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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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  • [RetractionIn] Blood. 2012 Aug 16;120(7):1533 [22753864.001]
  • (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. Healy J, Richer C, Bourgey M, Kritikou EA, Sinnett D: Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia. Haematologica; 2010 Sep;95(9):1608-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia.
  • Although childhood acute lymphoblastic leukemia is the most common pediatric cancer, its etiology remains poorly understood.
  • In an attempt to replicate the findings of 2 recent genome-wide association studies in a French-Canadian cohort, we confirmed the association of 5 SNPs [rs7073837 (P=4.2 x 10(-4)), rs10994982 (P=3.8 x 10(-4)), rs10740055 (P=1.6 x 10(-5)), rs10821936 (P=1.7 x 10(-7)) and rs7089424 (P=3.6 x 10(-7))] in the ARID5B gene with childhood acute lymphoblastic leukemia.
  • We also confirmed a selective effect for B-cell acute lymphoblastic leukemia with hyperdiploidy and report a putative gender-specific effect of ARID5B SNPs on acute lymphoblastic leukemia risk in males.
  • This study provides a strong rationale for more detailed analysis to identify the causal variants at this locus and to better understand the overall functional contribution of ARID5B to childhood acute lymphoblastic leukemia susceptibility.

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

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  • (PMID = 18554462.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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5. 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
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  • [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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6. 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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7. Jeha S, Behm F, Pei D, Sandlund JT, Ribeiro RC, Razzouk BI, Rubnitz JE, Hijiya N, Howard SC, Cheng C, Pui CH: Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3302-4
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  • [Title] Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • CD20 expression is associated with inferior survival in adults with acute lymphoblastic leukemia (ALL).
  • We analyzed the prognostic impact of CD20 expression in 353 children with B-cell precursor ALL treated in 3 consecutive St Jude Total Therapy studies.
  • There was no association between CD20 expression and E2A-PBX, TEL-AML1, ploidy, white blood cell count at diagnosis, or sex.
  • These data suggest that CD20 expression is not associated with inferior outcome in pediatric patients treated with contemporary regimens.

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  • (PMID = 16896151.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20
  • [Other-IDs] NLM/ PMC1895438
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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. 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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10. 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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11. 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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12. 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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13. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).

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  • (PMID = 27962529.001).
  • [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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14. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. 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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16. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.

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  • (PMID = 27962471.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • While the first course of chemotherapy successfully eradicated the cell line with the t(12;21), the second cell line with AML1 amplification remained latent during the time of complete remission and reappeared with a different immunophenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


18. 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
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  • [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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19. 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
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  • [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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20. 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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21. Tassano E, Acquila M, Tavella E, Micalizzi C, Panarello C, Morerio C: MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Aug;49(8):682-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia.
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus are common abnormalities in mature B-cell neoplasms.
  • Recent findings have also revealed their significant role in B-cell precursor acute lymphoblastic leukemia.
  • In this study, we describe a pediatric case of B-cell precursor acute lymphoblastic leukemia showing microRNA-125b-1 (MIR125B1) and BLID gene overexpression, resulting from a novel t(11;14)(q24.1;q32) translocation involving IGH.
  • [MeSH-major] BRCA2 Protein / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Child. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Female. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 20544842.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BLID protein, human; 0 / BRCA2 Protein; 0 / BRCA2 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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22. 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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23. Taylor GM, Hussain A, Lightfoot TJ, Birch JM, Eden TO, Greaves MF: HLA-associated susceptibility to childhood B-cell precursor ALL: definition and role of HLA-DPB1 supertypes. Br J Cancer; 2008 Mar 25;98(6):1125-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-associated susceptibility to childhood B-cell precursor ALL: definition and role of HLA-DPB1 supertypes.
  • Childhood B-cell precursor (BCP) ALL is thought to be caused by a delayed immune response to an unidentified postnatal infection.

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  • (PMID = 18334973.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen
  • [Other-IDs] NLM/ PMC2275491
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24. 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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25. 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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26. 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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27. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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28. Gaipa G, Basso G, Aliprandi S, Migliavacca M, Vallinoto C, Maglia O, Faini A, Veltroni M, Husak D, Schumich A, Ratei R, Biondi A, Dworzak MN, I-BFM-ALL-FCM-MRD-Study Group: Prednisone induces immunophenotypic modulation of CD10 and CD34 in nonapoptotic B-cell precursor acute lymphoblastic leukemia cells. Cytometry B Clin Cytom; 2008 May;74(3):150-5
Hazardous Substances Data Bank. PREDNISONE .

  • [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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29. 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
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] 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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30. 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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31. 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
  •  go-up   go-down


32. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


33. 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
MedlinePlus Health Information. consumer health - Down Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. Cardone M, Kandilci A, Carella C, Nilsson JA, Brennan JA, Sirma S, Ozbek U, Boyd K, Cleveland JL, Grosveld GC: The novel ETS factor TEL2 cooperates with Myc in B lymphomagenesis. Mol Cell Biol; 2005 Mar;25(6):2395-405
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors.
  • Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and MYC and/or MYCN in over one-third of B-ALL patients.
  • Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

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  • (PMID = 15743832.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076379; United States / NCI NIH HHS / CA / R01 CA76379-07; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01-CA72999-08
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ETV7 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1061619
  •  go-up   go-down


35. 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
MedlinePlus Health Information. consumer health - Down Syndrome.

  • [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
  •  go-up   go-down


36. 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
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  • [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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37. 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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38. Peter A, Heiden T, Taube T, Körner G, Seeger K: Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes. Eur J Haematol; 2009 Nov;83(5):420-32
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  • [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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39. He GS, Zhang XH, Yao L, Zhang R, Chen ZX, Wu DP, Sun AN, Jin ZM, Qiu HY, Hu XH: [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2009 Oct;30(10):675-7
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  • [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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40. 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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41. 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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  • [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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42. 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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  • [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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43. 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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44. 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


45. 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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46. Attarbaschi A, Mann G, König M, Steiner M, Dworzak MN, Gadner H, Haas OA, Austrian Berlin-Frankfurt-Münster Cooperative Study Group: Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases. Genes Chromosomes Cancer; 2006 Jun;45(6):608-11
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  • [Title] Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases.
  • Near-tetraploidy (82-94 chromosomes) makes up fewer than 1% of childhood acute lymphoblastic leukemia (ALL) cases and has been reportedly associated with a possibly poorer prognosis compared with other ploidy groups.
  • Fluorescence in situ hybridization revealed that eight of the nine B-cell precursor (BCP) cases and none of the three T-cell ALL cases had an ETV6/RUNX1 rearrangement.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / analysis. Polyploidy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / analysis. Repressor Proteins / analysis

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16552772.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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47. 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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48. 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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49. 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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50. Shiramizu B, Hu N, Frisque RJ, Nerurkar VR: High prevalence of human polyomavirus JC VP1 gene sequences in pediatric malignancies. Cell Mol Biol (Noisy-le-grand); 2007 May 15;53(3):4-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High prevalence of human polyomavirus JC VP1 gene sequences in pediatric malignancies.
  • The oncogenic potential of human polyomavirus JC (JCV), a ubiquitous virus that establishes infection during early childhood in approximately 70% of the human population, is unclear.
  • As a neurotropic virus, JCV has been implicated in pediatric central nervous system tumors and has been suggested to be a pathogenic agent in pediatric acute lymphoblastic leukemia.
  • Recent studies have demonstrated JCV gene sequences in pediatric medulloblastomas and among patients with colorectal cancer.
  • Since JCV is detected in B-lymphocytes, a retrospective analysis of pediatric B-cell and non-B-cell malignancies as well as other HIV-associated pediatric malignancies was conducted for the presence of JCV gene sequences.
  • DNA was extracted from 49 pediatric malignancies, including Hodgkin disease, non-Hodgkin lymphoma, large cell lymphoma and sarcoma.
  • A 215-bp region of the JCV VP1 gene was amplified from 26 (53%) pediatric tumor tissues.
  • Even though JCV TAg gene, which is similar to the SV40 TAg gene, is oncogenic in animal models, the presence of JCV gene sequences in pediatric malignancies does not prove causality.
  • In light of the available data on the presence of JCV in normal and cancerous colon epithelial tissue and our data on amplification of JCV from the cecum of an HIV-infected pediatric patient, further studies are warranted on the role of colon epithelium in the pathogenesis of JCV infection.

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  • (PMID = 17531143.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR003061-205811; United States / NINDS NIH HHS / NS / NS041833-03; United States / NINDS NIH HHS / NS / NS041833-02S1; United States / NINDS NIH HHS / NS / NS039406-01; United States / NINDS NIH HHS / NS / S11 NS041833-03; United States / NINDS NIH HHS / NS / U54 NS039406-05; United States / NCRR NIH HHS / RR / RR018727-039001; United States / NCRR NIH HHS / RR / RR018727-047376; United States / NCRR NIH HHS / RR / P20 RR018727-047376; United States / NINDS NIH HHS / NS / NS039406-05; United States / NINDS NIH HHS / NS / NS041833-04; United States / NCRR NIH HHS / RR / RR003061-217768; United States / NCRR NIH HHS / RR / P20 RR018727-039001; United States / NINDS NIH HHS / NS / S11 NS041833; United States / NINDS NIH HHS / NS / S11 NS041833-02S1; United States / NINDS NIH HHS / NS / NS041833-01; United States / NINDS NIH HHS / NS / U54 NS039406-01; United States / NCRR NIH HHS / RR / RR003061-198157; United States / NINDS NIH HHS / NS / NS039406-04; United States / NINDS NIH HHS / NS / S11 NS041833-04; United States / NINDS NIH HHS / NS / S11 NS041833-02; United States / NINDS NIH HHS / NS / NS041833-05; United States / NINDS NIH HHS / NS / U54 NS039406-03S1; United States / NINDS NIH HHS / NS / NS041833-02; United States / NCRR NIH HHS / RR / RR018727-029001; United States / NINDS NIH HHS / NS / NS039406-03; United States / NINDS NIH HHS / NS / NS041833-04S1; United States / NINDS NIH HHS / NS / NS039406-03S1; United States / NINDS NIH HHS / NS / U54 NS039406-02; United States / NCRR NIH HHS / RR / G12 RR003061-217768; United States / NCRR NIH HHS / RR / G12 RR003061-198157; United States / NINDS NIH HHS / NS / S11 NS041833-01; United States / NCRR NIH HHS / RR / P20 RR018727; United States / NCRR NIH HHS / RR / P20 RR018727-029001; United States / NCRR NIH HHS / RR / RR003061-205811; United States / NINDS NIH HHS / NS / S11 NS041833-04S1; United States / NCRR NIH HHS / RR / G12 RR003061; United States / NINDS NIH HHS / NS / U54 NS039406-03; United States / NINDS NIH HHS / NS / S11 NS41833; United States / NINDS NIH HHS / NS / U54 NS039406-04; United States / NINDS NIH HHS / NS / S11 NS041833-05; United States / NINDS NIH HHS / NS / NS039406-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Capsid Proteins; 0 / DNA Primers; 0 / VP1 protein, polyomavirus
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51. 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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52. 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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53. Fujita N, Mori T, Mitsui T, Inada H, Horibe K, Tsurusawa M, Lymphoma Committee of the Japanese Pediatric Leukemia/Lymphoma Study Group: The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan. Pediatr Blood Cancer; 2008 Aug;51(2):188-92
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  • [Title] The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan.
  • BACKGROUND: There have been excellent treatment results for children with B-cell non-Hodgkin lymphoma (B-NHL) and mature B-cell leukemia (B-ALL) in the last few decades.
  • Among 18 patients who had a chemotherapy-sensitive disease, 4 of 5 patients who underwent hematopoietic stem cell transplantation (HSCT) during remission survived without progression, while 3 of 12 patients who did not receive HSCT were alive without disease progression.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, B-Cell / therapy. Lymphoma, B-Cell / therapy


54. 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


55. Meeker ND, Yang JJ, Schiffman JD: Pharmacogenomics of pediatric acute lymphoblastic leukemia. Expert Opin Pharmacother; 2010 Jul;11(10):1621-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacogenomics of pediatric acute lymphoblastic leukemia.
  • IMPORTANCE OF THE FIELD: Pediatric acute lymphoblastic leukemia (ALL) represents one of the best examples of progress in disease treatment and improved outcome based in part upon the incorporation of the principles of pharmacogenomics.
  • Throughout the past several decades, clinical scientists have continued to refine risk stratification in clinical trials with the understanding that individual patients have different subtypes of pediatric ALL that will respond to therapy in different, but predictable ways.
  • AREAS COVERED IN THIS REVIEW: Discussed in this review are the most significant findings from pharmacogenomic studies of pediatric ALL from 1989 to the present.
  • Pharmacogenomic studies related to the drugs commonly used to treat pediatric ALL are covered in detail, including an emphasis on both genome-wide and candidate gene/pathway approaches.
  • TAKE HOME MESSAGE: The outcome for children with pediatric ALL has improved greatly, and this is in part due to the successful integration of data from pharmacogenomic studies into clinical trials.
  • [MeSH-major] Pharmacogenetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20429672.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 5J49Q6B70F / Vincristine; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 120
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56. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [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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57. Kiss F, Buslig J, Szegedi I, Scholtz B, Kappelmayer J, Kiss C: Early relapse after rituximab chemoimmunotherapy. Pediatr Blood Cancer; 2008 Feb;50(2):372-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In relapsed/refractory childhood acute lymphoblastic leukemia (ALL) of the B-cell lineage rituximab, a monoclonal anti-CD20 antibody was used successfully in some cases.
  • We report on a 15-year-old female with relapsed CD20-positive B-cell progenitor ALL treated with rituximab because of positive minimal residual disease signals after chemotherapy, as checked by flow cytometry and real time quantitative-PCR.
  • The patient died with fulminant aspergillosis before hematopoietic stem cell transplantation could be performed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Humans. Neoplasm, Residual / pathology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973316.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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58. 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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59. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • BACKGROUND AND OBJECTIVES: Impaired apoptosis, mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin, is thought to contribute to leukemic cell survival.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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60. Goldstone AH: Transplantations in adult acute lymphoblastic leukemia--grounds for optimism? Clin Lymphoma Myeloma; 2009;9 Suppl 3:S211-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transplantations in adult acute lymphoblastic leukemia--grounds for optimism?
  • The large MRC/ECOG Adult Acute Lymphoblastic Leukemia Study establishes the value of sibling donor allogeneic transplantation in patients with standard risk, demonstrating superior outcome to conventional chemotherapy.
  • If they are now treated on pediatric chemotherapy protocols, their outcome appears to improve significantly.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Medical Oncology / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19778843.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 6
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61. Forester CM, Braunreiter CL, Yaish H, Hedlund GL, Afify Z: Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia. Pediatr Radiol; 2009 Nov;39(11):1230-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia.
  • In children, leukemia is the most common malignancy, and approximately 75% of leukemias are acute lymphoblastic leukemia (ALL).
  • Central nervous system leukemia is found at diagnosis in fewer than 5% of children with ALL.
  • Leukemic intracranial masses have been described with acute myeloid leukemia, but ALL presenting as a mass lesion is rare.
  • We describe a unique case of an intracranial confirmed precursor B cell (pre-B) ALL mass in a 13-year-old girl that was diagnosed by brain CT, MRI and cerebral angiography, and confirmed by biopsy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Cerebral Angiography / methods. Magnetic Resonance Imaging / methods. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Tomography, X-Ray Computed / methods


62. Weng AP, Lau A: Notch signaling in T-cell acute lymphoblastic leukemia. Future Oncol; 2005 Aug;1(4):511-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is a form of pediatric leukemia that is thought to be caused by approximately 12 distinct chromosomal translocations that lead to aberrant expression of as many different cellular genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Notch / physiology

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  • (PMID = 16556027.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 118
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63. Radhakrishnan N, Sachdeva A, Oberoi J, Yadav SP: Conidiobolomycosis in relapsed acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Dec 15;53(7):1321-3
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  • [Title] Conidiobolomycosis in relapsed acute lymphoblastic leukemia.
  • Here we report the isolation of Conidiobolus coronatus, a rarely reported zygomycetes infection in a patient suffering from acute lymphoblastic leukemia.
  • [MeSH-major] Conidiobolus / isolation & purification. Maxillary Sinusitis / etiology. Orbital Cellulitis / etiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / complications. Zygomycosis / etiology

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19731329.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 7XU7A7DROE / Amphotericin B; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate
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64. Levine RL: Inherited susceptibility to pediatric acute lymphoblastic leukemia. Nat Genet; 2009 Sep;41(9):957-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inherited susceptibility to pediatric acute lymphoblastic leukemia.
  • Although genome-wide analyses have identified somatic alterations contributing to the pathogenesis of pediatric acute lymphoblastic leukemia (ALL), few studies have identified germline variants conferring risk of this disease.
  • [MeSH-major] Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Alleles. CCAAT-Enhancer-Binding Proteins / genetics. Case-Control Studies. Cell Line, Transformed. Cell Transformation, Viral. Child. Child, Preschool. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Gene Frequency. Genetic Variation. Genome-Wide Association Study. Germ-Line Mutation. Haplotypes. Herpesvirus 4, Human / physiology. Humans. Ikaros Transcription Factor / genetics. Oncogene Proteins, Fusion / genetics. Polymorphism, Single Nucleotide. Risk Factors. Transcription Factors / genetics

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  • (PMID = 19710713.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
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65. Abdelouahed K, Laghmari M, Tachfouti S, Cherkaoui W, Khorassani M, M'Seffer FA, Mohcine Z: [T-cell acute lymphoblastic leukemia /orbital lymphoblastic lymphoma in children]. J Fr Ophtalmol; 2005 Feb;28(2):197-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [T-cell acute lymphoblastic leukemia /orbital lymphoblastic lymphoma in children].
  • CASE: The authors report a case of an 6-year-old pediatric patient with a history of acute onset of proptosis of his right eye.
  • RESULTS: Incisional biopsy of the mass revealed after of histopathologic and immuno-histochemical evaluation a T-cell lymphoblastic lymphoma.
  • Systemic examination and bone marrow aspirate show a acute lymphoblastic leukemia.
  • CONCLUSION: Primary T-cell lymphoblastic lymphoma of the orbit is a rare entity in any age group, but it is very rare in children.
  • When tumors occurs in the orbit, it presents a challenging diagnosis problem, especially in pediatric patients.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Neoplasms, Multiple Primary. Orbital Neoplasms. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 15851954.001).
  • [ISSN] 0181-5512
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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66. Akiyama M, Yamada O, Agawa M, Yuza Y, Yanagisawa T, Eto Y, Yamada H: Effects of prednisolone on specifically expressed genes in pediatric acute B-lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Apr;30(4):313-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of prednisolone on specifically expressed genes in pediatric acute B-lymphoblastic leukemia.
  • Although glucocorticoid is essential in the treatment of pediatric acute lymphoblastic leukemia (ALL), their precise mechanisms of action remain unclear.
  • We used DNA microarray to evaluate prednisolone-regulated genes in pre-B-ALL cells from 2 pediatric patients.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. Lymphoma, B-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use

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  • (PMID = 18391702.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] VB0R961HZT / Prednisone
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67. Breakey VR, Abdelhaleem M, Weitzman S, Abla O: Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Dec;30(12):956-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia.
  • We report the clinical course of a child with precursor B-cell acute lymphoblastic leukemia who developed fever, hepatosplenomegaly, and refractory thrombocytopenia after initiation of chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphohistiocytosis, Hemophagocytic / chemically induced. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19131791.001).
  • [ISSN] 1536-3678
  • [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 / pegaspargase; 30IQX730WE / Polyethylene Glycols; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase
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68. Peterson MR, Noskoviak KJ, Newbury R: CD5-positive B-cell acute lymphoblastic leukemia. Pediatr Dev Pathol; 2007 Jan-Feb;10(1):41-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD5-positive B-cell acute lymphoblastic leukemia.
  • CD5-positive B-cell acute lymphoblastic leukemia (ALL) is an exceedingly rare entity, with only a single case report in the literature.
  • We report 2 additional cases of CD5-positive B-cell ALL in a 16-year-old male and a 15-year-old female.
  • We conclude that CD5-positive B-cell ALL is a rare, aggressive malignancy with a poor prognosis that presents in adolescence.
  • Pathologists and clinicians should be aware of this entity to avoid confusion with other small blue-cell tumors.
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Biopsy. Bone Marrow / pathology. Bone Marrow / surgery. Diagnosis, Differential. Diagnostic Errors. Female. Flow Cytometry. Humans. Immunohistochemistry. Leukemia / pathology. Lymphoma / pathology. Male. Prognosis. Sarcoma / pathology

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  • (PMID = 17378623.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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69. 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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70. Sallan SE: Myths and lessons from the adult/pediatric interface in acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2006;:128-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myths and lessons from the adult/pediatric interface in acute lymphoblastic leukemia.
  • The development of effective therapy for children with acute lymphoblastic leukemia (ALL) is one of the great successes of clinical oncology, with long-term survival achieved in over 80% of patients.
  • With an age-unrestricted, biology-based approach, we anticipate a better understanding about why these outcome differences exist, and think that by extending successful pediatric clinical programs to include adult patients with ALL, we can directly compare uniformly treated adults and children in terms of response to therapy, toxicity and underlying biology.

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  • (PMID = 17124051.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 68484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 17
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71. Curran MP, Perry CM: Clofarabine: in pediatric patients with acute lymphoblastic leukemia. Paediatr Drugs; 2005;7(4):259-64; discussion 265-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clofarabine: in pediatric patients with acute lymphoblastic leukemia.
  • Clofarabine also disrupts the integrity of mitochondrial membranes, resulting in programmed cell death.
  • In 61 pediatric patients with relapsed or refractory acute lymphoblastic leukemia treated with clofarabine 52 mg/m2 infused intravenously over 2 hours once daily for 5 days every 2-6 weeks, rates of complete remission, complete remission without platelet recovery, and partial remission were 12%, 8%, and 10%, respectively.
  • The most common adverse events associated with clofarabine 52 mg/m2 once daily for 5 days every 2-6 weeks in 96 patients with acute myelogenous or lymphoblastic leukemia (combined analysis of phase I/II trials) were hematologic events (including anemia, leukopenia, thrombocytopenia, neutropenia, and febrile neutro-penia), gastrointestinal events (including vomiting, nausea, and diarrhea), infections, and transient elevations in liver enzymes.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16117562.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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72. Morrissette JJ, Halligan GE, Punnett HH, McKenzie AS, Guerrero F, de Chadarévian JP: Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Aug;169(1):58-61
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  • [Title] Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia.
  • We describe the rare finding of a 33-month-old child neonatally diagnosed with Down syndrome, who presented with pre-B acute lymphoblastic leukemia (ALL) with a pretreatment bone marrow karyotype in which a low hypodiploid cell line (38 chromosomes) was identified in 17/19 cells studied.
  • The abnormal cell line retained the extra constitutional chromosome 21.
  • Hypodiploidy (loss of one or more chromosomes) is seen in approximately 5% of all childhood pre-B ALL cases and in approximately 2.2% cases of individuals with a constitutional trisomy 21.
  • Low hypodiploidy, associated with a high risk of relapse, is rare in pediatric ALL cases in the general population, and, to our knowledge, is previously unreported in patients with trisomy 21.

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  • (PMID = 16875938.001).
  • [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
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73. Cheok MH, Pottier N, Kager L, Evans WE: Pharmacogenetics in acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):39-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacogenetics in acute lymphoblastic leukemia.
  • Progress in the treatment of acute lymphoblastic leukemia (ALL) in children has been remarkable, from a disease being lethal four decades ago to current cure rates exceeding 80%.
  • However, despite these high cure rates, the annual number of children whose leukemia relapses after their initial therapy remains greater than that of new cases of most types of childhood cancers.
  • In this review, we summarize recent pharmacogenomic studies related to the treatment of pediatric ALL.
  • These studies illustrate the promise of pharmacogenomics to further advance the treatment of human cancers, with childhood leukemia serving as a paradigm.

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

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  • (PMID = 20435627.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2930948
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75. Al-Lamki Z, Wali YA, Wasifuddin SM, Zachariah M, Al-Mjeni R, Li C, Muralitharan S, Al-Kharusi K, Gunaratne P, Peterson L, Gibbs R, Gingras MC, Margolin JF: Identification of prognosis markers in pediatric high-risk acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2005 Oct-Nov;22(7):629-43
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  • [Title] Identification of prognosis markers in pediatric high-risk acute lymphoblastic leukemia.
  • Gene expression profiling may improve the understanding of the biology behind relapse in pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16166056.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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76. Renbarger JL, McCammack KC, Rouse CE, Hall SD: Effect of race on vincristine-associated neurotoxicity in pediatric acute lymphoblastic leukemia patients. Pediatr Blood Cancer; 2008 Apr;50(4):769-71
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of race on vincristine-associated neurotoxicity in pediatric acute lymphoblastic leukemia patients.
  • BACKGROUND: This report examines the association between race and vincristine-associated neurotoxicity in pediatric patients with precursor B cell acute lymphoblastic leukemia (preB ALL).
  • PROCEDURE: A retrospective analysis of vincristine-related side effects in pediatric patients treated for preB ALL was performed.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Continental Population Groups / ethnology. Neurotoxicity Syndromes / ethnology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine / adverse effects

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18085684.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / K23 RR019956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine
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77. Van Vlierberghe P, Palomero T, Khiabanian H, Van der Meulen J, Castillo M, Van Roy N, De Moerloose B, Philippé J, González-García S, Toribio ML, Taghon T, Zuurbier L, Cauwelier B, Harrison CJ, Schwab C, Pisecker M, Strehl S, Langerak AW, Gecz J, Sonneveld E, Pieters R, Paietta E, Rowe JM, Wiernik PH, Benoit Y, Soulier J, Poppe B, Yao X, Cordon-Cardo C, Meijerink J, Rabadan R, Speleman F, Ferrando A: PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Apr;42(4):338-42
SciCrunch. OMIM: Data: Gene Annotation .

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

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  • (PMID = 20228800.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364
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78. Al-Khabori M, Minden MD, Yee KW, Gupta V, Schimmer AD, Schuh AC, Xu W, Brandwein JM: Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2010 Jan;51(1):61-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia.
  • All patients with newly diagnosed T-cell acute lymphoblastic leukemia (T-ALL) and treated over a 17-year period at a single institution were retrospectively analyzed.
  • From 2000 to 2007, a pediatric-based protocol, DFCI (Dana Farber Cancer Institute), was used as the standard regimen for all patients (n = 32).
  • The results provide evidence supporting the superior efficacy of asparaginase-intensive pediatric-based regimens for adults with T-ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality


79. Lamb LS Jr, Neuberg R, Welsh J, Best R, Stetler-Stevenson M, Sorrell A: T-cell lymphoblastic leukemia/lymphoma syndrome with eosinophilia and acute myeloid leukemia. Cytometry B Clin Cytom; 2005 May;65(1):37-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic leukemia/lymphoma syndrome with eosinophilia and acute myeloid leukemia.
  • This case represents an example of an unusual T-cell lymphoblastic leukemia/lymphoma syndrome associated with eosinophilia and myeloid malignancy in a young boy.
  • This case is one of only five reported "leukemic" variants of the disease and demonstrates the importance of considering this poor prognostic diagnosis in pediatric acute lymphoblastic leukemia.
  • This case also illustrates the importance of an interactive multidisciplinary approach to the laboratory evaluation of a leukemia patient.
  • [MeSH-major] Eosinophilia / complications. Leukemia, Myeloid, Acute / complications. Leukemia-Lymphoma, Adult T-Cell / complications. Lymphoma / complications


80. Gutierrez A, Sanda T, Ma W, Zhang J, Grebliunaite R, Dahlberg S, Neuberg D, Protopopov A, Winter SS, Larson RS, Borowitz MJ, Silverman LB, Chin L, Hunger SP, Jamieson C, Sallan SE, Look AT: Inactivation of LEF1 in T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 08;115(14):2845-51
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of LEF1 in T-cell acute lymphoblastic leukemia.
  • To further unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performed high-resolution array comparative genomic hybridization on diagnostic specimens from 47 children with T-ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary samples.
  • [MeSH-major] Codon, Terminator. Lymphoid Enhancer-Binding Factor 1 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

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  • (PMID = 20124220.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / 5P01CA68484
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Codon, Terminator; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2854430
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81. Sahu GR, Das BR: Alteration of p73 in pediatric de novo acute lymphoblastic leukemia. Biochem Biophys Res Commun; 2005 Feb 18;327(3):750-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alteration of p73 in pediatric de novo acute lymphoblastic leukemia.
  • Aberrant DNA methylation of multiple promoter associated CpG islands is a frequent phenomenon in acute lymphoblastic leukemia (ALL).
  • One pediatric patient showed mutation in exon 4, two showed mutation in exon 5, and none of the patients showed mutation in exons 6 and 7.
  • However, p73 overexpression was observed in 58% of pediatric patients as demonstrated by immunocytochemistry and Western blot analysis.
  • Methylation of p73 does not play a role in pediatric ALL patients of our population.
  • This report is the first demonstrating the presence of p73 gene mutations in exons 4 and 5 with overexpression of p73 protein and absence of p73 methylation in pediatric ALL patients of eastern Indian population.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15649410.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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82. 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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83. Gill HK, Keoh TS, Dhaliwal JS, Moore S, Kim TS, Hassan R, Karim FA, Zakaria Z, Murad S, Mohamed M, Li Ho CM, Ibrahim H, Rahman EJ: TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2005 Jan 15;156(2):129-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia.
  • Eighty-eight multi-ethnic Malaysian pediatric acute lymphoblastic leukemia (ALL) patients were screened for the TEL-AML1 rearrangement by reverse transcription-polymerase chain reaction (RT-PCR).
  • All patients, including 1 with an unusual blast cell morphology who suffered an early relapse and death, were characteristic TEL-AML1 cases in cell count, age, ALL subset classification, and fusion transcript expressed.
  • This study shows that in Malaysia, TEL-AML1 is found in the same distinct ALL subset and at a similar frequency as in other diverse childhood ALL cohorts.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15642392.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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84. Aplenc R, Thompson J, Han P, La M, Zhao H, Lange B, Rebbeck T: Methylenetetrahydrofolate reductase polymorphisms and therapy response in pediatric acute lymphoblastic leukemia. Cancer Res; 2005 Mar 15;65(6):2482-7
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylenetetrahydrofolate reductase polymorphisms and therapy response in pediatric acute lymphoblastic leukemia.
  • A significant portion of patients treated for pediatric acute lymphoblastic leukemia (ALL) relapse.
  • Methotrexate (MTX), which interrupts folate metabolism, is a mainstay of pediatric ALL therapy.
  • These data provide evidence that the MTHFR C677T polymorphism is a common genetic variant conferring a moderate relative risk and a high attributable risk for relapse in pediatric ALL patients.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Methotrexate / therapeutic use. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology


85. Lowas SR, Marks D, Malempati S: Prevalence of transient hyperglycemia during induction chemotherapy for pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Jul;52(7):814-8
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of transient hyperglycemia during induction chemotherapy for pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Transient hyperglycemia (TH) is a recognized side effect of the corticosteroids and asparaginase given during induction chemotherapy for pediatric acute lymphoblastic leukemia (ALL).
  • This study examined the prevalence of TH in a cohort of pediatric ALL patients and the impact on TH of type of steroid or asparaginase used and of risk factors such as age, gender, and overweight.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hyperglycemia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19260096.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone
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86. Ponce-Torres E, Ruíz-Rodríguez Mdel S, Alejo-González F, Hernández-Sierra JF, Pozos-Guillén Ade J: Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia. J Clin Pediatr Dent; 2010;34(3):275-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia.
  • The purpose of this study was to determine the prevalence of oral manifestations in pediatric patients with acute lymphoblastic leukemia (ALL) receiving chemotherapy, and to evaluate the significance of independent risk factors (oral health, gender, age, time and type of treatment, and phase of chemotherapy).
  • The type of leukemia, gender and phase of chemotherapy were apparently associated with the presence of candidiasis, gingivitis, and periodontitis, and they could be considered risk factors for the development of oral manifestations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Mouth Diseases / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20578668.001).
  • [ISSN] 1053-4628
  • [Journal-full-title] The Journal of clinical pediatric dentistry
  • [ISO-abbreviation] J Clin Pediatr Dent
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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87. van Grotel M, van den Heuvel-Eibrink MM, van Wering ER, van Noesel MM, Kamps WA, Veerman AJ, Pieters R, Meijerink JP: CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Dec;51(6):737-40
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  • [Title] CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Children with T-lineage acute lymphoblastic leukemia (T-ALL) have an inferior outcome with combination chemotherapy compared to B-lineage ALL, and still about 30% of the patients relapse within the first 2 years following diagnosis.
  • As CD34 has been related with poor outcome in ALL in general, we investigated the prognostic significance of the stem cell marker CD34, as well as the association of CD34 positivity with the expression of several multidrug resistance (MDR) genes.
  • PROCEDURE: In this retrospective study, we investigated the prognostic significance of the expression of the early T-cell differentiation marker CD34 and the expression of MDR genes in relation to outcome in a cohort of 72 newly diagnosed pediatric T-ALL patients.
  • [MeSH-major] Antigens, CD34 / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 18683236.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Antigens, CD34; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1
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88. Hinds PS, Hockenberry MJ, Gattuso JS, Srivastava DK, Tong X, Jones H, West N, McCarthy KS, Sadeh A, Ash M, Fernandez C, Pui CH: Dexamethasone alters sleep and fatigue in pediatric patients with acute lymphoblastic leukemia. Cancer; 2007 Nov 15;110(10):2321-30
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  • [Title] Dexamethasone alters sleep and fatigue in pediatric patients with acute lymphoblastic leukemia.
  • BACKGROUND: Dexamethasone improves the cure rate of childhood acute lymphoblastic leukemia (ALL) but causes physical and behavioral adverse events.
  • The objective of the current study was to determine the effect of dexamethasone exposure on sleep and fatigue in pediatric patients with ALL.
  • METHODS: One hundred pediatric patients with low-risk or standard-risk ALL were enrolled on 1 of 3 protocols (St. Jude Total XV, Children's Oncology Group [COG] 9904, or COG 9905) at 3 institutions.
  • CONCLUSIONS: Dexamethasone treatment during continuation therapy for childhood ALL significantly and adversely altered sleep and fatigue, confirming that sleep and fatigue are behavioral responses to dexamethasone.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Dexamethasone / adverse effects. Fatigue / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sleep / drug effects

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17926333.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765; United States / NINR NIH HHS / NR / R01NR007610
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone
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89. Jessop M, Choo K, Little M: Acquired tracheoesophageal fistula during treatment for pediatric acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Dec;31(12):960-2
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  • [Title] Acquired tracheoesophageal fistula during treatment for pediatric acute lymphoblastic leukemia.
  • Management of pediatric malignancy can result in disruption of the integrity of the gastrointestinal mucosa through a variety of mechanisms.
  • We describe a pediatric oncology patient who developed a tracheoesophageal fistula as a complication of treatment for acute lymphoblastic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Tracheoesophageal Fistula / chemically induced

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  • (PMID = 19887961.001).
  • [ISSN] 1536-3678
  • [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
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90. 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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  • [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


91. Rytting M: Peg-asparaginase for acute lymphoblastic leukemia. Expert Opin Biol Ther; 2010 May;10(5):833-9
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  • [Title] Peg-asparaginase for acute lymphoblastic leukemia.
  • IMPORTANCE OF THE FIELD: Asparaginase is a prominent component of pediatric and adolescent treatment for acute lymphoblastic leukemia.
  • AREAS COVERED BY THIS REVIEW: The search terms used were asparaginase, leukemia, pegylated, oncaspar, adolescent and young adult.
  • WHAT THE READER WILL GAIN: The reader will gain knowledge of the tolerability and efficacy of pegylated asparaginase when treating acute lymphoblastic leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Asparaginase / therapeutic use. Polyethylene Glycols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20345338.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; EC 3.5.1.1 / Asparaginase
  • [Number-of-references] 33
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92. Crazzolara R, Bendall L: Emerging treatments in acute lymphoblastic leukemia. Curr Cancer Drug Targets; 2009 Feb;9(1):19-31
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  • [Title] Emerging treatments in acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a clonal proliferation of early B- and T-lymphocyte progenitors and results in the accumulation of leukemic blasts in the bone marrow and various extramedullary sites.
  • Despite current treatment protocols achieving rapid cytoreduction in the vast majority of patients, serious acute and late complications are frequent and resistance to chemotherapy often develops.
  • In contrast to the successes obtained with pediatric patients, treatment outcomes for adults remain poor with only 40% of patients being long-term survivors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19200049.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 136
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93. Devecioglu O, Anak S, Atay D, Aktan P, Devecioglu E, Ozalp B, Saribeyoglu E: Pediatric acute lymphoblastic leukemia complicated by secondary hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2009 Sep;53(3):491-2
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  • [Title] Pediatric acute lymphoblastic leukemia complicated by secondary hemophagocytic lymphohistiocytosis.
  • In this case, we report a child with acute lymphoblastic leukemia (ALL), who had three episodes of secondary HLH, possibly due to two different viral etiologies, namely CMV and RSV together with her malignancy, during her induction-consolidation treatment.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19459197.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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94. Wu P, Feng K, Li J, Xie Z, Xue P, Cai T, Cui Z, Chen X, Hou J, Zhang J, Yang F: Discovery and identification of potential biomarkers of pediatric acute lymphoblastic leukemia. Proteome Sci; 2009 Mar 16;7:7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discovery and identification of potential biomarkers of pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is a common form of cancer in children.
  • Noninvasive biomarkers for the early diagnosis of pediatric ALL are urgently needed.
  • The aim of this study was to discover potential protein biomarkers for pediatric ALL.
  • METHODS: Ninety-four pediatric ALL patients and 84 controls were randomly divided into a "training" set (45 ALL patients, 34 healthy controls) and a test set (49 ALL patients, 30 healthy controls and 30 pediatric acute myeloid leukemia (AML) patients).
  • RESULTS: A total of 7 protein peaks (9290 m/z, 7769 m/z, 15110 m/z, 7564 m/z, 4469 m/z, 8937 m/z, 8137 m/z) were found with differential expression levels in the sera of pediatric ALL patients and controls using SELDI-TOF-MS and then analyzed by BPS to construct a classification model in the "training" set.
  • Two candidate protein peaks (7769 and 9290 m/z) were found to be down-regulated in ALL patients, where these were identified as platelet factor 4 (PF4) and pro-platelet basic protein precursor (PBP).
  • CONCLUSION: Platelet factor (PF4), connective tissue activating peptide III (CTAP-III) and two fragments of C3a may be potential protein biomarkers of pediatric ALL and used to distinguish pediatric ALL patients from healthy controls and pediatric AML patients.
  • Further studies with additional populations or using pre-diagnostic sera are needed to confirm the importance of these findings as diagnostic markers of pediatric ALL.

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  • (PMID = 19291297.001).
  • [ISSN] 1477-5956
  • [Journal-full-title] Proteome science
  • [ISO-abbreviation] Proteome Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2662805
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95. Schraders M, van Reijmersdal SV, Kamping EJ, van Krieken JH, van Kessel AG, Groenen PJ, Hoogerbrugge PM, Kuiper RP: High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage. Cancer Genet Cytogenet; 2009 May;191(1):27-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage.
  • Lymphoblastic lymphoma (LBL) is one of the most frequent occurring pediatric non-Hodgkin lymphomas.
  • In the WHO classification scheme, pediatric LBL is considered to be the same disease entity as pediatric acute lymphoblastic leukemia (ALL).
  • However, it is unclear whether the genetic basis of pediatric LBL development is similar to that of pediatric ALL.
  • We performed genome-wide analyses of copy number aberrations in 12 T-LBL and 7 precursor B-cell LBL pediatric cases using high-resolution SNP-based array CGH.
  • These results show that, similar to T-ALL, the genomic alterations in T-LBL predominantly target genes involved in cell cycle progression.
  • The majority of precursor B-cell LBL was characterized by high-hyperdiploidy (71%), and showed high resemblance with high-hyperdiploid precursor B-cell ALL.
  • Taken together, our data suggest that pediatric LBL and ALL exhibit similar genomic abnormalities within confined immunophenotypic and cytogenetic subgroups, but that the representations of these subgroups differs between the two entities.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Gene Expression Profiling. Genome, Human / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Cell Cycle. Child. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 9 / genetics. Gene Duplication. Gene Expression Regulation, Leukemic. Humans. Polyploidy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes / pathology

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  • (PMID = 19389505.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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96. Butturini AM, Dorey FJ, Lange BJ, Henry DW, Gaynon PS, Fu C, Franklin J, Siegel SE, Seibel NL, Rogers PC, Sather H, Trigg M, Bleyer WA, Carroll WL: Obesity and outcome in pediatric acute lymphoblastic leukemia. J Clin Oncol; 2007 May 20;25(15):2063-9
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  • [Title] Obesity and outcome in pediatric acute lymphoblastic leukemia.
  • PURPOSE: To evaluate the effect of obesity (defined as a body mass index > 95th percentile for age and sex at diagnosis) on outcome of pediatric acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Obesity / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17513811.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA13539; United States / NCI NIH HHS / CA / CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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97. Graham DK, Salzberg DB, Kurtzberg J, Sather S, Matsushima GK, Keating AK, Liang X, Lovell MA, Williams SA, Dawson TL, Schell MJ, Anwar AA, Snodgrass HR, Earp HS: Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 May 1;12(9):2662-9
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  • [Title] Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia.
  • To determine if Mer expression is ectopic in T-cell acute lymphoblastic leukemia (ALL) and potentially important in leukemogenesis, we analyzed Mer expression in normal human thymocytes and lymphocytes and in pediatric ALL patient samples.
  • Mer expression in 34 T-cell ALL (T-ALL) patient samples was evaluated by reverse transcription-PCR, and Mer protein expression in a separate cohort of 16 patient samples was assayed by flow cytometry and Western blot.
  • CONCLUSIONS: Transforming Mer signals may contribute to T-cell leukemogenesis, and abnormal Mer expression may be a novel therapeutic target in pediatric ALL therapy.

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  • (PMID = 16675557.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA082086; United States / NCI NIH HHS / CA / CA 68346; United States / NCI NIH HHS / CA / P30 CA46934; United States / NCI NIH HHS / CA / T32CA8608604
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / RNA, Neoplasm; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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98. Styczynski J, Kurylak A, Wysocki M: Cytotoxicity of cortivazol in childhood acute lymphoblastic leukemia. Anticancer Res; 2005 May-Jun;25(3B):2253-8
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  • [Title] Cytotoxicity of cortivazol in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Glucocorticoids are the most important group of drugs used in the treatment of childhood acute lymphoblastic leukemia (ALL), however, resistance to this group remains the main obstacle in curing the disease.
  • AIM: Analysis of ex vivo sensitivity to cortivazol and other glucocorticoids in childhood acute lymphoblastic leukemia, as well as the relationship to anticancer therapy outcome.
  • Cell cycle before and after ex vivo glucocorticoid treatment was analyzed by flow cytometry.
  • CVZ, like other glucocorticoids, caused cell cycle arrest in the GI-phase, and increased the percentage of apoptotic cells to a greater extent than other glucocorticoids.
  • CONCLUSION: Cortivazol has potent antileukemic activity in childhood ALL.
  • Its activity is related to cell cycle arrest and induction of apoptosis.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pregnatrienes / pharmacology
  • [MeSH-minor] Adolescent. Cell Cycle / drug effects. Child. Child, Preschool. Drug Resistance, Neoplasm. Female. Glucocorticoids / pharmacology. Humans. Infant. Lymphocytes / drug effects. Lymphocytes / pathology. Male. Prednisolone / pharmacology. Prognosis

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  • (PMID = 16158972.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Pregnatrienes; 9PHQ9Y1OLM / Prednisolone; YM183K0H63 / cortivazol
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99. Diffner E, Gauffin F, Anagnostaki L, Nordgren A, Gustafsson B, Sander B, Gustafsson B, Persson JL: Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry. J Pediatr Hematol Oncol; 2009 Sep;31(9):696-701
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  • [Title] Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry.
  • We investigated the expression and clinical importance of VEGF and two of its receptors, VEGFR-1 and VEGFR-2, in childhood precursor B-cell acute lymphoblastic leukemia (pre-B ALL) by using immunohistochemistry.
  • These novel findings suggest that VEGFR-1 may have clinical importance in childhood pre-B ALL.
  • [MeSH-major] Immunoenzyme Techniques. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • (PMID = 19707156.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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100. André JM, Galambrun C, Trzeciak MC, Dargaud Y, Kaplan-Gouet C, Jallu V, Bertrand Y: Acquired Glanzmann's thrombasthenia associated with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 Oct;27(10):554-7
Genetic Alliance. consumer health - Thrombasthenia of Glanzmann and Naegeli.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired Glanzmann's thrombasthenia associated with acute lymphoblastic leukemia.
  • Acquired Glanzmann's thrombasthenia is an uncommon event in association with leukemia.
  • The authors describe a patient with acute lymphoblastic leukemia (ALL) who presented with severe hemorrhagic syndrome, without disseminated intravascular coagulation.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Thrombasthenia / etiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Thrombasthenia.
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  • (PMID = 16217260.001).
  • [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 / Autoantibodies; 0 / Platelet Glycoprotein GPIIb-IIIa Complex
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