider P, Nollau P, Horstmann M, Beverloo HB, van der Voort E, Valsecchi MG, de Lorenzo P, Sallan SE, Armstrong SA, Pieters R: Targeting FLT3 in primary MLL-gene-rearranged infant acute lymphoblastic leukemia. Blood; 2005 Oct 1;106(7):2484-90
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  • [Title] Targeting FLT3 in primary MLL-gene-rearranged infant acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) in infants is characterized by rearrangements of the mixed lineage leukemia (MLL) gene, drug resistance, and a poor treatment outcome.
  • Thus, PKC412-induced apoptosis in infant MLL cells is unlikely to be a consequence of FLT3 inhibition alone but may involve inhibition of multiple other kinases by this drug.
  • [MeSH-major] Gene Rearrangement. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15956279.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / Ligands; 0 / Tetrazolium Salts; 0 / Thiazoles; 120685-11-2 / 4'-N-benzoylstaurosporine; 298-93-1 / thiazolyl blue; 63231-63-0 / RNA; 9007-49-2 / DNA; H88EPA0A3N / Staurosporine
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83. Paulsson K, Cazier JB, Macdougall F, Stevens J, Stasevich I, Vrcelj N, Chaplin T, Lillington DM, Lister TA, Young BD: Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease. Proc Natl Acad Sci U S A; 2008 May 6;105(18):6708-13
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  • [Title] Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease.
  • We present here a genome-wide map of abnormalities found in diagnostic samples from 45 adults and adolescents with acute lymphoblastic leukemia (ALL).
  • Importantly, the pattern of deletions resembled that recently reported in pediatric ALL, suggesting that adult, adolescent, and childhood cases may be more similar on the genetic level than previously thought.
  • [MeSH-major] Gene Deletion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18458336.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE9611
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2373322
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84. Kanderová V, Hrusák O, Kalina T: Aberrantly expressed CEACAM6 is involved in the signaling leading to apoptosis of acute lymphoblastic leukemia cells. Exp Hematol; 2010 Aug;38(8):653-660.e1
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  • [Title] Aberrantly expressed CEACAM6 is involved in the signaling leading to apoptosis of acute lymphoblastic leukemia cells.
  • OBJECTIVE: The aberrant expression of myeloid antigens on acute lymphoblastic leukemia (ALL) cells is a well-documented phenomenon.
  • The granulocytic marker carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6, CD66c) is a GPI-anchored molecule that is reported to be the most frequently aberrantly expressed myeloid marker in ALL with a strong correlation with genotype.
  • However, CEACAM6 signaling resulted in an increase in apoptosis, unlike other GPI-anchored molecules, such as CD24.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Neoplasm / metabolism. Apoptosis. Cell Adhesion Molecules / metabolism. Gene Expression Regulation, Leukemic. MAP Kinase Signaling System. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • [Copyright] 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20380867.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Integrins; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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85. Zhu YM, Zhao WL, Fu JF, Shi JY, Pan Q, Hu J, Gao XD, Chen B, Li JM, Xiong SM, Gu LJ, Tang JY, Liang H, Jiang H, Xue YQ, Shen ZX, Chen Z, Chen SJ: NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis. Clin Cancer Res; 2006 May 15;12(10):3043-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • Interestingly, the statistically significant difference of survival according to NOTCH1 mutations was only observed in adult patients (>18 years) but not in pediatric patients (< or = 18 years), possibly due to the relatively good overall response of childhood T-ALL to the current chemotherapy.
  • CONCLUSION: NOTCH1 mutation is an important prognostic marker in T-ALL and its predictive value could be even further increased if coevaluated with other T-cell-related regulatory genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

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  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [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 / NOTCH1 protein, human; 0 / Receptor, Notch1
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86. Mullighan CG, Phillips LA, Su X, Ma J, Miller CB, Shurtleff SA, Downing JR: Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia. Science; 2008 Nov 28;322(5906):1377-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia.
  • Most children with acute lymphoblastic leukemia (ALL) can be cured, but the prognosis is dismal for the minority of patients who relapse after treatment.
  • To explore the genetic basis of relapse, we performed genome-wide DNA copy number analyses on matched diagnosis and relapse samples from 61 pediatric patients with ALL.
  • Most relapse samples lacked some of the CNAs present at diagnosis, which suggests that the cells responsible for relapse are ancestral to the primary leukemia cells.


87. Lowas S, Malempati S, Marks D: Body mass index predicts insulin resistance in survivors of pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Jul;53(1):58-63
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  • [Title] Body mass index predicts insulin resistance in survivors of pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Pediatric acute lymphoblastic leukemia (ALL) therapies have been associated with many late effects, including obesity, hyperglycemia, and insulin resistance.
  • [MeSH-major] Body Mass Index. Hyperglycemia / epidemiology. Insulin Resistance. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Survivors / statistics & numerical data

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
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  • (PMID = 19340854.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCRR NIH HHS / RR / UL1 RR024140-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS123017; NLM/ PMC3804011
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88. Panagopoulos I, Lilljebjörn H, Strömbeck B, Hjorth L, Olofsson T, Johansson B: MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia. Haematologica; 2006 Sep;91(9):1287-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia.
  • MLL/GAS7, resulting from t(11;17)(q23;p13), has been reported in one case of treatment-related acute myeloid leukemia (AML).
  • We present a de novo case of t(11;17)-positive pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Humans. Infant. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 16956839.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / GAS7 protein, human; 0 / MLL-GAS7 fusion protein; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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89. Chow EJ, Simmons JH, Roth CL, Baker KS, Hoffmeister PA, Sanders JE, Friedman DL: Increased cardiometabolic traits in pediatric survivors of acute lymphoblastic leukemia treated with total body irradiation. Biol Blood Marrow Transplant; 2010 Dec;16(12):1674-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased cardiometabolic traits in pediatric survivors of acute lymphoblastic leukemia treated with total body irradiation.
  • Survivors of childhood acute lymphoblastic leukemia (ALL) may face an increased risk of metabolic and cardiovascular late effects.
  • To determine the prevalence of and risk factors for adverse cardiometabolic traits in a contemporary cohort of pediatric ALL survivors, we recruited 48 off-therapy patients in remission treated with conventional chemotherapy and 26 treated with total body irradiation (TBI)-based hematopoietic cell transplantation (HCT) in this cross-sectional pilot study.
  • At a median age of 15 years (range, 8-21 years), HCT survivors were significantly more likely than non-HCT survivors to manifest multiple cardiometabolic traits, including central adiposity, hypertension, insulin resistance, and dyslipidemia.
  • Overall, 23.1% of HCT survivors met the criteria for metabolic syndrome (≥ 3 traits), compared with 4.2% of non-HCT survivors (P = .02).
  • Other risk factors included any cranial radiation exposure and family history of cardiometabolic disease.
  • In summary, pediatric ALL survivors exposed to TBI-based HCT as well as to any cranial radiation may manifest cardiometabolic traits at an early age and should be screened accordingly.

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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20685399.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024975-01; United States / NCRR NIH HHS / RR / UL1 RR025014-01; United States / NCRR NIH HHS / RR / TL1 RR024978; United States / NCRR NIH HHS / RR / KL2 RR024977; None / None / / UL1 RR025014-01; United States / NCRR NIH HHS / RR / UL1RR025014; United States / NCRR NIH HHS / RR / UL1RR024975; United States / NCRR NIH HHS / RR / UL1 RR025014; United States / NCRR NIH HHS / RR / UL1 RR024975
  • [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 / Leptin; 9007-41-4 / C-Reactive Protein
  • [Other-IDs] NLM/ NIHMS211258; NLM/ PMC2975816
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90. De Pittà C, Tombolan L, Campo Dell'Orto M, Accordi B, te Kronnie G, Romualdi C, Vitulo N, Basso G, Lanfranchi G: A leukemia-enriched cDNA microarray platform identifies new transcripts with relevance to the biology of pediatric acute lymphoblastic leukemia. Haematologica; 2005 Jul;90(7):890-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A leukemia-enriched cDNA microarray platform identifies new transcripts with relevance to the biology of pediatric acute lymphoblastic leukemia.
  • BACKGROUND AND OBJECTIVES: Microarray gene expression profiling has been widely applied to characterize hematologic malignancies, has attributed a molecular signature to leukemia subclasses and has allowed new subclasses to be distinguished.
  • To this end we used a unique leukemia-enriched cDNA microarray platform.
  • Using this platform we analyzed the expression profiles of 4,670 genes in bone marrow samples from 18 pediatric patients with acute lymphoblastic leukemia (ALL).
  • RESULTS: Expression profiling consistently distinguished the leukemia patients into three groups, those with T-ALL, B-ALL and B-ALL with MLL/AF4 rearrangement, in agreement with the clinical classification.
  • Our approach of using a unique platform has proven to be fruitful in identifying new genes and we suggest exploration of other malignancies using this approach.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Oligonucleotide Array Sequence Analysis / instrumentation. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentIn] Haematologica. 2005 Jul;90(7):866 [15996916.001]
  • (PMID = 15996926.001).
  • [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 / DNA, Complementary
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91. Sterba J, Dusek L, Demlova R, Valik D: Pretreatment plasma folate modulates the pharmacodynamic effect of high-dose methotrexate in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma: "folate overrescue" concept revisited. Clin Chem; 2006 Apr;52(4):692-700
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pretreatment plasma folate modulates the pharmacodynamic effect of high-dose methotrexate in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma: "folate overrescue" concept revisited.
  • BACKGROUND: To evaluate the influence of pretreatment plasma folate concentrations on methotrexate exposure in children with acute lymphoblastic leukemia/non-Hodgkin lymphoma treated with high-dose methotrexate, we assessed time profiles of plasma homocysteine, folate, and vitamin B(12) concentrations in children treated with high-dose methotrexate with leucovorin rescue.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Folic Acid / blood. Leucovorin / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vitamin B Complex / therapeutic use


92. Zibert A, Thomassen A, Müller L, Nguyen L, Glouchkova L, Fraefel C, Roskrow M, Meisel R, Dilloo D: Herpes simplex virus type-1 amplicon vectors for vaccine generation in acute lymphoblastic leukemia. Gene Ther; 2005 Dec;12(23):1707-17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Herpes simplex virus type-1 amplicon vectors for vaccine generation in acute lymphoblastic leukemia.
  • For leukemia vaccine generation, high-efficiency gene transfer is required to express immunomodulatory molecules that stimulate potent antileukemic immune responses.
  • In this context, herpes simplex virus type-1 (HSV-1)-derived vectors have proven to be a promising tool for genetic modification of lymphoblastic leukemia cells.
  • To explore the issue of immune-stimulation versus immune-suppression in immature lymphoblastic leukemia cells, two types of HSV-1 amplicon vectors, helper virus-dependent and helper virus-free that express the immunomodulatory molecules CD70 and IL-2, were compared with regard to their vector-associated immunomodulatory potential.
  • We first established that lymphoblastic cell lines and primary acute lymphoblastic leukemia (ALL) cells express HSV receptor genes.
  • Lymphoblastic cell lines were transduced with high efficiency, and in primary ALL cells high gene transfer rates of 47+/-15 and 42+/-14% were obtained with helper virus-dependent and -free HSV-1 amplicon vectors, respectively.
  • The efficacy of the two amplicon vectors to induce antineoplastic responses was assessed in a vaccine setting in mice with pre-existing highly malignant lymphoblastic disease.
  • Treatment of mice with vaccine cells transgenically expressing CD70+IL2 significantly suppressed lymphoblastic cell proliferation and improved survival.
  • Thus for vaccine generation in B lymphoblastic leukemia, the immunogenic potential of HSV-1 helper virus-dependent amplicon vectors does provide additional benefit to the high transduction efficiency of HSV-1-derived vectors.
  • [MeSH-major] Cancer Vaccines / genetics. Genetic Therapy / methods. Herpesvirus 1, Human / genetics. Immunotherapy / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16034459.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD70; 0 / CD70 protein, human; 0 / Cancer Vaccines; 0 / Interleukin-2; 0 / Membrane Proteins; 0 / Tnfsf7 protein, mouse; 0 / Tumor Necrosis Factors
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93. Szczepański T: Why and how to quantify minimal residual disease in acute lymphoblastic leukemia? Leukemia; 2007 Apr;21(4):622-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Why and how to quantify minimal residual disease in acute lymphoblastic leukemia?
  • Several studies have demonstrated that monitoring of minimal residual disease (MRD) in childhood and adult acute lymphoblastic leukemia (ALL) significantly correlates with clinical outcome.
  • Standardized MRD techniques form the basis for stratification of patients into the risk groups in new treatment protocols mainly in childhood ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 17301806.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 48
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94. Mullighan CG, Zhang J, Harvey RC, Collins-Underwood JR, Schulman BA, Phillips LA, Tasian SK, Loh ML, Su X, Liu W, Devidas M, Atlas SR, Chen IM, Clifford RJ, Gerhard DS, Carroll WL, Reaman GH, Smith M, Downing JR, Hunger SP, Willman CL: JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2009 Jun 9;106(23):9414-8
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  • [Title] JAK mutations in high-risk childhood acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) is a heterogeneous disease consisting of distinct clinical and biological subtypes that are characterized by specific chromosomal abnormalities or gene mutations.
  • We recently identified a poor prognostic subgroup of pediatric BCR-ABL1-negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1-positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype.
  • Here, we report activating mutations in the Janus kinases JAK1 (n = 3), JAK2 (n = 16), and JAK3 (n = 1) in 20 (10.7%) of 187 BCR-ABL1-negative, high-risk pediatric ALL cases.
  • The JAK-mutated cases had a gene expression signature similar to BCR-ABL1 pediatric ALL, and they had a poor outcome.

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  • (PMID = 19470474.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA118100; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / L40 CA142226; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / Howard Hughes Medical Institute / / ; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / U10 CA98543
  • [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 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2695045
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95. Schmiegelow K, Vestergaard T, Nielsen SM, Hjalgrim H: Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis. Leukemia; 2008 Dec;22(12):2137-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis.
  • The pattern of infections in the first years of life modulates our immune system, and a low incidence of infections has been linked to an increased risk of common childhood acute lymphoblastic leukemia (ALL).
  • We here present a new interpretation of these observations--the adrenal hypothesis--that proposes that the risk of childhood ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis that increase plasma cortisol levels.
  • [MeSH-major] Hypothalamo-Hypophyseal System / immunology. Infection / immunology. Pituitary-Adrenal System / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 18719616.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 50
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96. Hulleman E, Kazemier KM, Holleman A, VanderWeele DJ, Rudin CM, Broekhuis MJ, Evans WE, Pieters R, Den Boer ML: Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells. Blood; 2009 Feb 26;113(9):2014-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells.
  • Treatment failure in pediatric acute lymphoblastic leukemia (ALL) is related to cellular resistance to glucocorticoids (eg, prednisolone).
  • This sensitizing effect of the glycolysis inhibitors in glucocorticoid-resistant ALL cells was not found for other classes of antileukemic drugs (ie, vincristine and daunorubicin).
  • [MeSH-major] Drug Resistance, Neoplasm. Glycolysis / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Prednisolone / therapeutic use

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  • (PMID = 18978206.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 5J49Q6B70F / Vincristine; 9G2MP84A8W / Deoxyglucose; 9PHQ9Y1OLM / Prednisolone; IY9XDZ35W2 / Glucose; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ PMC4081395
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97. Kustanovich AM, Savitskaja TV, Bydanov OI, Belevtsev MV, Potapnev MP: Aberrant expression of tumor suppressor genes and their association with chimeric oncogenes in pediatric acute lymphoblastic leukemia. Leuk Res; 2005 Nov;29(11):1271-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of tumor suppressor genes and their association with chimeric oncogenes in pediatric acute lymphoblastic leukemia.
  • Aberrant expression of tumor suppressor genes WT 1, RB 1, p53, homozygous deletion of p16 gene and their relationship with expression of oncogenes BCR-ABL, TEL-AML 1, MLL-AF 4, E2A-PBX 1, SIL-TAL 1 were determined in bone marrow samples of children with de novo B-lineage (n=170) and T-lineage (n=25) acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Oncogenes / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15878620.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
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98. Luo XQ, Ke ZY, Guan XQ, Zhang YC, Huang LB, Zhu J: The comparison of outcome and cost of three protocols for childhood non-high risk acute lymphoblastic leukemia in China. Pediatr Blood Cancer; 2008 Aug;51(2):204-9
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  • [Title] The comparison of outcome and cost of three protocols for childhood non-high risk acute lymphoblastic leukemia in China.
  • OBJECTIVE: To compare the outcome and treatment cost of three protocols for childhood non-high risk acute lymphoblastic leukemia (ALL), and evaluate the feasibility of less intensive treatment protocol for low income families.
  • RESULTS: Among 243 patients, 19 abandoned treatment, 3 transferred to other hospitals, 48 were high-risk and were treated with the high risk protocol, and 4 had mature B-ALL.
  • A total of 169 cases were enrolled on non-high risk protocols: 46 treated on China-98 protocol, 73 on modified ALLIC BFM2002 and 50 from low income families on Economic Protocol.
  • The reduced intensity protocol appears to achieve reasonable EFS (72.8% at 4 years) for non-high risk ALL at a much lower cost.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


99. Treviño LR, Yang W, French D, Hunger SP, Carroll WL, Devidas M, Willman C, Neale G, Downing J, Raimondi SC, Pui CH, Evans WE, Relling MV: Germline genomic variants associated with childhood acute lymphoblastic leukemia. Nat Genet; 2009 Sep;41(9):1001-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Germline genomic variants associated with childhood acute lymphoblastic leukemia.
  • Using the Affymetrix 500K Mapping array and publicly available genotypes, we identified 18 SNPs whose allele frequency differed significantly(P < 1 x 10(-5)) between pediatric acute lymphoblastic leukemia (ALL) cases (n = 317) and non-ALL controls (n = 17,958).
  • Two SNPs in ARID5B not only differed between ALL and non-ALL groups (rs10821936, P = 1.4 x 10(-15), odds ratio (OR) = 1.91; rs10994982, P = 5.7 x 10(-9), OR = 1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P = 1.62 x 10(-5), OR = 2.17; rs10994982, P = 0.003, OR 1.72).
  • These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent validation cohort (n = 124 children with ALL; P = 0.003 and P = 0.0008, OR 2.45 and 2.86, respectively) and were associated with methotrexate accumulation and gene expression pattern in leukemic lymphoblasts.

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  • (PMID = 19684603.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH061675; United States / NIMH NIH HHS / MH / R01 MH059556; United States / NCI NIH HHS / CA / CA021765-259006; United States / NCI NIH HHS / CA / U10 CA098413-07; None / None / / U10 CA029139-22; None / None / / U10 CA098413-07; United States / NHLBI NIH HHS / HL / U01 HL65899; United States / NCI NIH HHS / CA / CA 078224; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / CA 36401; United States / NCI NIH HHS / CA / P30 CA021765-259006; United States / NCI NIH HHS / CA / R37 CA036401-24; United States / NIMH NIH HHS / MH / U01 MH046276; United States / NIMH NIH HHS / MH / R01 MH059535; United States / NIMH NIH HHS / MH / R01 MH059567; United States / NIMH NIH HHS / MH / R01 MH059545; United States / NIGMS NIH HHS / GM / GM061374-07; United States / NCI NIH HHS / CA / CA 51001; United States / NCI NIH HHS / CA / CA078224-10; United States / NHLBI NIH HHS / HL / U01 HL065899; United States / NIMH NIH HHS / MH / U01 MH079469; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / U10 CA098413; None / None / / R01 CA051001-15; United States / NIGMS NIH HHS / GM / U01GM61374; United States / NIGMS NIH HHS / GM / GM061393-100007; United States / NIMH NIH HHS / MH / R01 MH059548; United States / NIMH NIH HHS / MH / R01 MH067257; United States / NIMH NIH HHS / MH / R01 MH060870; United States / NIMH NIH HHS / MH / R01 MH081800; United States / NIMH NIH HHS / MH / R01 MH059534; United States / NIMH NIH HHS / MH / R01 MH059571; United States / NIMH NIH HHS / MH / R01 MH059565; United States / NCI NIH HHS / CA / CA036401-24; United States / NIGMS NIH HHS / GM / U01 GM061374-07; United States / NIMH NIH HHS / MH / U01 MH079470; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / R01 CA051001-15; United States / NIMH NIH HHS / MH / R01 MH059587; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIMH NIH HHS / MH / R01 MH059533; United States / NIGMS NIH HHS / GM / U01 GM061374; United States / NCI NIH HHS / CA / R01 CA078224-10; United States / NIMH NIH HHS / MH / R01 MH059586; United States / NCI NIH HHS / CA / U10 CA098543; United States / NHLBI NIH HHS / HL / U01 HL065899-07; United States / NHLBI NIH HHS / HL / HL065899-07; United States / NCI NIH HHS / CA / R01 CA051001; United States / NIMH NIH HHS / MH / Z01 MH002810; United States / NCI NIH HHS / CA / R01 CA036401; United States / NIMH NIH HHS / MH / R01 MH059566; United States / NIGMS NIH HHS / GM / U01 GM061393-100007; None / None / / U10 CA098543-07; United States / NIMH NIH HHS / MH / R01 MH059588; United States / NIMH NIH HHS / MH / U01 MH046318; United States / NCI NIH HHS / CA / U10 CA098543-07; United States / NIMH NIH HHS / MH / R01 MH059553; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / U10 CA029139-22; United States / NIMH NIH HHS / MH / R01 MH060879; United States / NIMH NIH HHS / MH / R01 MH060068
  • [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 / ARID5B protein, human; 0 / Antimetabolites, Antineoplastic; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / MKL1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators; 0 / Transcription Factors; 148971-36-2 / Ikaros Transcription Factor; 25513-46-6 / Polyglutamic Acid; EC 4.1.1.- / Dopa Decarboxylase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS134891; NLM/ PMC2762391
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100. Paulsson K, Forestier E, Lilljebjörn H, Heldrup J, Behrendtz M, Young BD, Johansson B: Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Dec 14;107(50):21719-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploid acute lymphoblastic leukemia (ALL) is one of the most common malignancies in children.
  • Other frequent abnormalities included whole-chromosome uniparental isodisomies (wUPIDs) 9 and 11, gain of 17q not associated with isochromosome formation, extra gain of part of 21q, deletions of ETS variant 6 (ETV6), cyclin-dependent kinase inhibitor 2A (CKDN2A) and paired box 5 (PAX5), and PAN3 poly(A) specific ribonuclease subunit homolog (PAN3) microdeletions.
  • Finally, two cases had partial deletions of AT rich interactive domain 5B (ARID5B), indicating that acquired as well as constitutional variants in this locus may be associated with pediatric ALL.
  • Here we provide a comprehensive characterization of the genetic landscape of high hyperdiploid childhood ALL, including the heterogeneous pattern of secondary genetic events.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics






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