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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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  • [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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  • [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. 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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  • [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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5. 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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  • 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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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
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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  • [Cites] Ann Oncol. 2003 Apr;14(4):520-35 [12649096.001]
  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]
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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. 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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8. 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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9. 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
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  • [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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10. 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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11. 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
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  • [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


12. 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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13. 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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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
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  • [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
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  • [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. 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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19. 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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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


21. 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
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] 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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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. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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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. 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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26. 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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27. 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
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [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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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 / / MRC/ G0300130; United Kingdom / Medical Research Council / / MRC/ MC/ U137686856
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. 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
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] 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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30. 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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31. 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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32. 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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33. 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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34. 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


35. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
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] 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. Correa-González LC, Mandeville PB, Manrique-Dueñas J, Alejo-González F, Salazar-Martínez A, de Pérez-Ramírez OJ, Hernández-Sierra JF: [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients]. Gac Med Mex; 2005 Nov-Dec;141(6):477-82
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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 pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients].
  • OBJECTIVE: To determine the prognostic value of preB immunophenotype and its variants on early treatment response among of acute pediatric lymphoblast leukemia.
  • PATIENTS AND METHODS: A case-control study nested in a cohort was carried out with male and female patients 15 years and younger with recently diagnosed pre-B lymphoblast leukemia.
  • A panel of B, T, monoclonal antibodies of the myelo-monocytic and megakaryocytic cell type was used.
  • CONCLUSIONS: We need to pay special emphasis on early treatment response in children with lymphoblast leukemia as our study did not corroborate the common finding that clinical factors and immune phenotype can be predictive factors.
  • [MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 16381501.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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42. 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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43. 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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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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45. O'Brien MM, Lee-Kim Y, George TI, McClain KL, Twist CJ, Jeng M: Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2008 Feb;50(2):381-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis.
  • Secondary HLH due to malignancy occurs most commonly with T or NK-cell lymphoid neoplasms.
  • HLH with B-cell malignancies is less common and HLH has rarely been described in association with precursor B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


46. 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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47. Mantadakis E, Danilatou V, Stiakaki E, Paterakis G, Papadhimitriou S, Kalmanti M: T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):354-7
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  • [Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.
  • We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.
  • Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.
  • This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16206214.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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48. 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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49. Torelli GF, Guarini A, Maggio R, Alfieri C, Vitale A, Foà R: Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission. Haematologica; 2005 Jun;90(6):785-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission.
  • The anti-leukemic activity of NK cells against acute myeloid leukemia (AML) blasts has been described, but very few data are available for acute lymphoid leukemia (ALL).
  • The present study was designed to investigate whether: (i) NK effectors could be expanded from adult and pediatric ALL patients in complete remission;.
  • (v) any differences in cytotoxic activity could be found between expanded effectors from adult and pediatric patients.
  • DESIGN AND METHODS: We co-cultured patients' peripheral blood mononuclear cells (PBMC) with the feeder cell line RPMI 8866 and analyzed the NK cells' expansion capacity by cell count and cytofluorimetric analyses.
  • 51Cr release assays, before and after stimulation with activating cytokines, were performed to analyze the cytotoxic potential of effector cells against tumor cell lines and autologous blast cells.
  • Patients' expanded cells showed cytotoxic activity against target cell lines comparable to that of normal donors.
  • No differences in expansion and cytotoxic activity were found between pediatric and adult patients.
  • [MeSH-major] Immunotherapy / methods. Killer Cells, Natural / cytology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 15951291.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Receptors, IgG
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50. Maecker B, Mougiakakos D, Zimmermann M, Behrens M, Hollander S, Schrauder A, Schrappe M, Welte K, Klein C: Dendritic cell deficiencies in pediatric acute lymphoblastic leukemia patients. Leukemia; 2006 Apr;20(4):645-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dendritic cell deficiencies in pediatric acute lymphoblastic leukemia patients.
  • Acute lymphoblastic leukemia (ALL) cells are particularly poor at generating anti-leukemia immunity, despite residing in lymphoid organs.
  • To assess a potential role of dendritic cells (DC) in poor anti-leukemia immunity, we analyzed peripheral blood DC in 55 pediatric ALL patients at the time of initial diagnosis and 19 age-matched healthy controls.
  • Thus, depletion of DC in B-lineage ALL patients may contribute to poor anti-leukemia immune responses.
  • [MeSH-major] Antigens, CD11c / biosynthesis. Dendritic Cells / immunology. Lectins, C-Type / biosynthesis. Membrane Glycoproteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Receptors, Immunologic / biosynthesis
  • [MeSH-minor] Adolescent. Antigens, CD / biosynthesis. Antigens, CD13 / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Count. Child. Child, Preschool. Cohort Studies. Female. Flow Cytometry / methods. Humans. Immunophenotyping. Leukocyte Count. Male. Monocytes / pathology. Neutrophils / pathology. Peroxidase / biosynthesis. Sensitivity and Specificity. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16498391.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11c; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CLEC4C protein, human; 0 / Lectins, C-Type; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 1.11.1.7 / Peroxidase; EC 3.4.11.2 / Antigens, CD13
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51. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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52. 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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53. 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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54. Shalapour S, Eckert C, Seeger K, Pfau M, Prada J, Henze G, Blankenstein T, Kammertoens T: Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia. J Mol Med (Berl); 2010 Mar;88(3):249-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.
  • Even though childhood ALL can be cured in a large number of patients, around 20% of the patients suffer a relapse after chemotherapy.
  • Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.
  • MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).
  • Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.
  • The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.
  • [MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [CommentIn] J Mol Med (Berl). 2010 Mar;88(3):219-22 [20135087.001]
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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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55. Unal S, Cetin M, Tuncer AM, Gümrük F, Yetgin S: The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients. Turk J Pediatr; 2008 Nov-Dec;50(6):533-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients.
  • The incidence of mixed-lineage leukemias in the pediatric age group was previously reported as 13.8% for myeloid antigen-positive ALL and 11.1% for lymphoid antigen-positive acute myeloid leukemia (AML).
  • Our study also supports most of the previous data and we postulate that myeloid antigen expression in pediatric ALL cases has insignificant effect on clinical presentation, relapse rates and survival.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19227415.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm
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56. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.


57. Paulsson K, Johansson B: High hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):637-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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58. 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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59. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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60. 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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61. 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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62. Yoda A, Yoda Y, Chiaretti S, Bar-Natan M, Mani K, Rodig SJ, West N, Xiao Y, Brown JR, Mitsiades C, Sattler M, Kutok JL, DeAngelo DJ, Wadleigh M, Piciocchi A, Dal Cin P, Bradner JE, Griffin JD, Anderson KC, Stone RM, Ritz J, Foà R, Aster JC, Frank DA, Weinstock DM: Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Jan 5;107(1):252-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia.
  • The prognosis for adults with precursor B-cell acute lymphoblastic leukemia (B-ALL) remains poor, in part from a lack of therapeutic targets.
  • We demonstrate that CRLF2 is overexpressed in approximately 15% of adult and high-risk pediatric B-ALL that lack MLL, TCF3, TEL, and BCR/ABL rearrangements, but not in B-ALL with these rearrangements or other lymphoid malignancies.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics. Signal Transduction / physiology


63. Dalle JH, Moghrabi A, Rousseau P, Leclerc JM, Barrette S, Bernstein ML, Champagne J, David M, Demers J, Duval M, Hume H, Meyer P, Champagne MA: Second induction in pediatric patients with recurrent acute lymphoid leukemia using DFCI-ALL protocols. J Pediatr Hematol Oncol; 2005 Feb;27(2):73-9
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  • [Title] Second induction in pediatric patients with recurrent acute lymphoid leukemia using DFCI-ALL protocols.
  • Between 15% and 30% of children with acute lymphoblastic leukemia (ALL) experience disease recurrence.
  • With the possible exception of patients presenting with late isolated extramedullary relapse, induction of second complete remission (CR) is employed as a stepping stone to allogeneic hematopoietic stem cell transplantation (HSCT).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Asparaginase / administration & dosage. Child. Child, Preschool. Cytarabine / administration & dosage. Doxorubicin / administration & dosage. Female. Humans. Infant. Male. Methotrexate / administration & dosage. Prednisone / administration & dosage. Recurrence. Retrospective Studies. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 15701980.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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64. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Such translocations result in gain of function fusion proteins that drive cell proliferation.
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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65. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
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  • [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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66. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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67. Panagopoulos I, Lilljebjörn H, Strömbeck B, Hjorth L, Olofsson T, Johansson B: MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia. Haematologica; 2006 Sep;91(9):1287-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia.
  • MLL/GAS7, resulting from t(11;17)(q23;p13), has been reported in one case of treatment-related acute myeloid leukemia (AML).
  • We present a de novo case of t(11;17)-positive pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Humans. Infant. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 16956839.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / GAS7 protein, human; 0 / MLL-GAS7 fusion protein; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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68. Gutierrez A, Sanda T, Ma W, Zhang J, Grebliunaite R, Dahlberg S, Neuberg D, Protopopov A, Winter SS, Larson RS, Borowitz MJ, Silverman LB, Chin L, Hunger SP, Jamieson C, Sallan SE, Look AT: Inactivation of LEF1 in T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 08;115(14):2845-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of LEF1 in T-cell acute lymphoblastic leukemia.
  • To further unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performed high-resolution array comparative genomic hybridization on diagnostic specimens from 47 children with T-ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary samples.
  • [MeSH-major] Codon, Terminator. Lymphoid Enhancer-Binding Factor 1 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

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  • (PMID = 20124220.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / 5P01CA68484
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Codon, Terminator; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2854430
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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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 / / 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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70. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


71. Riedt T, Ebinger M, Salih HR, Tomiuk J, Handgretinger R, Kanz L, Grünebach F, Lengerke C: Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia. Blood; 2009 Apr 23;113(17):4049-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia.
  • Previously, we reported that the murine homologues (Cdx1, Cdx2, and Cdx4) affect formation and differentiation of embryonic stem cell (ESC)-derived hematopoietic progenitor cells.
  • Consistent with the notion that embryonic pathways can reactivate during adult oncogenesis, recent studies suggest involvement of CDX2 in human acute myeloid leukemia (AML).
  • Here we study CDX2 in healthy and leukemic human lymphoid cells, and show that a majority of leukemic samples display various degrees of aberrant CDX2 expression.
  • Analysis of a cohort of 37 childhood acute lymphoblastic leukemia (ALL) patients treated in our hospital reveals that high CDX2 expression levels at diagnosis correlate with persistence of minimal residual disease (MRD) during the course of treatment.
  • Thus, CDX2 expression levels may serve as a marker for adverse prognosis in pediatric ALL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Homeodomain Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19218548.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
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72. 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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  • [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


73. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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74. 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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75. 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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76. 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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77. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • On the basis of the conventional cytogenetic analysis, molecular methods have improved pediatric hematologists/oncologist's ability to accurately and rapidly perform risk-stratification on patients with childhood ALL during the last few years.
  • The aim of the present study was to assess the demography of cytogenetic abnormalities in childhood ALL.
  • METHOD: The study subjects consisted of 124 newly diagnosed ALL patients younger than 16 years of age, who were diagnosed at the Department of Pediatric Hematology/Oncology, Soochow University Children's Hospital.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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78. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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79. 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
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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80. Amare Kadam PS, Raje GC, Pais AP, Banavali S: Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL. Cancer Genet Cytogenet; 2008 Apr 1;182(1):27-32
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  • [Title] Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
  • Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations.
  • ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18328947.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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81. Onda K, Iijima K, Katagiri YU, Okita H, Saito M, Shimizu T, Kiyokawa N: Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma. Int J Hematol; 2010 Jun;91(5):808-19
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  • [Title] Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma.
  • B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear.
  • We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells.
  • Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL.
  • BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells.
  • The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.
  • [MeSH-major] B-Cell Activating Factor / immunology. B-Cell Activation Factor Receptor / genetics. Burkitt Lymphoma / immunology. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / pathology
  • [MeSH-minor] Antigens, CD40 / immunology. Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans

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  • (PMID = 20428981.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / B-Cell Activating Factor; 0 / B-Cell Activation Factor Receptor
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82. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Of 200 cases, 9.0% aberrantly expressed T cell-associated antigens.
  • There were significant differences in antigen-expression patterns between adult and pediatric B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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83. 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
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  • [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

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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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84. Urs L, Stevens L, Kahwash SB: Leukemia presenting as solid tumors: report of four pediatric cases and review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):370-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia presenting as solid tumors: report of four pediatric cases and review of the literature.
  • Involvement of extramedullary tissue during the course of a leukemia is common and usually does not represent a major diagnostic challenge when the history is available and specimen triage is optimal.
  • In the lymphoid category, leukemia involvement of tissue is conventionally distinguished from lymphoma by establishing the presence of 20% or more blasts in the bone marrow.
  • A leukemia with an initial presentation outside the bone marrow mimicking a solid tumor is a rare but well-documented clinical encounter.
  • We report 4 case examples in the pediatric population, presenting in different anatomic sites.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Juvenile / pathology. Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 18179285.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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85. 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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  • (PMID = 16893464.001).
  • [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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86. O'Neil J, Look AT: Mechanisms of transcription factor deregulation in lymphoid cell transformation. Oncogene; 2007 Oct 15;26(47):6838-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of transcription factor deregulation in lymphoid cell transformation.
  • The most frequent targets of genetic alterations in human lymphoid leukemias are transcription factor genes with essential functions in blood cell development.
  • TAL1, LYL1, HOX11 and other transcription factors essential for normal hematopoiesis are often misexpressed in the thymus in T-cell acute lymphoblastic leukemia (T-ALL), leading to differentiation arrest and cell transformation.
  • The NOTCH1 gene, which is essential for key embryonic cell-fate decisions in multicellular organisms, was found to be activated by mutation in a large percentage of T-ALL patients.
  • Therefore, deregulated transcription and its consequent effects on key developmental pathways play a major role in the molecular pathogenesis of lymphoid malignancy.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Lymphocyte Subsets / metabolism. Lymphocyte Subsets / pathology. Transcription Factors / genetics

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  • (PMID = 17934490.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 170
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87. Jiang H, Gu LJ, Xue HL, Tang JY, Chen J, Pan C, Chen J: [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Aug;8(4):272-4
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  • [Title] [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia].
  • OBJECTIVE: To study the cellular activity of asparagine synthetase in different types of childhood acute lymphoblastic leukemia (ALL).
  • METHODS: The cellular activity of asparagine synthetase was detected by HPLC-FLD and Protein measurement in 28 ALL children (7 cases of T-ALL and 21 cases of B-lymphoid lineage ALL) before chemotherapy.
  • RESULTS: The asparagines synthetase activity levels in T-ALL children were significantly higher than those of the B-lymphoid lineage ALL patients, with the median activity level of 9.3 nM Asn/mg protein/hr vs 5.2 nM Asn/mg protein/hr (P < 0.05).
  • The distribution of the asparagine synthetase activity demonstrated a polymorphism in either T-ALL or B-lymphoid lineage ALL patients.
  • The asparagines synthetase activity levels in T-ALL are significantly higher than in B-lymphoid lineage ALL.
  • [MeSH-major] Aspartate-Ammonia Ligase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 16923354.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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88. Bachmann PS, Piazza RG, Janes ME, Wong NC, Davies C, Mogavero A, Bhadri VA, Szymanska B, Geninson G, Magistroni V, Cazzaniga G, Biondi A, Miranda-Saavedra D, Göttgens B, Saffery R, Craig JM, Marshall GM, Gambacorti-Passerini C, Pimanda JE, Lock RB: Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition. Blood; 2010 Oct 21;116(16):3013-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition.
  • Glucocorticoids play a critical role in the therapy of lymphoid malignancies, including pediatric acute lymphoblastic leukemia (ALL), although the mechanisms underlying cellular resistance remain unclear.
  • We report glucocorticoid resistance attributable to epigenetic silencing of the BIM gene in pediatric ALL biopsies and xenografts established in immune-deficient mice from direct patient explants as well as a therapeutic approach to reverse resistance in vivo.
  • These findings provide a novel therapeutic strategy to reverse glucocorticoid resistance and improve outcome for high-risk pediatric ALL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis Regulatory Proteins / genetics. Drug Resistance, Neoplasm. Gene Silencing. Glucocorticoids / therapeutic use. Histone Deacetylase Inhibitors / therapeutic use. Membrane Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 20647567.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0800784; United Kingdom / National Centre for the Replacement, Refinement and Reduction of Animals in Research / / NC3RS/ G0900729/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 58IFB293JI / vorinostat; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.98 / Histone Deacetylases
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89. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20920256.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2956734
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90. Taylor M, Harrison C, Eden T, Birch J, Greaves M, Lightfoot T, Hussain A, UKCCS Investigators: HLA-DPB1 supertype-associated protection from childhood leukaemia: relationship to leukaemia karyotype and implications for prevention. Cancer Immunol Immunother; 2008 Jan;57(1):53-61
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  • [Title] HLA-DPB1 supertype-associated protection from childhood leukaemia: relationship to leukaemia karyotype and implications for prevention.
  • Most childhood B cell precursor (BCP) acute lymphoblastic leukaemia (ALL) cases carry the reciprocal translocation t(12;21)(p13;q22) ( approximately 25%), or a high hyperdiploid (HeH) karyotype (30%).
  • Based on our previous analysis of HLA-DP in childhood ALL, and evidence from in vitro studies that TEL-AML1 can activate HLA-DP-restricted T cell responses, we hypothesised that the development of TEL-AML1+ ALL might be influenced by the child's DPB1 genotype.
  • To test this, we analysed the frequency of six HLA-DPB1 supertypes in a population-based series of childhood leukaemias (n = 776) classified by their karyotype (TEL-AML1+, HeH and others), in comparison with newborn controls (n = 864).
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genetic Predisposition to Disease. HLA-DP Antigens / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control

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  • (PMID = 17622527.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [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 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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91. Cairo MS, Gerrard M, Sposto R, Auperin A, Pinkerton CR, Michon J, Weston C, Perkins SL, Raphael M, McCarthy K, Patte C, FAB LMB96 International Study Committee: Results of a randomized international study of high-risk central nervous system B non-Hodgkin lymphoma and B acute lymphoblastic leukemia in children and adolescents. Blood; 2007 Apr 1;109(7):2736-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a randomized international study of high-risk central nervous system B non-Hodgkin lymphoma and B acute lymphoblastic leukemia in children and adolescents.
  • The prognosis for higher risk childhood B-cell non-Hodgkin lymphoma has improved over the past 20 years but the optimal intensity of treatment has yet to be determined.
  • Children 21 years old or younger with newly diagnosed B-cell non-Hodgkin lymphoma/B-cell acute lymphoblastic leukemia (B-NHL/B-ALL) with higher risk factors (bone marrow [BM] with or without CNS involvement) were randomized to standard intensity French-American-British/Lymphoma Malignancy B (FAB/LMB) therapy or reduced intensity (reduced cytarabine plus etoposide and deletion of 3 maintenance courses M2, M3, M4).
  • [MeSH-major] Burkitt Lymphoma / drug therapy. Central Nervous System Neoplasms / drug therapy. Lymphoma, B-Cell / drug therapy


92. Bernt KM, Armstrong SA: Leukemia stem cells and human acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):33-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia stem cells and human acute lymphoblastic leukemia.
  • Leukemia stem cells are fairly well described for acute myeloid leukemia (AML), but their existence and relevance for acute lymphoblastic leukemia (ALL) is less clear.
  • However, it has also been suggested that the majority of leukemic subfractions can propagate leukemia in the appropriate experimental setting, and that their hierarchical organization is less strict than in AML.
  • In addition, it is uncertain whether cancer stem cells arise from malignant transformation of a tissue-specific stem cell, or from committed progenitors or differentiated cells that re-acquire a stem cell-like program.
  • In common childhood ALL, current evidence points towards the cell of origin being a committed lymphoid progenitor.
  • In this review, we highlight recent findings relating to the question of leukemia stem cells in ALL.
  • [MeSH-major] Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19100366.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / T32 CA009172
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 44
  • [Other-IDs] NLM/ NIHMS89422; NLM/ PMC4031465
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93. Meleshko AN, Belevtsev MV, Savitskaja TV, Potapnev MP: The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression. Leuk Res; 2006 Jul;30(7):795-800
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 incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression.
  • Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangement is conventionally used for assessment of lymphoid malignant cells.
  • TCR genes rearrangements were reported to occur at high frequency in B-lineage acute lymphoblastic leukemia (ALL).
  • Therefore, we have analyzed 83 children with acute B-lineage ALL (67 de novo patients and 19 relapses) by PCR analysis for clonal IgH, incomplete TCRD (Vdelta2-Ddelta3 and Ddelta2-Ddelta3) and TCRG rearrangements.
  • It was shown that clonal cross-lineage TCR rearrangements were associated with more immature immunophenotype (CD34+, CD117+, CyIgM-) of leukemic cells from patients' bone marrow (BM) samples as compared to cell samples without cross-lineage TCR rearrangements.
  • [MeSH-major] Burkitt Lymphoma / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 16386788.001).
  • [ISSN] 0145-2126
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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94. Ek T, Pinkava M, Abrahamsson J: Ara-C fever and infections after high-dose ara-C treatment in pediatric lymphoid malignancies. J Pediatr Hematol Oncol; 2005 Jul;27(7):364-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ara-C fever and infections after high-dose ara-C treatment in pediatric lymphoid malignancies.
  • The objective of this study was to examine the incidence and characteristics of Ara-C-related fever and the frequency and severity of infections after single-drug, high-dose Ara-C treatment (HDAC) in children treated for acute lymphoblastic leukemia (ALL) or non-Hodgkin lymphoma (NHL).
  • Profound neutropenia and lymphopenia are causative factors for the high incidence of infections, but the risk of life-threatening complications after HDAC in children in remission of lymphoid malignancies is low, even without prophylactic use of colony-stimulating factors.
  • [MeSH-minor] Adolescent. Biomarkers / blood. C-Reactive Protein / analysis. Child. Child, Preschool. Fever / chemically induced. Humans. Infant. Leukocyte Count. Platelet Count. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Retrospective Studies

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  • (PMID = 16012325.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers; 04079A1RDZ / Cytarabine; 9007-41-4 / C-Reactive Protein
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95. 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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96. Stefan DC, Stones D: How much does it cost to treat children with Hodgkin lymphoma in Africa? Leuk Lymphoma; 2009 Feb;50(2):196-9
MedlinePlus Health Information. consumer health - Hodgkin Disease.

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  • Hodgkin lymphoma (HL) is a common B-cell childhood neoplasm and it has a higher incidence in the 0-14 year age group in developing countries compared to developed countries.

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  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):152-3 [19235011.001]
  • (PMID = 19197725.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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97. Sudhakar N, Nancy NK, Rajalekshmy KR, Rajkumar T: Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia. Iran J Immunol; 2009 Sep;6(3):141-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia.
  • BACKGROUND: Precursor B-Acute Lymphoblastic Leukemia (precursor B-ALL) occurs due to the uncontrolled proliferation of B-lymphoid precursors arrested at a particular stage of B-cell development.
  • Precursor-B-ALL is classified mainly into pro-B-ALL, common-ALL and pre-B-ALL.
  • The Common Acute Lymphoblastic Antigen CD10 is the marker for common-ALL.
  • OBJECTIVE: This study was aimed to examine the diversity of T-cell receptor Gamma (TCRG) and T-cell receptor Delta (TCRD) gene rearrangements in South Indian Common-ALL patients.
  • METHODS: Clonality of TCRG and TCRD was studied in 52 cases (pediatric=41 and adolescents and young adults=11) of common-ALL.
  • RESULTS: In pediatric common-ALL, clonal TCRG and TCRD gene rearrangements were detected in 19 (46.3%) and 18 (43.9%) cases respectively.
  • In the present study of common-ALL, the frequency of a TCRG rearrangement VII-J1.3/2.3 was significantly high in AYA compared to pediatric (36.3% vs 4.8%; p<0.025).
  • Thus, VII-J1.3/2.3 was highly diverse in AYA compared to pediatric.
  • That shows the difference in biology of the disease between pediatric and AYA in South Indian population.
  • [MeSH-major] Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 19801787.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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98. Mullighan CG, Downing JR: Global genomic characterization of acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):3-15
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

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  • (PMID = 19100363.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / P30 CA021765-30
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS168528; NLM/ PMC2834786
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99. Dorantes-Acosta E, Arreguin-Gonzalez F, Rodriguez-Osorio CA, Sadowinski S, Pelayo R, Medina-Sanson A: Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report. Cases J; 2009;2:154

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report.
  • Acute leukemia, the most common form of cancer in children, accounts for approximately 30% of all childhood malignancies, with acute lymphoblastic leukemia being five times more frequent than acute myeloid leukemia.
  • Lineage switch is the term that has been used to describe the phenomenon of acute leukemias that meet the standard French-American-British system criteria for a particular lineage (either lymphoid or myeloid) upon initial diagnosis, but meet the criteria for the opposite lineage at relapse.
  • Many reports have documented conversions of acute lymphoblastic leukemia to acute myeloid leukemia.
  • Here, we report the case of a 4-year-old child with acute myeloid leukemia, which upon relapse switched to acute lymphoblastic leukemia.

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  • (PMID = 19946525.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2783110
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100. Park JA, Ghim TT, Bae Kw, Im HJ, Jang SS, Park CJ, Chi HS, Seo JJ: Stem cell transplant in the treatment of childhood biphenotypic acute leukemia. Pediatr Blood Cancer; 2009 Sep;53(3):444-52
Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell transplant in the treatment of childhood biphenotypic acute leukemia.
  • BACKGROUND: Many studies have found that biphenotypic acute leukemia (BAL) is associated with a poor outcome.
  • RESULTS: BAL constituted 4.4% of all acute childhood leukemia cases.
  • In terms of immunophenotype, 14 patients had leukemia with myeloid plus B-lymphoid (M + B) marker, 7 with myeloid plus T-lymphoid (M + T) marker, and 4 with myeloid plus B-lymphoid and T-lymphoid (M + B + T) markers.
  • Hematopoietic stem cell transplantation (HSCT) did not improve either overall survival or event-free survival compared to chemotherapy alone (hazard ratio 0.98, 95% CI 0.35-2.76, P = 0.966; hazard ratio 1.07, 95% CI 0.41-2.78, P = 0.88).
  • CONCLUSIONS: Treatment outcomes in childhood BAL patients differed by immunophenotype and cytogenetics.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 19489056.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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