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

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  • (PMID = 20460642.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2930966
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2. Usvasalo A, Räty R, Knuutila S, Vettenranta K, Harila-Saari A, Jantunen E, Kauppila M, Koistinen P, Parto K, Riikonen P, Salmi TT, Silvennoinen R, Elonen E, Saarinen-Pihkala UM: Acute lymphoblastic leukemia in adolescents and young adults in Finland. Haematologica; 2008 Aug;93(8):1161-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia in adolescents and young adults in Finland.
  • BACKGROUND: Interest has recently been paid to adolescents and young adults with acute lymphoblastic leukemia, particularly because all reports so far published indicate that these patients have a better outcome when treated with pediatric rather than adult therapeutic protocols.
  • There are different biological subtypes of acute lymphoblastic leukemia with distinct features and prognoses; the distribution of these subtypes is not well known among adolescents.
  • We, therefore, studied acute lymphoblastic leukemia in adolescents and young adults aged 10 to 25 years in Finland.
  • DESIGN AND METHODS: This population-based study included 225 consecutive patients aged 10-25 years diagnosed with acute lymphoblastic leukemia during 1990-2004.
  • One hundred and twenty-eight patients (10-16 years) were treated with pediatric Nordic (NOPHO) protocols, and 97 patients (17-25 years) with Finnish Leukemia Group National protocols.
  • Good prognostic features were TEL-AML1, hyperdiploidy, and pediatric intermediate risk stratification.
  • CONCLUSIONS: Unlike all previous studies, we found that the outcome of adolescents and young adults with acute lymphoblastic leukemia treated with pediatric or adult therapeutic protocols was comparable.
  • The success of the adult acute lymphoblastic leukemia therapy emphasizes the benefit of central referral of patients to academic centers and adherence to research protocols.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Blast Crisis. Child. Disease-Free Survival. Female. Finland. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / mortality. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukocyte Count. Male. Phenotype. Philadelphia Chromosome. Survival Analysis

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  • [CommentIn] Haematologica. 2008 Aug;93(8):1124-8 [18669975.001]
  • (PMID = 18556413.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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3. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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4. Aldrich MC, Zhang L, Wiemels JL, Ma X, Loh ML, Metayer C, Selvin S, Feusner J, Smith MT, Buffler PA: Cytogenetics of Hispanic and White children with acute lymphoblastic leukemia in California. Cancer Epidemiol Biomarkers Prev; 2006 Mar;15(3):578-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics of Hispanic and White children with acute lymphoblastic leukemia in California.
  • Epidemiologic studies of childhood leukemia have made limited use of tumor genetic characteristics, which may be related to disease etiology.
  • We characterized the cytogenetics of 543 childhood leukemia patients (0-14 years of age) enrolled in the Northern California Childhood Leukemia Study, an approximately population-based study comprised primarily of Hispanics (42%) and non-Hispanic Whites (41%), and compared the cytogenetic profiles between these two ethnic groups.
  • The ploidy levels most frequently observed among acute lymphoblastic leukemia patients were high hyperdiploidy (51-67 chromosomes) and pseudodiploidy (34% and 27%, respectively).
  • Among B-lineage acute lymphoblastic leukemia patients, the percentage of TEL-AML1 translocations was significantly lower in Hispanics (13%) than in non-Hispanic Whites (24%; P = 0.01).
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. European Continental Ancestry Group / genetics. Genetic Predisposition to Disease / epidemiology. Hispanic Americans / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ethnology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16537719.001).
  • [ISSN] 1055-9965
  • [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
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Genetic Markers; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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5. Zemanova Z, Michalova K, Sindelarova L, Smisek P, Brezinova J, Ransdorfova S, Vavra V, Dohnalova A, Stary J: Prognostic value of structural chromosomal rearrangements and small cell clones with high hyperdiploidy in children with acute lymphoblastic leukemia. Leuk Res; 2005 Mar;29(3):273-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of structural chromosomal rearrangements and small cell clones with high hyperdiploidy in children with acute lymphoblastic leukemia.
  • In this study, 107 children with acute lymphoblastic leukemia (ALL) were analysed for the presence of hyperdiploidy by cytogenetics and interphase fluorescence in situ hybridisation (I-FISH).
  • Clones with high hyperdiploidy (>50 chromosomes) (HeH) were found in 46 patients (43%).
  • [MeSH-major] Chromosome Aberrations. DNA, Neoplasm / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15661262.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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6. Wiemels JL, Zhang Y, Chang J, Zheng S, Metayer C, Zhang L, Smith MT, Ma X, Selvin S, Buffler PA, Wiencke JK: RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia. Leukemia; 2005 Mar;19(3):415-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia.
  • We explored the relationship of RAS gene mutations with epidemiologic and cytogenetic factors in a case series of children with leukemia.
  • Diagnostic bone marrow samples from 191 incident leukemia cases from the Northern California Childhood Leukemia Study were typed for NRAS and KRAS codon 12 and 13 mutations.
  • Among the 142 B-cell acute lymphoblastic leukemia (ALL) cases, RAS mutations were more common among Hispanic children (P=0.11) or children born to mothers <30 years (P=0.007).
  • Those with hyperdiploidy at diagnosis (>50 chromosomes) had the highest rates of RAS mutation (P=0.02).
  • A multivariable model confirmed the significant associations between RAS mutation and both maternal age and hyperdiploidy.
  • Interestingly, smoking of the father in the 3 months prior to pregnancy was reported less frequently among hyperdiploid leukemia patients than among those without hyperdiploidy (P=0.02).
  • The data suggest that RAS and high hyperdiploidy may be cooperative genetic events to produce the leukemia subtype; and furthermore, that maternal age and paternal preconception smoking or other factors associated with these parameters are critical in the etiology of subtypes of childhood leukemia.
  • [MeSH-major] Genes, ras / genetics. Mutation. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15674422.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCHHSTP CDC HHS / PS / PS42 ES04705; United States / NCI NIH HHS / CA / R01 CA89032; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
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7. Healey K, Gray SL, Halligan GE, McKenzie AS, de Chadarévian JP, Morrissette JJ: Hyperdiploidy with trisomy 9 and deletion of the CDKN2A locus in T-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Apr 15;190(2):121-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperdiploidy with trisomy 9 and deletion of the CDKN2A locus in T-cell acute lymphoblastic leukemia.
  • We describe the rare finding of a T-cell acute lymphoblastic leukemia (T-ALL) and a pretreatment bone marrow karyotype mosaic for four distinct cell lines in a 4-year-old boy.
  • This case represents a rare case of hyperdiploidy in T-ALL, and characterizes the clonal evolution of the 9p21 deletion leading to the abnormal karyotype.
  • [MeSH-major] Gene Deletion. Genes, p16. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Trisomy / genetics

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  • (PMID = 19380031.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Iwamoto S, Mihara K, Downing JR, Pui CH, Campana D: Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase. J Clin Invest; 2007 Apr;117(4):1049-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase.
  • Because of their low asparagine synthetase (ASNS) expression and asparagine biosynthesis, acute lymphoblastic leukemia (ALL) cells are exquisitely sensitive to asparagine depletion.
  • In 288 children with ALL, cellular ASNS expression was more likely to be high in T-lineage ALL and low in B-lineage ALL with TEL-AML1 or hyperdiploidy.

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  • (PMID = 17380207.001).
  • [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 / CA21765; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA58297; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA058297; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7006-34-0 / Asparagine; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
  • [Other-IDs] NLM/ PMC1821067
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9. Gruhn B, Taub JW, Ge Y, Beck JF, Zell R, Häfer R, Hermann FH, Debatin KM, Steinbach D: Prenatal origin of childhood acute lymphoblastic leukemia, association with birth weight and hyperdiploidy. Leukemia; 2008 Sep;22(9):1692-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prenatal origin of childhood acute lymphoblastic leukemia, association with birth weight and hyperdiploidy.
  • Recent studies with very small numbers of patients showed that in some cases of childhood acute lymphoblastic leukemia (ALL), preleukemic cells are detectable on Guthrie cards that were used for newborn screening.
  • Positive screening cards were not associated with patient's age at diagnosis but were almost always found in patients with hyperdiploidy (10/11; 91%; P=0.04).
  • In the search for causes of childhood leukemia we should concentrate on prenatal factors as well as postnatal factors.
  • Our results suggest that autologous cord bloods could be a poor choice as the source of stem cells for transplantation in leukemia, which may contain preleukemic cells.
  • Pending the development of suitable methods, childhood leukemia is a potentially screenable disease.
  • [MeSH-major] Aneuploidy. Birth Weight. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Preleukemia / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains. Infant. Infant, Newborn. Male. Neonatal Screening. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / etiology. Retrospective Studies


10. Liang DC, Shih LY, Yang CP, Hung IJ, Liu HC, Jaing TH, Yeh TC, Liang ST, Chang CL, Lee EH, Lai CL, Chang WH: Frequencies of ETV6-RUNX1 fusion and hyperdiploidy in pediatric acute lymphoblastic leukemia are lower in far east than west. Pediatr Blood Cancer; 2010 Sep;55(3):430-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequencies of ETV6-RUNX1 fusion and hyperdiploidy in pediatric acute lymphoblastic leukemia are lower in far east than west.
  • BACKGROUND: Both ETV6-RUNX1 (TEL-AML1) fusion and hyperdiploidy (>50 chromosomes) in transformed lymphoblasts are favorable genetic features in childhood acute lymphoblastic leukemia (ALL).
  • PROCEDURE: Among 433 Taiwanese children with ALL diagnosed at our hospitals between 1997 and 2007, the ETV6-RUNX1 fusion was found in 15.8%, and hyperdiploidy (>50 chromosomes) in 14.1% of the patients.
  • These frequencies were lower than those reported in the West, leading us to conduct a meta-analysis of ETV6-RUNX1 fusion and hyperdiploidy frequencies in childhood ALL based on published reports.
  • Similarly, the frequency of hyperdiploidy in Japan and Taiwan was 14.3% (333/2,334, range: 12-20%, median 16%), significantly lower than the 25.2% in the West (5,173/20,510, range: 18-34%, median 23.5%; P < 0.001, odds ratio = 2.0, 95% CI: 1.8-2.3).
  • CONCLUSIONS: This meta-analysis demonstrates lower frequencies of ETV6-RUNX1 fusion and hyperdiploidy among leukemia patients in the Far East compared with the West.
  • [MeSH-major] Diploidy. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658612.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Meta-Analysis
  • [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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11. Sunil SK, Prakash PN, Hariharan S, Vinod G, Preethi RT, Geetha N, Ankathil R: Adult acute lymphoblastic leukemia with near haploidy, hyperdiploidy and Ph positive lines: a rare entity with poor prognosis. Leuk Lymphoma; 2006 Mar;47(3):561-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult acute lymphoblastic leukemia with near haploidy, hyperdiploidy and Ph positive lines: a rare entity with poor prognosis.
  • Chromosomal ploidies provide a wealth of information with respect to the prognosis of patients with acute lymphoblastic leukemia (ALL).
  • The prognosis is favourable in hyperdiploidy (>50 ALL), whereas pseudodiploidy and hypodiploidy have an overall poor clinical outcome.
  • This is an extremely rare malignancy with an adverse clinical course compared to other lymphoblastic leukemias.
  • [MeSH-major] Philadelphia Chromosome. Ploidies. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16396782.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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12. Nygaard U, Larsen J, Kristensen TD, Wesenberg F, Jonsson OG, Carlsen NT, Forestier E, Kirchhoff M, Larsen JK, Schmiegelow K, Christensen IJ: Flow cytometric DNA index, G-band karyotyping, and comparative genomic hybridization in detection of high hyperdiploidy in childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2006 Mar;28(3):134-40
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  • [Title] Flow cytometric DNA index, G-band karyotyping, and comparative genomic hybridization in detection of high hyperdiploidy in childhood acute lymphoblastic leukemia.
  • High hyperdiploid acute lymphoblastic leukemia in children is related to a good outcome.
  • Twenty-six girls and 34 boys with acute lymphoblastic leukemia diagnosed in 1998 to 1999 were analyzed by FCM, GBK, and HR-CGH.
  • However, in 4 of 18 patients, high hyperdiploidy was overlooked by GBK or HR-CGH, and even when FCM was applied, 2 of 18 patients with high hyperdiploidy by GBK and/or HR-CGH were classified as nonhigh hyperdiploid.
  • Thus, both GBK and HR-CGH overlook patients with high hyperdiploidy, and FCM only detects all high hyperdiploid patients if small high hyperdiploid clones are included.
  • [MeSH-major] DNA, Neoplasm / analysis. Flow Cytometry. Karyotyping. Nucleic Acid Hybridization. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16679935.001).
  • [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 / DNA, Neoplasm
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13. van Delft FW, Bellotti T, Luo Z, Jones LK, Patel N, Yiannikouris O, Hill AS, Hubank M, Kempski H, Fletcher D, Chaplin T, Foot N, Young BD, Hann IM, Gammerman A, Saha V: Prospective gene expression analysis accurately subtypes acute leukaemia in children and establishes a commonality between hyperdiploidy and t(12;21) in acute lymphoblastic leukaemia. Br J Haematol; 2005 Jul;130(1):26-35
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  • [Title] Prospective gene expression analysis accurately subtypes acute leukaemia in children and establishes a commonality between hyperdiploidy and t(12;21) in acute lymphoblastic leukaemia.
  • We have prospectively analysed and correlated the gene expression profiles of children presenting with acute leukaemia to the Royal London and Great Ormond Street Hospitals with morphological diagnosis, immunophenotype and karyotype.
  • Total RNA extracted from freshly sorted blast cells was obtained from 84 lymphoblastic [acute lymphoblastic leukaemia (ALL)], 20 myeloid [acute myeloid leukaemia (AML)] and three unclassified acute leukaemias and hybridised to the high density Affymetrix U133A oligonucleotide array.
  • A novel 50-gene set accurately identified all patients with ALL and AML and predicted for a diagnosis of AML in three patients with unclassified acute leukaemia.
  • A unique gene set was derived for each of eight subtypes of acute leukaemia within our data set.
  • A common profile for children with ALL with an ETV6-RUNX1 fusion, amplification or deletion of ETV6, amplification of RUNX1 or hyperdiploidy with an additional chromosome 21 was identified.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Analysis of Variance. Child. Chromosome Banding. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / genetics. Diagnosis, Differential. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia / genetics. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics. Ploidies. Principal Component Analysis. Prospective Studies. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-ets. Repressor Proteins / genetics. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Telomeric Repeat Binding Protein 2 / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • (PMID = 15982341.001).
  • [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] Journal Article; 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 / ETS translocation variant 6 protein; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Telomeric Repeat Binding Protein 2; 0 / Transcription Factors
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14. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • We noticed a relative increase of karyotypes that did not fall into the classic ALL cytogenetic subgroups (high hyperdiploidy, t(12;21), t(9;22), 11q23, t(1;19), <45 chromosomes) in a group of 29 patients at relapse (38%) compared to 130 patients at presentation (30%).
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics


15. De Braekeleer E, Basinko A, Douet-Guilbert N, Morel F, Le Bris MJ, Berthou C, Morice P, Férec C, De Braekeleer M: Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008. Cancer Genet Cytogenet; 2010 Jul 1;200(1):8-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008.
  • The detection of chromosome abnormalities by conventional cytogenetics, now combined with analyses using fluorescence in situ hybridization (FISH), is an important component in assessing the risk stratification of acute lymphoblastic leukemia (ALL).
  • As previously reported, the incidence of high hyperdiploidy (51-67 chromosomes) was higher among children, whereas pseudodiploidy and hypodiploidy were higher among those >15 years of age.
  • [MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Histone-Lysine N-Methyltransferase. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Recurrence. Time Factors. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20513528.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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16. Schraders M, van Reijmersdal SV, Kamping EJ, van Krieken JH, van Kessel AG, Groenen PJ, Hoogerbrugge PM, Kuiper RP: High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage. Cancer Genet Cytogenet; 2009 May;191(1):27-33
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  • [Title] High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage.
  • Lymphoblastic lymphoma (LBL) is one of the most frequent occurring pediatric non-Hodgkin lymphomas.
  • In the WHO classification scheme, pediatric LBL is considered to be the same disease entity as pediatric acute lymphoblastic leukemia (ALL).
  • The majority of precursor B-cell LBL was characterized by high-hyperdiploidy (71%), and showed high resemblance with high-hyperdiploid precursor B-cell ALL.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Gene Expression Profiling. Genome, Human / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Cell Cycle. Child. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 9 / genetics. Gene Duplication. Gene Expression Regulation, Leukemic. Humans. Polyploidy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes / pathology

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  • (PMID = 19389505.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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17. Shafer D, Wu H, Al-Saleem T, Reddy K, Borghaei H, Lessin S, Smith M: Cutaneous precursor B-cell lymphoblastic lymphoma in 2 adult patients: clinicopathologic and molecular cytogenetic studies with a review of the literature. Arch Dermatol; 2008 Sep;144(9):1155-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous precursor B-cell lymphoblastic lymphoma in 2 adult patients: clinicopathologic and molecular cytogenetic studies with a review of the literature.
  • BACKGROUND: Precursor B-cell lymphoblastic lymphoma (B-LBL) is an uncommon high-grade neoplasm of immature B cells.
  • In contrast to the more common lymphoblastic lymphoma of T-cell lineage, B-LBL can be an extranodal disease, with a propensity to involve skin and bone.
  • Fluorescence in situ hybridization studies, not previously reported in primary cutaneous B-LBL to our knowledge, demonstrated rearrangement of the MLL gene in one patient and possible hyperdiploidy in the other, both reported in precursor acute lymphoblastic leukemia.
  • Precursor B-cell lymphoblastic lymphoma is more common in children and in young adults, with a tropism for the head and neck region.
  • Although there is a suggestion in a limited number of patients that abbreviated therapy may provide long-term disease control, the risk of relapse remains significant, particularly if a patient's condition is misdiagnosed and the patient is treated as having mature B-cell lymphoma.
  • In the absence of prospective studies for this population, patients with B-LBL are treated currently with intensive acute lymphoblastic leukemia regimens.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Skin Neoplasms / genetics. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Back. Cytogenetic Analysis. Diploidy. Forehead. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Scalp. Skin / pathology

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  • (PMID = 18794461.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 25
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18. Braoudaki M, Karpusas M, Katsibardi K, Papathanassiou Ch, Karamolegou K, Tzortzatou-Stathopoulou F: Frequency of FLT3 mutations in childhood acute lymphoblastic leukemia. Med Oncol; 2009 Dec;26(4):460-2
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  • [Title] Frequency of FLT3 mutations in childhood acute lymphoblastic leukemia.
  • FLT3 mutations are occasionally observed in acute lymphoblastic leukemia (ALL).
  • This is in accordance to previous studies indicating a higher incidence in the patient subgroup associated with hyperdiploidy.
  • [MeSH-major] Mutation / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [Cites] Blood. 2005 Jan 15;105(2):812-20 [15374878.001]
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  • (PMID = 19085113.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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19. Udayakumar AM, Bashir WA, Pathare AV, Wali YA, Zacharia M, Khan AA, Soliman H, Al-Lamki Z, Raeburn JA: Cytogenetic profile of childhood acute lymphoblastic leukemia in Oman. Arch Med Res; 2007 Apr;38(3):305-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic profile of childhood acute lymphoblastic leukemia in Oman.
  • BACKGROUND: Chromosomal abnormalities have important diagnostic and prognostic significance in acute lymphoblastic leukemia (ALL).
  • RESULTS: Among Omani children examined with ALL, 47 (81%) patients yielded results, with 26 (55.3%) showing an abnormal karyotype [10 (21.3%) pseudodiploid, 2 (4.3%) hypodiploid and 14 (29.7%) hyperdiploidy] and 21 (44.6%) had normal diploidy.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17350480.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Ceppi F, Brown A, Betts DR, Niggli F, Popovic MB: Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua. Pediatr Blood Cancer; 2009 Dec 15;53(7):1238-41
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  • [Title] Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua.
  • BACKGROUND: Within the frame of a twinning programme with Nicaragua, The La Mascota project, we evaluated in our study the contribution of cytogenetic characterization of acute lymphoblastic leukemia (ALL) as prognostic factor compared to clinical, morphological, and immunohistochemical parameters.
  • FISH analysis demonstrated a TEL/AML1 fusion in 9/66 (14%), BCR/ABL fusion in 1 (1.5%), MLL rearrangement in 2 (3.1%), iAMP21 in 2 (3.1%), MYC rearrangement in 1 (1.5%), and high-hyperdiploidy in 16 (24%).
  • All patients but two with TEL/AML1 fusion and high-hyperdiploidy were clinically and hematologically in the standard risk group whereas those with poor cytogenetic factors had clinical high-risk features and were treated intensively.
  • CONCLUSIONS: Compared to Europe, the ALL population in Nicaragua is older, has a higher proportion of poor prognostic clinical and hematological features and receives more intensive treatment, while patients with TEL/AML1 translocations and high-hyperdiploidy are clinically in the standard risk group.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Aneuploidy. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Hepatomegaly / epidemiology. Hepatomegaly / etiology. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Nicaragua / epidemiology. Oncogene Proteins, Fusion / genetics. Prognosis. Prospective Studies. Risk. Splenomegaly / epidemiology. Splenomegaly / etiology

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19672974.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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21. Brown P, Levis M, Shurtleff S, Campana D, Downing J, Small D: FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with high levels of FLT3 expression. Blood; 2005 Jan 15;105(2):812-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with high levels of FLT3 expression.
  • FMS-like tyrosine kinase 3 (FLT3) is almost universally expressed in B-precursor childhood acute lymphoblastic leukemia (ALL).
  • Cases of ALL with MLL gene rearrangements and those with high hyperdiploidy (> 50 chromosomes) express the highest levels of FLT3, and activating mutations of FLT3 occur in 18% of MLL-rearranged and 28% of hyperdiploid ALL cases.
  • Sensitivity to FLT3 inhibition was particularly high in samples with MLL gene rearrangements (82%, n = 11; P = .0005), high hyperdiploidy (100%, n = 5; P = .0007), and/or FLT3 mutations (100%, n = 4; P = .0021).
  • [MeSH-major] Carbazoles / pharmacology. Gene Expression Regulation, Leukemic. Indoles / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Age Factors. Apoptosis / drug effects. Child. DNA-Binding Proteins / genetics. Enzyme Inhibitors / pharmacology. Gene Rearrangement. Genotype. Histone-Lysine N-Methyltransferase. Humans. Infant. Myeloid-Lymphoid Leukemia Protein. Phenotype. Ploidies. Proto-Oncogenes / genetics. Transcription Factors / genetics. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3

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  • (PMID = 15374878.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA095600; United States / NCI NIH HHS / CA / CA60441; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCI NIH HHS / CA / CA91177
  • [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 / Carbazoles; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; DO989GC5D1 / lestaurtinib; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The DNA methylome of pediatric acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy, with high hyperdiploidy [51-67 chromosomes] and the t(12;21)(p13;q22) [ETV6/RUNX1 fusion] representing the most frequent abnormalities.
  • [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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23. Liu XP, Zhu XF, Wang JX, Mi YC, Zou Y, Chen YM, Li CW, Dai Y, Qin S, Xiao JG, Xu FY, Gong JY, Wang SP, Yu CL, Fan J: [A comparative cytogenetic analysis in large scale between adult and childhood patients with acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1399-404
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A comparative cytogenetic analysis in large scale between adult and childhood patients with acute lymphoblastic leukemia].
  • This study was purposed to comparatively analyze the cytogenetic characteristics between 566 cases of adult acute lymphoblastic leukemia (aALL) and 586 cases of childhood acute lymphoblastic leukemia (cALL).
  • The result showed that the difference of chromosome abnormality between cALL and aALL was statistically significant.
  • The percentage of abnormal karyotypes in aALL was 62.0%, including mainly t(9;22)(q34;q11), hypodiploidy, hyperdiploidy (47 - 50), abn(6q), abn(9p) and -7, most of which conferring an unfavorable prognosis.
  • The percentage of abnormal karyotypes in cALL was 39.2%, composed mainly of high hyperdiploidy, hypodiploidy, TEL/AML1(+), +8, hyperdiploidy (47 - 50) and +21, etc, most of which conferring a favorable prognosis.
  • The incidences of abnormal karyotypes, total hypodiploidy, total hyperdiploidy (47 - 50), t(9;22)(q34;q11), -7, abn(7q), abn(14q32) and +Ph in aALL were significantly higher than those of cALL (p < 0.05), whereas the incidences of normal karyotype (N), high hyperdiploidy, +8, +21*2 and TEL/AML1(+) in cALL were significantly higher than those of aALL (p < 0.05).
  • The significant difference of chromosome abnormality exists between aALL and cALL.

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  • (PMID = 20030914.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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24. 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.
  • Of 15 patients with B-lineage ALL, 11 (73.3%) had an ETV6-RUNX1 (previously TEL-AML1 and then ETV6-CBFA2) fusion.
  • Patients with near-triploidy or near-tetraploidy were more likely than those with high-hyperdiploidy (51-67 chromosomes) (n = 159) to be female (P = 0.05) and have T-lineage ALL (P = 0.02), L2 morphology (P < 0.0001), or the ETV6-RUNX1 fusion (P < 0.0001).
  • The 5-year event-free survival estimates (+/- SE) were 75% +/- 19% for patients with near-triploidy, 93% +/- 7% for those with near-tetraploidy, and 84% +/- 3% for those with high-hyperdiploidy.
  • Although near-triploidy and near-tetraploidy are biologically different from high-hyperdiploidy, the favorable outcomes of patients with any one of these abnormalities suggest that patients with B-lineage ALL and a DNA index >or= 1.16 can be included in the low-risk arm of treatment protocols.
  • [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


25. Milani L, Lundmark A, Kiialainen A, Nordlund J, Flaegstad T, Forestier E, Heyman M, Jonmundsson G, Kanerva J, Schmiegelow K, Söderhäll S, Gustafsson MG, Lönnerholm G, Syvänen AC: DNA methylation for subtype classification and prediction of treatment outcome in patients with childhood acute lymphoblastic leukemia. Blood; 2010 Feb 11;115(6):1214-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation for subtype classification and prediction of treatment outcome in patients with childhood acute lymphoblastic leukemia.
  • Despite improvements in the prognosis of childhood acute lymphoblastic leukemia (ALL), subgroups of patients would benefit from alternative treatment approaches.
  • It also stratified patients with high hyperdiploidy and t(12;21) ALL into 2 subgroups with different probability of relapse.
  • We also identified 20 individual genes with DNA methylation levels that predicted relapse of leukemia.
  • [MeSH-major] CpG Islands. DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


26. 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.
  • [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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27. Paulsson K, Mörse H, Fioretos T, Behrendtz M, Strömbeck B, Johansson B: Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2005 Oct;44(2):113-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy (>50 chromosomes) in childhood acute lymphoblastic leukemia (ALL) is characterized by nonrandom multiple trisomies and tetrasomies involving in particular chromosomes X, 4, 6, 8, 10, 14, 17, 18, and 21.
  • These data strongly suggest that hyperdiploidy in childhood ALL generally arises by a simultaneous gain of all additional chromosomes in a single abnormal mitosis.
  • [MeSH-major] Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15942938.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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28. Moorman AV, Chilton L, Wilkinson J, Ensor HM, Bown N, Proctor SJ: A population-based cytogenetic study of adults with acute lymphoblastic leukemia. Blood; 2010 Jan 14;115(2):206-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A population-based cytogenetic study of adults with acute lymphoblastic leukemia.
  • Chromosomal abnormalities are increasingly used to risk stratify adults with acute lymphoblastic leukemia.
  • High hyperdiploidy occurred in 13% of patients younger than 20 years of age but in only 5% of older patients.
  • These population-based results demonstrate the cytogenetic heterogeneity of adult acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Translocation, Genetic

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  • [CommentIn] Blood. 2010 Aug 12;116(6):1011; author reply 1012 [20705768.001]
  • [ErratumIn] Blood. 2010 Aug 12;116(6):1017
  • (PMID = 19897583.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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29. Strefford JC, van Delft FW, Robinson HM, Worley H, Yiannikouris O, Selzer R, Richmond T, Hann I, Bellotti T, Raghavan M, Young BD, Saha V, Harrison CJ: Complex genomic alterations and gene expression in acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21. Proc Natl Acad Sci U S A; 2006 May 23;103(21):8167-72
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  • [Title] Complex genomic alterations and gene expression in acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21.
  • We have previously identified a unique subtype of acute lymphoblastic leukemia (ALL) associated with a poor outcome and characterized by intrachromosomal amplification of chromosome 21 including the RUNX1 gene (iAMP21).
  • A unique subset of differentially expressed genes, outside the CRA and CRD, were identified when gene expression signatures of iAMP21 were compared to ALL samples with ETV6-RUNX1 fusion (n = 21) or high hyperdiploidy with additional chromosomes 21 (n = 23).
  • [MeSH-major] Chromosomes, Human, Pair 21. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16702559.001).
  • [ISSN] 0027-8424
  • [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 Kingdom / Cancer Research UK / / 14840; United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1472447
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30. Papaemmanuil E, Hosking FJ, Vijayakrishnan J, Price A, Olver B, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Tomlinson IP, Taylor M, Greaves M, Houlston RS: Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia. Nat Genet; 2009 Sep;41(9):1006-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia.
  • To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls.
  • The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy.
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 7. Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 19684604.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Bloodwise / / 13027; United Kingdom / Medical Research Council / / G0000934; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ EMS27409; NLM/ PMC4915548
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31. Paulsson K, Heidenblad M, Mörse H, Borg A, Fioretos T, Johansson B: Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia. Leukemia; 2006 Nov;20(11):2002-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy, characterized by non-random trisomies, is the largest cytogenetic subgroup in childhood acute lymphoblastic leukemia (ALL).
  • In conclusion, the array CGH analyses revealed putative leukemia-associated submicroscopic imbalances and rearrangements in 2/8 (25%) hyperdiploid ALLs.
  • [MeSH-major] Genomics / methods. In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic


32. Heerema NA, Raimondi SC, Anderson JR, Biegel J, Camitta BM, Cooley LD, Gaynon PS, Hirsch B, Magenis RE, McGavran L, Patil S, Pettenati MJ, Pullen J, Rao K, Roulston D, Schneider NR, Shuster JJ, Sanger W, Sutcliffe MJ, van Tuinen P, Watson MS, Carroll AJ: Specific extra chromosomes occur in a modal number dependent pattern in pediatric acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2007 Jul;46(7):684-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific extra chromosomes occur in a modal number dependent pattern in pediatric acute lymphoblastic leukemia.
  • Children with acute lymphoblastic leukemia (ALL) and high hyperdiploidy (>50 chromosomes) are considered to have a relatively good prognosis.
  • Karyotypes of 2,339 children with ALL and high hyperdiploidy at diagnosis showed a distinct nonrandom sequential pattern of gain for each chromosome as MN increased, with four groups of gain: chromosomes 21, X, 14, 6, 18, 4, 17, and 10 at MN 51-54; chromosomes 8, 5, 11, and 12 at MN 57-60; chromosomes 2, 3, 9,16, and 22 at MN 63-67; chromosomes 1, 7 13, 15, 19, and 20 at MN 68-79, and Y only at MN >or=80.
  • These results are consistent with different origins of high hyperdiploidy, near-trisomy, and near-tetrasomy.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17431878.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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33. Liang DC, Yang CP, Lin DT, Hung IJ, Lin KH, Chen JS, Hsiao CC, Chang TT, Peng CT, Lin MT, Chang TK, Jaing TH, Liu HC, Wang LY, Yeh TC, Jou ST, Lu MY, Cheng CN, Sheen JM, Chiou SS, Wu KH, Hung GY, Chen RL, Chen SH, Cheng SN, Chang YH, Chen BW, Ho WL, Wang JL, Lin ST, Hsieh YL, Wang SC, Chang HH, Yang YL, Huang FL, Chang CY, Chang WH, Lin KS: Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia. Leukemia; 2010 Feb;24(2):397-405
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  • [Title] Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia.
  • The long-term outcome of 1390 children with acute lymphoblastic leukemia (ALL), treated in two successive clinical trials (Taiwan Pediatric Oncology Group (TPOG)-ALL-97 and TPOG-ALL-2002) between 1997 and 2007, is reported.
  • High-risk B-lineage ALL, T-cell, CD10 negativity, t(9;22), infant, and higher leukocyte count were consistently adverse factors, whereas hyperdiploidy >50 was a consistently favorable factor.
  • Although long-term outcome in TPOG clinical trials is comparable with results being reported worldwide, the persistent strength of certain prognostic variables and the lower frequencies of favorable outcome predictors, such as ETV6-RUNX1 and hyperdiploidy >50, in Taiwanese children warrant renewed effort to cure a higher proportion of patients while preserving their quality of life.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


34. Al-Bahar S, Zámecníkova A, Pandita R: Frequency and type of chromosomal abnormalities in childhood acute lymphoblastic leukemia patients in Kuwait: a six-year retrospective study. Med Princ Pract; 2010;19(3):176-81
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  • [Title] Frequency and type of chromosomal abnormalities in childhood acute lymphoblastic leukemia patients in Kuwait: a six-year retrospective study.
  • OBJECTIVE: To characterize the frequency of genetic profiles in pediatric acute lymphoblastic leukemia (ALL) patients in Kuwait.
  • RESULTS: Recurring aberrations, observed in 123 (75%) patients, included hyperdiploidy (n=68, 41%), tetraploidy (n=12, 7.3%), hypodiploidy (n=2, 1.2%), TEL-AML1 fusion (n=11, 7%), mixed-lineage leukemia rearrangement (n=6, 3.6%), t(9;22) (n=4, 2.4%), t(1;19) (n=3, 1.8%), t(8;14) or t(8;22) (n=2, 1.2%), +21 (n=2, 1.2%), del(6) (n=2, 1.2%) and miscellaneous abnormalities (n=9, 5%).
  • The highest observed numerical chromosome abnormality was high hyperdiploidy in 89 patients (54%) with abnormal karyotype while the TEL-AML fusion was the highest observed structural abnormality.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20357498.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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35. Appel IM, Kazemier KM, Boos J, Lanvers C, Huijmans J, Veerman AJ, van Wering E, den Boer ML, Pieters R: Pharmacokinetic, pharmacodynamic and intracellular effects of PEG-asparaginase in newly diagnosed childhood acute lymphoblastic leukemia: results from a single agent window study. Leukemia; 2008 Sep;22(9):1665-79
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  • [Title] Pharmacokinetic, pharmacodynamic and intracellular effects of PEG-asparaginase in newly diagnosed childhood acute lymphoblastic leukemia: results from a single agent window study.
  • L-asparaginase is an effective drug for treatment of children with acute lymphoblastic leukemia (ALL).
  • The in vivo window response was significantly related to immunophenotype and genotype: 26/38 common/pre B-ALL cases, especially those with hyperdiploidy and TELAML1 rearrangement, demonstrated a good clinical response compared to 8/17 T-ALL (P=0.01) and BCRABL-positive ALL (P=0.04).
  • [MeSH-major] Asparaginase / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18580955.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids; 30IQX730WE / Polyethylene Glycols; EC 3.5.1.1 / Asparaginase
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36. Mancini M, Scappaticci D, Cimino G, Nanni M, Derme V, Elia L, Tafuri A, Vignetti M, Vitale A, Cuneo A, Castoldi G, Saglio G, Pane F, Mecucci C, Camera A, Specchia G, Tedeschi A, Di Raimondo F, Fioritoni G, Fabbiano F, Marmont F, Ferrara F, Cascavilla N, Todeschini G, Nobile F, Kropp MG, Leoni P, Tabilio A, Luppi M, Annino L, Mandelli F, Foà R: A comprehensive genetic classification of adult acute lymphoblastic leukemia (ALL): analysis of the GIMEMA 0496 protocol. Blood; 2005 May 1;105(9):3434-41
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  • [Title] A comprehensive genetic classification of adult acute lymphoblastic leukemia (ALL): analysis of the GIMEMA 0496 protocol.
  • The Gruppo Italiano Malattie Ematologiche dell'Adulto (GIMEMA) 0496 protocol, through the central handling of bone marrow samples at presentation, allowed us to combine cytogenetic and molecular information on a large series of adults with acute lymphoblastic leukemia (ALL) treated homogeneously, enabling us to define as broadly as possible their genetic profile and to determine the impact on outcome of the cytogenetic-molecular signature.
  • The t(9;22)/BCR-ABL, t(4;11)/MLL-AF4, t(1; 19)/E2A-PBX1 defined a group with dismal prognosis (median DFS, 7 months), whereas 6q deletions, miscellaneous aberrations, and hyperdiploidy predicted an intermediate prognosis (median DFS, 19 months).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15650057.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
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37. Nachman J: Clinical characteristics, biologic features and outcome for young adult patients with acute lymphoblastic leukaemia. Br J Haematol; 2005 Jul;130(2):166-73
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  • [Title] Clinical characteristics, biologic features and outcome for young adult patients with acute lymphoblastic leukaemia.
  • Young adult patients with acute lymphoblastic leukaemia (ALL) represent a unique epidemiologic subgroup in that therapy may be provided by either adult or paediatric oncologists.
  • 21) hyperdiploidy, a slightly increased incidence of the t(9;22), and an increased frequency of T cell immunophenotype.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16029445.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 29
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38. Sulong S, Moorman AV, Irving JA, Strefford JC, Konn ZJ, Case MC, Minto L, Barber KE, Parker H, Wright SL, Stewart AR, Bailey S, Bown NP, Hall AG, Harrison CJ: A comprehensive analysis of the CDKN2A gene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups. Blood; 2009 Jan 1;113(1):100-7
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  • [Title] A comprehensive analysis of the CDKN2A gene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups.
  • We assessed the principal mode of inactivation in childhood acute lymphoblastic leukemia (ALL) and frequency in biologically relevant subgroups.
  • Patients with high hyperdiploidy, ETV6-RUNX1, or 11q23/MLL rearrangements had low rates of deletion (11%, 15%, 13%), whereas patients with t(9;22), t(1;19), TLX3, or TLX1 rearrangements had higher frequencies (61%, 42%, 78%, and 89%).
  • In conclusion, CDKN2A deletion is a significant secondary abnormality in childhood ALL strongly correlated with phenotype and genotype.
  • [MeSH-major] Gene Deletion. Gene Dosage. Gene Expression Regulation, Leukemic. Genes, p16. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


39. Moorman AV, Ensor HM, Richards SM, Chilton L, Schwab C, Kinsey SE, Vora A, Mitchell CD, Harrison CJ: Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial. Lancet Oncol; 2010 May;11(5):429-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial.
  • BACKGROUND: Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease markers and indicators of outcomes.
  • METHODS: We analysed cytogenetic data from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medical Research Council ALL97/99 study and followed up for a median time of 8.2 years.
  • FINDINGS: Two chromosomal abnormalities were associated with a significantly better outcome (ETV6-RUNX1, hazard ratio [HR] 0.51, 95% CI 0.38-0.70 and high hyperdiploidy, 0.60, 0.47-0.78), whereas five abnormalities were associated with an increased risk of relapse (intrachromosomal amplification of chromosome 21 [iAMP21], 6.04, 3.90-9.35; t(9;22), 3.55, 2.21-5.72; MLL translocations, 2.98, 1.71-5.20; abnormal 17p, 2.09, 1.30-3.37; and loss of 13q, 1.87, 1.09-3.20).
  • Multivariate analysis incorporating age, white-cell count, and treatment parameters showed that six cytogenetic abnormalities (ETV6-RUNX1, high hyperdiploidy, iAMP21, t(9;22), loss of 13q, and abnormal 17p) retained their significance for effect on relapse risk.
  • FUNDING: Leukaemia and Lymphoma Research (LLR).
  • [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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40. Piloto O, Nguyen B, Huso D, Kim KT, Li Y, Witte L, Hicklin DJ, Brown P, Small D: IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples. Cancer Res; 2006 May 1;66(9):4843-51
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  • [Title] IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples.
  • The class III receptor tyrosine kinase FLT3 is expressed on the blasts of >90% of patients with B-lineage acute lymphoblastic leukemias (ALL).
  • In addition, it is expressed at extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy and is sometimes mutated in these same patients.
  • Through antibody-dependent, cell-mediated cytotoxicity, such an antibody could still prove efficacious against leukemia cells in vivo.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / immunology

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  • (PMID = 16651440.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCRR NIH HHS / RR / RR00171
  • [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 / Antibodies, Monoclonal; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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41. Yang YL, Lin SR, Chen JS, Hsiao CC, Lin KH, Sheen JM, Cheng CN, Wu KH, Lin SW, Yu SL, Chen HY, Lu MY, Chang HH, Yen CT, Lin JF, Su YH, Li YP, Lin CY, Jou ST, Lin DT: Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Nov;32(8):e323-30
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  • [Title] Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia.
  • BACKGROUND: The classification of B-lineage acute lymphoblastic leukemia (ALL) by specific chromosomal translocations has prognostic implications for risk-directed therapy.
  • Patients with t(12;21)/ETV6-RUNX1 fusion, hyperdiploidy, and t(1;19)/TCF-PBX1 fusion had the most favorable outcomes, whereas those with the t(9;22)/BCR-ABL1 fusion or t(4;11) and other MLL gene rearrangement had poor prognosis (P<0.001 for EFS and OS).
  • CONCLUSIONS: The biological factors of leukemia cells are associated with treatment outcomes in childhood ALL.
  • [MeSH-major] Genetic Testing / methods. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Cell Lineage / genetics. Child. Child, Preschool. Chimera. Core Binding Factor Alpha 2 Subunit. Female. Fusion Proteins, bcr-abl / genetics. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction / methods. Prognosis. Risk Factors. Sensitivity and Specificity. Taiwan / epidemiology

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  • (PMID = 20930648.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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42. Sutcliffe MJ, Shuster JJ, Sather HN, Camitta BM, Pullen J, Schultz KR, Borowitz MJ, Gaynon PS, Carroll AJ, Heerema NA: High concordance from independent studies by the Children's Cancer Group (CCG) and Pediatric Oncology Group (POG) associating favorable prognosis with combined trisomies 4, 10, and 17 in children with NCI Standard-Risk B-precursor Acute Lymphoblastic Leukemia: a Children's Oncology Group (COG) initiative. Leukemia; 2005 May;19(5):734-40
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  • [Title] High concordance from independent studies by the Children's Cancer Group (CCG) and Pediatric Oncology Group (POG) associating favorable prognosis with combined trisomies 4, 10, and 17 in children with NCI Standard-Risk B-precursor Acute Lymphoblastic Leukemia: a Children's Oncology Group (COG) initiative.
  • Chromosome aberrations have a major role in pediatric acute lymphoblastic leukemia (ALL) risk assignment.
  • POG analyses also demonstrated hyperdiploidy (> or =53 chromosomes) was less of an independently significant prognostic factor in the absence of these key trisomies.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 4 / genetics. Trisomy / genetics

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  • (PMID = 15789069.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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43. Blandin AT, Mühlematter D, Bougeon S, Gogniat C, Porter S, Beyer V, Parlier V, Beckmann JS, van Melle G, Jotterand M: Automated four-color interphase fluorescence in situ hybridization approach for the simultaneous detection of specific aneuploidies of diagnostic and prognostic significance in high hyperdiploid acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2008 Oct 15;186(2):69-77
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  • [Title] Automated four-color interphase fluorescence in situ hybridization approach for the simultaneous detection of specific aneuploidies of diagnostic and prognostic significance in high hyperdiploid acute lymphoblastic leukemia.
  • In high hyperdiploid acute lymphoblastic leukemia (ALL), the concurrence of specific trisomies confers a more favorable outcome than hyperdiploidy alone.
  • [MeSH-major] Aneuploidy. In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18940469.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Gmidène A, Sennana H, Elghezal H, Ziraoui S, Youssef YB, Elloumi M, Issaoui L, Harrabi I, Raynaud S, Saad A: Cytogenetic analysis of 298 newly diagnosed cases of acute lymphoblastic leukaemia in Tunisia. Hematol Oncol; 2008 Jun;26(2):91-7
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  • [Title] Cytogenetic analysis of 298 newly diagnosed cases of acute lymphoblastic leukaemia in Tunisia.
  • Genetic changes associated with Acute Lymphoblastic Leukaemia (ALL) provide diagnostic and prognostic information with a direct impact on patient management.
  • Some chromosomal abnormalities especially hyperdiploidy, 19p13 abnormalities, 8q24 translocations, 12p, 6q deletions and TCR rearrangements occur at a lower incidence compared to that reported in other populations.
  • [MeSH-major] Chromosomes / ultrastructure. Cytogenetics / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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  • (PMID = 18271061.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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45. Harrison CJ, Haas O, Harbott J, Biondi A, Stanulla M, Trka J, Izraeli S, Biology and Diagnosis Committee of International Berlin-Frankfürt-Münster study group: Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group. Br J Haematol; 2010 Oct;151(2):132-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group.
  • Treatment of childhood acute lymphoblastic leukaemia (ALL) has improved considerably in recent years.
  • Here we review the current diagnostic criteria of genetic abnormalities in precursor B-ALL (BCP-ALL), including the relevant technical approaches and the application of the most appropriate methods for the detection of each abnormality.
  • The abnormalities with the most significant impact for treatment and management of BCP-ALL are t(9;22)(q34;q11)/BCR-ABL1, t(4;11)(q21;q23)/MLL-AFF1 and near-haploidy/low hypodiploidy for high risk stratification and, to a lesser extent, t(12;21)(p13;q22)/ETV6-RUNX1 and high hyperdiploidy for good risk management.
  • [MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20701601.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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46. Manabe A, Ohara A, Hasegawa D, Koh K, Saito T, Kiyokawa N, Kikuchi A, Takahashi H, Ikuta K, Hayashi Y, Hanada R, Tsuchida M, Tokyo Children's Cancer Study Group: Significance of the complete clearance of peripheral blasts after 7 days of prednisolone treatment in children with acute lymphoblastic leukemia: the Tokyo Children's Cancer Study Group Study L99-15. Haematologica; 2008 Aug;93(8):1155-60
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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 the complete clearance of peripheral blasts after 7 days of prednisolone treatment in children with acute lymphoblastic leukemia: the Tokyo Children's Cancer Study Group Study L99-15.
  • BACKGROUND: Treatment response has become one of the most important prognostic factors in childhood acute lymphoblastic leukemia.
  • We evaluated the significance of the complete clearance of peripheral leukemic blasts on survival in children with acute lymphoblastic leukemia.
  • DESIGN AND METHODS: Seven hundred and fifty-four children diagnosed with acute lymphoblastic leukemia, consecutively enrolled from 1999 to 2003 in the TCCSG L99-15 study, were eligible for analysis.
  • The event-free survival for Day8NoBlasts patients with B-lineage acute lymphoblastic leukemia and T-cell acute lymphoblastic leukemia was 89.8+/-2.1% (n=226) and 95.7+/-4.3% (n=23), respectively.
  • In a multivariate analysis, age at diagnosis, the initial white blood cell count, immunophenotype, and gender did not remain as independent risk factors for treatment failure, whereas Day8NoBlasts and marked hyperdiploidy (more than 50 chromosomes) became statistically significant.
  • CONCLUSIONS: Children with Day8NoBlasts constituted one third of all the cases with childhood acute lymphoblastic leukemia with an excellent outcome, and should be candidates for curative management with less intensive treatment.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Blast Crisis / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisolone / therapeutic use

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  • [CommentIn] Haematologica. 2008 Aug;93(8):1124-8 [18669975.001]
  • (PMID = 18519521.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9PHQ9Y1OLM / Prednisolone
  • [Investigator] Isoyama K; Kinoshita A; Kamijo T; Kumagai MA; Yabe H; Morimoto T; Maeda M; Sugita K; Noguchi Y; Kaneko T; Sugita K; Sotomatsu M; Kajiwara M; Okimoto Y; Ohta S; Saito M; Fukushima T
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47. Gaikwad A, Rye CL, Devidas M, Heerema NA, Carroll AJ, Izraeli S, Plon SE, Basso G, Pession A, Rabin KR: Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia. Br J Haematol; 2009 Mar;144(6):930-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia.
  • Recurrent, prognostically significant chromosomal abnormalities occur in approximately 75% of paediatric acute lymphoblastic leukaemia (ALL), but only infrequently in children with Down syndrome (DS) and ALL.
  • Mutations were overrepresented in males (P < 0.03), occurred once in association with high hyperdiploidy and were not significantly correlated with age, initial white blood count, or event-free survival.

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  • [Cites] Blood. 2007 Mar 1;109(5):2202-4 [17068151.001]
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  • (PMID = 19120350.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / K12 CA090433-06; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ NIHMS127709; NLM/ PMC2724897
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48. Hamouda F, El-Sissy AH, Radwan AK, Hussein H, Gadallah FH, Al-Sharkawy N, Sedhom E, Ebeid E, Salem SI: Correlation of karyotype and immunophenotype in childhood acute lymphoblastic leukemia; experience at the National Cancer Institute, Cairo University, Egypt. J Egypt Natl Canc Inst; 2007 Jun;19(2):87-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of karyotype and immunophenotype in childhood acute lymphoblastic leukemia; experience at the National Cancer Institute, Cairo University, Egypt.
  • Hyperdiploidy was found in 31.5% of CALLA positive early pre B cases and was associated with favorable prognostic features and DFS of 66.6% at 12 months.
  • Hyperdiploidy of >50 chromosome represented 62.5% of hyperdipoid cases, 80% of them were CALLA positive early pre B ALL carrying good risk features.
  • CONCLUSION: CALLA early pre B phenotype has a positive impact on chromosomal pattern having best outcome among patients with hyperdiploidy.
  • [MeSH-major] Antigens, Neoplasm / analysis. Immunophenotyping / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19034338.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
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49. Hamerschlak N: Leukemia: genetics and prognostic factors. J Pediatr (Rio J); 2008 Aug;84(4 Suppl):S52-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia: genetics and prognostic factors.
  • OBJECTIVE: To present the implications of genetics, particularly of cytogenetic techniques, for the diagnosis and prognosis of leukemia.
  • Nowel and David Hungerford of the 9:22 translocation (the Philadelphia chromosome), genetics has come to play an important role in hematology, in this case making it possible to diagnose chronic myeloid leukemia and opening doors to research avenues for the whole field of oncology.
  • One point of great interest refers to the implications of these findings for the prognosis of a range of types of leukemia.
  • In acute myeloid leukemia, the karyotype is of fundamental importance to postremission treatment decisions, and molecular factors determine the treatment of individuals with normal karyotypes.
  • In chronic myeloid leukemia, clonal evolution is associated with progression to the blast crisis.
  • Finally, in acute lymphoblastic leukemia, factors such as hyperdiploidy and t 12:21 are associated with good prognosis, whereas carriers of t 4:11 and t 9:22 are considered high risk patients.
  • CONCLUSIONS: Genetics has come to stay as far as hematology and, in particular, the management of leukemia and its prognostic factors are concerned.
  • [MeSH-major] Cytogenetic Analysis. Leukemia / genetics
  • [MeSH-minor] Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis

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  • (PMID = 18830516.001).
  • [ISSN] 1678-4782
  • [Journal-full-title] Jornal de pediatria
  • [ISO-abbreviation] J Pediatr (Rio J)
  • [Language] eng; por
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 30
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50. Lo KC, Chalker J, Strehl S, Neat M, Smith O, Dastugue N, Kearney L, Izraeli S, Kempski H, Cowell JK: Array comparative genome hybridization analysis of acute lymphoblastic leukaemia and acute megakaryoblastic leukaemia in patients with Down syndrome. Br J Haematol; 2008 Sep;142(6):934-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array comparative genome hybridization analysis of acute lymphoblastic leukaemia and acute megakaryoblastic leukaemia in patients with Down syndrome.
  • Twenty-five cases of B-cell precursor acute lymphoblastic leukaemia (ALL) from Down syndrome (DS) patients were analyzed using array comparative genomic hybridization (aCGH) and compared with two other subgroups of non-DS patients with ALL; five cases with high-hyperdiploidy (HH) and nine cases with ETV6-RUNX1 positive clones.
  • Seven cases of DS-acute megakaryoblastic leukaemia (AMKL) were also included, DS-ALL cases showed relatively stable karyotypes with cryptic losses and gains that most frequently involved chromosomes X, 1, 2, 9, 11, 16, and 17.
  • [MeSH-major] Chromosome Aberrations. Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentIn] Br J Haematol. 2009 Jun;146(1):113-5 [19344409.001]
  • (PMID = 18557744.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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51. Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B: Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study. Blood; 2008 Feb 1;111(3):1575-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
  • Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


52. Rachieru-Sourisseau P, Baranger L, Dastugue N, Robert A, Geneviève F, Kuhlein E, Chassevent A: DNA Index in childhood acute lymphoblastic leukaemia: a karyotypic method to validate the flow cytometric measurement. Int J Lab Hematol; 2010 Jun;32(3):288-98

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA Index in childhood acute lymphoblastic leukaemia: a karyotypic method to validate the flow cytometric measurement.
  • The DNA index (DI) is a prognostic factor in childhood acute lymphoblastic leukemia (ALL).
  • The accuracy of DI measurement is important for treatment stratification: hyperdiploidy with DI > or = 1.16 is predictive of favorable prognosis whereas hypodiploidy is associated with poor prognosis.
  • [MeSH-major] DNA / analysis. Flow Cytometry / methods. Karyotyping / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19793113.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 9007-49-2 / DNA
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53. Greaves M: Darwin and evolutionary tales in leukemia. The Ham-Wasserman Lecture. Hematology Am Soc Hematol Educ Program; 2009;:3-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Darwin and evolutionary tales in leukemia. The Ham-Wasserman Lecture.
  • The evolutionary, natural history of childhood acute lymphoblastic leukemia (ALL) is almost entirely covert, clinically silent and well advanced by the point of diagnosis.
  • (ii) archived neonatal blood spots or Guthrie cards from individuals who later developed leukemia; and (iii) stored, viable cord blood cells.
  • These studies indicate prenatal initiation of leukemia by chromosome translocation and gene fusion (or hyperdiploidy) and the post-natal acquisition of multiple, gene copy number alterations (CNAs), mostly deletions.

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  • (PMID = 20008176.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Lectures; 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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54. Kawamata N, Ogawa S, Zimmermann M, Kato M, Sanada M, Hemminki K, Yamatomo G, Nannya Y, Koehler R, Flohr T, Miller CW, Harbott J, Ludwig WD, Stanulla M, Schrappe M, Bartram CR, Koeffler HP: Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray. Blood; 2008 Jan 15;111(2):776-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray.
  • Pediatric acute lymphoblastic leukemia (ALL) is a malignant disease resulting from accumulation of genetic alterations.
  • Three common genetic alterations were found: deletion of ETV6, deletion of p16INK4A, and hyperdiploidy, as well as a number of novel recurrent genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 17890455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2200831
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55. Moorman AV, Harrison CJ, Buck GA, Richards SM, Secker-Walker LM, Martineau M, Vance GH, Cherry AM, Higgins RR, Fielding AK, Foroni L, Paietta E, Tallman MS, Litzow MR, Wiernik PH, Rowe JM, Goldstone AH, Dewald GW, Adult Leukaemia Working Party, Medical Research Council/National Cancer Research Institute: Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial. Blood; 2007 Apr 15;109(8):3189-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial.
  • However, its usefulness in adult acute lymphoblastic leukemia (ALL) is generally limited to the presence of the Philadelphia (Ph) chromosome because of the low incidence of other recurrent abnormalities.
  • In contrast, patients with high hyperdiploidy or a del(9p) had a significantly improved outcome.
  • [MeSH-major] Chromosome Deletion. Philadelphia Chromosome. Ploidies. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17170120.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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56. Kuchinskaya E, Heyman M, Nordgren A, Schoumans J, Staaf J, Borg A, Söderhäll S, Grandér D, Nordenskjöld M, Blennow E: Array-CGH reveals hidden gene dose changes in children with acute lymphoblastic leukaemia and a normal or failed karyotype by G-banding. Br J Haematol; 2008 Mar;140(5):572-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array-CGH reveals hidden gene dose changes in children with acute lymphoblastic leukaemia and a normal or failed karyotype by G-banding.
  • A tiling path 33K BAC array was used to study 28 children with acute lymphoblastic leukaemia (ALL) who had normal or failed G-banded karyotypes.
  • Molecular cytogenetic and array comparative genomic hybridization results enabled the division of B-precursor ALL patients into five groups: high hyperdiploidy, intrachromosomal amplification of 21q, ETV6/RUNX1 rearrangement, others and no CNA.
  • [MeSH-major] Chromosome Aberrations. Gene Dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18275435.001).
  • [ISSN] 1365-2141
  • [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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57. 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.
  • Cytogenetic analysis revealed hyperdiploidy (n=6), del(7) in two cases and del(11)(q23) in seven cases.
  • [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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58. Chang HH, Lu MY, Jou ST, Lin KH, Tien HF, Lin DT: Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience. Pediatr Hematol Oncol; 2006 Sep;23(6):495-506
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience.
  • Analysis of ploidy revealed 16 (20.5%) patients with normal diploidy, 28 (35.9%) with pseudodiploidy, 6 (7.7%) with hyperdiploidy (47-50), 19 (24.4%) with hyperdiploidy (> 50), and 9 (9.4%) hypodiploidy.
  • [MeSH-major] Chromosome Aberrations / statistics & numerical data. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16849281.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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59. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • In Cox multivariate analysis, longer duration of oral 6-mercaptopurine (6MP)/methotrexate (MTX) maintenance therapy (P = .02; longest for standard-risk patients) and presence of high hyperdiploidy (P = .07) were related to increased risk of SMN.

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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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60. Krishnan S, Wade R, Moorman AV, Mitchell C, Kinsey SE, Eden TO, Parker C, Vora A, Richards S, Saha V: Temporal changes in the incidence and pattern of central nervous system relapses in children with acute lymphoblastic leukaemia treated on four consecutive Medical Research Council trials, 1985-2001. Leukemia; 2010 Feb;24(2):450-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temporal changes in the incidence and pattern of central nervous system relapses in children with acute lymphoblastic leukaemia treated on four consecutive Medical Research Council trials, 1985-2001.
  • Despite the success of contemporary treatment protocols in childhood acute lymphoblastic leukaemia (ALL), relapse within the central nervous system (CNS) remains a challenge.
  • In ETV6-RUNX1 ALL, relapse patterns mirrored overall trends whereas in high hyperdiploidy (HH) ALL, these seem to have plateaued over the latter two trial periods.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / epidemiology. Neoplasm Recurrence, Local / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 20016529.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United Kingdom / Cancer Research UK / / A7923; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / G0300130; United Kingdom / Cancer Research UK / / ; United Kingdom / Cancer Research UK / / A6791; United Kingdom / Cancer Research UK / / 14840
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2820451; NLM/ UKMS28095
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61. Gindina TL, Mamaev NN, Zubaĭdullina SR, Kondakova EV: [Acute lymphoblastic leukemias with translocations (1;19)(q23;p13): a description of 3 new cases and a review of the literature]. Ter Arkh; 2010;82(11):63-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute lymphoblastic leukemias with translocations (1;19)(q23;p13): a description of 3 new cases and a review of the literature].
  • AIM: To discuss the specific features of the cytogenetics and clinical manifestations of acute lymphoblastic leukemias (ALL) with balanced and unbalanced translocations (1;19)(q23; p13).
  • It is commonly concurrent with other karyotypic changes, namely, 6q deletion, 1q trisomy, and high hyperdiploidy.
  • [MeSH-major] Chromosomes, Human, Pair 1 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 21381353.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
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62. Mori T, Nishimura N, Hasegawa D, Kawasaki K, Kosaka Y, Uchide K, Yanai T, Hayakawa A, Takeshima Y, Nishio H, Matsuo M: Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia. Leuk Res; 2010 Oct;34(10):1398-401

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia.
  • Most chromosomal rearrangements including the mixed lineage leukemia (MLL) gene are manifested as leukemia and predict a poor prognosis.
  • Here we report a case of a 3-year old boy bearing a novel MLL-rearrangement with the suppressor of actin mutations 1-like (SACM1L) gene in the absence of leukemia.
  • Bone marrow cells harboring the MLL-SACM1L rearrangement appeared during chemotherapy for acute lymphoblastic leukemia with hyperdiploidy and were continuously detected over 7 years without clonal expansion.
  • [MeSH-major] Gene Rearrangement. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20553989.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Membrane Proteins; 0 / SACM1L protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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63. Guo Y, Chen YM, Zou Y, Chen XJ, Zhang L, Wang SC, Zhu XF: [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Oct;11(10):793-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study].
  • OBJECTIVE: To investigate the biologic features of childhood acute leukemia in the northern region of China through a small cohort study in a single center.
  • METHODS: The medical records of 688 children with acute leukemia (age< or =15 years) who were initially diagnosed at Blood Disease Hospital of Chinese Academy of Medical Sciences from October 2003 to June 2006 were retrospectively studied.
  • RESULTS: Four hundred children were diagnosed as acute lymphoblastic leukemia (ALL), with a peak incidence at ages of 1-4 years.
  • In the 154 patients with cytogenetic data, high hyperdiploidy was presented in 13.0% of patients, low hyperdiploidy in 3.9%, pseudodiploidy in 5.2%, and hypodiploidy in 5.8%.
  • E2A-PBX1 fusion gene was expressed in 3.9% of children with B-cell ALL.
  • Two hundred and twenty-two children were diagnosed as acute myeloid leukemia (AML), with a peak incidence at ages of 10-15 years.
  • Acute hybrid leukemia (AHL) was confirmed in 24 children (4.2%), with a median age of 9 years.
  • CONCLUSIONS: There are differences in the biologic features of childhood acute leukemia between the northern region of China and other regions and races, which suggests that there might be differences in the pathogenesis of childhood acute leukemia in different environmental exposures.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19849934.001).
  • [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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64. Kim SR, Kim HJ, Kim SH: [Clinical utility of fluorescence in-situ hybridization profile test in detecting genetic aberrations in acute leukemia]. Korean J Lab Med; 2009 Oct;29(5):371-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical utility of fluorescence in-situ hybridization profile test in detecting genetic aberrations in acute leukemia].
  • BACKGROUND: Cytogenetic abnormalities are one of the most reliable prognostic factors in acute leukemia.
  • The objective of this study was to investigate the utility of FISH profile analyses in the initial diagnosis of acute leukemia.
  • METHODS: Two hundred and forty one de novo acute leukemia patients diagnosed from January, 2002 to November, 2007 were included.
  • For acute lymphoblastic leukemia profile test, FISH probes for BCR/ABL, TEL/AML1, MLL gene rearrangement and CDKN2A deletion were used.
  • For acute myeloid leukemia profile test, probes for AML1/ETO, MLL and CBFbeta gene rearrangement were used.
  • Among these 51 cases, TEL/AML1 abnormalities were detected in 44.3%, followed by the abnormal CDKN2A signal (24.6%) and hyperdiploidy (18.0%).
  • CONCLUSIONS: FISH analysis as a profile test detected additional genetic aberrations in a significant proportion of acute leukemia, and was effective especially in detecting cryptic translocations, submicroscopic deletions and complex karyotypes.
  • Our study supports the need to incorporate FISH profile test at initial work up in acute leukemia.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor beta Subunit / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Proto-Oncogene Proteins c-bcr / genetics

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  • (PMID = 19893343.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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65. 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).
  • We were thus able to define amplification of AML1 as a new recurrent abnormality in ALL, associated with a poor prognosis.
  • Amplification involving the ABL gene, a rare recurrent abnormality confined to T ALL patients, was identified for the first time.
  • The use of centromeric probes revealed significant hidden high hyperdiploidy of 33% and 59%, respectively, in patients with normal (n = 21/64) or failed (n = 32/54) cytogenetic results.
  • The iFISH contributed significantly to the high success rate of 91% (n = 2114/2323) and the remarkable abnormality detection rate of 89% (n = 1879/2114).
  • [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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66. Menendez P, Catalina P, Rodríguez R, Melen GJ, Bueno C, Arriero M, García-Sánchez F, Lassaletta A, García-Sanz R, García-Castro J: Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene. J Exp Med; 2009 Dec 21;206(13):3131-41
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  • [Title] Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene.
  • MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero.
  • Fusion genes were absent in BM-MSCs of childhood leukemias carrying TEL-AML1, BCR-ABL, AML1-ETO, MLL-AF9, MLL-AF10, MLL-ENL or hyperdiploidy.
  • The absence of monoclonal rearrangements in MLL-AF4(+) BM-MSCs precludes the possibility of cellular plasticity or de-differentiation of B-ALL blasts and suggests that MLL-AF4 might arise in a population of prehematopoietic precursors.
  • [MeSH-major] Mesenchymal Stromal Cells / metabolism. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19995953.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2806455
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67. Chang P, Kang M, Xiao A, Chang J, Feusner J, Buffler P, Wiemels J: FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia. BMC Cancer; 2010 Sep 27;10:513
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  • [Title] FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia.
  • BACKGROUND: Mutations in FLT3 result in activated tyrosine kinase activity, cell growth stimulation, and a poor prognosis among various subtypes of leukemia.
  • We evaluated the prevalence and timing of origin of FLT3 mutations in a population series of childhood leukemia patients from Northern California.
  • METHODS: We screened and sequenced FLT3 mutations (point mutations and internal tandem duplications, ITDs) among 517 childhood leukemia patients, and assessed whether these mutations occurred before or after birth using sensitive "backtracking" methods.
  • Among AMLs, FLT3 mutations were more common in older patients, and among ALLs, FLT3 mutations were more common in patients with high hyperdiploidy (3.7%) than those without this cytogenetic feature (1.4%).

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  • (PMID = 20875128.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NIEHS NIH HHS / ES / P42ES0470; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / R01CA89032; United States / NIEHS NIH HHS / ES / R01ES09137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2955609
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68. Andersson A, Olofsson T, Lindgren D, Nilsson B, Ritz C, Edén P, Lassen C, Råde J, Fontes M, Mörse H, Heldrup J, Behrendtz M, Mitelman F, Höglund M, Johansson B, Fioretos T: Molecular signatures in childhood acute leukemia and their correlations to expression patterns in normal hematopoietic subpopulations. Proc Natl Acad Sci U S A; 2005 Dec 27;102(52):19069-74
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  • [Title] Molecular signatures in childhood acute leukemia and their correlations to expression patterns in normal hematopoietic subpopulations.
  • Global expression profiles of a consecutive series of 121 childhood acute leukemias (87 B lineage acute lymphoblastic leukemias, 11 T cell acute lymphoblastic leukemias, and 23 acute myeloid leukemias), six normal bone marrows, and 10 normal hematopoietic subpopulations of different lineages and maturations were ascertained by using 27K cDNA microarrays.
  • Unsupervised analyses revealed segregation according to lineages and primary genetic changes, i.e., TCF3(E2A)/PBX1, IGH@/MYC, ETV6(TEL)/RUNX1(AML1), 11q23/MLL, and hyperdiploidy (>50 chromosomes).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / genetics
  • [MeSH-minor] Bone Marrow / metabolism. Bone Marrow Cells / cytology. Cell Line. Cell Lineage. Chromosome Aberrations. Cluster Analysis. DNA, Complementary / metabolism. Gene Expression Regulation. Genes, Neoplasm. Hematopoiesis. Hematopoietic Stem Cells / cytology. Hematopoietic System / metabolism. Humans. Leukemia, Myeloid, Acute / genetics. Models, Genetic. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Ploidies. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Principal Component Analysis. Transcription Factors / chemistry


69. Ahmad F, Dalvi R, Chavan D, Das BR, Mandava S: Cytogenetic profile of acute lymphocytic leukemia patients: report of a novel translocation t(4;13) (q21 x 3; q35) from an Indian population. Hematology; 2008 Feb;13(1):28-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic profile of acute lymphocytic leukemia patients: report of a novel translocation t(4;13) (q21 x 3; q35) from an Indian population.
  • Acute lymphocytic leukemia (ALL) is a malignant neoplasm characterized by clonal proliferation, decreased apoptosis and accumulation of immature lymphoid cells in the bone marrow as well as the peripheral blood.
  • Various other abnormalities were hyperdiploidy (20 x 68%), hypodiploidy (10 x 34%), t(8;14) (3 x 44%), t(9;22) (6 x 9%), t(4;16) (3 x 44%), t(7;10) (3 x 44%) and gain of chromosome 8, 13, 16, and 22 was seen in one case each (3 x 44%).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 4 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 18534063.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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70. Bassal M, La MK, Whitlock JA, Sather HN, Heerema NA, Gaynon PS, Stork LC: Lymphoblast biology and outcome among children with Down syndrome and ALL treated on CCG-1952. Pediatr Blood Cancer; 2005 Jan;44(1):21-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Patients with Down syndrome (DS) and standard risk (SR) acute lymphoblastic leukemia (ALL-DS) are reported to have inferior event free (EFS) and overall survival (OS) compared to patients without DS (ALL-NDS).
  • DS patients were less likely to have either favorable (hyperdiploidy, triple trisomy of chromosomes 4, 10, and 17, TEL-AML1 rearrangement) or unfavorable (T-cell ALL, hypodiploidy, adverse translocations) biologic features.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Down Syndrome / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368546.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
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71. Soszynska K, Mucha B, Debski R, Skonieczka K, Duszenko E, Koltan A, Wysocki M, Haus O: The application of conventional cytogenetics, FISH, and RT-PCR to detect genetic changes in 70 children with ALL. Ann Hematol; 2008 Dec;87(12):991-1002
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated bone marrow cells of 70 acute lymphoblastic leukemia children by conventional cytogenetics (CC), fluorescence in situ hybridization (FISH), and reverse transcription polymerase chain reaction (RT-PCR) methods.
  • Hyperdiploidy>50 chromosomes was present in nine cases, hyperdiploidy 47-50 chromosomes in six, pseudodiploidy in 15, and hypodiploidy in five.
  • The outcome was the best for the children with hyperdiploidy>50 chromosomes without structural changes.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Genes, abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18633615.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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72. 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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  • 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.
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • 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.
  • [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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73. Fronkova E, Mejstrikova E, Avigad S, Chik KW, Castillo L, Manor S, Reznickova L, Valova T, Zdrahalova K, Hrusak O, Jabali Y, Schrappe M, Conter V, Izraeli S, Li CK, Stark B, Stary J, Trka J: Minimal residual disease (MRD) analysis in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: is it possible to avoid MRD testing? Leukemia; 2008 May;22(5):989-97
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  • There were no significant associations with gender or hyperdiploidy in the study group, or with TEL/AML1 fusion within BCP-ALL.
  • [MeSH-major] Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 18305563.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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74. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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75. Brown A, Niggli F, Hengartner H, Caflisch U, Nobile L, Kuhne T, Angst R, Bourquin JP, Betts D: Characterization of high-hyperdiploidy in childhood acute lymphoblastic leukemia with gain of a single chromosome 21. Leuk Lymphoma; 2007 Dec;48(12):2457-60
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  • [Title] Characterization of high-hyperdiploidy in childhood acute lymphoblastic leukemia with gain of a single chromosome 21.
  • [MeSH-major] Chromosomes, Human, Pair 21. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18067025.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
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