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1. Linger RM, DeRyckere D, Brandão L, Sawczyn KK, Jacobsen KM, Liang X, Keating AK, Graham DK: Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia. Blood; 2009 Sep 24;114(13):2678-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is currently treated with an intense regimen of chemotherapy yielding cure rates near 80%.
  • Here, we report ectopic expression of the receptor tyrosine kinase Mer in pediatric B-cell ALL.
  • Inhibition of Mer prevented Erk 1/2 activation, increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and delayed disease onset in a mouse model of leukemia.

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  • (PMID = 19643988.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / F32 HL096416; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U24 CA114766; United States / NHLBI NIH HHS / HL / F32HL096416; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC2927045
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2. Prasad RB, Hosking FJ, Vijayakrishnan J, Papaemmanuil E, Koehler R, Greaves M, Sheridan E, Gast A, Kinsey SE, Lightfoot T, Roman E, Taylor M, Pritchard-Jones K, Stanulla M, Schrappe M, Bartram CR, Houlston RS, Kumar R, Hemminki K: Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood. Blood; 2010 Mar 4;115(9):1765-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood.
  • Recent genome-wide association data have implicated genetic variation at 7p12.2 (IKZF1), 10q21.2 (ARIDB5), and 14q11.2 (CEBPE) in the etiology of B-cell childhood acute lymphoblastic leukemia (ALL).
  • To verify and further examine the relationship between these variants and ALL risk, we genotyped 1384 cases of precursor B-cell childhood ALL and 1877 controls from Germany and the United Kingdom.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 7 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20042726.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
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3. Healy J, Richer C, Bourgey M, Kritikou EA, Sinnett D: Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia. Haematologica; 2010 Sep;95(9):1608-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia.
  • Although childhood acute lymphoblastic leukemia is the most common pediatric cancer, its etiology remains poorly understood.
  • In an attempt to replicate the findings of 2 recent genome-wide association studies in a French-Canadian cohort, we confirmed the association of 5 SNPs [rs7073837 (P=4.2 x 10(-4)), rs10994982 (P=3.8 x 10(-4)), rs10740055 (P=1.6 x 10(-5)), rs10821936 (P=1.7 x 10(-7)) and rs7089424 (P=3.6 x 10(-7))] in the ARID5B gene with childhood acute lymphoblastic leukemia.
  • We also confirmed a selective effect for B-cell acute lymphoblastic leukemia with hyperdiploidy and report a putative gender-specific effect of ARID5B SNPs on acute lymphoblastic leukemia risk in males.
  • This study provides a strong rationale for more detailed analysis to identify the causal variants at this locus and to better understand the overall functional contribution of ARID5B to childhood acute lymphoblastic leukemia susceptibility.

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  • (PMID = 20460642.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2930966
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4. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M, Jiang LM: [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):333-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To study the role of minimal residual disease (MRD) in the evaluation of therapeutic effectiveness of childhood B-cell acute lymphoblastic leukemia (ALL).
  • METHODS: MRD testing was performed in 124 children with B-cell ALL, who were newly diagnosed and enrolled in the ALL-XH-99 treatment protocol from September 2001 to April 2005MRD was determined by 4-color flow cytometry in the different time points during the treatment period.
  • Multivariate analysis confirmed that the MRD level after induction chemotherapy together with the reaction to prednisone, the bone marrow features on the 19th day of induction, and the fusion gene with BCR-ABL or MLL-AF4 had prognostic significance in childhood B-cell ALL.
  • CONCLUSIONS: The MRD level in the whole course of therapy is an important outcome indicator in childhood B cell ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18554462.001).
  • [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
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5. Tie LJ, Gu LJ, Chen J, Jiang LM, Dong L, Pan C, Ye H, Song DL, Xue HL, Tang JY, Wang YP, Chen J: [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Feb;27(2):120-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To assess the prognostic value of minimal residual disease (MRD) in childhood B-cell acute lymphoblastic leukemia (ALL) after induction chemotherapy.
  • CONCLUSION: The MRD level at achieving CR is one of important prognostic factor in the treatment of childhood B-cell ALL, and might be used to assess the early treatment response.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, B-Cell / drug therapy. Neoplasm, Residual

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  • (PMID = 16732969.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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6. Jeha S, Behm F, Pei D, Sandlund JT, Ribeiro RC, Razzouk BI, Rubnitz JE, Hijiya N, Howard SC, Cheng C, Pui CH: Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3302-4
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  • [Title] Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • CD20 expression is associated with inferior survival in adults with acute lymphoblastic leukemia (ALL).
  • We analyzed the prognostic impact of CD20 expression in 353 children with B-cell precursor ALL treated in 3 consecutive St Jude Total Therapy studies.
  • There was no association between CD20 expression and E2A-PBX, TEL-AML1, ploidy, white blood cell count at diagnosis, or sex.
  • These data suggest that CD20 expression is not associated with inferior outcome in pediatric patients treated with contemporary regimens.

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  • (PMID = 16896151.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20
  • [Other-IDs] NLM/ PMC1895438
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7. Taylor GM, Hussain A, Lightfoot TJ, Birch JM, Eden TO, Greaves MF: HLA-associated susceptibility to childhood B-cell precursor ALL: definition and role of HLA-DPB1 supertypes. Br J Cancer; 2008 Mar 25;98(6):1125-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-associated susceptibility to childhood B-cell precursor ALL: definition and role of HLA-DPB1 supertypes.
  • Childhood B-cell precursor (BCP) ALL is thought to be caused by a delayed immune response to an unidentified postnatal infection.

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  • (PMID = 18334973.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen
  • [Other-IDs] NLM/ PMC2275491
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8. Cardone M, Kandilci A, Carella C, Nilsson JA, Brennan JA, Sirma S, Ozbek U, Boyd K, Cleveland JL, Grosveld GC: The novel ETS factor TEL2 cooperates with Myc in B lymphomagenesis. Mol Cell Biol; 2005 Mar;25(6):2395-405
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors.
  • Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and MYC and/or MYCN in over one-third of B-ALL patients.
  • Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

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  • (PMID = 15743832.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076379; United States / NCI NIH HHS / CA / R01 CA76379-07; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01-CA72999-08
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ETV7 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1061619
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9. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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10. Chatterton Z, Morenos L, Saffery R, Craig JM, Ashley D, Wong NC: DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia. Epigenomics; 2010 Oct;2(5):697-708
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common cancer in children in the modern world.
  • A number of DNA methylation and miRNA profiling studies have investigated the role of both in childhood ALL.
  • [MeSH-major] DNA Methylation / physiology. Epigenesis, Genetic / physiology. High-Throughput Screening Assays / methods. MicroRNAs / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 22122053.001).
  • [ISSN] 1750-192X
  • [Journal-full-title] Epigenomics
  • [ISO-abbreviation] Epigenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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11. Ju X, Li D, Shi Q, Hou H, Sun N, Shen B: Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2009 Jan;26(1):1-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • The analysis of differential microRNA expression profiles may be a powerful tool to allow us insight on the mechanisms of childhood B-cell precursor acute lymphoblastic leukemia (pre-B-ALL).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Computational Biology. Gene Expression Profiling. Hematopoiesis / genetics. Humans. Infant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19206004.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN222 microRNA, human; 0 / MIRN373 microRNA, human; 0 / MIRN451 microRNA, human; 0 / MicroRNAs
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12. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • While the first course of chemotherapy successfully eradicated the cell line with the t(12;21), the second cell line with AML1 amplification remained latent during the time of complete remission and reappeared with a different immunophenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


13. Fridberg M, Kjellström S, Anagnostaki L, Skogvall I, Mustelin T, Wiebe T, Persson JL, Dictor M, Wingren AG: Immunohistochemical analyses of phosphatases in childhood B-cell lymphoma: lower expression of PTEN and HePTP and higher number of positive cells for nuclear SHP2 in B-cell lymphoma cases compared to controls. Pediatr Hematol Oncol; 2008 Sep;25(6):528-40
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] Immunohistochemical analyses of phosphatases in childhood B-cell lymphoma: lower expression of PTEN and HePTP and higher number of positive cells for nuclear SHP2 in B-cell lymphoma cases compared to controls.
  • Although many pediatric B-cell lymphoma patients are being cured today, much is still unknown about the pathogenesis of this disease.
  • The authors have analyzed 26 pediatric B-cell lymphoma cases for the expression of a panel of phosphatases and report a statistically significant lower expression intensity of PTEN and HePTP and higher nuclear SHP2 expression in B-cell lymphoma cases compared to lymphoid tissue.
  • Knowledge about the expression of key regulatory proteins in pediatric B-cell lymphomas is necessary for revealing the complex molecular background of this disease.
  • [MeSH-major] Lymphoma, B-Cell / genetics. PTEN Phosphohydrolase / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / biosynthesis. Protein Tyrosine Phosphatases, Non-Receptor / metabolism

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  • (PMID = 18728972.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.3.48 / PTPN7 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases, Non-Receptor; EC 3.1.3.67 / PTEN Phosphohydrolase
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14. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.
  • Bone marrow karyotype in combination with molecular cytogenetic techniques like FISH should be done for improvement in sensitivity and accurate cytogenetic analysis in childhood ALL patients for proper identification of prognostic group for optimum treatment.
  • This is one of the few reported studies worldwide for amplification of RUNX1 gene from Indian subcontinent in childhood BCP-ALL.

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  • (PMID = 27960689.001).
  • [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. Zhang LP, Cheng YF, Liu GL, Lu AD, Liu YR, Wang H: [The clinical significance of detecting minimal residual disease in acute childhood B-cell lymphoblastic leukemia with flow cytometry]. Zhonghua Er Ke Za Zhi; 2005 Jul;43(7):481-5
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The clinical significance of detecting minimal residual disease in acute childhood B-cell lymphoblastic leukemia with flow cytometry].
  • OBJECTIVE: Flow cytometry may be used to detect minimal residual disease (MRD) in acute lymphoblastic leukemia because leukemic cells often display aberrant phenotypes when compared to normal cells.
  • The investigators also aimed to study the value of the detection of MRD by flow cytometry in childhood B-ALL without effective antibody combinations.
  • METHODS: Thirty-six cases of childhood B-ALL with effective antibody combinations were performed MRD analysis after induction therapy.
  • (1) Forty-two cases of childhood B-ALL were screened for antibody combinations of interest and were identified in 86% (36/42) of the cases.
  • CONCLUSION:. (1) Flow cytometry is a sensitive and specific method for detecting MRD of childhood ALL, and could predict the coming relapse. (2) Patients with MRD levels > 10(-3) had poor prognosis. (3) The levels of MRD at month 9 and 12 had prognostic value. (4) The value of antibody combinations consisting of CD(45)/CD(19)/CD(10)/CD(34) and CD(45)/CD(19)/CD(20)/CD(22) should be further investigated in patients without effective antibody combinations.
  • [MeSH-major] B-Lymphocyte Subsets / immunology. Flow Cytometry. Immunophenotyping. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16083543.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] China
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16. Attias D, Weitzman S: The efficacy of rituximab in high-grade pediatric B-cell lymphoma/leukemia: a review of available evidence. Curr Opin Pediatr; 2008 Feb;20(1):17-22
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The efficacy of rituximab in high-grade pediatric B-cell lymphoma/leukemia: a review of available evidence.
  • PURPOSE OF REVIEW: This review evaluates whether rituximab has efficacy in high-grade pediatric B-cell lymphoma/leukemia.
  • Current pediatric protocols for CD20+ B-cell lymphoma/leukemia significantly improve survival, but with major morbidity.
  • To assess whether rituximab has efficacy in very high-grade pediatric disease, all published data on rituximab therapy for Burkitt's lymphoma/B acute lymphoblastic leukaemia (B-ALL) and pediatric patients with relapsed/refractory large B-cell lymphoma were reviewed.
  • Minimal pediatric data have been published, but 19 children with mature B-cell lymphoma/B-ALL received rituximab, alone or in combination with chemotherapy, as salvage therapy, after failure of intensive chemotherapy.
  • Although positive reporting bias is suspected, it appears that rituximab, even as monotherapy, has efficacy in heavily pretreated pediatric patients with high-grade B-lymphoma/B-ALL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy

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  • (PMID = 18197034.001).
  • [ISSN] 1040-8703
  • [Journal-full-title] Current opinion in pediatrics
  • [ISO-abbreviation] Curr. Opin. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 53
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17. Csinady E, van der Velden VH, Joas R, Fischer S, de Vries JF, Beverloo HB, König M, Pötschger U, van Dongen JJ, Mann G, Haas OA, Panzer-Grümayer ER: Chromosome 14 copy number-dependent IGH gene rearrangement patterns in high hyperdiploid childhood B-cell precursor ALL: implications for leukemia biology and minimal residual disease analysis. Leukemia; 2009 May;23(5):870-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 14 copy number-dependent IGH gene rearrangement patterns in high hyperdiploid childhood B-cell precursor ALL: implications for leukemia biology and minimal residual disease analysis.
  • Childhood B-cell precursor acute lymphoblastic leukemia (BCP ALL) is generally a clonal disease in which the number of IGH rearrangements per cell does not exceed the number of the IGH alleles on chromosome 14.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Gene Dosage / genetics. Gene Rearrangement. Immunoglobulin Heavy Chains / genetics. Neoplasm, Residual / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19148138.001).
  • [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 / Immunoglobulin Heavy Chains
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18. Xu C, Zhao HJ, Jiang LM, Yuan XJ, Li L, Tang JY, Shen LS: [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):717-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia].
  • This study was aimed to investigate the value of CD58 in evaluation of early therapeutic effect on childhood B-ALL.
  • The expression features of CD58 in 135 cases of childhood B-ALL were analyzed by four-color flow cytometry; MRD detection protocol for B-ALL using CD58/CD10/CD34/CD19 combination was established; the correlation between the expression features of CD58 and MRD detection was analyzed for the early therapeutic response in childhood B-ALL.
  • The CD58 over expression may be considered as a marker of a favorable prognosis in childhood B-ALL.

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  • (PMID = 16928307.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD58; 0 / Biomarkers, Tumor
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19. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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20. Haltrich I, Csóka M, Kovács G, Fekete G: [Intrachromosomal amplification of AML1 gene in childhood acute lymphoblastic leukemia]. Orv Hetil; 2008 Jun 15;149(24):1143-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intrachromosomal amplification of AML1 gene in childhood acute lymphoblastic leukemia].
  • [Transliterated title] AML1-gén intrakromoszomális amplifikációja gyermekkori acut lymphoid leukaemiában.
  • The introduction of routine molecular cytogenetic assays enabled us to reveal hitherto unknown genetic disorders of childhood acute leukemias.
  • In our present study we review a novel cytogenetic mutation typical for childhood B-cell ALL, the intrachromosomal amplification of chromosome 21, which requires high-risk therapy irrespective of other risk factors, and which is associated with a cryptic 12;21 translocation of good prognostic value.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Amplification. Genetic Markers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18539581.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Genetic Markers; 0 / RUNX1 protein, human
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21. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


22. Hill A, Short MA, Varghese C, Kusumakumary P, Kumari P, Morgan GJ: The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India. Haematologica; 2005 Mar;90(3):414-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India.
  • t(12;21) (TEL/AML1) is the most common genetic event in childhood B-cell acute lymphoblastic leukemia (B-ALL) in Western countries.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Child. Humans. Incidence. India / epidemiology. Leukemia, B-Cell. Molecular Epidemiology

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  • (PMID = 15749681.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
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23. Gudowius S, Recker K, Laws HJ, Dirksen U, Tröger A, Wieczorek U, Furlan S, Göbel U, Hanenberg H: Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL. Klin Padiatr; 2006 Nov-Dec;218(6):327-33
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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 candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL.
  • BACKGROUND: Contemporary risk adapted treatment protocols for childhood acute lymphoblastic leukemia (ALL) rely on accurate risk assessment strategies for disease re-occurrence by incorporating clinical parameters as well as immunological, molecular and cytogenetic features of the blasts at initial manifestation.
  • PATIENTS AND METHODS: In order to identify target antigen structures, we analyzed the immunological expression profiles of blasts from 181 patients with B-cell precursor ALL treated at our institution in 11 years according to the CoALL-92/97/03 protocols.
  • CD20 was expressed on 11-37 % of B-cell precursor ALL samples.
  • CONCLUSIONS: These analyses clearly identified the three antigens CD19, CD22 and HLA-DR present on blasts in more than 90 % of patients as potential target structures for targeted therapies with native or toxin-bound monoclonal antibodies in childhood ALL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD19 / analysis. Burkitt Lymphoma / immunology. HLA-DR Antigens / analysis. Immunotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sialic Acid Binding Ig-like Lectin 2 / analysis

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  • (PMID = 17080335.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 2
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24. Bernaldez-Rios R, Ortega-Alvarez MC, Perez-Saldivar ML, Alatoma-Medina NE, Del Campo-Martinez Mde L, Rodriguez-Zepeda Mdel C, Montero-Ponce I, Franco-Ornelas S, Fernandez-Castillo G, Nuñez-Villegas NN, Taboada-Flores MA, Flores-Lujano J, Argüelles-Sanchez ME, Juarez-Ocaña S, Fajardo-Gutierrez A, Mejia-Arangure JM: The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City. J Pediatr Hematol Oncol; 2008 Mar;30(3):199-203
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City.
  • The objective of this population-based survey was to assess the peak age of incidence of B-cell precursor acute lymphoblastic leukemia (ALL) in children in Mexico City (MC).
  • All patients were classified according to their immunophenotype, and only B-cell precursor and T-lineage were analyzed.
  • The frequency of B-cell precursor ALL was 76.1%, whereas T lineage ALL showed a frequency of 23.6%.
  • B-cell precursor ALL was the major contributor to peak age; T lineage ALL showed a peak among 1 and 3 years of age.
  • We conclude that the age peak for children with ALL in MC is within the ranges reported for developed countries and that B-cell precursor ALL is the main contributor to these peak.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18376281.001).
  • [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
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25. Cocco C, Canale S, Frasson C, Di Carlo E, Ognio E, Ribatti D, Prigione I, Basso G, Airoldi I: Interleukin-23 acts as antitumor agent on childhood B-acute lymphoblastic leukemia cells. Blood; 2010 Nov 11;116(19):3887-98
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-23 acts as antitumor agent on childhood B-acute lymphoblastic leukemia cells.
  • The aim of this study was to investigate the potential direct antitumor activity of IL-23 in pediatric B-acute lymphoblastic leukemia (B-ALL) cells and to unravel the molecular mechanisms involved.
  • Here, we show, for the first time, that IL-23R is up-regulated in primary B-ALL cells, compared with normal early B lymphocytes, and that IL-23 dampens directly tumor growth in vitro and in vivo through the inhibition of tumor cell proliferation and induction of apoptosis.
  • The latter finding is related to IL-23-induced up-regulation of miR15a expression and the consequent down-regulation of BCL-2 protein expression in pediatric B-ALL cells.
  • [MeSH-major] Interleukin-23 Subunit p19 / immunology. Interleukin-23 Subunit p19 / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Gene Expression / drug effects. Genes, bcl-2 / drug effects. Humans. In Vitro Techniques. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. MicroRNAs / antagonists & inhibitors. MicroRNAs / genetics. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / pharmacology. Signal Transduction / immunology

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  • (PMID = 20671120.001).
  • [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 / IL23A protein, human; 0 / Interleukin-23 Subunit p19; 0 / MIRN15 microRNA, human; 0 / MicroRNAs; 0 / Recombinant Proteins
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26. He GS, Zhang XH, Yao L, Zhang R, Chen ZX, Wu DP, Sun AN, Jin ZM, Qiu HY, Hu XH: [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2009 Oct;30(10):675-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review].
  • OBJECTIVE: To report a case of T cell acute lymphoblastic leukemia (ALL) with t(1;19)(q23;pl3) and E2A-PBX1 fusion gene, which is a characteristic translocation of childhood B cell ALL (B-ALL).
  • The leukemic cells expressed T cell markers.
  • CONCLUSION: t(1;19)E2A-PBX1(+) can be implicated in adult T-ALL, besides childhood B-ALL.
  • [MeSH-major] Homeodomain Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19954663.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 146150-85-8 / E2A-Pbx1 fusion protein
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27. Tassano E, Acquila M, Tavella E, Micalizzi C, Panarello C, Morerio C: MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Aug;49(8):682-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia.
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus are common abnormalities in mature B-cell neoplasms.
  • Recent findings have also revealed their significant role in B-cell precursor acute lymphoblastic leukemia.
  • In this study, we describe a pediatric case of B-cell precursor acute lymphoblastic leukemia showing microRNA-125b-1 (MIR125B1) and BLID gene overexpression, resulting from a novel t(11;14)(q24.1;q32) translocation involving IGH.
  • [MeSH-major] BRCA2 Protein / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Child. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Female. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 20544842.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BLID protein, human; 0 / BRCA2 Protein; 0 / BRCA2 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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28. Moorman AV, Ensor HM, Richards SM, Chilton L, Schwab C, Kinsey SE, Vora A, Mitchell CD, Harrison CJ: Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial. Lancet Oncol; 2010 May;11(5):429-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial.
  • BACKGROUND: Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease markers and indicators of outcomes.
  • METHODS: We analysed cytogenetic data from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medical Research Council ALL97/99 study and followed up for a median time of 8.2 years.
  • Multivariate analysis incorporating age, white-cell count, and treatment parameters showed that six cytogenetic abnormalities (ETV6-RUNX1, high hyperdiploidy, iAMP21, t(9;22), loss of 13q, and abnormal 17p) retained their significance for effect on relapse risk.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [CommentIn] Lancet Oncol. 2010 May;11(5):403-4 [20409755.001]
  • [ErratumIn] Lancet Oncol. 2010 Jun;11(6):516
  • (PMID = 20409752.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300130; United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. Jetsrisuparb A, Wiangnon S, Komvilaisak P, Kularbkaew C, Yutanawiboonchai W, Mairieng E: Rituximab combined with CHOP for successful treatment of aggressive recurrent, pediatric B-cell large cell non-Hodgkin's lymphoma. J Pediatr Hematol Oncol; 2005 Apr;27(4):223-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab combined with CHOP for successful treatment of aggressive recurrent, pediatric B-cell large cell non-Hodgkin's lymphoma.
  • This report is the first to describe the successful treatment of a 14-year-old boy with aggressive recurrent, CD20-positive, B-cell large cell non-Hodgkin's lymphoma.
  • Rituximab and CHOP in addition to chemotherapy may be an alternative treatment for aggressive recurrent, pediatric CD20-positive B-cell large cell non-Hodgkin's lymphoma if highly intensive chemotherapy and stem cell transplantation are not available.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 15838396.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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30. Dworzak MN, Schumich A, Printz D, Pötschger U, Husak Z, Attarbaschi A, Basso G, Gaipa G, Ratei R, Mann G, Gadner H: CD20 up-regulation in pediatric B-cell precursor acute lymphoblastic leukemia during induction treatment: setting the stage for anti-CD20 directed immunotherapy. Blood; 2008 Nov 15;112(10):3982-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD20 up-regulation in pediatric B-cell precursor acute lymphoblastic leukemia during induction treatment: setting the stage for anti-CD20 directed immunotherapy.
  • CD20 is expressed in approximately one- half of pediatric acute lymphoblastic leukemia (ALL) cases with B-cell precursor (BCP) origin.
  • To understand the impact of this on the potential effectiveness of anti-CD20 immunotherapy, we studied 237 CD10(+) pediatric BCP-ALL patients with Berlin-Frankfurt-Munster (BFM)-type therapy.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antigens, CD20 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Gene Expression Regulation, Leukemic / drug effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18780832.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00430118
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
  • [Other-IDs] NLM/ PMC2581996
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31. Karadeniz C, Oguz A, Citak EC, Uluoglu O, Okur V, Demirci S, Okur A, Aksakal N: Clinical characteristics and treatment results of pediatric B-cell non-Hodgkin lymphoma patients in a single center. Pediatr Hematol Oncol; 2007 Sep;24(6):417-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and treatment results of pediatric B-cell non-Hodgkin lymphoma patients in a single center.
  • The aim of this study was to evaluate and compare the clinical characteristics of the B-cell non-Hodgkin lymphoma (NHL) patients and therapeutic efficacy of modified NHL BFM-90 and NHL BFM-95 protocols in the authors' center.
  • Forty-five patients were treated with modified B-cell BFM-90 and 16 patients were treated with B-cell BFM-95 regimens.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy

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  • (PMID = 17710659.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Diuretics; 0 / Neoplasm Proteins; 5J49Q6B70F / Vincristine; 63CZ7GJN5I / Allopurinol; 8MDF5V39QO / Sodium Bicarbonate; EC 1.1.1.27 / L-Lactate Dehydrogenase; Q573I9DVLP / Leucovorin; YL5FZ2Y5U1 / Methotrexate
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32. Ahmad N, Zaidi A, Badar F, Maaz AU, Akram MS: Clinical characteristics and outcome analysis of pediatric B-cell non-Hodgkin's lymphoma. Experience with FAB-LMB 96 and UKCCSG B-cell NHL guidelines in a developing country. Asia Pac J Clin Oncol; 2010 Mar;6(1):49-56

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and outcome analysis of pediatric B-cell non-Hodgkin's lymphoma. Experience with FAB-LMB 96 and UKCCSG B-cell NHL guidelines in a developing country.
  • AIM: To analyze the clinical characteristics of B-cell non-Hodgkin's lymphoma (NHL) patients and the therapeutic efficacy of French-American-British Lymphoma Malins de Burkitt 96 and the recent United Kingdom Children's Cancer Study Group B-cell NHL guidelines in the tertiary care hospital of a developing country.
  • METHODS: Patients aged < or =18 years registered at our hospital between January 1995 and December 2006 with histologically proved B-Cell NHL were selected for retrospective analysis.
  • Of these 95 had Burkitt's lymphoma, 22 diffuse large B-cell lymphoma and five had B-cell NHL not otherwise specified.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / mortality. Practice Guidelines as Topic

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  • (PMID = 20398038.001).
  • [ISSN] 1743-7563
  • [Journal-full-title] Asia-Pacific journal of clinical oncology
  • [ISO-abbreviation] Asia Pac J Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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33. Kikuchi A, Mori T, Fujimoto J, Kumagai M, Sunami S, Okimoto Y, Tsuchida M: Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol. Leuk Lymphoma; 2008 Apr;49(4):757-62
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  • [Title] Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol.
  • From June 1996 to January 2001, 91 patients with B-cell non-Hodgkin lymphoma or B-cell acute lymphoblastic leukemia up to 18 years of age were enrolled in Tokyo Children's Cancer Study Group (TCCSG) NHL B9604 protocol study.
  • The TCCSG NHL B9604 protocol achieved an excellent treatment outcome especially in patients with the most advanced disease (Group D: high BM blast cell burden and/or central nervous system involvement).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Lymphoma, B-Cell / drug therapy


34. Harrison CJ, Haas O, Harbott J, Biondi A, Stanulla M, Trka J, Izraeli S, Biology and Diagnosis Committee of International Berlin-Frankfürt-Münster study group: Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group. Br J Haematol; 2010 Oct;151(2):132-42
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  • [Title] Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group.
  • Treatment of childhood acute lymphoblastic leukaemia (ALL) has improved considerably in recent years.
  • Here we review the current diagnostic criteria of genetic abnormalities in precursor B-ALL (BCP-ALL), including the relevant technical approaches and the application of the most appropriate methods for the detection of each abnormality.
  • [MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20701601.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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35. Forestier E, Andersen MK, Autio K, Blennow E, Borgström G, Golovleva I, Heim S, Heinonen K, Hovland R, Johannsson JH, Kerndrup G, Nordgren A, Rosenquist R, Swolin B, Johansson B, Nordic Society of Pediatric Hematology and Oncology (NOPHO), Swedish Cytogenetic Leukemia Study Group (SCLSG), NOPHO Leukemia Cytogenetic Study Group (NLCSG): Cytogenetic patterns in ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia: A Nordic series of 245 cases and review of the literature. Genes Chromosomes Cancer; 2007 May;46(5):440-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic patterns in ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia: A Nordic series of 245 cases and review of the literature.
  • Between 1992 and 2004, 1,140 children (1 to<15 years) were diagnosed with B-cell precursor acute lymphoblastic leukemia (ALL) in the Nordic countries.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Leukemia, Lymphoid / genetics. Transcription Factors / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17285576.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ETV1 protein, human; 0 / RUNX1 protein, human; 0 / Transcription Factors
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36. Attarbaschi A, Mann G, König M, Steiner M, Dworzak MN, Gadner H, Haas OA, Austrian Berlin-Frankfurt-Münster Cooperative Study Group: Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases. Genes Chromosomes Cancer; 2006 Jun;45(6):608-11
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  • [Title] Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases.
  • Near-tetraploidy (82-94 chromosomes) makes up fewer than 1% of childhood acute lymphoblastic leukemia (ALL) cases and has been reportedly associated with a possibly poorer prognosis compared with other ploidy groups.
  • Fluorescence in situ hybridization revealed that eight of the nine B-cell precursor (BCP) cases and none of the three T-cell ALL cases had an ETV6/RUNX1 rearrangement.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / analysis. Polyploidy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / analysis. Repressor Proteins / analysis

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16552772.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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37. Pichler H, Möricke A, Mann G, Teigler-Schlegel A, Niggli F, Nebral K, König M, Inthal A, Krehan D, Dworzak MN, Janousek D, Harbott J, Schrappe M, Gadner H, Strehl S, Haas OA, Panzer-Grümayer R, Attarbaschi A, Berlin-Frankfurt-Münster (BFM) Study Group: Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy. Br J Haematol; 2010 Apr;149(1):93-100
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  • [Title] Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy.
  • The presence of a dicentric chromosome dic(9;20) has been reported to have an unfavourable prognosis in children with B-cell precursor acute lymphoblastic leukaemia (BCP-ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20067563.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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38. Schoumans J, Johansson B, Corcoran M, Kuchinskaya E, Golovleva I, Grandér D, Forestier E, Staaf J, Borg A, Gustafsson B, Blennow E, Nordgren A: Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2. Br J Haematol; 2006 Nov;135(4):492-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2.
  • Although the dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in paediatric B-cell precursor acute lymphoblastic leukaemia (BCP ALL), occurring in approximately 2% of the cases, its molecular genetic consequences have not been elucidated.
  • In the present study, high-resolution genome-wide array-based comparative genomic hybridisation (array-CGH) and fluorescence in situ hybridisation (FISH) were used to characterise the 9p and 20q breakpoints (BPs) in seven childhood BCP ALLs with dic(9;20), which was shown to be unbalanced in all of them, resulting in loss of 9p13.2-pter.
  • One of the ALLs, shown to have a complex dic(9;20), was further investigated by FISH, revealing a rearrangement of the haemapoietic cell kinase isoform p61 (HCK) gene at 20q11.

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  • (PMID = 16999846.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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39. Fujita N, Mori T, Mitsui T, Inada H, Horibe K, Tsurusawa M, Lymphoma Committee of the Japanese Pediatric Leukemia/Lymphoma Study Group: The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan. Pediatr Blood Cancer; 2008 Aug;51(2):188-92
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  • [Title] The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan.
  • BACKGROUND: There have been excellent treatment results for children with B-cell non-Hodgkin lymphoma (B-NHL) and mature B-cell leukemia (B-ALL) in the last few decades.
  • Among 18 patients who had a chemotherapy-sensitive disease, 4 of 5 patients who underwent hematopoietic stem cell transplantation (HSCT) during remission survived without progression, while 3 of 12 patients who did not receive HSCT were alive without disease progression.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, B-Cell / therapy. Lymphoma, B-Cell / therapy


40. Mussolin L, Pillon M, Conter V, Piglione M, Lo Nigro L, Pierani P, Micalizzi C, Buffardi S, Basso G, Zanesco L, Rosolen A: Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood. J Clin Oncol; 2007 Nov 20;25(33):5254-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood.
  • PURPOSE: To study the prevalence of t(8;14) at diagnosis and the response kinetics to treatment of minimal residual disease (MRD) in B-cell acute lymphoblastic leukemia (B-ALL) patients and determine its impact on prognosis.
  • PATIENTS AND METHODS: A total of 68 children affected by de novo B-ALL enrolled onto the Berlin-Frankfurt-Muenster-based Italian Association of Pediatric Hematology and Oncology LNH-97 clinical protocol were studied.
  • [MeSH-major] Burkitt Lymphoma / mortality. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Translocation, Genetic

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  • (PMID = 18024872.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
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41. Forsythe A, Breland T, Majumdar S, Elkin TD, Johnson D, Megason G: Gender differences in incidence rates of childhood B-precursor acute lymphocytic leukemia in Mississippi. J Pediatr Oncol Nurs; 2010 May-Jun;27(3):164-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gender differences in incidence rates of childhood B-precursor acute lymphocytic leukemia in Mississippi.
  • The authors studied pediatric patients with B-precursor acute lymphocytic leukemia (ALL) to determine whether Mississippi's gender incidences correlate with national statistics.
  • A retrospective chart review was performed of pediatric B-precursor ALL patients diagnosed at the Children's Cancer Clinic at the University of Mississippi Medical Center from 1995 to 2005.
  • However, the national average includes T-cell ALL, which is known to be significantly more prevalent in boys.
  • Of greater significance, boys were noted to present with high-risk B-precursor ALL 4 times more than girls, suggesting the need for further investigation into possible causes of this phenomenon.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Academic Medical Centers. Bias (Epidemiology). Causality. Chi-Square Distribution. Child. Female. Humans. Incidence. Male. Mississippi / epidemiology. Population Surveillance. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Prevalence. Retrospective Studies. Risk Assessment. Sex Distribution. United States / epidemiology

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  • (PMID = 20164246.001).
  • [ISSN] 1532-8457
  • [Journal-full-title] Journal of pediatric oncology nursing : official journal of the Association of Pediatric Oncology Nurses
  • [ISO-abbreviation] J Pediatr Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Fasano RE, Bergen DC: Intractable epilepsy in patients treated for childhood acute lymphocytic leukemia. Seizure; 2009 May;18(4):298-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intractable epilepsy in patients treated for childhood acute lymphocytic leukemia.
  • PURPOSE: In the 1970s and 80s, standard treatment for childhood acute lymphocytic leukemia (ALL) included both intrathecal methotrexate and whole-brain irradiation.
  • During acute treatment, seizures were not uncommon.
  • We describe five patients who were treated for acute lymphocytic leukemia as children, who later developed intractable epilepsy.
  • RESULTS: All of the patients were diagnosed with leukemia before age seven.
  • CONCLUSIONS: Successful treatment for childhood leukemia may be followed by signs of late cerebral injury including intractable epilepsy.
  • [MeSH-major] Antirheumatic Agents / adverse effects. Cranial Irradiation / adverse effects. Epilepsy / etiology. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19041267.001).
  • [ISSN] 1059-1311
  • [Journal-full-title] Seizure
  • [ISO-abbreviation] Seizure
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; YL5FZ2Y5U1 / Methotrexate
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43. Spinola-Castro AM, Siviero-Miachon AA, Andreoni S, Tosta-Hernandez PD, Macedo CR, Lee ML: Transient hyperglycemia during childhood acute lymphocytic leukemia chemotherapy: an old event revisited. Clin Adv Hematol Oncol; 2009 Jul;7(7):465-72
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  • [Title] Transient hyperglycemia during childhood acute lymphocytic leukemia chemotherapy: an old event revisited.
  • Hyperglycemia has been described as a common event occurring during acute lymphocytic leukemia chemotherapy.
  • Our goal was to compare clinical and laboratory findings between hyperglycemic episodes occurring during childhood acute lymphocytic leukemia induction chemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Glucocorticoids / adverse effects. Hyperglycemia / chemically induced. Neoplasm Recurrence, Local. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19701154.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Glucose; 0 / Glucocorticoids; EC 3.2.1.- / Amylases
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44. Robinson KE, Livesay KL, Campbell LK, Scaduto M, Cannistraci CJ, Anderson AW, Whitlock JA, Compas BE: Working memory in survivors of childhood acute lymphocytic leukemia: functional neuroimaging analyses. Pediatr Blood Cancer; 2010 Apr;54(4):585-90
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  • [Title] Working memory in survivors of childhood acute lymphocytic leukemia: functional neuroimaging analyses.
  • BACKGROUND: Research on the physical and psychological late effects of treatment of childhood cancer has led to the identification of significant long-term neurocognitive deficits experienced by some survivors, particularly in the areas of memory and executive functioning.
  • PROCEDURE: This study used functional neuroimaging techniques to examine working memory and executive functioning deficits of survivors of childhood acute lymphocytic leukemia (ALL), as compared to age- and gender-matched healthy controls.
  • CONCLUSIONS: These results support the theory of compensatory activation in necessary brain regions in order to complete tasks in pediatric ALL survivors, similar to that observed in multiple sclerosis patients.

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  • (PMID = 19953649.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA068485-13S4; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / CA068485; United States / NCI NIH HHS / CA / P30 CA068485-13S4
  • [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; 04079A1RDZ / Cytarabine; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS183910; NLM/ PMC2901833
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45. Campbell LK, Scaduto M, Van Slyke D, Niarhos F, Whitlock JA, Compas BE: Executive function, coping, and behavior in survivors of childhood acute lymphocytic leukemia. J Pediatr Psychol; 2009 Apr;34(3):317-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Executive function, coping, and behavior in survivors of childhood acute lymphocytic leukemia.
  • OBJECTIVE: To examine the role of executive function in coping and behavioral outcomes in childhood acute lymphocytic leukemia (ALL) survivors.
  • Directions for future research on executive function deficits and coping skills in survivors of pediatric ALL are suggested.
  • [MeSH-major] Adaptation, Psychological. Cognition. Emotions. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology. Stress, Psychological / etiology. Survivors / psychology

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  • (PMID = 18667478.001).
  • [ISSN] 1465-735X
  • [Journal-full-title] Journal of pediatric psychology
  • [ISO-abbreviation] J Pediatr Psychol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2722127
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46. Jacobs JE, Hastings C: Isolated extramedullary relapse in childhood acute lymphocytic leukemia. Curr Hematol Malig Rep; 2010 Oct;5(4):185-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated extramedullary relapse in childhood acute lymphocytic leukemia.
  • Although the vast majority of children with acute lymphocytic leukemia attain remission with modern therapies, an unacceptably high number will suffer a disease relapse.
  • Finally, the evolution of leukemia therapy is reviewed, bringing into focus the goals and challenges of future therapeutic endeavors.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 20717757.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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47. Baris S, Celkan T, Batar B, Guven M, Ozdil M, Ozkan A, Apak H, Yildiz I: Association between genetic polymorphism in DNA repair genes and risk of B-cell lymphoma. Pediatr Hematol Oncol; 2009 Sep;26(6):467-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between genetic polymorphism in DNA repair genes and risk of B-cell lymphoma.
  • OBJECTIVES: The authors evaluated the possible effect of DNA repair genes, XPD (Xeroderma pigmentosum group D) codon (312 and 751) and XRCC1 (X-ray repair cross-complementing group 1) codon (194 and 399) SNPs (single-nucleotide polymorphisms) on the risk of childhood B-cell lymphoma.
  • RESULTS: The authors observed no association between variation in the XPD codon Asp312Asn, Lys751Gln, and XRCC1 codon Arg399Gln polymorphisms and B-cell lymphoma for any parameter.
  • The frequency of XRCC1 194Arg/Trp genotype in B-cell lymphoma was significantly lower than that in controls (p = .005).
  • CONCLUSIONS: XRCC1 194Trp allele may be associated with a protective effect against development of childhood B-cell lymphoma.
  • [MeSH-major] DNA Repair / genetics. DNA-Binding Proteins / genetics. Lymphoma, B-Cell / genetics. Polymorphism, Single Nucleotide / genetics. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 19657998.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein
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48. Lyu CJ, Rha SY, Won SC: Clinical role of bone marrow angiogenesis in childhood acute lymphocytic leukemia. Yonsei Med J; 2007 Apr 30;48(2):171-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical role of bone marrow angiogenesis in childhood acute lymphocytic leukemia.
  • But, until today, the importance of theses factors on leukemia, especially childhood acute lymphocytic leukemia (ALL) has received limited attention.
  • CONCLUSION: Our data suggest that the increased levels of VEGF and bFGF in bone marrow may play an important role in prognosis of childhood ALL.
  • [MeSH-major] Bone Marrow / blood supply. Neovascularization, Pathologic / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 17461513.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC2628125
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49. Catusse J, Wollner S, Leick M, Schröttner P, Schraufstätter I, Burger M: Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells. J Cell Physiol; 2010 Nov;225(3):792-800
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells.
  • Elevated levels of CCL18 have been described in various diseases including childhood acute lymphocytic leukemia (ALL) but its functions remain poorly characterized.
  • CXCL12 is a pivotal chemokine for hematopoiesis and B cell homing processes.
  • We demonstrate that CCL18 interferes with CXCL12-mediated pre-B ALL cell activation.
  • CXCL12-induced calcium mobilization, chemotaxis, pseudo-emperipolesis and cellular proliferation could be significantly reduced by CCL18 in pre-B ALL cell lines.
  • [MeSH-major] Chemokines, CC / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology. Receptors, CXCR4 / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Apoptosis. COS Cells. Calcium Signaling. Cell Line, Tumor. Cell Proliferation. Cercopithecus aethiops. Chemokine CXCL12 / metabolism. Chemotaxis, Leukocyte. Estradiol / metabolism. Estrogen Antagonists / pharmacology. Humans. Ligands. Lymphocyte Activation. Receptors, Estrogen. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Recombinant Proteins / metabolism. Transfection

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20568229.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL18 protein, human; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Estrogen Antagonists; 0 / GPER protein, human; 0 / Ligands; 0 / Receptors, CXCR4; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol
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50. Tissing WJ, Lauten M, Meijerink JP, den Boer ML, Koper JW, Sonneveld P, Pieters R: Expression of the glucocorticoid receptor and its isoforms in relation to glucocorticoid resistance in childhood acute lymphocytic leukemia. Haematologica; 2005 Sep;90(9):1279-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the glucocorticoid receptor and its isoforms in relation to glucocorticoid resistance in childhood acute lymphocytic leukemia.
  • In vitro prednisolone resistance is a poor prognostic factor in the treatment of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisolone / therapeutic use. Receptors, Glucocorticoid / biosynthesis

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  • (PMID = 16154856.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Protein Isoforms; 0 / Receptors, Glucocorticoid; 9PHQ9Y1OLM / Prednisolone
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51. Akbayram S, Doğan M, Akgün C, Erbey F, Caksen H, Oner AF: Use of rituximab in three children with relapsed/refractory Burkitt lymphoma. Target Oncol; 2010 Dec;5(4):291-4
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  • Monoclonal antibodies have provided new promise for patients with B-cell malignancies.
  • Rituximab is a monoclonal antibody against B-lymphocytes that express CD20; it is used for the treatment of patients with relapsed or refractory B-cell non-Hodgkin lymphoma.
  • In this article, we reported three children with primary refractory/relapsed B-cell-non-Hodgkin lymphoma, who were successfully treated with a combination of intensive chemotherapy protocol plus rituximab.
  • Our aim is to emphasize the importance of use of rituximab in the treatment of childhood B-cell non-Hodgkin lymphoma.

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  • (PMID = 20859698.001).
  • [ISSN] 1776-260X
  • [Journal-full-title] Targeted oncology
  • [ISO-abbreviation] Target Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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52. Sonabend RY, McKay SV, Okcu MF, Yan J, Haymond MW, Margolin JF: Hyperglycemia during induction therapy is associated with increased infectious complications in childhood acute lymphocytic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):387-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperglycemia during induction therapy is associated with increased infectious complications in childhood acute lymphocytic leukemia.
  • BACKGROUND: Children with acute lymphocytic leukemia (ALL) are at high risk for developing hyperglycemia.
  • [MeSH-major] Hyperglycemia / complications. Infection / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 18523991.001).
  • [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 / Blood Glucose
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53. Kim AS, Eastmond DA, Preston RJ: Childhood acute lymphocytic leukemia and perspectives on risk assessment of early-life stage exposures. Mutat Res; 2006 Nov-Dec;613(2-3):138-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute lymphocytic leukemia and perspectives on risk assessment of early-life stage exposures.
  • For these reasons, we evaluated childhood acute lymphocytic leukemia (ALL) studies from the point of view of mechanism and etiology.
  • ALL is the most common form of childhood cancer proposed to result from a prenatal primary event and a postnatal second event.
  • The possibility of using fusion genes alone as biomarkers of response is also discussed because they can serve as predictors of key events in the development of a mode of action (a sequence of key events, starting with interaction of an agent with a cell, ultimately resulting in cancer formation) for particular environmental exposures.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17049456.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 174
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54. Rowe JM, Goldstone AH: How I treat acute lymphocytic leukemia in adults. Blood; 2007 Oct 1;110(7):2268-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How I treat acute lymphocytic leukemia in adults.
  • The treatment of newly diagnosed acute lymphocytic leukemia (ALL) in adults remains unsatisfactory.
  • Not withstanding the outstanding progress in curing childhood ALL, only approximately one third of adults younger than 60 years can be cured, and the overall published survival curves have not changed significantly during the past 15 years.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [ErratumIn] Blood. 2010 Sep 2;116(9):1627. Dosage error in article text
  • (PMID = 17596539.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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55. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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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 B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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56. Hosking FJ, Papaemmanuil E, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Taylor M, Tomlinson IP, Greaves M, Houlston RS: Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk. Blood; 2010 Jun 3;115(22):4472-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk.
  • To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs.

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  • (PMID = 20231427.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
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57. Barakat M, Elkhayat Z, Kholoussi N, Elnady H, Ismail M, Raafat J: Monitoring treatment response of childhood acute lymphocytic leukemia with certain molecular and biochemical markers. J Biochem Mol Toxicol; 2010 Nov-Dec;24(6):343-50
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  • [Title] Monitoring treatment response of childhood acute lymphocytic leukemia with certain molecular and biochemical markers.
  • Apoptosis is the primary mechanism through which most chemotherapeutic agents induce tumor cell death.
  • The purpose of this study was to monitor the expression of pro- and anti-apoptotic proteins CD(95) , Bcl-2, as well as copper and zinc levels in the peripheral blood of children with acute lymphocytic leukemia (ALL) prior to and 6 months after the beginning of chemotherapy.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / blood. Biomarkers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • [Copyright] Copyright © 2010 Wiley Periodicals, Inc.
  • (PMID = 21182165.001).
  • [ISSN] 1099-0461
  • [Journal-full-title] Journal of biochemical and molecular toxicology
  • [ISO-abbreviation] J. Biochem. Mol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers; 0 / Proto-Oncogene Proteins c-bcl-2; 789U1901C5 / Copper; J41CSQ7QDS / Zinc
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58. Ribeiro KB, Buffler PA, Metayer C: Socioeconomic status and childhood acute lymphocytic leukemia incidence in São Paulo, Brazil. Int J Cancer; 2008 Oct 15;123(8):1907-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Socioeconomic status and childhood acute lymphocytic leukemia incidence in São Paulo, Brazil.
  • To investigate the association of childhood ALL and SES, we collected data on 507 children aged 0-14 years diagnosed with ALL between 1997 and 2002 from the population-based Cancer Registry of São Paulo, Brazil, covering 96 districts.
  • Lower incidence rates of childhood ALL were also found in areas with high percentages of households with more than 7 persons (>or=5.7%) compared with areas where there were <or=2.2% (RR = 0.32, 95% CI 0.25-0.43).
  • Population-based attributes for SES and household size may be useful surrogate markers of early exposure to childhood infections, which has been found to decrease the risk of ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18688860.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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59. Zhang ZX, Cao LZ, Huang Q, Yang MH, Wang Z, Yu Y: [Detection of human cyclin C gene expression in childhood acute lymphocytic leukemia using real-time fluorescence quantitative PCR]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Feb;10(1):14-6
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  • [Title] [Detection of human cyclin C gene expression in childhood acute lymphocytic leukemia using real-time fluorescence quantitative PCR].
  • OBJECTIVE: To explore the relationship between human cyclin C (CCNC) gene and childhood acute lymphocytic leukemia (ALL).
  • METHODS: The total RNA isolated from myeloid tissues of normal children and of children with newly diagnosed ALL and from ALL cell line 6T-CEM was reversely transcribed into cDNA.
  • CONCLUSIONS: CCNC gene shows lower expression in children with newly diagnosed ALL, suggesting that it may be a tumor suppressing gene in childhood ALL.
  • [MeSH-major] Cyclins / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18289462.001).
  • [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 / CCNC protein, human; 0 / Cyclin C; 0 / Cyclins
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60. Sehgal S, Mujtaba S, Gupta D, Aggarwal R, Marwaha RK: High incidence of Epstein Barr virus infection in childhood acute lymphocytic leukemia: a preliminary study. Indian J Pathol Microbiol; 2010 Jan-Mar;53(1):63-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High incidence of Epstein Barr virus infection in childhood acute lymphocytic leukemia: a preliminary study.
  • OBJECTIVE: The study aims to investigate the association of EBV in childhood leukemia.
  • MATERIAL AND METHODS: Patients attending pediatric oncology services of the referral center have been included in the study.
  • Twenty-five consecutive pediatric patients with acute lymphocytic lukemia (ALL) were subjected to EBV studies employing sensitive polymerase chain reaction followed by hybridization for presence of Bam H1-W region of EBV genome and detection of anti Z EBV replication activator (ZEBRA) antibodies using Western blot.
  • [MeSH-major] Epstein-Barr Virus Infections / epidemiology. Herpesvirus 4, Human / isolation & purification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology

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  • [CommentIn] Indian J Pathol Microbiol. 2010 Oct-Dec;53(4):890-1 [21045472.001]
  • (PMID = 20090225.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / DNA, Viral
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61. Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ: [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Oct;10(5):620-4
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  • [Title] [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
  • OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The cell proliferation was detected with MTT.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Humans. Infant. Jurkat Cells. Male. RNA, Messenger / analysis

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  • (PMID = 18947485.001).
  • [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 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
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62. Lee DS, Kim YR, Cho HK, Lee CK, Lee JH, Cho HI: The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL). Cancer Genet Cytogenet; 2005 Oct 15;162(2):176-8
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  • [Title] The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL).
  • TEL/AML1 (also known as ETV6/RUNX1) rearrangement is the most frequent genetic change in childhood B-acute lymphoblastic leukemia (ALL) and is associated with a favorable prognosis.
  • TEL/AML1 rearrangement is not unique in childhood ALL, and cryptic TEL deletion without TEL/AML1 rearrangement was more frequent than the TEL/AML1 rearrangement in adult ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 16213368.001).
  • [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 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
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63. Goto H, Naruto T, Tanoshima R, Kato H, Yokosuka T, Yanagimachi M, Fujii H, Yokota S, Komine H: Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children. Leuk Res; 2009 Oct;33(10):1386-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children.
  • Sensitivity to 10 anticancer drugs was evaluated in 6 childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cell lines.
  • Authenticity of newly established cell lines was confirmed by genomic fingerprinting.
  • This cell line panel offers an in vitro model for the development of new therapies for childhood BCP-ALL.
  • [MeSH-major] B-Lymphocytes / pathology. DNA Fingerprinting / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Survival / drug effects. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Leukocyte Count. Male. Prednisolone / pharmacology

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  • (PMID = 19157546.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 9PHQ9Y1OLM / Prednisolone
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64. Steiner M, Attarbaschi A, König M, Nebral K, Gadner H, Haas OA, Mann G, Austrian Berlin-Frankfurt-Münster Group: Equal frequency of TEL/AML1 rearrangements in children with acute lymphoblastic leukemia with and without Down syndrome. Pediatr Hematol Oncol; 2005 Apr-May;22(3):229-34
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  • [Title] Equal frequency of TEL/AML1 rearrangements in children with acute lymphoblastic leukemia with and without Down syndrome.
  • Constitutional trisomy 21 is the most prominent predisposing factor to childhood leukemia, whereas the t(12;21)(p13;q22) with its molecular genetic counterpart, the TEL/AML1 fusion gene, is the most common acquired chromosomal rearrangement in childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL).
  • Accordingly, they were able to analyze 8 of 10 individuals with DS and a BCP ALL, two of whom who suffered from a TEL/AML1+ leukemia.
  • Based on this observation they concluded that individuals with BCP leukemia and a constitutional trisomy 21 may have similar likelihood to have a TEL/AML1 rearrangement as BCP ALL patients without this specific predisposing factor.
  • [MeSH-major] Down Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [RepublishedFrom] Pediatr Hematol Oncol. 2005 Jan-Feb;22(1):11-6 [15770827.001]
  • (PMID = 16020107.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Corrected and Republished Article; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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65. Russo V, Scott IU, Querques G, Stella A, Barone A, Delle Noci N: Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients. Eur J Ophthalmol; 2008 Jul-Aug;18(4):619-23
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  • [Title] Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients.
  • PURPOSE: To investigate the association between presence of orbital or ocular lesions and type and stage of leukemia and to investigate whether orbital and ocular lesions are significant in predicting leukemia prognosis.
  • METHODS: The authors evaluated 180 patients with acute childhood leukemia.
  • Lesions associated with leukemia may be classified as specific (due to leukemic infiltration of various ocular tissues), nonspecific (due to one of the secondary complications), or iatrogenic manifestations caused by chemotherapy.
  • Children with presenting white blood cell count below 50,000 mm3 are considered at standard risk for treatment failure, while all others are considered at high risk for treatment failure.
  • RESULTS: Specific lesions were noted in 66% of patients with acute myeloid leukemia (AML) and 11.5% patients with acute lymphocytic leukemia (ALL) (p<0.05), and were more severe in patients with high risk leukemia than in patients with standard risk leukemia.
  • [MeSH-major] Eye Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Orbital Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 18609485.001).
  • [ISSN] 1120-6721
  • [Journal-full-title] European journal of ophthalmology
  • [ISO-abbreviation] Eur J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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66. Reddy H, Jamil K: Polymorphisms in the MTHFR gene and their possible association with susceptibility to childhood acute lymphocytic leukemia in an Indian population. Leuk Lymphoma; 2006 Jul;47(7):1333-9
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  • [Title] Polymorphisms in the MTHFR gene and their possible association with susceptibility to childhood acute lymphocytic leukemia in an Indian population.
  • Acute lymphocytic leukemia (ALL) is the most common pediatric cancer worldwide, and is particularly more common in the Indian population.
  • [MeSH-major] Genetic Predisposition to Disease. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentIn] Leuk Lymphoma. 2006 Jul;47(7):1203-4 [16923547.001]
  • (PMID = 16923565.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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67. 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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  • [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]
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  • (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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68. Pais AP, Amare Kadam PS, Raje GC, Banavali S, Parikh P, Kurkure P, Arora B, Gujral S, Kumar SA, Badrinath Y: RUNX1 aberrations in ETV6/RUNX1-positive and ETV6/RUNX1-negative patients: its hemato-pathological and prognostic significance in a large cohort (619 cases) of ALL. Pediatr Hematol Oncol; 2008 Sep;25(6):582-97

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A large-cohort study (619) of acute lymphoblastic leukemia (ALL) revealed an ETV6/RUNX1 (previously known as TEL/AML1) incidence of 18% in pediatric B-cell precussor ALL, indicating no geographical heterogeinity.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18728978.001).
  • [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 / 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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69. Gaipa G, Basso G, Aliprandi S, Migliavacca M, Vallinoto C, Maglia O, Faini A, Veltroni M, Husak D, Schumich A, Ratei R, Biondi A, Dworzak MN, I-BFM-ALL-FCM-MRD-Study Group: Prednisone induces immunophenotypic modulation of CD10 and CD34 in nonapoptotic B-cell precursor acute lymphoblastic leukemia cells. Cytometry B Clin Cytom; 2008 May;74(3):150-5
Hazardous Substances Data Bank. PREDNISONE .

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  • [Title] Prednisone induces immunophenotypic modulation of CD10 and CD34 in nonapoptotic B-cell precursor acute lymphoblastic leukemia cells.
  • BACKGROUND: Immunophenotypic modulation is induced by steroids in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) patients during remission induction therapy.
  • RESULTS: Leukemia samples that sustained the treatment in vitro with prednisone, showed significative reduction of CD10 and CD34 expression compared with control, and it was comparable with that observed in residual leukemic cells of the same patients in BM at day 15 of treatment.
  • [MeSH-major] Antigens, CD34 / metabolism. Neprilysin / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / drug effects. Precursor Cells, B-Lymphoid / immunology. Prednisone / pharmacology
  • [MeSH-minor] Adolescent. Cell Culture Techniques. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Remission Induction

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  • [Copyright] (c) 2008 Clinical Cytometry Society
  • (PMID = 18271020.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 3.4.24.11 / Neprilysin; VB0R961HZT / Prednisone
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70. Cox CV, Blair A: A primitive cell origin for B-cell precursor ALL? Stem Cell Rev; 2005;1(3):189-96

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A primitive cell origin for B-cell precursor ALL?
  • A stem cell origin has been described for both acute and chronic myelogenous leukemias.
  • In contrast, childhood B-cell precursor acute lymphoblastic leukemia (ALL) is thought to arise in committed B-lineage cells.
  • Evidence suggests that some subtypes of childhood ALL have a primitive cell origin and share many immunophenotypic characteristics with normal progenitor cells.
  • These leukemic stem cells may be resistant to current therapeutic strategies designed to kill the bulk ALL cell population and subsequent relapses may arise from this population.
  • [MeSH-major] Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Burkitt Lymphoma / immunology. Gene Expression Regulation, Leukemic / immunology. Neoplastic Stem Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Animals. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Proliferation. Humans. Recurrence

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  • (PMID = 17142855.001).
  • [ISSN] 1550-8943
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
  • [Number-of-references] 54
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71. Azevedo-Silva F, Camargo Bd, Pombo-de-Oliveira MS: Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia. Braz J Med Biol Res; 2010 Mar;43(3):226-9
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  • [Title] Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia.
  • Acute leukemia is the most frequent cancer in children.
  • Recently, a new hypothesis was proposed for the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The so-called 'adrenal hypothesis' emphasized the role of endogenous cortisol in the etiology of B-cell precursor ALL.
  • The adrenal hypothesis proposes that the risk of childhood B-cell precursor ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis.


72. Paulsson K, Johansson B: High hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):637-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy (51-67 chromosomes) is the most common cytogenetic abnormality pattern in childhood B-cell precursor acute lymphoblastic leukemia (ALL), occurring in 25-30% of such cases.
  • Despite the high frequency of this karyotypic subgroup, many questions remain regarding the epidemiology, etiology, presence of other genetic changes, the time and cell of origin, and the formation and pathogenetic consequences of high hyperdiploidy.
  • However, during the last few years, several studies have addressed some of these important issues, and these, as well as previous reports on high hyperdiploid childhood ALL, are reviewed herein.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 19415723.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 195
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73. Jalali GR, An Q, Konn ZJ, Worley H, Wright SL, Harrison CJ, Strefford JC, Martineau M: Disruption of ETV6 in intron 2 results in upregulatory and insertional events in childhood acute lymphoblastic leukaemia. Leukemia; 2008 Jan;22(1):114-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of ETV6 in intron 2 results in upregulatory and insertional events in childhood acute lymphoblastic leukaemia.
  • We describe four cases of childhood B-cell progenitor acute lymphoblastic leukaemia (BCP-ALL) and one of T-cell (T-ALL) with unexpected numbers of interphase signals for ETV6 with an ETV6-RUNX1 fusion probe.
  • Fluorescence in situ hybridisation (FISH), array comparative genomic hybridization (aCGH) and Molecular Copy-Number Counting (MCC) results were concordant for the T-cell case.
  • [MeSH-major] Chromosome Aberrations. Introns / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 17972957.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / TLX3 protein, human
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74. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
Hazardous Substances Data Bank. FOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • We sequenced the translocation breakpoints of 56 patients with childhood ALL or AML harboring t(12;21), t(8;21), t(15;17), inv(16), and t(1;19), and demonstrated, with the notable exception of t(1;19), that these rearrangements are commonly detected in the neonatal blood spots (Guthrie cards) of the cases.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
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75. Steiner M, Attarbaschi A, König M, Gadner H, Haas OA, Mann G: Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome. Pediatr Hematol Oncol; 2005 Jan-Feb;22(1):11-6
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  • [Title] Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome.
  • Constitutional trisomy 21 is the most prominent predisposing factor to childhood leukemia, whereas the t(12;21)(p13;q22) with its molecular genetic counterpart, the TEL/AML1 fusion gene, is the most common acquired chromosomal rearrangement in childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL).
  • Accordingly, they were able to analyze 8 of 10 individuals with DS and a BCP ALL, including 2 who suffered from a TEL/AML1+ leukemia.
  • Based on this observation we concluded that individuals with a constitutional trisomy 21 may have the similar likelihood to develop a TEL/AML1+ leukemia as BCP ALL patients without this specific predisposingfactor.
  • [MeSH-major] Down Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [RepublishedIn] Pediatr Hematol Oncol. 2005 Apr-May;22(3):229-34 [16020107.001]
  • (PMID = 15770827.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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76. 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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  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • BACKGROUND AND OBJECTIVES: Impaired apoptosis, mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin, is thought to contribute to leukemic cell survival.
  • 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.
  • [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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77. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; 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 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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78. Bener A, Hoffmann GF, Afify Z, Rasul K, Tewfik I: Does prolonged breastfeeding reduce the risk for childhood leukemia and lymphomas? Minerva Pediatr; 2008 Apr;60(2):155-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does prolonged breastfeeding reduce the risk for childhood leukemia and lymphomas?
  • AIM: Prolonged breastfeeding was shown to reduce the risk of childhood acute leukemia.
  • The aim of the study was to investigate the protective effect of longer breastfeeding on the risk of lymphoid malignancies in children and its dependent socio-economic factors.
  • METHODS: The study group comprised of 169 patients with acute lymphocytic leukemia (ALL), Hodgkin's (HL) and non-Hodgkin's lymphoma (NHL), age =or<15 years, and 169 healthy controls, matched to patients by age and sex.
  • In multivariate analysis, statistically significant risk factors for the development of childhood lymphoid malignancy were: a shorter duration of breastfeeding, lower age and level of education of mother and higher income, larger size of accommodation and birth order in the family.
  • Additional factors found to be associated with an elevated risk of lymphoid malignancy were low age and low education of mother.
  • All these factors can be related to an increased risk of early childhood infections.
  • [MeSH-major] Breast Feeding. Hodgkin Disease / prevention & control. Lymphoma, Non-Hodgkin / prevention & control. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control

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  • (PMID = 18449131.001).
  • [ISSN] 0026-4946
  • [Journal-full-title] Minerva pediatrica
  • [ISO-abbreviation] Minerva Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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79. Luo CY, Li BS, Jiang H, Gu LJ: [Study of the correlation between the expression level of asparagine synthetase and the outcome of children with acute lymphocytic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jul;29(7):446-9

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  • [Title] [Study of the correlation between the expression level of asparagine synthetase and the outcome of children with acute lymphocytic leukemia].
  • OBJECTIVE: To determine whether the high level of asparagine synthetase (AS) expression in childhood acute lymphocytic leukemia (ALL) is associated with an inferior prognosis.
  • [MeSH-major] Aspartate-Ammonia Ligase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 19035175.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 6.3.1.1 / Aspartate-Ammonia Ligase
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80. Campbell LK, Scaduto M, Sharp W, Dufton L, Van Slyke D, Whitlock JA, Compas B: A meta-analysis of the neurocognitive sequelae of treatment for childhood acute lymphocytic leukemia. Pediatr Blood Cancer; 2007 Jul;49(1):65-73
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  • [Title] A meta-analysis of the neurocognitive sequelae of treatment for childhood acute lymphocytic leukemia.
  • BACKGROUND: Impaired neurocognitive functioning is one increasingly recognized long-term consequence of childhood ALL treatment.
  • PROCEDURE: A comprehensive meta-analytic review of the long-term neurocognitive effects of childhood ALL was conducted.
  • Studies were included if they were published in English, reported original quantitative data on the post-treatment neurocognitive functioning of childhood ALL patients in first remission and control groups, and used neurocognitive measures with adequate psychometric properties and published normative data.
  • Neurocognitive assessment plays a critical role in determining what remedial or specialized instruction is needed in childhood ALL survivors and should be included as a standard part of long-term follow-up care.
  • [MeSH-major] Cognition Disorders / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16628558.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Meta-Analysis
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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81. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism. Cell Communication. Cell Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate

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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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82. Krstic AD, Impera L, Guc-Scekic M, Lakic N, Djokic D, Slavkovic B, Storlazzi CT: A complex rearrangement involving cryptic deletion of ETV6 and CDKN1B genes in a case of childhood acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Dec;195(2):125-31
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  • [Title] A complex rearrangement involving cryptic deletion of ETV6 and CDKN1B genes in a case of childhood acute lymphoblastic leukemia.
  • We report on a case of childhood B-cell lineage acute lymphoblastic leukemia (ALL).
  • The deleted segment on 12p contains several genes, among the tumor suppressor genes ETV6 and CDKN1B, which are frequently involved in 12p abnormalities in childhood ALL.
  • Thus, the present study documents the loss of both ETV6 and CDKN1B genes accompanying the occurrence of a complex rearrangement involving chromosomes 3 and 12 in a case of childhood ALL.
  • [MeSH-major] Gene Deletion. Intracellular Signaling Peptides and Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • [ErratumIn] Cancer Genet Cytogenet. 2010 Apr 1;198(1):76
  • (PMID = 19963112.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / ETS translocation variant 6 protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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83. Krapf G, Kaindl U, Kilbey A, Fuka G, Inthal A, Joas R, Mann G, Neil JC, Haas OA, Panzer-Grümayer ER: ETV6/RUNX1 abrogates mitotic checkpoint function and targets its key player MAD2L1. Oncogene; 2010 Jun 03;29(22):3307-12
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  • Approximately 25% of childhood B-cell precursor acute lymphoblastic leukemia have an ETV6/RUNX1 (E/R) gene fusion that results from a t(12;21).
  • This genetic subgroup of leukemia is associated with near-triploidy, near-tetraploidy, and trisomy 21 as rather specific types of secondary changes.
  • Consistent with this notion, E/R-expressing diploid murine and human cell lines have decreased proportions of cells with 4N DNA content and a lower mitotic index when treated with spindle toxins.
  • [MeSH-major] Calcium-Binding Proteins / genetics. Cell Cycle Proteins / genetics. Mitosis / genetics. Oncogene Proteins, Fusion / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Core Binding Factor Alpha 2 Subunit. Gene Fusion. Gene Rearrangement. Humans. Karyotyping. Mad2 Proteins. Promoter Regions, Genetic

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  • (PMID = 20190817.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 17551
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MAD2L1 protein, human; 0 / Mad2 Proteins; 0 / Oncogene Proteins, Fusion; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ EMS32872; NLM/ PMC4194424
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84. Citak EC, Oguz A, Karadeniz C, Akyurek N: Role of gelatinases (MMP-2 and MMP-9), TIMP-1, vascular endothelial growth factor (VEGF), and microvessel density on the clinicopathological behavior of childhood non-Hodgkin lymphoma. Pediatr Hematol Oncol; 2008 Jan-Feb;25(1):55-66
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  • [Title] Role of gelatinases (MMP-2 and MMP-9), TIMP-1, vascular endothelial growth factor (VEGF), and microvessel density on the clinicopathological behavior of childhood non-Hodgkin lymphoma.
  • The present study was carried out to clarify the role of matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), vascular endothelial growth factor (VEGF), and microvessel density (MVD) in the clinicopathologic behavior of childhood B-cell non-Hodgkin lymphoma (NHL).
  • The results showed that angiogenesis and angiogenic factors might have a role in development and clinical behavior of childhood NHL.
  • Larger series of patients are needed to determine the prognostic value of angiogenesis in childhood non-Hodgkin lymphoma.
  • [MeSH-major] Angiogenic Proteins / analysis. Lymphoma, B-Cell / diagnosis. Neovascularization, Pathologic


85. Crazzolara R, Cisterne A, Thien M, Hewson J, Baraz R, Bradstock KF, Bendall LJ: Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia. Blood; 2009 Apr 2;113(14):3297-306
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia.
  • Despite advances in the treatment of acute lymphoblastic leukemia (ALL), the majority of children who relapse still die of ALL.
  • We investigated the effects of the mammalian target of rapamycin inhibitor, RAD001 (Everolimus), in a nonobese diabetic/severe combined immunodeficiency model of human childhood B-cell progenitor ALL.
  • RAD001 induced a cell-cycle arrest in the G(0/1) phase with associated dephosphorylation of the retinoblastoma protein, and reduced levels of cyclin-dependent kinases 4 and 6.
  • In conclusion, we have demonstrated activity of RAD001 in an in vivo leukemia model supporting further clinical development of target of rapamycin inhibitors for the treatment of patients with ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / analogs & derivatives. Vincristine / administration & dosage


86. Forestier E, Gauffin F, Andersen MK, Autio K, Borgström G, Golovleva I, Gustafsson B, Heim S, Heinonen K, Heyman M, Hovland R, Johannsson JH, Kerndrup G, Rosenquist R, Schoumans J, Swolin B, Johansson B, Nordgren A, Nordic Society of Pediatric Hematology and Oncology, Swedish Cytogenetic Leukemia Study Group, NOPHO Leukemia Cytogenetic Study Group: Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukemias: a Nordic series of 24 cases and review of the literature. Genes Chromosomes Cancer; 2008 Feb;47(2):149-58
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  • [Title] Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukemias: a Nordic series of 24 cases and review of the literature.
  • Although dic(9;20)(p13.2;q11.2) is a characteristic abnormality in childhood B-cell precursor acute lymphoblastic leukemias (BCP ALL), little is known about its clinical impact or the type and frequency of additional aberrations it may occur together with.
  • We here review the clinical and cytogenetic features of a Nordic pediatric series of 24 patients with dic(9;20)-positive BCP ALL diagnosed 1996-2006, constituting 1.3% of the BCP ALL, as well as 47 childhood cases from the literature.
  • Consistent immunophenotypic features of the Nordic cases included positivity for HLA-DR, CD10, CD19, CD20, and CD22 and negativity for T-cell and myeloid markers; no detailed immunophenotypes were reported for the previously published cases.
  • The median patient age was 3 years, the female/male ratio was 2.0, the median white blood cell count was 24 x 10(9)/l, 11% had central nervous system involvement, and 5% had a mediastinal mass at diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Cytogenetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17990329.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 38
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87. Isoda T, Ito S, Kajiwara M, Nagasawa M: Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment. Pediatr Int; 2007 Dec;49(6):1018-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment.
  • Methotrexate (MTX) is a key drug in the chemotherapy for childhood acute lymphocytic leukemia (ALL).
  • [MeSH-major] Acute Kidney Injury / chemically induced. Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18045317.001).
  • [ISSN] 1328-8067
  • [Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society
  • [ISO-abbreviation] Pediatr Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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88. Olsen M, Madsen HO, Hjalgrim H, Gregers J, Rostgaard K, Schmiegelow K: Preleukemic TEL-AML1-positive clones at cell level of 10(-3) to 10(-4) do not persist into adulthood. J Pediatr Hematol Oncol; 2006 Nov;28(11):734-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preleukemic TEL-AML1-positive clones at cell level of 10(-3) to 10(-4) do not persist into adulthood.
  • The TEL-AML1 translocation, t(12;21)(p13;q22), is one of the most frequent genetic aberrations in childhood B-cell precursor acute lymphoblastic leukemia (ALL), where it occurs in 25% of all cases.
  • Evidence suggests that the TEL-AML1 translocation occurs in utero in 1% of all newborn children at cell levels of 10 to 10.
  • The observed prevalence of TEL-AML1-positive cells in healthy adults is of the same order of magnitude as the prevalence reported in healthy newborns, but the observed cell level of 10 to 10 is much lower.
  • These data indicates that prenatal TEL-AML1 subclones does not persist throughout adult life at cell levels of 10 to 10.
  • The findings are compatible with the risk of t(12;21)(p13;q22) ALL correlating with the total number of TEL-AML1-positive cells in peripheral blood in both childhood and adulthood.
  • [MeSH-minor] Adult. Blood Donors. Child. Female. Humans. Male. Middle Aged. Nucleic Acid Hybridization / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17114960.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; 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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89. D'Amico G, Bonamino M, Dander E, Marin V, Basso G, Balduzzi A, Biagi E, Biondi A: T cells stimulated by CD40L positive leukemic blasts-pulsed dendritic cells meet optimal functional requirements for adoptive T-cell therapy. Leukemia; 2006 Nov;20(11):2015-24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cells stimulated by CD40L positive leukemic blasts-pulsed dendritic cells meet optimal functional requirements for adoptive T-cell therapy.
  • Adoptive T-cell immunotherapy may provide complementary therapy for childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • In this study, we have analyzed the functional characteristics of anti-BCP-ALL effector T cells generated by co-culturing T lymphocytes and dendritic cells (DC) from allogeneic human stem cell transplantation (HSCT) donors.
  • Anti-BCP-ALL T cells expressed CD49d and CXCR4 (implicated in the recruitment to bone marrow), and CD62L and CCR7 (involved in the migration to lymphoid organs).
  • These effectors are fully equipped to reach leukemia-infiltrated tissues and have characteristics to support and orchestrate the anti-tumor immune-response.
  • [MeSH-major] Adoptive Transfer / methods. CD40 Ligand / metabolism. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Th1 Cells / immunology
  • [MeSH-minor] Antigen-Presenting Cells / cytology. Antigen-Presenting Cells / immunology. B-Lymphocytes / cytology. B-Lymphocytes / immunology. Bone Marrow Cells / cytology. Cell Communication / immunology. Cell Lineage / immunology. Cell Movement / immunology. Cells, Cultured. Child. Coculture Techniques. Humans. Immunologic Memory. Immunophenotyping

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  • (PMID = 16990769.001).
  • [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] 147205-72-9 / CD40 Ligand
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90. Taylor GM, Hussain A, Verhage V, Thompson PD, Fergusson WD, Watkins G, Lightfoot T, Harrison CJ, Birch JM, UKCCS Investigators: Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601. Leukemia; 2009 May;23(5):863-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601.
  • We previously reported that susceptibility to childhood B cell precursor ALL (BCP ALL) is associated with HLA-DPB1 alleles having glutamic acid (E) rather than lysine (K) in the P4 antigenic peptide-binding pocket.
  • Here, we report that only one of seven alleles with the DP6 supertype (DPB1(*)0601) is associated with childhood leukaemia (leukaemia vs controls: odds ratio, 95% confidence interval [OR, CI]: 4.6, 2.0-10.4; corrected P=0.019), but not with childhood solid tumours or lymphomas.
  • Sequencing the coding region of DPB1(*)0601 revealed an exon 1-4 haplotype [T-DEAV-KIL-RVI] shared with DPB1(*)0301 and 0901, but no evidence of germline mutations in childhood leukaemia.
  • These results suggest that the DPbeta0601 molecule may be functionally involved in childhood leukaemia.
  • Analysis of peptide binding and T-cell activation by DPbeta0601-peptide complexes should help determine its role in childhood leukaemia causation.
  • [MeSH-major] HLA-DP Antigens / genetics. Haplotypes / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19148140.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen
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91. Hou Y, Hu Q, Liu AG, Zhang LQ, Liu SY: [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Apr;8(2):101-4
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  • [Title] [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy].
  • OBJECTIVE: Survivin, a unique member of the inhibitor of apoptosis protein (IAP) family, plays an important role in regulating both apoptosis and cell division.
  • METHODS: The expression of survivin protein was detected by immunohistochemical assay in bone marrow cells from 62 children with acute leukemia and 40 hospitalized children who did not have leukemia (Control group), and in a human acute T lymphocytic leukemia cell line (Molt-4 cells) treated in vitro with daunorubicin (DNR).
  • Cell apoptosis was detected using flow cytometry.
  • RESULTS: Survivin protein was expressed in 41.9% of the 62 children with acute leukemia but in only 5.0% of the Control group (chi(2)=16.66; P < 0.01).
  • The expression rate of survivin was 46.2% in cytoplasm and 53.9% in nucleus in the children with acute leukemia (chi(2)0.3077; P> 0.05).
  • DNR treatment also induced survivin transllocation from cytoplasm to nucleus and cell apoptosis in a time and dosage-dependent manner.
  • CONCLUSIONS: Survivin may play an important role in the development and prognosis of childhood acute leukemia.
  • The different expression pattern of survivin in the cytoplasm and the nucleus may be associated with therapeutic efficacy and prognosis in acute leukemia.
  • DNR may reduce the survivin expression in leukemic cells and induce cell apoptosis.
  • [MeSH-major] Bone Marrow Cells / chemistry. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16613699.001).
  • [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 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; ZS7284E0ZP / Daunorubicin
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92. Accordi B, Espina V, Giordan M, VanMeter A, Milani G, Galla L, Ruzzene M, Sciro M, Trentin L, De Maria R, te Kronnie G, Petricoin E, Liotta L, Basso G: Functional protein network activation mapping reveals new potential molecular drug targets for poor prognosis pediatric BCP-ALL. PLoS One; 2010;5(10):e13552
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  • [Title] Functional protein network activation mapping reveals new potential molecular drug targets for poor prognosis pediatric BCP-ALL.
  • BACKGROUND: In spite of leukemia therapy improvements obtained over the last decades, therapy is not yet effective in all cases.
  • Current approaches in Acute Lymphoblastic Leukemia (ALL) research focus on identifying new molecular targets to improve outcome for patients with a dismal prognosis.
  • METHODOLOGY/PRINCIPAL FINDINGS: We employed Reverse Phase Protein Microarrays to identify aberrantly activated proteins in 118 pediatric B-cell precursor (BCP)-ALL patients.
  • We observed an increased activation/expression of several pathways involved in cell proliferation in poor clinical prognosis patients.
  • [MeSH-major] Leukemia, B-Cell / drug therapy
  • [MeSH-minor] Adenylate Kinase / metabolism. Blotting, Western. Cell Line, Tumor. Child. Child, Preschool. Humans. Immunoprecipitation. Infant. Neoplasm Proteins / metabolism. Prednisone / therapeutic use. Prognosis. Proteomics. Signal Transduction

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  • (PMID = 21042412.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; EC 2.7.4.3 / Adenylate Kinase; VB0R961HZT / Prednisone
  • [Other-IDs] NLM/ PMC2958847
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93. Peter A, Heiden T, Taube T, Körner G, Seeger K: Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes. Eur J Haematol; 2009 Nov;83(5):420-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes.
  • OBJECTIVES: TEL/AML1 (ETV6/RUNX1) fusion resulting from the translocation t(12;21)(p13;q22) constitutes the most common chimeric fusion gene in initial childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) (19-27%) and has been associated with good prognosis.
  • They also show that it is important to consider combined mutations in the analysis of this leukemia entity.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Dosage. In Situ Hybridization, Fluorescence. Interphase. Mutation. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19594616.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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94. Stachel D, Albert M, Meilbeck R, Kreutzer B, Haas RJ, Schmid I: Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL). Eur J Med Res; 2006 Mar 27;11(3):102-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL).
  • Samples from 49 consecutive pediatric patients with B cell precursor acute lymphocytic leukemia (BCP ALL) were analyzed by semiquantitative RT-PCR.
  • We identified interleukin (IL)-10 expression as a significant adverse prognostic indicator in childhood BCP-ALL.
  • Taqman RT-PCR of sorted cell populations showed that IL-10 mRNA was synthetized almost exclusively by NK or T cells.
  • These findings emphasize the role of the immune system for the outcome of childhood ALL.
  • [MeSH-major] Bone Marrow Cells / immunology. Burkitt Lymphoma / genetics. Burkitt Lymphoma / immunology. Cytokines / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Th2 Cells / immunology

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  • (PMID = 16751110.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Cytokines; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4
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95. Eby GA: Treatment of acute lymphocytic leukemia using zinc adjuvant with chemotherapy and radiation--a case history and hypothesis. Med Hypotheses; 2005;64(6):1124-6
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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 acute lymphocytic leukemia using zinc adjuvant with chemotherapy and radiation--a case history and hypothesis.
  • Low blood levels of zinc are often noted in acute lymphocytic leukemia (ALL), but zinc is not administered as part of any modern chemotherapy program in the treatment of ALL.
  • The result was a bone marrow remission from 95+% blast cells to an observed zero blast cell count in both hips within the first 14 days of treatment which never relapsed.
  • In addition to the reduction of blast cells to an observed count of zero (not a single leukemic or normal blast), red blood cell production and other hemopoietic functions returned to normal at a clinically remarkable rate.
  • The extremely broad role of zinc in pre-leukemic adverse health conditions, viral, fungal and tumoral immunity, hemopoietics, cell growth, division and differentiation, genetics and chemotherapy interactions are considered.
  • Since treatment with zinc and other identified deficient nutrients, particularly magnesium, did not appear injurious in ALL and they appear to be highly beneficial, controlled clinical studies of zinc (3.18 mg/kg body weight/day) with magnesium (8.0 mg/kg body weight/day) as adjuvants to chemotherapy in the treatment of childhood ALL are suggested.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gluconates / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Zinc / physiology

  • Hazardous Substances Data Bank. AMMONIUM GLUCONATE .
  • Hazardous Substances Data Bank. POTASSIUM GLUCONATE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. GLUCONIC ACID .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • Hazardous Substances Data Bank. MANGANESE GLUCONATE .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
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  • (PMID = 15823699.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Chickenpox Vaccine; 0 / Gluconates; 5J49Q6B70F / Vincristine; E7WED276I5 / 6-Mercaptopurine; J41CSQ7QDS / Zinc; R4R8J0Q44B / gluconic acid; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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96. Kang R, Tang DL, Cao LZ, Yu Y, Zhang GY, Xiao XZ: [High mobility group box 1 is increased in children with acute lymphocytic leukemia and stimulates the release of tumor necrosis factor-alpha in leukemic cell]. Zhonghua Er Ke Za Zhi; 2007 May;45(5):329-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [High mobility group box 1 is increased in children with acute lymphocytic leukemia and stimulates the release of tumor necrosis factor-alpha in leukemic cell].
  • OBJECTIVE: Cytokine mediated cell immunity is the main mode of anti-tumor immunity in organism, and the disequilibrium of cytokine network is the main cause of tumor cells escaping immunologic surveillance.
  • In the present study, the investigators explored the clinical significance of alteration in the serum levels of HMGB1 in childhood acute lymphocytic leukemia (ALL) and the mechanism of HMGB1-induced tumor necrosis factor (TNF)-alpha secretion in leukemic cells.
  • METHODS: The serum levels of HMGB1 in healthy children and childhood ALL were assayed by Western blotting.
  • TNF-alpha started to become detectable at 2 h and was still increasing at 16 h after HMGB1 (1 microg/ml) treatment in K562 cell culture.
  • CONCLUSIONS: The measurement of serum HMGB1 is helpful to evaluate the prognosis of the childhood ALL.
  • [MeSH-major] HMGB1 Protein / metabolism. Imidazoles / pharmacology. JNK Mitogen-Activated Protein Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein Kinase Inhibitors / pharmacology. Pyridines / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Child. Cytokines / metabolism. Humans. Mitogen-Activated Protein Kinase Kinases / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Signal Transduction / drug effects

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  • (PMID = 17697615.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cytokines; 0 / HMGB1 Protein; 0 / Imidazoles; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / SB 203580; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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97. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • In comparison with that of B cell ALL (B-ALL), the percentages of age older than 10 years, initial WBC count more than 50 x 10(9)/ L, prednisone poor response (PPR), and failed to achieve remission at day 19 of induction chemotherapy in the T-ALLs were all higher.
  • CONCLUSION: There were statistic differences between T-cell and B-cell childhood ALLs in age, initial WBC count, early response to therapy, and eight-year EFS and RFS.
  • Childhood T-ALL was associated with a worse prognosis than other sub-types of childhood ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Karyotyping. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • (PMID = 19563031.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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98. Hassan R, White LR, Stefanoff CG, de Oliveira DE, Felisbino FE, Klumb CE, Bacchi CE, Seuánez HN, Zalcberg IR: Epstein-Barr virus (EBV) detection and typing by PCR: a contribution to diagnostic screening of EBV-positive Burkitt's lymphoma. Diagn Pathol; 2006 Aug 07;1:17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We performed a systematic comparison between RISH and PCR for EBV detection, in a group of childhood B-cell Non-Hodgkin lymphomas (NHL), aiming to validate PCR as a first, rapid method for the diagnosis of EBV-associated B-cell NHL.
  • METHODS: EBV infection was investigated in formalin fixed paraffin-embedded tumor samples of 41 children with B-cell NHL, including 35 Burkitt's lymphoma (BL), from Rio de Janeiro, Brazil, by in situ hybridization of EBV-encoded small RNA (EBER-RISH) and PCR assays based on EBNA2 amplification.

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  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA082274
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1559641
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99. Clark BR, Ferketich AK, Fisher JL, Ruymann FB, Harris RE, Wilkins JR 3rd: Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio. Pediatr Blood Cancer; 2007 Nov;49(6):797-802
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio.
  • BACKGROUND: This ecologic study examined the geographic distribution of childhood leukemias in Ohio, 1996-2000, among children aged 0-19 for evidence that population mixing may be a factor.
  • RESULTS: Of the 585 cases, 73.3% were acute lymphocytic leukemia (ALL), 16.6% acute myelogenous leukemia (AML), 3.2% acute monocytic leukemia (AMoL), and 2.6% chronic myelogenous leukemia (CML).
  • Rates for total leukemia burden were significantly below national levels for all races (P = 0.00001), likely due to poor ascertainment of cases.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Population Density. Population Dynamics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Rural Population. Urban Population


100. Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB: Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids. Cancer Cell Int; 2007 Nov 28;7:18
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  • Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
  • GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.
  • Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).
  • To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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  • (PMID = 18045478.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041407
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2228275
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