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1. Tie LJ, Gu LJ, Jiang LM, Zhao JC, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP: [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):246-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: Minimal residual disease (MRD) is one of the most important prognostic factors in childhood acute lymphoblastic leukemia (ALL).
  • Using sets of combined antibodies, immunophenotypic expression of leukemia cells was observed in 95 of 106 B-lineage ALL cases (89.6%).
  • [MeSH-major] Flow Cytometry / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19374803.001).
  • [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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2. Hosono N, Kishi S, Iho S, Urasaki Y, Yoshida A, Kurooka H, Yokota Y, Ueda T: Glutathione S-transferase M1 inhibits dexamethasone-induced apoptosis in association with the suppression of Bim through dual mechanisms in a lymphoblastic leukemia cell line. Cancer Sci; 2010 Mar;101(3):767-73
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  • [Title] Glutathione S-transferase M1 inhibits dexamethasone-induced apoptosis in association with the suppression of Bim through dual mechanisms in a lymphoblastic leukemia cell line.
  • Recently GSTM1 has been reported to be a significant risk factor for hematological relapse in childhood acute lymphoblastic leukemia, although the underlying mechanism remains largely unknown.
  • Glucocorticoids play a crucial role in the treatment of childhood acute lymphoblastic leukemia, therefore we hypothesized that GSTM1 plays important roles in glucocorticoid-induced apoptotic pathways.
  • To clarify the relationship between GSTM1 and drug resistance, GSTM1 was transfected into a T-acute lymphoblastic leukemia cell line, CCRF-CEM (CEM), and we established the GSTM1-expressing cell lines CEM/M1-4 and CEM/M1-9.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / antagonists & inhibitors. Dexamethasone / pharmacology. Glutathione Transferase / physiology. Membrane Proteins / antagonists & inhibitors. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins / antagonists & inhibitors

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  • (PMID = 20067466.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / NF-kappa B p50 Subunit; 0 / Proto-Oncogene Proteins; 5072-26-4 / Buthionine Sulfoximine; 7S5I7G3JQL / Dexamethasone; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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3. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt. Hematology; 2006 Oct;11(5):341-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Initially low Hb < 8 gm/dl, high WBCs and platelet counts > 50,000/mm(3) also showed better but non-significant remission rates.
  • CONCLUSIONS: Cytogenetic and molecular characterizations of childhood ALL may add prognostic criteria for optimal therapy allocation.
  • [MeSH-major] Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


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4. Moorman AV, Raimondi SC, Pui CH, Baruchel A, Biondi A, Carroll AJ, Forestier E, Gaynon PS, Harbott J, Harms DO, Heerema N, Pieters R, Schrappe M, Silverman LB, Vilmer E, Harrison CJ, Ponte di Legno Working Group: No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities. Leukemia; 2005 Apr;19(4):557-63
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  • [Title] No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities.
  • This study characterized the additional chromosomal abnormalities (ACA) associated with 11q23 rearrangements in 450 infants and children with acute lymphoblastic leukemia (ALL) and examined the impact of these ACA on survival.
  • This study has conclusively demonstrated that there is no prognostic effect of secondary chromosomal changes in association with 11q23 abnormalities in childhood ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 15744345.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA78224; United States / NIGMS NIH HHS / GM / GM61393
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
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5. 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.
  • 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 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

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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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6. Halton J, Gaboury I, Grant R, Alos N, Cummings EA, Matzinger M, Shenouda N, Lentle B, Abish S, Atkinson S, Cairney E, Dix D, Israels S, Stephure D, Wilson B, Hay J, Moher D, Rauch F, Siminoski K, Ward LM, Canadian STOPP Consortium: Advanced vertebral fracture among newly diagnosed children with acute lymphoblastic leukemia: results of the Canadian Steroid-Associated Osteoporosis in the Pediatric Population (STOPP) research program. J Bone Miner Res; 2009 Jul;24(7):1326-34
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  • [Title] Advanced vertebral fracture among newly diagnosed children with acute lymphoblastic leukemia: results of the Canadian Steroid-Associated Osteoporosis in the Pediatric Population (STOPP) research program.
  • Vertebral compression is a serious complication of childhood acute lymphoblastic leukemia (ALL).
  • Whether the fractures will resolve through bone growth during or after leukemia chemotherapy remains to be determined.

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  • (PMID = 19210218.001).
  • [ISSN] 1523-4681
  • [Journal-full-title] Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • [ISO-abbreviation] J. Bone Miner. Res.
  • [Language] ENG
  • [Grant] None / None / / 64285-1; Canada / Canadian Institutes of Health Research / / 64285-1
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids
  • [Other-IDs] NLM/ CAMS3788; NLM/ PMC3890351
  • [Investigator] Sykes E; Scharke M; Konji V; Riddell C; Ward LM; Feber J; Gaboury I; Halton J; Matzinger M; Moher D; Roth J; Shenouda N; Stephure D; Kloiber R; Lewis V; Midgley J; Miettunen P; Cabral D; Dix DB; Nadel HR; White C; Lentle BC; Hay J; Clarson C; Cairney E; Filler G; Grimmer J; Sparrow K; Cummings E; Fernandez C; Huber AM; Lang B; O'Brien K; Ross A; Atkinson S; Arora S; Barr R; Coblentz C; Dent PB; Webber C; Rodd C; Abish S; Bell L; Scuccimarri R; Rauch F; Glorieux F; Alos N; Dubois J; Laverdière C; Phan V; Saint-Cyr C; Couch R; Ellsworth J; LeBlanc C; Pinsk M; Siminoski K; Wilson B; Grant R; Charron M; Hebert D; Taback S; Blydt-Hansen T; Israels S; Oen K; Reed M
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7. Bungaro S, Dell'Orto MC, Zangrando A, Basso D, Gorletta T, Lo Nigro L, Leszl A, Young BD, Basso G, Bicciato S, Biondi A, te Kronnie G, Cazzaniga G: Integration of genomic and gene expression data of childhood ALL without known aberrations identifies subgroups with specific genetic hallmarks. Genes Chromosomes Cancer; 2009 Jan;48(1):22-38
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  • [Title] Integration of genomic and gene expression data of childhood ALL without known aberrations identifies subgroups with specific genetic hallmarks.
  • Pediatric acute lymphoblastic leukemia (ALL) comprises genetically distinct subtypes.
  • To identify genomic aberrancies in childhood ALL patients nonclassifiable by conventional methods, we performed a single nucleotide polymorphisms (SNP) array-based genomic analysis of leukemic cells from 29 cases.
  • [MeSH-major] Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18803328.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Calcium-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Genetic Markers; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / PAX5 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Smad1 Protein; 134324-36-0 / Serrate proteins
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8. Hundsdoerfer P, Dietrich I, Schmelz K, Eckert C, Henze G: XIAP expression is post-transcriptionally upregulated in childhood ALL and is associated with glucocorticoid response in T-cell ALL. Pediatr Blood Cancer; 2010 Aug;55(2):260-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] XIAP expression is post-transcriptionally upregulated in childhood ALL and is associated with glucocorticoid response in T-cell ALL.
  • BACKGROUND: Resistance to glucocorticoid induced apoptosis is one of the major risk factors for relapse and poor outcome in childhood acute lymphoblastic leukemia (ALL).
  • PROCEDURE: XIAP protein and mRNA expression were determined in leukemic blasts of 51 childhood ALL patients and normal bone marrow mononuclear cells.
  • RESULTS: XIAP protein but not mRNA expression was found to be highly increased in childhood ALL compared to control bone marrow mononuclear cells (MNC) (median: 3.5 vs. 0.14 ng/10(5) MNC, P < 0.0001) indicating a post-transcriptional regulation of XIAP expression.
  • CONCLUSION: In childhood ALL compared to control bone marrow, the expression of the apoptosis inhibitor XIAP is highly increased by post-transcriptional regulation.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Glucocorticoids / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. X-Linked Inhibitor of Apoptosis Protein / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Bone Marrow Cells / pathology. Bone Marrow Examination. Child. Drug Resistance. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Male. Monocytes / pathology. Pharmacogenetics. Prognosis. RNA, Messenger / analysis. Treatment Outcome. Up-Regulation


9. Aricó M, Baruchel A, Bertrand Y, Biondi A, Conter V, Eden T, Gadner H, Gaynon P, Horibe K, Hunger SP, Janka-Schaub G, Masera G, Nachman J, Pieters R, Schrappe M, Schmiegelow K, Valsecchi MG, Pui CH: The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005. Leukemia; 2005 Jul;19(7):1145-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005.
  • Between 1995 and 2004, six International Childhood Acute Lymphoblastic Leukemia (ALL) Workshop have been held, and the completion of several collaborative projects has established the clinical relevance and treatment options for several specific genetic subtypes of ALL.
  • [MeSH-major] Neoplasm, Residual / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15902295.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61393; United States / NIGMS NIH HHS / GM / GM61374
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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10. Glouchkova L, Ackermann B, Zibert A, Meisel R, Siepermann M, Janka-Schaub GE, Goebel U, Troeger A, Dilloo D: The CD70/CD27 pathway is critical for stimulation of an effective cytotoxic T cell response against B cell precursor acute lymphoblastic leukemia. J Immunol; 2009 Jan 1;182(1):718-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The CD70/CD27 pathway is critical for stimulation of an effective cytotoxic T cell response against B cell precursor acute lymphoblastic leukemia.
  • However, in B cell precursor acute lymphoblastic leukemia, the most common childhood malignancy, the role of CD70 in stimulation of antileukemic T cell responses has so far not been delineated.
  • Herein we demonstrate that in B cell precursor acute lymphoblastic leukemia expression of CD70 is low but can be induced upon blast activation via CD40.
  • Modulation of the CD70/CD27 pathway may thus represent a novel therapeutic approach for augmenting magnitude and quality of the antileukemic response in B cell precursor acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, CD27 / physiology. Antigens, CD70 / physiology. Lymphocyte Activation / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 19109206.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD70; 0 / CD70 protein, human
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11. Escherich G, Horstmann MA, Zimmermann M, Janka-Schaub GE, COALL study group: Cooperative study group for childhood acute lymphoblastic leukaemia (COALL): long-term results of trials 82,85,89,92 and 97. Leukemia; 2010 Feb;24(2):298-308
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperative study group for childhood acute lymphoblastic leukaemia (COALL): long-term results of trials 82,85,89,92 and 97.
  • In this study, the long-term outcome of 1818 patients treated in five consecutive clinical trials (the cooperative study group for childhood acute lymphoblastic leukaemia (COALL) 82, 85, 89, 92 and 97) from 24 cooperating centres in Germany is reported.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasm Recurrence, Local / therapy. Neoplasm, Residual / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20016530.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Pongratz; Otte J; Jorch N; Spaar HJ; Lieber T; Siegert; Göbel U; Janssen G; Beck JF; Weigel S; Streitberger; Nürnberger W; von Klinggräff C; Westerbeck K; Thomas P; Völpel S; Weissbach G; Bierbach U; Gutjahr P; Althaus I; Roos R; Klose P; Graubner U; Schmidt I; Haas; Drescher; Müller H; Kolb R; Wolff J; Peters O; Weber J; Dohrn
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12. Strehl S, Nebral K, König M, Harbott J, Strobl H, Ratei R, Struski S, Bielorai B, Lessard M, Zimmermann M, Haas OA, Izraeli S: ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations. Clin Cancer Res; 2008 Feb 15;14(4):977-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations.
  • Cytogenetic analysis of six cases of childhood acute lymphoblastic leukemia revealed a novel recurrent t(8;12)(q13;p13), suggesting involvement of ETV6.
  • RESULTS: We have identified a novel recurrent t(8;12)(q13;p13), which results in a fusion between the transcriptional repressor ETV6 (TEL) and the transcriptional coactivator NCOA2 (TIF2) in six cases of childhood leukemia expressing both T-lymphoid and myeloid antigens.
  • In addition, ETV6-NCOA2 leukemia shows a high frequency of heterozygous activating NOTCH1 mutations, which disrupt the heterodimerization or the PEST domains.
  • CONCLUSIONS: The ETV6-NCOA2 fusion may define a novel subgroup of acute leukemia with T-lymphoid and myeloid features, which is associated with a high prevalence of NOTCH1 mutations.
  • [MeSH-major] Nuclear Receptor Coactivator 2 / genetics. Oncogene Fusion / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18281529.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / NCOA2 protein, human; 0 / NOTCH1 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Receptor, Notch1; 0 / Repressor Proteins
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13. Familiades J, Bousquet M, Lafage-Pochitaloff M, Béné MC, Beldjord K, De Vos J, Dastugue N, Coyaud E, Struski S, Quelen C, Prade-Houdellier N, Dobbelstein S, Cayuela JM, Soulier J, Grardel N, Preudhomme C, Cavé H, Blanchet O, Lhéritier V, Delannoy A, Chalandon Y, Ifrah N, Pigneux A, Brousset P, Macintyre EA, Huguet F, Dombret H, Broccardo C, Delabesse E: PAX5 mutations occur frequently in adult B-cell progenitor acute lymphoblastic leukemia and PAX5 haploinsufficiency is associated with BCR-ABL1 and TCF3-PBX1 fusion genes: a GRAALL study. Leukemia; 2009 Nov;23(11):1989-98
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  • [Title] PAX5 mutations occur frequently in adult B-cell progenitor acute lymphoblastic leukemia and PAX5 haploinsufficiency is associated with BCR-ABL1 and TCF3-PBX1 fusion genes: a GRAALL study.
  • Adult and child B-cell progenitor acute lymphoblastic leukemia (BCP-ALL) differ in terms of incidence and prognosis.
  • A genome-wide analysis using oligo SNP arrays recently demonstrated that PAX5 (paired-box domain 5) is the main target of somatic mutations in childhood BCP-ALL being altered in 38.9% of the cases.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. DNA-Binding Proteins / genetics. Fusion Proteins, bcr-abl / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 19587702.001).
  • [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 / Antineoplastic Agents; 0 / B-Cell-Specific Activator Protein; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / Immunoglobulin Heavy Chains; 0 / PAX5 protein, human; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / TCF3 protein, human; 0 / pbx1 protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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14. Butrón Valdez K, Ramírez Galves M, Germes Piña F, Ramos Martínez E, Zamora Perea A: [Systemic lymphoma cells with T precursor condition of extreme female genital tract. A case report and literature review]. Ginecol Obstet Mex; 2009 Jun;77(6):291-9
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  • Primary female genital tract non Hodgkin's lymphoma is a rare presentation for a common disease in the childhood, and its classification as primary extranodal lymphoma is still controversial.
  • There are a few cases reported as a primary precursor B-cell lymphoblastic lymphoma of the female genital tract, but there is not any case reported as primary precursor T-cell lymphoblastic lymphoma of the ovary in childhood.
  • The chemotherapy regimen comprised of CHOP (Cyclophosphamide, Hydroxydaunorubicin, Oncovin, Prednisone/Prednisolone) and methotrexate, 3 months later presents left facial hemiparesia follow by right facial hemiparesia, 7 months later presents more Central Nervous System (CNS) complications and apparently was complicated with acute lymphocitic leukemia and after 16 months from the diagnosis, following by a torpid evolution, the pacient finally died.
  • [MeSH-major] Genital Neoplasms, Female. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 19681371.001).
  • [ISSN] 0300-9041
  • [Journal-full-title] Ginecología y obstetricia de México
  • [ISO-abbreviation] Ginecol Obstet Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Number-of-references] 19
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15. Jamroziak K, Robak T: Inheritance and clinical outcome in childhood acute lymphoblastic leukemia. Leuk Res; 2009 Jul;33(7):889-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inheritance and clinical outcome in childhood acute lymphoblastic leukemia.
  • [MeSH-major] Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


16. Harrison CJ, Moorman AV, Barber KE, Broadfield ZJ, Cheung KL, Harris RL, Jalali GR, Robinson HM, Strefford JC, Stewart A, Wright S, Griffiths M, Ross FM, Harewood L, Martineau M: Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study. Br J Haematol; 2005 May;129(4):520-30
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  • [Title] Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study.
  • Summary Interphase fluorescence in situ hybridization (iFISH) was used independently to reveal chromosomal abnormalities of prognostic importance in a large, consecutive series of children (n = 2367) with acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Cytogenetic Analysis. DNA-Binding Proteins / genetics. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Gene Rearrangement. Genes, abl. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Interphase. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogenes / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics

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  • (PMID = 15877734.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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17. Sherborne AL, Hosking FJ, Prasad RB, Kumar R, Koehler R, Vijayakrishnan J, Papaemmanuil E, Bartram CR, Stanulla M, Schrappe M, Gast A, Dobbins SE, Ma Y, Sheridan E, Taylor M, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Moorman AV, Harrison CJ, Tomlinson IP, Richards S, Zimmermann M, Szalai C, Semsei AF, Erdelyi DJ, Krajinovic M, Sinnett D, Healy J, Gonzalez Neira A, Kawamata N, Ogawa S, Koeffler HP, Hemminki K, Greaves M, Houlston RS: Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk. Nat Genet; 2010 Jun;42(6):492-4
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  • [Title] Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
  • Using data from a genome-wide association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398 controls and with validation in samples totaling 2,386 cases and 2,419 controls, we have shown that common variation at 9p21.3 (rs3731217, intron 1 of CDKN2A) influences acute lymphoblastic leukemia risk (odds ratio = 0.71, P = 3.01 x 10(-11)), irrespective of cell lineage.
  • [MeSH-major] Chromosomes, Human, Pair 9. Genes, p16. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20453839.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA026038-31; United Kingdom / Cancer Research UK / / C1298/A8362; United States / NIGMS NIH HHS / GM / T32 GM008243; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / R01 CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS400186; NLM/ PMC3434228
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18. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Almost 80% of the non-Down B-cell precursor ALL cases in the 2 to 7 years frequency peak group who had aberrant cytogenetic results had either a high-hyperdiploid clone (51 to 61 chromosomes) or a translocation t(12;21)(p13;q22).
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16912588.001).
  • [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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19. van der Velden VH, Hoogeveen PG, Pieters R, van Dongen JJ: Impact of two independent bone marrow samples on minimal residual disease monitoring in childhood acute lymphoblastic leukaemia. Br J Haematol; 2006 May;133(4):382-8
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  • [Title] Impact of two independent bone marrow samples on minimal residual disease monitoring in childhood acute lymphoblastic leukaemia.
  • Minimal residual disease (MRD) diagnostics are used for risk group stratification in several acute lymphoblastic leukaemia (ALL) treatment protocols.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16643444.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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20. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
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  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [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 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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21. Heinsohn S, Golta S, Kabisch H, zur Stadt U: Standardized detection of Simian virus 40 by real-time quantitative polymerase chain reaction in pediatric malignancies. Haematologica; 2005 Jan;90(1):94-9
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  • [Title] Standardized detection of Simian virus 40 by real-time quantitative polymerase chain reaction in pediatric malignancies.
  • DNA samples from 149 healthy controls, from 26 fresh frozen childhood cases of acute lymphoblastic leukemia (ALL) (B-, BCP- and T-ALL) and from 12 paraffin-embedded osteosarcomas were investigated.
  • Various amounts of SV40 were detectable in 20/26 (77%) childhood ALL samples of German origin and, in part, high amounts were visible in 11/12 (92%) paraffin embedded Hungarian osteosarcomas.
  • [MeSH-major] Osteosarcoma / virology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology. Simian virus 40 / isolation & purification

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  • [CommentIn] Haematologica. 2005 Jan;90(1):6 [15644307.001]
  • (PMID = 15642675.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA, Viral
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22. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
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  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • RESULTS: Survivin overexpression, with an up to ten-fold increase of the normal level, was detected in 65% of the leukemic samples in contrast to negligible expression in non-malignant hematopoietic cells.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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23. Xu XJ, Tang YM, Song H, Shi SW, Yang SL, Shen HQ, Wei J, Xu WQ, Pan BH, Zhao FY: [Monitoring of minimal residual disease in children with acute lymphoblastic leukemia and its prognostic significance]. Zhonghua Er Ke Za Zhi; 2010 Mar;48(3):180-4
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  • [Title] [Monitoring of minimal residual disease in children with acute lymphoblastic leukemia and its prognostic significance].
  • OBJECTIVE: Monitoring of minimal residual disease (MRD) is proven to be increasingly valuable for predicting relapse and outcome of childhood acute lymphoblastic leukemia (ALL) and is used to identify patients' risk groups in several current clinical trials.
  • The aim of this study was to investigate the predictive values of different MRD levels detected at different chemotherapy phases in childhood ALL.
  • All the patients were treated with modified National Protocol of Childhood ALL in China 1997.
  • All samples were stained with a panel of four colour combinations of fluorochrome conjugated monoclonal antibodies according to the leukemia-associated immunophenotype (LAIP) defined at diagnosis and analyzed by multi-parametric flow cytometry.
  • CONCLUSION: Dynamic MRD detection by multi-parametric flow cytometry is highly predictive of outcome for childhood ALL, and the cut-off values at different time points were different.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 20426951.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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24. Tedeschi R, Luostarinen T, Marus A, Bzhalava D, Ogmundsdottir HM, Dillner J, De Paoli P, Surcel HM, Pukkala E, Lehtinen M, Lehtinen T: No risk of maternal EBV infection for childhood leukemia. Cancer Epidemiol Biomarkers Prev; 2009 Oct;18(10):2790-2
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  • [Title] No risk of maternal EBV infection for childhood leukemia.
  • We performed a large nested case-control study within the Finnish and Icelandic maternity cohorts to verify/falsify the association of maternal EBV infection with an increased risk of acute lymphoblastic leukemia (ALL) in the offspring found in previous studies.
  • For each index mother of a leukemia case, three matched control mothers with cancer-free offspring were identified.
  • First trimester sera from 561 ALL and 144 non-ALL index mothers and from 2,105 control mothers were analyzed for antibodies to EBV viral capsid antigen (IgG and IgM), early antigen (IgG) and ZEBRA protein (IgG).
  • [MeSH-major] Epstein-Barr Virus Infections / epidemiology. Herpesvirus 4, Human / isolation & purification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology. Pregnancy Complications, Infectious / epidemiology. Pregnancy Complications, Infectious / virology

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  • (PMID = 19755652.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Capsid Proteins; 0 / Epstein-Barr viral capsid antigen
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25. Beesley AH, Cummings AJ, Freitas JR, Hoffmann K, Firth MJ, Ford J, de Klerk NH, Kees UR: The gene expression signature of relapse in paediatric acute lymphoblastic leukaemia: implications for mechanisms of therapy failure. Br J Haematol; 2005 Nov;131(4):447-56
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  • [Title] The gene expression signature of relapse in paediatric acute lymphoblastic leukaemia: implications for mechanisms of therapy failure.
  • Despite significant improvements in the treatment of childhood acute lymphoblastic leukaemia (ALL), the prognosis for relapsing patients remains poor.
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Antigens, CD147 / genetics. Antigens, CD147 / metabolism. Cell Division / genetics. Child. Child, Preschool. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Humans. Infant. Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Prognosis. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Treatment Failure. Treatment Outcome

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  • [CommentIn] Br J Haematol. 2006 Oct;135(2):274-5 [16965384.001]
  • (PMID = 16281934.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BSG protein, human; 0 / Neoplasm Proteins; 136894-56-9 / Antigens, CD147
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26. Tsuchida M, Ohara A, Manabe A, Kumagai M, Shimada H, Kikuchi A, Mori T, Saito M, Akiyama M, Fukushima T, Koike K, Shiobara M, Ogawa C, Kanazawa T, Noguchi Y, Oota S, Okimoto Y, Yabe H, Kajiwara M, Tomizawa D, Ko K, Sugita K, Kaneko T, Maeda M, Inukai T, Goto H, Takahashi H, Isoyama K, Hayashi Y, Hosoya R, Hanada R, Tokyo Children's Cancer Study Group: Long-term results of Tokyo Children's Cancer Study Group trials for childhood acute lymphoblastic leukemia, 1984-1999. Leukemia; 2010 Feb;24(2):383-96
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  • [Title] Long-term results of Tokyo Children's Cancer Study Group trials for childhood acute lymphoblastic leukemia, 1984-1999.
  • We report the long-term results of Tokyo Children's Cancer Study Group's studies L84-11, L89-12, L92-13, and L95-14 for 1846 children with acute lymphoblastic leukemia, which were conducted between 1984 and 1999.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20033052.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Kigasawa H; Hashiyama M; Migita M; Matsui A; Yoshihawa H; Kawaguchi H; Makimoto A; Hosono A; Takagi K; Morinaga S; Kiyotani C; Shiota Y; Moriwaki K; Mochizuki S; Toyama D; Kato Y; Hoshi Y; Gunji Y; Kashii Y; Morimoto T; Saito M; Fujimura J; Ishimoto K; Isoyama K; Yamamoto M; Hirota T; Koike K; Yanagisawa R; Ishii E; Kinoshita A; Kondo K; Morimoto M; Ishida Y; Ozawa M; Hasegawa D; Kamiya T; Ochiai H; Sato Y; Sakao E; Ito K; Sunami K; Igarashi T; Komori I; Kakuta H; Kato S; Morimoto K; Yabe M; Mizutani S; Nagasawa M; Koana S; Kashiwagi Y; Takita J; Kato KM; Ooki K; Wada E; Kato F; Kojima Y; Mitsui K; Uchino Y; Watanabe A; Fukushima K; Kurosawa H; Hagisawa S; Sato Y; Fukuoka K; Sugita M; Kaku H; Kawamura M; Fukunaga Y; Migita S; Ueda T; Asano K; Sugita K; Goi K; Fugii H; Ikuta K; Yanagimachi M; Yokosuka T; Kai S; Goto A; Tanaka F; Tsuji K; Ebihara Y; Nakadate N; Ishiguro Y; Suzuki T; Nakao S; Sotomatsu M; Paku A; Bessho F; Yoshino H; Ishii M; Genma Y; Kogawa K; Tsuji Y; Imai K; Sawa F
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27. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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28. Gill HK, Keoh TS, Dhaliwal JS, Moore S, Kim TS, Hassan R, Karim FA, Zakaria Z, Murad S, Mohamed M, Li Ho CM, Ibrahim H, Rahman EJ: TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2005 Jan 15;156(2):129-33
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  • [Title] TEL-AML1 frequency in multi-ethnic Malaysian pediatric acute lymphoblastic leukemia.
  • Eighty-eight multi-ethnic Malaysian pediatric acute lymphoblastic leukemia (ALL) patients were screened for the TEL-AML1 rearrangement by reverse transcription-polymerase chain reaction (RT-PCR).
  • This study shows that in Malaysia, TEL-AML1 is found in the same distinct ALL subset and at a similar frequency as in other diverse childhood ALL cohorts.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15642392.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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29. Paulsson K, Cazier JB, Macdougall F, Stevens J, Stasevich I, Vrcelj N, Chaplin T, Lillington DM, Lister TA, Young BD: Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease. Proc Natl Acad Sci U S A; 2008 May 06;105(18):6708-13
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  • [Title] Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease.
  • We present here a genome-wide map of abnormalities found in diagnostic samples from 45 adults and adolescents with acute lymphoblastic leukemia (ALL).
  • Importantly, the pattern of deletions resembled that recently reported in pediatric ALL, suggesting that adult, adolescent, and childhood cases may be more similar on the genetic level than previously thought.
  • [MeSH-major] Gene Deletion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18458336.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE9611
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2373322
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30. Schiffman JD, Wang Y, McPherson LA, Welch K, Zhang N, Davis R, Lacayo NJ, Dahl GV, Faham M, Ford JM, Ji HP: Molecular inversion probes reveal patterns of 9p21 deletion and copy number aberrations in childhood leukemia. Cancer Genet Cytogenet; 2009 Aug;193(1):9-18
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  • [Title] Molecular inversion probes reveal patterns of 9p21 deletion and copy number aberrations in childhood leukemia.
  • Childhood leukemia, which accounts for >30% of newly diagnosed childhood malignancies, is one of the leading causes of death for children with cancer.
  • In this pilot study, 45 pediatric leukemia samples were analyzed for gene copy aberrations using novel molecular inversion probe (MIP) technology.
  • Acute leukemia subtypes included precursor B-cell acute lymphoblastic leukemia (ALL) (n=23), precursor T-cell ALL (n=6), and acute myeloid leukemia (n=14).

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  • (PMID = 19602459.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / P01 HG000205; United States / NHGRI NIH HHS / HG / 2P01HG000205; United States / NCI NIH HHS / CA / CA96879; United States / NHGRI NIH HHS / HG / P01 HG000205-20; United States / NCI NIH HHS / CA / K08 CA096879
  • [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 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS151549; NLM/ PMC2776674
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31. Wu S, Gessner R, Taube T, Korte A, von Stackelberg A, Kirchner R, Henze G, Seeger K: Chemokine IL-8 and chemokine receptor CXCR3 and CXCR4 gene expression in childhood acute lymphoblastic leukemia at first relapse. J Pediatr Hematol Oncol; 2006 Apr;28(4):216-20
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  • [Title] Chemokine IL-8 and chemokine receptor CXCR3 and CXCR4 gene expression in childhood acute lymphoblastic leukemia at first relapse.
  • In this study, we examined the gene expression of interleukin (IL)-8, CXCR3, and CXCR4 in leukemic cells from 100 children with relapsed B-cell progenitors (BCP) acute lymphoblastic leukemia (ALL), using quantitative real-time polymerase chain reaction (RT-PCR).
  • [MeSH-major] Bone Marrow / pathology. Gene Expression Regulation, Neoplastic. Interleukin-8 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, CXCR4 / genetics. Receptors, Chemokine / genetics

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  • (PMID = 16679918.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCR3 protein, human; 0 / DNA Primers; 0 / Interleukin-8; 0 / RNA, Neoplasm; 0 / Receptors, CXCR3; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine
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32. 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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  • [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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33. Emerenciano M, Agudelo Arias DP, Coser VM, de Brito GD, Macedo Silva ML, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia. Pediatr Blood Cancer; 2006 Oct 15;47(5):549-54
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  • [Title] Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • BACKGROUND: Chromosome abnormalities often occur prenatally in childhood leukemia, characterizing an early event in leukemogenesis.
  • We describe the molecular cytogenetic findings of 207 infant acute leukemia (IAL) cases included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • PROCEDURE: The diagnosis of Acute Lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) was made according to morphology and immunophenotyping classification, followed by conventional karyotyping.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16261608.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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34. Kabuto M, Nitta H, Yamamoto S, Yamaguchi N, Akiba S, Honda Y, Hagihara J, Isaka K, Saito T, Ojima T, Nakamura Y, Mizoue T, Ito S, Eboshida A, Yamazaki S, Sokejima S, Kurokawa Y, Kubo O: Childhood leukemia and magnetic fields in Japan: a case-control study of childhood leukemia and residential power-frequency magnetic fields in Japan. Int J Cancer; 2006 Aug 1;119(3):643-50
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  • [Title] Childhood leukemia and magnetic fields in Japan: a case-control study of childhood leukemia and residential power-frequency magnetic fields in Japan.
  • We analyzed 312 case children (0-15 years old) newly diagnosed with acute lymphoblastic leukemia (ALL) or acute myelocytic leukemia (AML) in 1999-2001 (2.3 years) and 603 controls matched for gender, age and residential area.
  • Most of the leukemia cases in the highest exposure category had MF levels far above 0.4 microT.
  • Our results provided additional evidence that high MF exposure was associated with a higher risk of childhood leukemia, particularly of ALL.
  • [MeSH-major] Electromagnetic Fields / adverse effects. Leukemia, Myeloid / etiology. Leukemia, Radiation-Induced / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Acute Disease. Case-Control Studies. Child. Child, Preschool. Environmental Exposure / adverse effects. Female. Geography. Housing / standards. Humans. Infant. Japan / epidemiology. Logistic Models. Male. Odds Ratio. Risk Factors. Seasons

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16496405.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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35. Mkrtchyan H, Garcia Ney DR, de Ventura ES, Liehr T, Felix GR, Marques-Salles Tde J, Abdelhay E, Macedo Silva ML: Molecular cytogenetic studies characterize a near-triploid complex karyotype in a child with acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 Feb;197(1):71-4
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  • [Title] Molecular cytogenetic studies characterize a near-triploid complex karyotype in a child with acute lymphoblastic leukemia.
  • High hyperdiploidy with modal chromosome numbers between 50 and 65 is common in childhood acute lymphoblastic leukemia (ALL), occurring in 25-30% of the cases.
  • By contrast, near triploidy and tetraploidy are found in <1% of childhood ALL.
  • [MeSH-major] Chromosome Aberrations. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20113840.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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36. Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG: A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial. Lancet; 2007 Jul 21;370(9583):240-50
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  • [Title] A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
  • BACKGROUND: Acute lymphoblastic leukaemia in infants younger than 1 year is rare, and infants with the disease have worse outcomes than do older children.
  • We initiated an international study to investigate the effects of a new hybrid treatment protocol with elements designed to treat both acute lymphoblastic leukaemia and acute myeloid leukaemia, and to identify any prognostic factors for outcome in infants.
  • Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given a hybrid regimen based on the standard protocol for acute lymphoblastic leukaemia, with some elements designed for treatment of acute myeloid leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [CommentIn] Lancet. 2007 Jul 21;370(9583):198-200 [17658376.001]
  • (PMID = 17658395.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
  • [Grant] United Kingdom / Medical Research Council / / G0300130
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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37. Dunwell T, Hesson L, Rauch TA, Wang L, Clark RE, Dallol A, Gentle D, Catchpoole D, Maher ER, Pfeifer GP, Latif F: A genome-wide screen identifies frequently methylated genes in haematological and epithelial cancers. Mol Cancer; 2010;9:44
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  • RESULTS: Here we report for the first time the use of the MIRA assay (methylated CpG island recovery assay) in combination with genome-wide CpG island arrays to identify epigenetic molecular markers in childhood acute lymphoblastic leukemia (ALL) on a genome-wide scale.
  • We identified 30 genes demonstrating methylation frequencies of > or =25% in childhood ALL, nine genes showed significantly different methylation frequencies in B vs T-ALL.
  • For majority of the genes expression could be restored in methylated leukemia lines after treatment with 5-azaDC.
  • In chronic myeloid leukemia (CML) two of the genes, (TFAP2A and EBF2), demonstrated increased methylation in blast crisis compared to chronic phase (P < 0.05).
  • CONCLUSION: In summary we have identified a large number of genes showing frequent methylation in childhood ALL, methylation status of two of these genes is associated with advanced disease in CML and methylation status of another gene is associated with prognosis.
  • [MeSH-minor] Blast Crisis / genetics. Cell Line, Tumor. Child. Cloning, Molecular. DNA, Neoplasm / genetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Reproducibility of Results. Sequence Analysis, DNA. Sulfites / metabolism

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  • (PMID = 20184741.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Sulfites; OJ9787WBLU / hydrogen sulfite
  • [Other-IDs] NLM/ PMC2838813
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38. Holleman A, den Boer ML, de Menezes RX, Cheok MH, Cheng C, Kazemier KM, Janka-Schaub GE, Göbel U, Graubner UB, Evans WE, Pieters R: The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia. Blood; 2006 Jan 15;107(2):769-76
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  • [Title] The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) consists of various subtypes that respond differently to cytotoxic drugs and therefore have a markedly different clinical outcome.
  • In conclusion, ALL subtypes have a unique expression pattern of apoptosis genes and our data suggest that selective genes are linked to cellular drug resistance and prognosis in childhood B-lineage ALL.
  • [MeSH-major] Apoptosis. Cell Lineage. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


39. 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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  • [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).
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology


40. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6
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  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • We used standard methods to explore NOTCH1 mutations and other specific molecular markers in 15 early childhood T-ALL cases.
  • Despite being found in a lower frequency than that described for overall pediatric T-ALL, NOTCH1 alterations were the most frequent ones.
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19631984.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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41. Raimondi SC, Zhou Y, Shurtleff SA, Rubnitz JE, Pui CH, Behm FG: Near-triploidy and near-tetraploidy in childhood acute lymphoblastic leukemia: association with B-lineage blast cells carrying the ETV6-RUNX1 fusion, T-lineage immunophenotype, and favorable outcome. Cancer Genet Cytogenet; 2006 Aug;169(1):50-7
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  • [Title] Near-triploidy and near-tetraploidy in childhood acute lymphoblastic leukemia: association with B-lineage blast cells carrying the ETV6-RUNX1 fusion, T-lineage immunophenotype, and favorable outcome.
  • The prognostic significance of near-triploidy (68-80 chromosomes) and near-tetraploidy (>80 chromosomes) in childhood acute lymphoblastic leukemia (ALL) is unclear.
  • [MeSH-major] B-Lymphocytes / immunology. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. T-Lymphocytes / immunology


42. Campana D: Minimal residual disease in acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2010;2010:7-12
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  • [Title] Minimal residual disease in acute lymphoblastic leukemia.
  • In patients with acute lymphoblastic leukemia (ALL), treatment response is increasingly evaluated with minimal residual disease (MRD) assays.
  • ALL cells can be recognized by their clonal rearrangement of immunoglobulin and T-cell receptor genes, expression of gene fusions, and leukemia-associated immunophenotypes.
  • The vast majority of cases have antigen-receptor gene rearrangements and leukemia immunophenotypes for MRD monitoring; about half of the cases currently have suitable gene fusions.
  • The clinical significance of MRD has been conclusively demonstrated in both childhood and adult ALL.

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  • (PMID = 21239764.001).
  • [ISSN] 1520-4383
  • [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 / CA21765; United States / NCI NIH HHS / CA / CA60419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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43. Frost BM, Forestier E, Gustafsson G, Nygren P, Hellebostad M, Jonmundsson G, Kanerva J, Schmiegelow K, Larsson R, Lönnerholm G, Nordic Society for Paediatric Haematology and Oncology: Translocation t(1;19) is related to low cellular drug resistance in childhood acute lymphoblastic leukaemia. Leukemia; 2005 Jan;19(1):165-9
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  • [Title] Translocation t(1;19) is related to low cellular drug resistance in childhood acute lymphoblastic leukaemia.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Drug Resistance, Neoplasm / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 15526029.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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44. Wang CH, Wu KH, Yang YL, Peng CT, Wang RF, Tsai CW, Tsai RY, Lin DT, Tsai FJ, Bau DT: Association study of cyclooxygenase 2 single nucleotide polymorphisms and childhood acute lymphoblastic leukemia in Taiwan. Anticancer Res; 2010 Sep;30(9):3649-53
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  • [Title] Association study of cyclooxygenase 2 single nucleotide polymorphisms and childhood acute lymphoblastic leukemia in Taiwan.
  • AIM: The relationship between COX-2 gene and childhood leukemia risk is ambiguous.
  • In this study, the association of genotypic polymorphisms in cyclooxygenase 2 (Cox-2) with childhood leukemia were investigated.
  • MATERIALS AND METHODS: A total of 266 patients with childhood leukemia and 266 healthy controls recruited from the China Medical Hospital in central Taiwan were genotyped by PCR-RFLP method.
  • Six polymorphic variants of Cox-2 were investigated, including G-1195A, G-765C, T+8473C, intron 1, intron 5, and intron 6, and the associations of specific genotypes with susceptibility to childhood leukemia were analysed.
  • RESULTS: The data showed that although there was no difference in the distribution for each genotype of Cox-2 G-1195A, G-765C, T+8473C, intron 1, intron 5, and intron 6, between the childhood leukemia and control groups (p>0.05), the analysis of combined effect for COX-2 G-765C and intron 6 showed that individuals with GC at G-765C and GG or AG+AA at intron 6 present a slightly higher potential for developing childhood leukemia than other groups.
  • CONCLUSION: These findings suggest that the C allele of COX-2 G-765C may be responsible for childhood leukemia and may be useful in early detection of child leukemia.
  • [MeSH-major] Cyclooxygenase 2 / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20944149.001).
  • [ISSN] 1791-7530
  • [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] EC 1.14.99.1 / Cyclooxygenase 2
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45. Palle J, Frost BM, Forestier E, Gustafsson G, Nygren P, Hellebostad M, Jonsson OG, Kanerva J, Schmiegelow K, Larsson R, Lönnerholm G, Nordic Society for Paediatric Haematology and Oncology: Cellular drug sensitivity in MLL-rearranged childhood acute leukaemia is correlated to partner genes and cell lineage. Br J Haematol; 2005 Apr;129(2):189-98
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  • [Title] Cellular drug sensitivity in MLL-rearranged childhood acute leukaemia is correlated to partner genes and cell lineage.
  • Rearrangements in the 11q23 region, the site of the mixed lineage leukaemia (MLL) gene, are found in both childhood acute myeloid (AML) and lymphoblastic (ALL) leukaemia.
  • In AML, children with t(9;11) (n = 10) were significantly more sensitive to cytarabine (P < 0.001) and doxorubicin (P = 0.005) than non-11q23 rearranged patients (n = 108).
  • Children with other 11q23 rearrangements (n = 14) differed less from non-rearranged children.
  • [MeSH-major] DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Agents / pharmacology. Cell Lineage. Child. Child, Preschool. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Cytarabine / pharmacology. Cytotoxicity Tests, Immunologic. Doxorubicin / pharmacology. Female. Fluorometry. Glucocorticoids / pharmacology. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein. Prospective Studies. Statistics, Nonparametric. Translocation, Genetic

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  • (PMID = 15813846.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Glucocorticoids; 0 / MLL protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 80168379AG / Doxorubicin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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46. Latino-Martel P, Chan DS, Druesne-Pecollo N, Barrandon E, Hercberg S, Norat T: Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis. Cancer Epidemiol Biomarkers Prev; 2010 May;19(5):1238-60
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  • [Title] Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis.
  • BACKGROUND: Leukemia is the most frequently occurring cancer in children.
  • Although its etiology is largely unknown, leukemia is believed to result from an interaction between genetic and environmental factors.
  • METHODS: To assess the association between maternal alcohol consumption during pregnancy and childhood leukemia, a systematic review and meta-analysis of published studies was done.
  • Analyses were conducted by type of leukemia, children's age at diagnosis, and type of alcoholic beverage and trimester of pregnancy at alcohol use.
  • Alcohol intake during pregnancy (yes versus no) was statistically significantly associated with childhood acute myeloid leukemia (AML) [odds ratio (OR), 1.56; 95% confidence interval (CI), 1.13-2.15] but not with acute lymphoblastic leukemia (OR, 1.10; 95% CI, 0.93-1.29).
  • IMPACT: Avoidance of maternal alcohol drinking during pregnancy might contribute to a decrease in the risk of childhood AML.
  • [MeSH-major] Alcohol Drinking / adverse effects. Leukemia / chemically induced. Prenatal Exposure Delayed Effects

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  • [Copyright] Copyright (c) 2010 AACR
  • (PMID = 20447918.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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47. 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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  • [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.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [CommentIn] Lancet Oncol. 2010 May;11(5):403-4 [20409755.001]
  • [ErratumIn] Lancet Oncol. 2010 Jun;11(6):516
  • (PMID = 20409752.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300130; United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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48. Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M: Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica. J Pediatr Hematol Oncol; 2009 Feb;31(2):131-5
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  • [Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
  • In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).
  • Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.
  • We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).
  • The observed rate of leukemia was 52.2 cases per million children per year.
  • Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
  • The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

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  • (PMID = 19194200.001).
  • [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 / Oncogene Proteins, Fusion
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49. Laane E, Panaretakis T, Pokrovskaja K, Buentke E, Corcoran M, Söderhäll S, Heyman M, Mazur J, Zhivotovsky B, Porwit A, Grandér D: Dexamethasone-induced apoptosis in acute lymphoblastic leukemia involves differential regulation of Bcl-2 family members. Haematologica; 2007 Nov;92(11):1460-9
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  • [Title] Dexamethasone-induced apoptosis in acute lymphoblastic leukemia involves differential regulation of Bcl-2 family members.
  • BACKGROUND AND OBJECTIVES: The mechanism of glucocorticoid -induced apoptosis is not fully understood and early predictive assays based on apoptotic markers for clinical outcome in acute lymphoblastic leukemia (ALL) are scarce.
  • DESIGN AND METHODS: Primary childhood ALL samples, the pre-B ALL cell line RS(4;11), and the T-ALL cell line CCRF-CEM were used.
  • [MeSH-major] Apoptosis / drug effects. Dexamethasone / pharmacology. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins c-bcl-2 / genetics

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  • (PMID = 18024393.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 7S5I7G3JQL / Dexamethasone; EC 3.4.22.- / Caspases
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50. Mitchell C, Payne J, Wade R, Vora A, Kinsey S, Richards S, Eden T: The impact of risk stratification by early bone-marrow response in childhood lymphoblastic leukaemia: results from the United Kingdom Medical Research Council trial ALL97 and ALL97/99. Br J Haematol; 2009 Aug;146(4):424-36
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  • [Title] The impact of risk stratification by early bone-marrow response in childhood lymphoblastic leukaemia: results from the United Kingdom Medical Research Council trial ALL97 and ALL97/99.
  • The 1997 acute lymphoblastic leukaemia (ALL) trial (ALL97) was a randomised comparison of prednisolone versus dexamethasone and of 6-mercaptopurine versus 6-thioguanine.
  • During the first 2 years of the trial, review of survival data showed the preceding trial, UKALL XI, was no better than its predecessor and that survival for childhood ALL in the UK had not improved in the fashion witnessed by other cooperative treatment groups.
  • There were no significant differences for non-CNS relapse, induction deaths or deaths in remission between the two phases of the trial.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Cells / immunology. Immunosuppressive Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19549269.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300130; United Kingdom / Medical Research Council / / MC/ U137686856; United Kingdom / Medical Research Council / / 98223452
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
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51. Schotte D, Chau JC, Sylvester G, Liu G, Chen C, van der Velden VH, Broekhuis MJ, Peters TC, Pieters R, den Boer ML: Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):313-22
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  • [Title] Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia.
  • To identify miRNAs relevant to pediatric acute lymphoblastic leukemia (ALL), we cloned 105 known and 8 new miRNA genes expressed in patients' leukemia cells.
  • Eight miRNAs were differentially expressed between MLL and non-MLL precursor B-ALL cases (P<0.05).
  • The expression did not correlate with the maturation status of leukemia cells based on immunoglobulin and T-cell receptor rearrangements, immunophenotype or MLL-fusion partner.
  • [MeSH-major] MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Cloning, Molecular. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Myeloid-Lymphoid Leukemia Protein / genetics


52. Kager L, Cheok M, Yang W, Zaza G, Cheng Q, Panetta JC, Pui CH, Downing JR, Relling MV, Evans WE: Folate pathway gene expression differs in subtypes of acute lymphoblastic leukemia and influences methotrexate pharmacodynamics. J Clin Invest; 2005 Jan;115(1):110-7
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  • [Title] Folate pathway gene expression differs in subtypes of acute lymphoblastic leukemia and influences methotrexate pharmacodynamics.
  • The ability of leukemia cells to accumulate methotrexate polyglutamate (MTXPG) is an important determinant of the antileukemic effects of methotrexate (MTX).
  • We measured in vivo MTXPG accumulation in leukemia cells from 101 children with acute lymphoblastic leukemia (ALL) and established that B-lineage ALL with either TEL-AML1 or E2A-PBX1 gene fusion, or T-lineage ALL, accumulates significantly lower MTXPG compared with B-lineage ALL without these genetic abnormalities or compared with hyperdiploid (fewer than 50 chromosomes) ALL.
  • To elucidate mechanisms underlying these differences in MTXPG accumulation, we used oligonucleotide microarrays to analyze expression of 32 folate pathway genes in diagnostic leukemia cells from 197 children.
  • These findings reveal distinct mechanisms of subtype-specific differences in MTXPG accumulation and point to new strategies to overcome these potential causes of treatment failure in childhood ALL.

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  • (PMID = 15630450.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA71907-07; United States / NCI NIH HHS / CA / R37 CA36401; United States / NCI NIH HHS / CA / P01 CA071907; 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 / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA78224; United States / NCI NIH HHS / CA / R01 CA51001
  • [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 / RNA, Messenger; 25513-46-6 / Polyglutamic Acid; 82334-40-5 / methotrexate polyglutamate; 9007-49-2 / DNA; 935E97BOY8 / Folic Acid; EC 2.1.1.45 / Thymidylate Synthase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC539195
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53. Moreno DA, Scrideli CA, Cortez MA, de Paula Queiroz R, Valera ET, da Silva Silveira V, Yunes JA, Brandalise SR, Tone LG: Differential expression of HDAC3, HDAC7 and HDAC9 is associated with prognosis and survival in childhood acute lymphoblastic leukaemia. Br J Haematol; 2010 Sep;150(6):665-73
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  • [Title] Differential expression of HDAC3, HDAC7 and HDAC9 is associated with prognosis and survival in childhood acute lymphoblastic leukaemia.
  • We evaluated the mRNA gene expression profile of 12 HDAC genes by quantitative real-time polymerase chain reaction in 94 consecutive childhood acute lymphoblastic leukaemia (ALL) samples and its association with clinical/biological features and survival.
  • Our data suggest that higher expression of HDAC7 and HDAC9 is associated with poor prognosis in childhood ALL and could be promising therapeutic targets for the treatment of refractory childhood ALL.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Histone Deacetylases / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20636436.001).
  • [ISSN] 1365-2141
  • [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 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Repressor Proteins; EC 3.5.1.98 / HDAC7 protein, human; EC 3.5.1.98 / HDAC9 protein, human; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
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54. Schmiegelow K, Al-Modhwahi I, Andersen MK, Behrendtz M, Forestier E, Hasle H, Heyman M, Kristinsson J, Nersting J, Nygaard R, Svendsen AL, Vettenranta K, Weinshilboum R, Nordic Society for Paediatric Haematology and Oncology: Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Blood; 2009 Jun 11;113(24):6077-84
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  • [Title] Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Among 1614 children with acute lymphoblastic leukemia (ALL) treated with the Nordic Society for Paediatric Haematology and Oncology (NOPHO) ALL-92 protocol, 20 patients developed a second malignant neoplasm (SMN) with a cumulative risk of 1.6% at 12 years from the diagnosis of ALL.
  • Nine of the 16 acute myeloid leukemias or myelodysplastic syndromes had monosomy 7 (n = 7) or 7q deletions (n = 2).
  • This study indicates that the duration and intensity of 6MP/MTX maintenance therapy of childhood ALL may influence the risk of SMNs in childhood ALL.

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  • [CommentIn] Blood. 2009 Jun 11;113(24):6258; author reply 6258-9 [19520817.001]
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  • (PMID = 19224761.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2699230
  • [Investigator] Schmiegelow K; Hejl M; Østergård M; Schrøder H; Pihkala U; Ilanmaa E; Antila K; Korpela K; Vuorinen O; Perkkiö M; Kojo N; Nyman R; Pere M; Lanning M; Niemi A; Vuoristo A; Niemi S; Isotalo J; Laapas H; Mäkipernaa A; Salmi T; Varsamäki T; Kristinsson J; Zeller B; Danielsen O; Madsen B; Nielsen B; Stensvold K; Lund JH; Danielsen K; Brekke P; Stamnes O; Glomstein A; Widing E; Hapnes C; Stokland T; Kolmannskog S; Halvorsen B; Spangen S; Carlsson G; Bergkvist M; Skanka N; Korlén B; Dimberg A; Adrian BA; Mellander L; Aronson S; Jensen D; Winiarski J; Lagerwall A; Jonsson NO; Cervin T; Samuelsson U; Berg A; Nilsson H; Behrendtz M; Wiebe T; Ljung R; Tessin I; Ljungren CG; Dohlwitz A; Christensen HO; Ronge E; Berglund M; Björk O; Fransson D; Eriksson M; Forestier E; Kreuger A; Blomgren M; Rönnblad B; Eriksson B; Berg T; Hedling L; Forsberg T; Lindquist B; Kriström B; Hjalmars U
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55. Plasschaert SL, de Bont ES, Boezen M, vander Kolk DM, Daenen SM, Faber KN, Kamps WA, de Vries EG, Vellenga E: Expression of multidrug resistance-associated proteins predicts prognosis in childhood and adult acute lymphoblastic leukemia. Clin Cancer Res; 2005 Dec 15;11(24 Pt 1):8661-8
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  • [Title] Expression of multidrug resistance-associated proteins predicts prognosis in childhood and adult acute lymphoblastic leukemia.
  • PURPOSE: Patients with acute lymphoblastic leukemia (ALL) are treated with a variety of chemotherapeutic drugs, which can be transported by six multidrug resistance-associated proteins (MRP).
  • [MeSH-major] Multidrug Resistance-Associated Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16361551.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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56. Davidsson J, Lilljebjörn H, Andersson A, Veerla S, Heldrup J, Behrendtz M, Fioretos T, Johansson B: The DNA methylome of pediatric acute lymphoblastic leukemia. Hum Mol Genet; 2009 Nov 1;18(21):4054-65
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  • [Title] The DNA methylome of pediatric acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy, with high hyperdiploidy [51-67 chromosomes] and the t(12;21)(p13;q22) [ETV6/RUNX1 fusion] representing the most frequent abnormalities.
  • [MeSH-major] CpG Islands / genetics. DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19679565.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BBC3 protein, human; 0 / CAV1 protein, human; 0 / CDK2AP1 protein, human; 0 / Caveolin 1; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / PRKCDBP protein, human; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / Tumor Suppressor Proteins; 0 / bcl-Associated Death Protein; 117896-08-9 / nucleophosmin; EC 3.1.2.- / THEM4 protein, human; EC 3.1.2.- / Thiolester Hydrolases
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57. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
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  • [Title] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


58. Mullighan CG, Zhang J, Harvey RC, Collins-Underwood JR, Schulman BA, Phillips LA, Tasian SK, Loh ML, Su X, Liu W, Devidas M, Atlas SR, Chen IM, Clifford RJ, Gerhard DS, Carroll WL, Reaman GH, Smith M, Downing JR, Hunger SP, Willman CL: JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2009 Jun 9;106(23):9414-8
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  • [Title] JAK mutations in high-risk childhood acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) is a heterogeneous disease consisting of distinct clinical and biological subtypes that are characterized by specific chromosomal abnormalities or gene mutations.
  • We recently identified a poor prognostic subgroup of pediatric BCR-ABL1-negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1-positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype.
  • Here, we report activating mutations in the Janus kinases JAK1 (n = 3), JAK2 (n = 16), and JAK3 (n = 1) in 20 (10.7%) of 187 BCR-ABL1-negative, high-risk pediatric ALL cases.
  • The JAK-mutated cases had a gene expression signature similar to BCR-ABL1 pediatric ALL, and they had a poor outcome.

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  • (PMID = 19470474.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA118100; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / L40 CA142226; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / Howard Hughes Medical Institute / / ; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2695045
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59. Lee KM, Ward MH, Han S, Ahn HS, Kang HJ, Choi HS, Shin HY, Koo HH, Seo JJ, Choi JE, Ahn YO, Kang D: Paternal smoking, genetic polymorphisms in CYP1A1 and childhood leukemia risk. Leuk Res; 2009 Feb;33(2):250-8
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  • [Title] Paternal smoking, genetic polymorphisms in CYP1A1 and childhood leukemia risk.
  • We conducted a case-control study to evaluate the association between paternal smoking and childhood leukemia and to evaluate potential modification by polymorphisms in CYP1A1.
  • Histologically confirmed childhood leukemia cases (n=164) and non-cancer controls (n=164) were recruited from three teaching hospitals in Seoul, Korea.
  • We also conducted a meta-analysis of 12 studies that have reported the association between paternal smoking and childhood leukemia risk.
  • Paternal smoking at home was associated with all leukemias (OR=1.8, 95% CI=1.1-2.8) and acute lymphoblastic leukemia (ALL) (2.0, 1.2-3.4).
  • The meta-analysis showed that overall paternal smoking (1.13, 1.04-1.24) and smoking before the pregnancy of the child (1.12, 1.04-1.21) were significantly associated with childhood leukemia risk.
  • Our results suggest that paternal smoking is a risk factor for childhood leukemia and the effect may be modified by CYP1A1 genotype.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Fathers. Leukemia / etiology. Polymorphism, Genetic. Smoking / adverse effects
  • [MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Environmental Exposure. Female. Genotype. Haplotypes. Humans. Infant. Male. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Risk Factors


60. Brassesco MS, Montaldi AP, Gras DE, Camparoto ML, Martinez-Rossi NM, Scrideli CA, Tone LG, Sakamoto-Hojo ET: Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors. Mutagenesis; 2009 Mar;24(2):153-60
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  • [Title] Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors.
  • The successful treatment of paediatric malignancies by multimodal therapy has improved outcomes for children with cancer, especially those with acute lymphoblastic leukaemia (ALL).
  • Depending on dosage, 2-12% of patients treated with topoisomerase II inhibitors and/or alkylating agents develop treatment-related acute myeloid leukaemia characterized by translocations at 11q23.
  • Our goal was to study MLL rearrangements in peripheral lymphocytes using cytogenetic and molecular methods in order to evaluate the late effects of cancer therapy in patients previously treated for childhood ALL.
  • Our results indicate an increase in MLL aberrations in childhood ALL survivors years after completion of therapy.
  • [MeSH-major] Cytogenetic Analysis. Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Survivors

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  • (PMID = 19028982.001).
  • [ISSN] 1464-3804
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; 957E6438QA / Teniposide
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61. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia. Indian J Pediatr; 2007 Mar;74(3):255-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • RESULTS: Cases aged 50.000/mm3 also showed better but non-significant remission rates.
  • CONCLUSION: Some cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17401264.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
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62. Salzer WL, Devidas M, Carroll WL, Winick N, Pullen J, Hunger SP, Camitta BA: Long-term results of the pediatric oncology group studies for childhood acute lymphoblastic leukemia 1984-2001: a report from the children's oncology group. Leukemia; 2010 Feb;24(2):355-70
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  • [Title] Long-term results of the pediatric oncology group studies for childhood acute lymphoblastic leukemia 1984-2001: a report from the children's oncology group.
  • From 1984 to 2001, the Pediatric Oncology Group (POG) conducted 12 acute lymphoblastic leukemia (ALL) studies.
  • Ten-year event-free survival (EFS) for patients >12 months of age with B-precursor ALL on acute leukemia in children 14, 15 and 16 series were 66.7+/-1.2%, 68.1+/-1.4% and 73.2+/-2.1%, respectively.
  • There was a non-significant improvement in EFS for infants (10-year EFS 17.7+/-7.2-31.9+/-8.3%).

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  • (PMID = 20016527.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / CA 29139; United States / NCI NIH HHS / CA / U10 CA030969-22; United States / NCI NIH HHS / CA / U10 CA029139-22; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / CA 30969; United States / NCI NIH HHS / CA / U10 CA029139; United States / NCI NIH HHS / CA / U10 CA098543-07; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA030969; United States / NCI NIH HHS / CA / U10 CA098413-07; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS158683; NLM/ PMC4300959
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63. Möricke A, Zimmermann M, Reiter A, Henze G, Schrauder A, Gadner H, Ludwig WD, Ritter J, Harbott J, Mann G, Klingebiel T, Zintl F, Niemeyer C, Kremens B, Niggli F, Niethammer D, Welte K, Stanulla M, Odenwald E, Riehm H, Schrappe M: Long-term results of five consecutive trials in childhood acute lymphoblastic leukemia performed by the ALL-BFM study group from 1981 to 2000. Leukemia; 2010 Feb;24(2):265-84
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  • [Title] Long-term results of five consecutive trials in childhood acute lymphoblastic leukemia performed by the ALL-BFM study group from 1981 to 2000.
  • Between 1981 and 2000, 6609 children (<18 years of age) were treated in five consecutive trials of the Berlin-Frankfurt-Münster (BFM) study group for childhood acute lymphoblastic leukemia (ALL).
  • In parallel to relapse reduction, major efforts focused on reducing acute and late toxicity through advanced risk adaptation of treatment.
  • (1) preventive cranial radiotherapy could be safely reduced to 12 Gy in T-ALL and high-risk (HR) ALL patients, and eliminated in non- HR non-T-ALL patients, if it was replaced by high-dose and intrathecal (IT) MTX;.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation


64. Hou X, Wang S, Zhou Y, Xu Z, Zou Y, Zhu X, Han M, Pang T, Han ZC: Cyclin D1 gene polymorphism and susceptibility to childhood acute lymphoblastic leukemia in a Chinese population. Int J Hematol; 2005 Oct;82(3):206-9
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  • [Title] Cyclin D1 gene polymorphism and susceptibility to childhood acute lymphoblastic leukemia in a Chinese population.
  • Correlation between genetic polymorphism of A870G of CCND1 and clinical outcome among patients with acute lymphoblastic leukemia (ALL) has been reported.
  • [MeSH-major] Cyclin D1 / genetics. Exons / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


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

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16435384.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
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66. Karrman K, Forestier E, Heyman M, Andersen MK, Autio K, Blennow E, Borgström G, Ehrencrona H, Golovleva I, Heim S, Heinonen K, Hovland R, Johannsson JH, Kerndrup G, Nordgren A, Palmqvist L, Johansson B, Nordic Society of Pediatric Hematology, Oncology (NOPHO), Swedish Cytogenetic Leukemia Study Group (SCLSG), NOPHO Leukemia Cytogenetic Study Group (NLCSG): Clinical and cytogenetic features of a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias: rare T-cell receptor gene rearrangements are associated with poor outcome. Genes Chromosomes Cancer; 2009 Sep;48(9):795-805
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  • [Title] Clinical and cytogenetic features of a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias: rare T-cell receptor gene rearrangements are associated with poor outcome.
  • Clinical characteristics and cytogenetic aberrations were ascertained and reviewed in a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias (T-ALLs) diagnosed between 1992 and 2006 in the Nordic countries.
  • In conclusion, in this large series of childhood T-ALLs from the Nordic countries, the cytogenetic findings were not associated with risk of therapy failure with the exception of the TCR;other group.
  • [MeSH-major] Chromosome Aberrations. Gene Rearrangement, T-Lymphocyte. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 19530250.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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67. Sawada A, Sakata N, Kishimoto T, Higuchi B, Koyama M, Kondo O, Sato E, Okamura T, Yasui M, Inoue M, Yoshioka A, Kawa K: Significance of four MRD markers in MRD-based treatment strategy for childhood acute lymphoblastic leukemia. Leuk Res; 2009 Dec;33(12):1710-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of four MRD markers in MRD-based treatment strategy for childhood acute lymphoblastic leukemia.
  • [MeSH-major] Biomarkers, Tumor / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • (PMID = 19596431.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
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68. 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
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  • 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.
  • 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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69. Hubacek P, Muzikova K, Hrdlickova A, Cinek O, Hyncicova K, Hrstkova H, Sedlacek P, Stary J: Prevalence of HHV-6 integrated chromosomally among children treated for acute lymphoblastic or myeloid leukemia in the Czech Republic. J Med Virol; 2009 Feb;81(2):258-63
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  • [Title] Prevalence of HHV-6 integrated chromosomally among children treated for acute lymphoblastic or myeloid leukemia in the Czech Republic.
  • Stored DNA samples taken originally for detection of fusion genes and minimal residual disease from 339 pediatric patients treated for leukemia in the Czech Republic between the years 1995-2007 were tested retrospectively.
  • The prevalence of CI-HHV-6 in childhood leukemia does not differ from that published for other patients or healthy populations.
  • [MeSH-major] Chromosomes / virology. Herpesviridae Infections / epidemiology. Herpesvirus 6, Human / genetics. Herpesvirus 6, Human / isolation & purification. Leukemia, Myeloid / virology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / virology. Virus Integration / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 19107978.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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70. von Goessel H, Jacobs U, Semper S, Krumbholz M, Langer T, Keller T, Schrauder A, van der Velden VH, van Dongen JJ, Harbott J, Panzer-Grümayer ER, Schrappe M, Rascher W, Metzler M: Cluster analysis of genomic ETV6-RUNX1 (TEL-AML1) fusion sites in childhood acute lymphoblastic leukemia. Leuk Res; 2009 Aug;33(8):1082-8
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  • [Title] Cluster analysis of genomic ETV6-RUNX1 (TEL-AML1) fusion sites in childhood acute lymphoblastic leukemia.
  • Fusion between ETV6 and RUNX1 defines the largest genetic subgroup in childhood ALL.
  • [MeSH-major] Biomarkers, Tumor / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19081626.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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71. Molteni CG, Te Kronnie G, Bicciato S, Villa T, Tartaglia M, Basso G, Biondi A, Cazzaniga G: PTPN11 mutations in childhood acute lymphoblastic leukemia occur as a secondary event associated with high hyperdiploidy. Leukemia; 2010 Jan;24(1):232-5
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  • [Title] PTPN11 mutations in childhood acute lymphoblastic leukemia occur as a secondary event associated with high hyperdiploidy.
  • [MeSH-major] Diploidy. Mutation. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics

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  • (PMID = 19776760.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP07115
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
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72. Pérez-Vera P, Montero-Ruiz O, Frías S, Ulloa-Avilés V, Cárdenas-Cardós R, Paredes-Aguilera R, Rivera-Luna R, Carnevale A: Detection of ETV6 and RUNX1 gene rearrangements using fluorescence in situ hybridization in Mexican patients with acute lymphoblastic leukemia: experience at a single institution. Cancer Genet Cytogenet; 2005 Oct 15;162(2):140-5
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  • [Title] Detection of ETV6 and RUNX1 gene rearrangements using fluorescence in situ hybridization in Mexican patients with acute lymphoblastic leukemia: experience at a single institution.
  • The t(12;21) produces the gene fusion ETV6/RUNX1 and is a frequent rearrangement in childhood ALL, associated with a good prognosis.
  • [MeSH-major] Gene Rearrangement. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 16213362.001).
  • [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 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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73. Paulsson K, Jonson T, Ora I, Olofsson T, Panagopoulos I, Johansson B: Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemias. Br J Haematol; 2007 Jul;138(2):196-201
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  • [Title] Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemias.
  • The t(1;19)(q23;p13), one of the most common translocations in childhood and adult acute lymphoblastic leukaemias (ALLs), usually results in fusion of exons 1-16 of TCF3 (previously E2A) and exons 3-9 of PBX1.
  • This confirms that most t(1;19) rearrangements may arise by a combination of illegitimate V(D)J recombination and non-homologous end joining.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. DNA-Binding Proteins / genetics. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic / genetics

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  • (PMID = 17593026.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TCF3 protein, human; 0 / pbx1 protein, human
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74. Assumpção JG, Ganazza MA, de Araújo M, Silva AS, Scrideli CA, Brandalise SR, Yunes JA: Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in childhood acute lymphoblastic leukemia using a low-cost PCR strategy. Pediatr Blood Cancer; 2010 Dec 15;55(7):1278-86
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  • [Title] Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in childhood acute lymphoblastic leukemia using a low-cost PCR strategy.
  • BACKGROUND: Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements function as specific markers for minimal residual disease (MRD), which is one of the best predictors of outcome in childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, T-Cell Receptor / genetics. Immunoglobulins / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Clone Cells. Humans. Neoplasm, Residual. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Prognosis

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  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 20730889.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins
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75. Porto L, Preibisch C, Hattingen E, Bartels M, Lehrnbecher T, Dewitz R, Zanella F, Good C, Lanfermann H, DuMesnil R, Kieslich M: Voxel-based morphometry and diffusion-tensor MR imaging of the brain in long-term survivors of childhood leukemia. Eur Radiol; 2008 Nov;18(11):2691-700
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  • [Title] Voxel-based morphometry and diffusion-tensor MR imaging of the brain in long-term survivors of childhood leukemia.
  • The aims of this study were to detect morphological changes in neuroanatomical components in adult survivors of acute lymphoblastic leukemia (ALL).
  • Voxel-based morphometry (VBM) can be used to detect subtle structural changes in brain morphology and via analysis of fractional anisotropy (FA), diffusion-tensor imaging (DTI) can non-invasively probe white matter (WM) integrity.
  • Ten ALL survivors received chemotherapy and irradiation; ten survivors received chemotherapy alone during childhood.
  • Survivors of childhood ALL who underwent cranial irradiation during childhood had smaller WM volumes and reduced GM concentration within the caudate nucleus and thalamus.
  • [MeSH-major] Brain / pathology. Diffusion Magnetic Resonance Imaging / methods. Imaging, Three-Dimensional / methods. Leukemia / diagnosis

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  • (PMID = 18491104.001).
  • [ISSN] 1432-1084
  • [Journal-full-title] European radiology
  • [ISO-abbreviation] Eur Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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76. Yeung J, Kempski H, Neat M, Bailey S, Smith O, Brady HJ: Characterization of the t(17;19) translocation by gene-specific fluorescent in situ hybridization-based cytogenetics and detection of the E2A-HLF fusion transcript and protein in patients' cells. Haematologica; 2006 Mar;91(3):422-4
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  • This is the first report to comprehensively characterize the E2A-HLF fusion generated from the t(17;19)(q22;p13) translocation in childhood B-lineage acute lymphoblastic leukemia.
  • [MeSH-minor] Adolescent. Child, Preschool. Cytogenetic Analysis / methods. Female. Humans. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16531271.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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77. Gaipa G, Basso G, Maglia O, Leoni V, Faini A, Cazzaniga G, Bugarin C, Veltroni M, Michelotto B, Ratei R, Coliva T, Valsecchi MG, Biondi A, Dworzak MN, I-BFM-ALL-FCM-MRD Study Group: Drug-induced immunophenotypic modulation in childhood ALL: implications for minimal residual disease detection. Leukemia; 2005 Jan;19(1):49-56
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  • [Title] Drug-induced immunophenotypic modulation in childhood ALL: implications for minimal residual disease detection.
  • However, we previously noticed modulation of surface antigen expression in acute lymphoblastic leukemia (ALL) during the early treatment.
  • [MeSH-major] Neoplasm, Residual. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • [CommentIn] Leukemia. 2005 Oct;19(10):1858 [16107890.001]
  • [CommentIn] Leukemia. 2005 Oct;19(10):1845-7 [16107891.001]
  • (PMID = 15538405.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
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78. Roy A, Bradburn M, Moorman AV, Burrett J, Love S, Kinsey SE, Mitchell C, Vora A, Eden T, Lilleyman JS, Hann I, Saha V, Medical Research Council Childhood Leukaemia Working Party: Early response to induction is predictive of survival in childhood Philadelphia chromosome positive acute lymphoblastic leukaemia: results of the Medical Research Council ALL 97 trial. Br J Haematol; 2005 Apr;129(1):35-44
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  • [Title] Early response to induction is predictive of survival in childhood Philadelphia chromosome positive acute lymphoblastic leukaemia: results of the Medical Research Council ALL 97 trial.
  • We report on the outcome of children with Philadelphia positive acute lymphoblastic leukaemia (Ph+ ALL) treated on the UK Medical Research Council (MRC) trial for childhood ALL, MRC ALL 97, between January 1997 and June 2002.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15801953.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 14840
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin
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79. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
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  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • CONCLUSION: There were statistic differences between T-cell and B-cell childhood ALLs in age, initial WBC count, early response to therapy, and eight-year EFS and RFS.
  • Childhood T-ALL was associated with a worse prognosis than other sub-types of childhood ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Karyotyping. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis

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  • (PMID = 19563031.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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80. Gandemer V, Rio AG, de Tayrac M, Sibut V, Mottier S, Ly Sunnaram B, Henry C, Monnier A, Berthou C, Le Gall E, Le Treut A, Schmitt C, Le Gall JY, Mosser J, Galibert MD: Five distinct biological processes and 14 differentially expressed genes characterize TEL/AML1-positive leukemia. BMC Genomics; 2007;8:385
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  • [Title] Five distinct biological processes and 14 differentially expressed genes characterize TEL/AML1-positive leukemia.
  • BACKGROUND: The t(12;21)(p13;q22) translocation is found in 20 to 25% of cases of childhood B-lineage acute lymphoblastic leukemia (B-ALL).
  • RESULTS: We compared the leukemia cell gene expression profiles of 16 TEL/AML1-positive ALL patients to those of 44 TEL/AML1-negative patients, whose blast cells did not contain any additional recurrent translocation.
  • CONCLUSION: Gene expression analyses of leukemia cells from 60 children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes, associated with 14 validated genes characterizing and highlighting the biology of the TEL/AML1-positive ALL sub-group.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Profiling / methods. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17956600.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [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 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ PMC2211320
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81. Hagedorn N, Acquaviva C, Fronkova E, von Stackelberg A, Barth A, zur Stadt U, Schrauder A, Trka J, Gaspar N, Seeger K, Henze G, Cavé H, Eckert C, Resistant Disease Committee of the International BFM study group: Submicroscopic bone marrow involvement in isolated extramedullary relapses in childhood acute lymphoblastic leukemia: a more precise definition of "isolated" and its possible clinical implications, a collaborative study of the Resistant Disease Committee of the International BFM study group. Blood; 2007 Dec 1;110(12):4022-9
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  • [Title] Submicroscopic bone marrow involvement in isolated extramedullary relapses in childhood acute lymphoblastic leukemia: a more precise definition of "isolated" and its possible clinical implications, a collaborative study of the Resistant Disease Committee of the International BFM study group.
  • This study investigates the extent of bone marrow (BM) involvement at diagnosis of apparent isolated extramedullary (AIEM) relapses of childhood acute lymphoblastic leukemia (ALL) and its relation to prognosis.
  • [MeSH-major] Bone Marrow. Gene Rearrangement, B-Lymphocyte / genetics. Polymerase Chain Reaction. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics


82. Agirre X, Román-Gómez J, Jiménez-Velasco A, Garate L, Montiel-Duarte C, Navarro G, Vázquez I, Zalacain M, Calasanz MJ, Heiniger A, Torres A, Minna JD, Prósper F: ASPP1, a common activator of TP53, is inactivated by aberrant methylation of its promoter in acute lymphoblastic leukemia. Oncogene; 2006 Mar 23;25(13):1862-70
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  • [Title] ASPP1, a common activator of TP53, is inactivated by aberrant methylation of its promoter in acute lymphoblastic leukemia.
  • We have analyzed the regulation and expression of ASPP members, genes implicated in the regulation of the apoptotic function of the TP53 tumor-suppressor gene, in acute lymphoblastic leukemia (ALL).
  • Methylation was significantly higher in adult ALL vs childhood ALL (32 vs 17%, P = 0.03) and T-ALL vs B-ALL (50 vs 9%, P = 0.001).
  • [MeSH-major] Carrier Proteins / biosynthesis. Carrier Proteins / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [ErratumIn] Oncogene. 2013 Feb 7;32(6):803
  • (PMID = 16314841.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / Carrier Proteins; 0 / PPP1R13B protein, human
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83. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • LAF4 is the first gene fused with both AML1 and MLL in acute leukemia.
  • Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Child. DNA Mutational Analysis / methods. DNA, Complementary / analysis. Humans. Male. Models, Biological. Molecular Sequence Data

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  • (PMID = 17968322.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AFF3 protein, human; 0 / AML1-LAF4 fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
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84. Mussolin L, Pillon M, Conter V, Piglione M, Lo Nigro L, Pierani P, Micalizzi C, Buffardi S, Basso G, Zanesco L, Rosolen A: Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood. J Clin Oncol; 2007 Nov 20;25(33):5254-61
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  • [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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85. Dohnal AM, Inthal A, Felzmann T, Glatt S, Sommergruber W, Mann G, Gadner H, Panzer-Grümayer ER: Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL. Int J Cancer; 2006 Dec 15;119(12):2870-7
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  • [Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.
  • The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).
  • Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17016825.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
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86. van Scherpenzeel Thim V, Remacle S, Picard J, Cornu G, Gofflot F, Rezsohazy R, Verellen-Dumoulin C: Mutation analysis of the HOX paralogous 4-13 genes in children with acute lymphoid malignancies: identification of a novel germline mutation of HOXD4 leading to a partial loss-of-function. Hum Mutat; 2005 Apr;25(4):384-95
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  • [Title] Mutation analysis of the HOX paralogous 4-13 genes in children with acute lymphoid malignancies: identification of a novel germline mutation of HOXD4 leading to a partial loss-of-function.
  • The molecular basis of susceptibility to childhood malignant hemopathy remains largely unknown.
  • We aimed to explore the possibility that germline alterations of HOX genes might be involved in childhood acute lymphoid malignancies.
  • A cohort of 86 children diagnosed with acute lymphoid malignancy was studied, 20 of them concurrently presenting a congenital anomaly of the skeleton.
  • While 13 changes were also observed in healthy controls, three variants were exclusively found in acute lymphoid malignancy cases.
  • These comprised the germline c.242A>T (p.Glu81Val) missense mutation of HOXD4, detected in two children diagnosed with acute lymphoblastic leukemia (ALL).
  • The p.Glu81Val mutation of HOXD4 thus results in a partial loss-of-function, which might be involved in childhood ALL.
  • [MeSH-major] Germ-Line Mutation. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 15776434.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Databank-accession-numbers] OMIM/ 142981; RefSeq/ NM/ 014621
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HOXD1 protein, human; 0 / Homeodomain Proteins; 0 / Hoxd4 protein, mouse; 0 / Transcription Factors
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87. Pottier N, Cheok MH, Yang W, Assem M, Tracey L, Obenauer JC, Panetta JC, Relling MV, Evans WE: Expression of SMARCB1 modulates steroid sensitivity in human lymphoblastoid cells: identification of a promoter SNP that alters PARP1 binding and SMARCB1 expression. Hum Mol Genet; 2007 Oct 1;16(19):2261-71
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  • Although cure rate of childhood acute lymphoblastic leukemia (ALL) has surpassed 80%, drug resistance remains a major cause of treatment failure.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Gene Expression / drug effects. Poly(ADP-ribose) Polymerases / genetics. Steroids / pharmacology. Transcription Factors / genetics

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  • (PMID = 17616514.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765; United States / NCI NIH HHS / CA / R01 CA51001; United States / NCI NIH HHS / CA / R01 CA78224; United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NIGMS NIH HHS / GM / U01 GM61394
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / SMARCB1 protein, human; 0 / Steroids; 0 / Transcription Factors; 9PHQ9Y1OLM / Prednisolone; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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88. Kerst G, Kreyenberg H, Roth C, Well C, Dietz K, Coustan-Smith E, Campana D, Koscielniak E, Niemeyer C, Schlegel PG, Müller I, Niethammer D, Bader P: Concurrent detection of minimal residual disease (MRD) in childhood acute lymphoblastic leukaemia by flow cytometry and real-time PCR. Br J Haematol; 2005 Mar;128(6):774-82
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  • [Title] Concurrent detection of minimal residual disease (MRD) in childhood acute lymphoblastic leukaemia by flow cytometry and real-time PCR.
  • Minimal (i.e. submicroscopic) residual disease (MRD) predicts outcome in childhood acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Biomarkers, Tumor / analysis. Flow Cytometry / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15755280.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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89. Stevens B, Croxford R, McKeever P, Yamada J, Booth M, Daub S, Gafni A, Gammon J, Greenberg M: Hospital and home chemotherapy for children with leukemia: a randomized cross-over study. Pediatr Blood Cancer; 2006 Sep;47(3):285-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hospital and home chemotherapy for children with leukemia: a randomized cross-over study.
  • BACKGROUND: The study objective was to compare a hospital-based and a home-based chemotherapy program for children with acute lymphoblastic leukemia (ALL) in relation to Quality of Life (QOL), safety, caregiver burden, and costs.
  • PROCEDURE: A randomized cross-over trial (RCT) design with repeated measures was conducted with 23 children with ALL who attended the oncology outpatient clinic of a metropolitan university affiliated tertiary level pediatric hospital and who also received home visits from a community health services care provider in central Canada.
  • These data provide important information to families and caregivers as they consider home or hospital-based therapy in childhood ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Home Care Services, Hospital-Based. Oncology Service, Hospital. Outcome and Process Assessment (Health Care). Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Age Factors. Cost of Illness. Cross-Over Studies. Family Health. Health Care Costs. Hospitals, Pediatric. Humans. Ontario. Quality of Life. Safety. Sickness Impact Profile. Surveys and Questionnaires

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  • [CommentIn] Pediatr Blood Cancer. 2006 Sep;47(3):237-8 [16435381.001]
  • (PMID = 16200556.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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90. Cario G, Zimmermann M, Romey R, Gesk S, Vater I, Harbott J, Schrauder A, Moericke A, Izraeli S, Akasaka T, Dyer MJ, Siebert R, Schrappe M, Stanulla M: Presence of the P2RY8-CRLF2 rearrangement is associated with a poor prognosis in non-high-risk precursor B-cell acute lymphoblastic leukemia in children treated according to the ALL-BFM 2000 protocol. Blood; 2010 Jul 01;115(26):5393-7
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  • [Title] Presence of the P2RY8-CRLF2 rearrangement is associated with a poor prognosis in non-high-risk precursor B-cell acute lymphoblastic leukemia in children treated according to the ALL-BFM 2000 protocol.
  • High-level expression of the cytokine receptor-like factor 2 gene, CRLF2, in precursor B-cell acute lymphoblastic leukemia (pB-ALL) was shown to be caused by a translocation involving the IGH@ locus or a deletion juxtaposing CRLF2 with the P2RY8 promoter.
  • To assess its possible prognostic value, CRLF2 expression was analyzed in 555 childhood pB-ALL patients treated according to the Acute Lymphoblastic Leukemia Berlin-Frankfurt-Münster 2000 (ALL-BFM 2000) protocol.
  • This difference was mainly attributable to an extremely high incidence of relapse (71% +/- 19%) in non-high-risk patients with P2RY8-CRLF2 rearrangement.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics. Receptors, Purinergic P2 / genetics

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  • (PMID = 20378752.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRLF2 protein, human; 0 / Receptors, Cytokine; 0 / Receptors, Purinergic P2
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91. Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ: [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Oct;10(5):620-4
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  • [Title] [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
  • OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology

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  • (PMID = 18947485.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
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92. Thörn I, Botling J, Hermansson M, Lönnerholm G, Sundström C, Rosenquist R, Barbany G: Monitoring minimal residual disease with flow cytometry, antigen-receptor gene rearrangements and fusion transcript quantification in Philadelphia-positive childhood acute lymphoblastic leukemia. Leuk Res; 2009 Aug;33(8):1047-54
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  • [Title] Monitoring minimal residual disease with flow cytometry, antigen-receptor gene rearrangements and fusion transcript quantification in Philadelphia-positive childhood acute lymphoblastic leukemia.
  • In this study, we followed minimal residual disease (MRD) in eight children with Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL) using (i) flow cytometry (FCM), (ii) real-time quantitative PCR of IG/TCR gene rearrangements and (iii) RT-PCR detecting fusion gene transcripts.
  • [MeSH-major] Flow Cytometry / methods. Gene Expression Regulation, Leukemic. Gene Rearrangement, T-Lymphocyte. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-abl / biosynthesis. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19157547.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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93. Taylor GM, Hussain A, Verhage V, Thompson PD, Fergusson WD, Watkins G, Lightfoot T, Harrison CJ, Birch JM, UKCCS Investigators: Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601. Leukemia; 2009 May;23(5):863-9
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  • [Title] Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601.
  • We previously reported that susceptibility to childhood B cell precursor ALL (BCP ALL) is associated with HLA-DPB1 alleles having glutamic acid (E) rather than lysine (K) in the P4 antigenic peptide-binding pocket.
  • Clustering approximately 90% of DPB1 alleles into DPB69E (DP2, 6, 8) and DPB69K (DP1, 3, 4) supertypes revealed that DP2 and DP8 are associated with BCP ALL, but DP6 is also associated with non-BCP leukaemia.
  • Here, we report that only one of seven alleles with the DP6 supertype (DPB1(*)0601) is associated with childhood leukaemia (leukaemia vs controls: odds ratio, 95% confidence interval [OR, CI]: 4.6, 2.0-10.4; corrected P=0.019), but not with childhood solid tumours or lymphomas.
  • Sequencing the coding region of DPB1(*)0601 revealed an exon 1-4 haplotype [T-DEAV-KIL-RVI] shared with DPB1(*)0301 and 0901, but no evidence of germline mutations in childhood leukaemia.
  • These results suggest that the DPbeta0601 molecule may be functionally involved in childhood leukaemia.
  • Analysis of peptide binding and T-cell activation by DPbeta0601-peptide complexes should help determine its role in childhood leukaemia causation.
  • [MeSH-major] HLA-DP Antigens / genetics. Haplotypes / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19148140.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen
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94. Zuna J, Burjanivova T, Mejstrikova E, Zemanova Z, Muzikova K, Meyer C, Horsley SW, Kearney L, Colman S, Ptoszkova H, Marschalek R, Hrusak O, Stary J, Greaves M, Trka J: Covert preleukemia driven by MLL gene fusion. Genes Chromosomes Cancer; 2009 Jan;48(1):98-107
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  • Acute leukemia is considered to be a two- or multiple-step process.
  • We demonstrate here a striking sequence of events, which include a covert, protracted preleukemic phase characterized by a dominant MLL/FOXO3A clone with intact myeloid differentiation and the subsequent acquisition of a secondary genetic abnormality, leading to overt lymphoblastic leukemia.
  • Backtracking of the secondary acute lymphoblastic leukemia (sALL) with the MLL rearrangement showed no blasts in the bone marrow (BM) during the protracted preleukemic phase.
  • These data provide insight into the dynamics of leukemogenesis in secondary leukemia with MLL rearrangement.
  • [MeSH-major] Gene Fusion. Leukemia, Promyelocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics

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  • (PMID = 18932267.001).
  • [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 / Biomarkers, Tumor; 0 / FOXO3 protein, human; 0 / Forkhead Transcription Factors; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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95. Tedeschi R, Bloigu A, Ogmundsdottir HM, Marus A, Dillner J, dePaoli P, Gudnadottir M, Koskela P, Pukkala E, Lehtinen T, Lehtinen M: Activation of maternal Epstein-Barr virus infection and risk of acute leukemia in the offspring. Am J Epidemiol; 2007 Jan 15;165(2):134-7
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  • [Title] Activation of maternal Epstein-Barr virus infection and risk of acute leukemia in the offspring.
  • After identifying an association between maternal Epstein-Barr virus (EBV) reactivation and acute lymphoblastic leukemia (ALL), the authors analyzed a nested case-control study within Finnish and Icelandic maternity cohorts with 7 million years of follow-up to confirm EBV's role in ALL.
  • Offspring of 550,000 mothers were followed up to age 15 years during 1975-1997 by national cancer registries to identify leukemia cases.
  • First-trimester sera from mothers of 304 ALL cases and 39 non-ALL cases and from 943 mothers of controls were analyzed for antibodies to viral capsid antigen, early antigen, and EBV transactivator protein ZEBRA.
  • Both ZEBRA immunoglobulin G antibodies and viral capsid antigen immunoglobulin M antibodies were associated with an increased risk of non-ALL in the offspring (odds ratio = 4.5, 95% confidence interval: 1.3, 16; odds ratio = 5.6, 95% confidence interval: 1.1, 29, respectively), suggesting EBV reactivation in the mothers of non-ALL cases.
  • EBV reactivation may be associated with a proportion of childhood leukemia.
  • [MeSH-major] Antigens, Viral / immunology. Capsid Proteins / immunology. Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / immunology. Maternal Exposure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 17005627.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Antigens, Viral; 0 / Capsid Proteins; 0 / Epstein-Barr viral capsid antigen; 0 / Immunoglobulin G
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96. Steiner M, Attarbaschi A, König M, Gadner H, Haas OA, Mann G: Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome. Pediatr Hematol Oncol; 2005 Jan-Feb;22(1):11-6
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  • [Title] Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome.
  • Constitutional trisomy 21 is the most prominent predisposing factor to childhood leukemia, whereas the t(12;21)(p13;q22) with its molecular genetic counterpart, the TEL/AML1 fusion gene, is the most common acquired chromosomal rearrangement in childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL).
  • Accordingly, they were able to analyze 8 of 10 individuals with DS and a BCP ALL, including 2 who suffered from a TEL/AML1+ leukemia.
  • Based on this observation we concluded that individuals with a constitutional trisomy 21 may have the similar likelihood to develop a TEL/AML1+ leukemia as BCP ALL patients without this specific predisposingfactor.
  • [MeSH-major] Down Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [RepublishedIn] Pediatr Hematol Oncol. 2005 Apr-May;22(3):229-34 [16020107.001]
  • (PMID = 15770827.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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97. Luria D, Rosenthal E, Steinberg D, Kodman Y, Safanaiev M, Amariglio N, Avigad S, Stark B, Izraeli S, Israel National Study Group of Childhood ALL: Prospective comparison of two flow cytometry methodologies for monitoring minimal residual disease in a multicenter treatment protocol of childhood acute lymphoblastic leukemia. Cytometry B Clin Cytom; 2010 Nov;78(6):365-71
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  • [Title] Prospective comparison of two flow cytometry methodologies for monitoring minimal residual disease in a multicenter treatment protocol of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Minimal residual disease (MRD) is a powerful prognostic indicator in childhood acute lymphoblastic leukemia (ALL).
  • METHODS: We compared FC-MRD of identical bone marrow samples processed as either Ficoll separated mononuclear cells or lyse and wash nucleated cells (NC) in two central laboratories of a national multicenter childhood ALL study.
  • CONCLUSIONS: FC-MRD analysis of childhood ALL is a robust method during the earliest phases of induction therapy in a multicentric setting.
  • [MeSH-major] Flow Cytometry / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] © 2010 International Clinical Cytometry Society.
  • (PMID = 20632326.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Dina A; Gali A; Ami B; Bella B; Yoav B; Ronit E; Herzel G; Yosef K; Hagit M; Dalia S; Michael W
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98. Kadan-Lottick NS, Brouwers P, Breiger D, Kaleita T, Dziura J, Northrup V, Chen L, Nicoletti M, Bostrom B, Stork L, Neglia JP: Comparison of neurocognitive functioning in children previously randomly assigned to intrathecal methotrexate compared with triple intrathecal therapy for the treatment of childhood acute lymphoblastic leukemia. J Clin Oncol; 2009 Dec 10;27(35):5986-92
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  • [Title] Comparison of neurocognitive functioning in children previously randomly assigned to intrathecal methotrexate compared with triple intrathecal therapy for the treatment of childhood acute lymphoblastic leukemia.
  • PURPOSE: For the majority of children with acute lymphoblastic leukemia (ALL), CNS prophylaxis consists of either intrathecal (IT) methotrexate or triple IT therapy (ie, methotrexate with both cytarabine and hydrocortisone).
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cognition / drug effects. Methotrexate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


99. Kawaguchi H, Taketani T, Hongo T, Park MJ, Koh K, Ida K, Kobayashi M, Takita J, Taki T, Yoshino H, Bessho F, Hayashi Y: In vitro drug resistance to imatinib and mutation of ABL gene in childhood Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Feb;46(2):273-6
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  • [Title] In vitro drug resistance to imatinib and mutation of ABL gene in childhood Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia.
  • Imatinib, the ABL kinase inhibitor, is used not only for Philadelphia chromosome-positive (Ph + ) chronic myelogenous leukemia, but also for Ph + acute lymphoblastic leukemia (ALL), although resistance to the drug tends to develop in an early stage of the clinical course.
  • We describe a childhood refractory Ph + ALL patient in whom progressive resistance to imatinib was correlated with the appearance of a mutation in the BCR-ABL kinase domain and in vitro drug resistance to imatinib as determined by the methyl-thiazol-tetrazolium (MTT) assay.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Genes, abl / genetics. Mutation, Missense. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use


100. Starkova J, Zamostna B, Mejstrikova E, Krejci R, Drabkin HA, Trka J: HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL. Pediatr Blood Cancer; 2010 Dec 1;55(6):1072-82
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  • [Title] HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL.
  • However, HOX expression patterns in leukemia cells compared to normal lymphoid progenitors have not been systematically studied in acute lymphoblastic leukemia (ALL) subtypes.
  • PROCEDURE: The RNA expression levels of HOXA, HOXB, and CDX1/2 genes were analyzed by qRT-PCR in a cohort of 61 diagnostic pediatric ALL samples and FACS-sorted subpopulations of normal lymphoid progenitors.
  • HOXA7 gene was low expressed at the RNA level in patients with hyperdiploid leukemia, whereas HOXB7 and CDX2 genes were low expressed in TEL/AML1-positive and BCR/ABL-positive cases, respectively.
  • In contrast to previous findings in acute myeloid leukemia, high HOXA RNA expression was associated with an excellent prognosis in Cox's regression model (P = 0.03).
  • CONCLUSIONS: HOX gene RNA expression cannot discriminate leukemia subgroups or relative maturity of leukemic cells.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 20672366.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / HOXB2 protein, human; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
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