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

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  • (PMID = 19100367.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA036401-25; United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA21765; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA036401-25; United States / NCI NIH HHS / CA / R01 CA78224
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 120
  • [Other-IDs] NLM/ NIHMS89418; NLM/ PMC2665795
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7. Bhojwani D, Howard SC, Pui CH: High-risk childhood acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S222-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-risk childhood acute lymphoblastic leukemia.
  • Although most children with acute lymphoblastic leukemia (ALL) are cured, certain subsets have a high risk of relapse.
  • Infants with mixed-lineage leukemia (MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
  • Hybrid protocols incorporating drugs effective for acute myeloid leukemia could improve survival, a strategy being tested in international trials.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
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  • (PMID = 19778845.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS163517; NLM/ PMC2814411
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8. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • RESULTS: Hemoglobin levels at diagnosis were distributed in a non-random pattern.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • On the other hand, the inverse relationship between severity of anemia and survival found within specific subgroups suggests that very low hemoglobin levels at diagnosis are associated with more advanced disease in these subgroups.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome


9. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia. Indian J Pediatr; 2007 Mar;74(3):255-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • RESULTS: Cases aged 50.000/mm3 also showed better but non-significant remission rates.
  • Most of the present cases were L2 with better remission compared to other immunophenotypes.
  • CONCLUSION: Some cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17401264.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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10. Dunwell TL, Hesson LB, Pavlova T, Zabarovska V, Kashuba V, Catchpoole D, Chiaramonte R, Brini AT, Griffiths M, Maher ER, Zabarovsky E, Latif F: Epigenetic analysis of childhood acute lymphoblastic leukemia. Epigenetics; 2009 Apr 1;4(3):185-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic analysis of childhood acute lymphoblastic leukemia.
  • We used a chromosome 3 wide NotI microarray for identification of epigenetically inactivated genes in childhood acute lymphoblastic leukemia (ALL).
  • Three novel genes demonstrated frequent methylation in childhood ALL.
  • In our series of childhood ALL BNC1 was frequently methylated in both T (77%) and B-ALL (79%), whilst MSX1 showed T-ALL (25%) specific methylation.
  • The methylation of the above five genes was cancer specific and expression of the genes could be restored in methylated leukemia cell lines treated with 5-aza-2'-deoxycytidine.
  • This is the first report demonstrating frequent epigenetic inactivation of PPP2R3A, FBLN2, THRB, BNC1 and MSX1 in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


11. Jiang H, Gu LJ, Xue HL, Tang JY, Chen J, Pan C, Chen J, Xu C, Dong L, Zhou M: [Prognostic factors for childhood acute non-mature B-lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):290-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic factors for childhood acute non-mature B-lymphoblastic leukemia].
  • OBJECTIVE: To study the prognostic factors for events-free survival (EFS) in children with acute non-mature B-lymphoblastic leukemia.
  • METHODS: One hundred and sixty-one children with newly diagnosed acute non-mature B-lymphoblastic leukemia received the ALL-XH-99 protocol treatment.
  • Immunophenotype, myeloid-associated antigen and the risk grade of disease were also related to the EFS (P<0.05).
  • CONCLUSIONS: WBC >or=50 x 10(9)/L, Cmu positive, BCR/ABL or MLL/AF4 positive and MRD positive have important prognostic values in childhood acute non-mature B-lymphoblastic leukemia.
  • [MeSH-major] Burkitt Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Genes, abl. Humans. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm, Residual. Oncogene Proteins, Fusion / genetics. Prognosis. Regression Analysis


12. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • Non-classical cytogenetic aberrations in these 29 patients were mostly found on chromosomes 1, 2, 7, 9, 13, 14, and 17.
  • From 29 patients with non-classical cytogenetic aberrations, only 8 (28%) had been stratified to a high risk-arm on the first treatment protocol, suggesting that this subgroup might benefit from the identification of new prognostic markers in future studies.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


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

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  • (PMID = 19415723.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 195
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1
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4. Stanulla M, Schrappe M: Treatment of childhood acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):52-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood.
  • Studies in ALL have been a model for clinical and basic research beyond pediatric hemato-oncology.
  • As a result of sustained and well-organized research efforts since the early 1960s, childhood ALL now can be successfully treated in about 80% of patients by the application of intensive combination chemotherapy regimens, which in specific patient subgroups may need to be supplemented with radiation therapy and/or hematopoietic stem cell transplantation.
  • Thus, future research must extend our molecular understanding of leukemia and host factors in order to even more specifically identify the mechanisms underlying the differences in treatment response and outcome, and to finally address the therapeutic needs of the individual child.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19100368.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 101
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15. Nebral K, Denk D, Attarbaschi A, König M, Mann G, Haas OA, Strehl S: Incidence and diversity of PAX5 fusion genes in childhood acute lymphoblastic leukemia. Leukemia; 2009 Jan;23(1):134-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence and diversity of PAX5 fusion genes in childhood acute lymphoblastic leukemia.
  • PAX5, a master regulator of B-cell development, was recently shown to be involved in several leukemia-associated rearrangements, which result in fusion genes encoding chimeric proteins that antagonize PAX5 transcriptional activity.
  • In a population-based fluorescence in situ hybridization screening study of 446 childhood acute lymphoblastic leukemia (ALL) patients, we now show that PAX5 rearrangements occur at an incidence of about 2.5% of B-cell precursor ALL.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19020546.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Oncogene Proteins, Fusion; 0 / PAX5 protein, human; 0 / Transcription Factors
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16. Davidsen ML, Dalhoff K, Schmiegelow K: Pharmacogenetics influence treatment efficacy in childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Nov;30(11):831-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacogenetics influence treatment efficacy in childhood acute lymphoblastic leukemia.
  • As most childhood acute lymphoblastic leukemia treatment protocols include up to 13 different chemotherapeutic agents, the impact of individual SNPs has been difficult to evaluate.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasm Proteins / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


17. Nurmio M, Keros V, Lähteenmäki P, Salmi T, Kallajoki M, Jahnukainen K: Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility. J Clin Endocrinol Metab; 2009 Jun;94(6):2119-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility.
  • CONTEXT: Isolation of spermatogonial stem cells before potentially sterilizing cancer therapy, followed by transplantation of these cells into the testis after such treatment, may be an effective approach to prevent infertility among prepubertal boys suffering from acute lymphoblastic leukemia (ALL).
  • A key clinical consideration in this context is the timing of biopsy, if collection of spermatogonia could be delayed from diagnosis to the later phase of leukemia treatment, better patient selection could be offered.
  • OBJECTIVE: The objective of the study was to examine the routine testicular biopsy material collected to detect testicular leukemia to evaluate if treatment for leukemia affects numbers and maturation of the spermatogonia during the prepubertal period.
  • No significant alteration in spermatogonial numbers was associated with testicular leukemia.
  • CONCLUSION: Treatment for childhood leukemia without high-dose cyclophosphamide seldom depletes the spermatogonial stem cell pool totally.
  • [MeSH-major] Cyclophosphamide / adverse effects. Fertility / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatogonia / pathology

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  • (PMID = 19318447.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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18. Hosking FJ, Papaemmanuil E, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Taylor M, Tomlinson IP, Greaves M, Houlston RS: Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk. Blood; 2010 Jun 3;115(22):4472-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk.
  • To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs.

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  • (PMID = 20231427.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
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19. Sherborne AL, Hosking FJ, Prasad RB, Kumar R, Koehler R, Vijayakrishnan J, Papaemmanuil E, Bartram CR, Stanulla M, Schrappe M, Gast A, Dobbins SE, Ma Y, Sheridan E, Taylor M, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Moorman AV, Harrison CJ, Tomlinson IP, Richards S, Zimmermann M, Szalai C, Semsei AF, Erdelyi DJ, Krajinovic M, Sinnett D, Healy J, Gonzalez Neira A, Kawamata N, Ogawa S, Koeffler HP, Hemminki K, Greaves M, Houlston RS: Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk. Nat Genet; 2010 Jun;42(6):492-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
  • Using data from a genome-wide association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398 controls and with validation in samples totaling 2,386 cases and 2,419 controls, we have shown that common variation at 9p21.3 (rs3731217, intron 1 of CDKN2A) influences acute lymphoblastic leukemia risk (odds ratio = 0.71, P = 3.01 x 10(-11)), irrespective of cell lineage.
  • [MeSH-major] Chromosomes, Human, Pair 9. Genes, p16. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20453839.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA026038-31; United Kingdom / Cancer Research UK / / C1298/A8362; United States / NIGMS NIH HHS / GM / T32 GM008243; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / R01 CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS400186; NLM/ PMC3434228
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20. Harila MJ, Winqvist S, Lanning M, Bloigu R, Harila-Saari AH: Progressive neurocognitive impairment in young adult survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Aug;53(2):156-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Progressive neurocognitive impairment in young adult survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Despite the extensive literature on neuropsychological sequelae after treatment of childhood acute lymphoblastic leukemia (ALL), the very-long-term neurocognitive outcome of the survivors is poorly studied.
  • We assessed neuropsychological functioning in a population-based cohort of young adult childhood ALL survivors.
  • The mean VIQ test scores were 91, 100, and 109 (P < 0.001), and the mean PIQ test scores 100, 111, and 118 (P < 0.001) for the irradiated survivors, non-irradiated survivors and controls, respectively.
  • A significant decline in PIQ and VIQ test scores was observed in the irradiated survivor group during the follow-up period, but only in VIQ in the non-irradiated group.
  • CONCLUSIONS: Survivors of childhood ALL suffer from long-lasting progressive neuropsychological impairment, especially when treatment includes cranial irradiation.
  • [MeSH-major] Brain Neoplasms / complications. Cognition Disorders / epidemiology. Cognition Disorders / etiology. Cranial Irradiation / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


21. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


22. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt. Hematology; 2006 Oct;11(5):341-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Initially low Hb < 8 gm/dl, high WBCs and platelet counts > 50,000/mm(3) also showed better but non-significant remission rates.
  • Most of our cases were L(2) with better remission compared to other immunophenotypes.
  • CONCLUSIONS: Cytogenetic and molecular characterizations of childhood ALL may add prognostic criteria for optimal therapy allocation.
  • [MeSH-major] Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17607584.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
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23. Pui CH: Recent research advances in childhood acute lymphoblastic leukemia. J Formos Med Assoc; 2010 Nov;109(11):777-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent research advances in childhood acute lymphoblastic leukemia.
  • Recent progress in risk-adapted treatment for childhood acute lymphoblastic leukemia has secured 5-year event-free survival rates of approximately 80% and 5-year survival rates approaching 90%.
  • As high-resolution, genome-wide analyses of leukemic and normal host cells continue to identify novel subtypes of lymphoblastic leukemia and provide new insights into leukemogenesis, we can look forward to the time when all cases of this disease will be classified according to specific genetic abnormalities, some of which will yield "druggable" targets for more effective and less toxic treatments.
  • Meanwhile, it is sobering to consider that a significant fraction of leukemia survivors will develop serious health problems within 30 years of their initial diagnosis.
  • The ultimate challenge is to gain a clear understanding of the factors that give rise to childhood leukemia in the first place, and enable preventive strategies to be devised and implemented.

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  • [Copyright] Copyright © 2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.
  • (PMID = 21126650.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Singapore
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24. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19526524.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Razzouk BI, Rose SR, Hongeng S, Wallace D, Smeltzer MP, Zacher M, Pui CH, Hudson MM: Obesity in survivors of childhood acute lymphoblastic leukemia and lymphoma. J Clin Oncol; 2007 Apr 1;25(10):1183-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Obesity in survivors of childhood acute lymphoblastic leukemia and lymphoma.
  • PURPOSE: We evaluated the long-term effects of treatment on the body mass index (BMI) of children with acute lymphoblastic leukemia (ALL) or lymphoblastic lymphoma who received one of three CNS-directed therapies: intrathecal methotrexate with intravenous high-dose methotrexate (1 g/m2), intrathecal methotrexate with 18 Gy cranial radiation, or intrathecal methotrexate with 24 Gy cranial radiation.
  • CONCLUSION: BMI weight category at diagnosis, rather than type of CNS treatment received, predicted adult weight in long-term survivors of childhood hematologic malignancies.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Cranial Irradiation / adverse effects. Methotrexate / adverse effects. Obesity / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


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

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16435384.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
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27. Graubner UB, Porzig S, Jorch N, Kolb R, Wessalowski R, Escherich G, Janka GE: Impact of reduction of therapy on infectious complications in childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Feb;50(2):259-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of reduction of therapy on infectious complications in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Infections are a major cause of morbidity and mortality in childhood acute lymphoblastic leukemia (ALL) and only limited information is available on infectious complications.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Infection / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / microbiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17635005.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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28. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt. Hematology; 2007 Apr;12(2):103-11
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt.
  • The objective of the work was to evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Initially low HB < 8 gm/dl, high WBCs and platelet counts >50.000/mm(3) also showed better but non-significant remission rates.
  • Most of our cases were L(2) with better remission compared to other immunophenotypes.
  • Our conclusions were that cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Aneuploidy. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17454190.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
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29. Banklau C, Jindadamrongwech S, Sawangpanich R, Apibal S, Hongeng S, Paisooksantivatana K, Pakakasama S: Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia. Hematol Oncol Stem Cell Ther; 2010;3(3):103-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia.
  • Currently, treatment of childhood acute lymphoblastic leukemia (ALL) includes cytarabine, especially in high-risk patients.
  • PATIENTS AND METHODS: We included children diagnosed with ALL and lymphoblastic lymphoma (LL) stage III and IV.
  • CONCLUSION: The dCK-360G allele was found to increase the risk of mucositis after exposure to low-dose cytarabine in childhood ALL therapy.
  • [MeSH-major] Cytarabine / therapeutic use. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20890066.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.48 / Antigens, CD45; EC 3.5.4.5 / Cytidine Deaminase
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30. 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.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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31. Chang JS, Wiemels JL, Chokkalingam AP, Metayer C, Barcellos LF, Hansen HM, Aldrich MC, Guha N, Urayama KY, Scélo G, Green J, May SL, Kiley VA, Wiencke JK, Buffler PA: Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2010 Sep;19(9):2152-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia.
  • BACKGROUND: Childhood acute lymphoblastic leukemia (ALL) has been hypothesized to have an infection- and immune-related etiology.
  • The lack of immune priming in early childhood may result in abnormal immune responses to infections later in life and increase ALL risk.
  • METHODS: The current analyses examined the association between childhood ALL and 208 single-nucleotide polymorphisms (SNP) of 29 adaptive immune function genes among 377 ALL cases and 448 healthy controls.
  • This increased risk was stronger among firstborn children of all ethnicities and among non-Hispanic children with less day care attendance, consistent with the hypothesis about the role of early immune modulation in the development of childhood ALL.
  • Haplotype analyses identified additional regions of CD28, FCGR2, GATA3, IL2RA, STAT4, and STAT6 associated with childhood ALL.
  • CONCLUSION: Polymorphisms of genes on the adaptive immunity pathway are associated with childhood ALL risk.
  • IMPACT: Results of this study support an immune-related etiology of childhood ALL.

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  • [Copyright] (c) 2010 AACR.
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  • (PMID = 20716621.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES009137-08; United States / NIEHS NIH HHS / ES / ES009137-10; United States / NIEHS NIH HHS / ES / P42 ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-01A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S20023; United States / NIEHS NIH HHS / ES / ES009137-05S1; United States / NIEHS NIH HHS / ES / P42 ES004705-200023; United States / NIEHS NIH HHS / ES / P42 ES004705-220023; United States / NIEHS NIH HHS / ES / ES009137-02; United States / NIEHS NIH HHS / ES / ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-01A1; United States / NIEHS NIH HHS / ES / R01 ES009137-02; United States / NIEHS NIH HHS / ES / R01 ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NIEHS NIH HHS / ES / ES004705-22S30023; United States / NIEHS NIH HHS / ES / R01 ES009137-10S1; United States / NIEHS NIH HHS / ES / ES009137-03S1; United States / NIEHS NIH HHS / ES / R01 ES009137-07; United States / NIEHS NIH HHS / ES / ES004705-190023; United States / NIEHS NIH HHS / ES / ES004705-200023; United States / NIEHS NIH HHS / ES / R01 ES009137-05S1; United States / NIEHS NIH HHS / ES / R01 ES009137-10; United States / NIEHS NIH HHS / ES / ES004705-230023; United States / NIEHS NIH HHS / ES / PS42ES04705; United States / NIEHS NIH HHS / ES / ES004705-210023; United States / NIEHS NIH HHS / ES / ES009137-06A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S30023; United States / NIEHS NIH HHS / ES / P42 ES004705-210023; United States / NIEHS NIH HHS / ES / R01 ES009137-03S1; United States / NIEHS NIH HHS / ES / P42 ES004705-230023; United States / NIEHS NIH HHS / ES / ES009137-07; United States / NIEHS NIH HHS / ES / R01 ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-09; United States / NIEHS NIH HHS / ES / ES004705-220023; United States / NIEHS NIH HHS / ES / R01ES09137; United States / NIEHS NIH HHS / ES / ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-06A1; United States / NIEHS NIH HHS / ES / ES004705-22S20023; United States / NIEHS NIH HHS / ES / R01 ES009137; United States / NIEHS NIH HHS / ES / ES009137-10S1; United States / NIEHS NIH HHS / ES / R01 ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705-190023; United States / NIEHS NIH HHS / ES / R01 ES009137-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS220398; NLM/ PMC3257312
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32. Schmiegelow K, Vestergaard T, Nielsen SM, Hjalgrim H: Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis. Leukemia; 2008 Dec;22(12):2137-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis.
  • The pattern of infections in the first years of life modulates our immune system, and a low incidence of infections has been linked to an increased risk of common childhood acute lymphoblastic leukemia (ALL).
  • We here present a new interpretation of these observations--the adrenal hypothesis--that proposes that the risk of childhood ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis that increase plasma cortisol levels.
  • [MeSH-major] Hypothalamo-Hypophyseal System / immunology. Infection / immunology. Pituitary-Adrenal System / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 18719616.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 50
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33. Kwan ML, Jensen CD, Block G, Hudes ML, Chu LW, Buffler PA: Maternal diet and risk of childhood acute lymphoblastic leukemia. Public Health Rep; 2009 Jul-Aug;124(4):503-14
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  • [Title] Maternal diet and risk of childhood acute lymphoblastic leukemia.
  • OBJECTIVE: Intrauterine environmental factors, including maternal diet, may play an etiologic role in acute lymphoblastic leukemia (ALL), a common childhood cancer.
  • Expanding on previous findings from phase 1 of the Northern California Childhood Leukemia Study (NCCLS), a population-based case-control study, we sought to further elucidate and replicate the relationships between maternal diet and ALL risk.
  • CONCLUSIONS: These data suggest that it may be prudent for women to consume a diet rich in vegetables and adequate in protein prior to and during pregnancy as a possible means of reducing childhood ALL risk in their offspring.
  • [MeSH-major] Feeding Behavior. Mothers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 19618787.001).
  • [ISSN] 0033-3549
  • [Journal-full-title] Public health reports (Washington, D.C. : 1974)
  • [ISO-abbreviation] Public Health Rep
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / R01 ES009137; 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] United States
  • [Other-IDs] NLM/ PMC2693164
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34. Crazzolara R, Bradstock KF, Bendall LJ: RAD001 (Everolimus) induces autophagy in acute lymphoblastic leukemia. Autophagy; 2009 Jul;5(5):727-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RAD001 (Everolimus) induces autophagy in acute lymphoblastic leukemia.
  • The elimination of tumor cells by apoptosis is the main mechanism of action of chemotherapeutic drugs used in current treatment protocols of acute lymphoblastic leukemia (ALL).
  • Despite the rapid cytoreduction achieved, serious acute and late complications are frequent, and resistance to chemotherapy develops.
  • In the present study we have evaluated the efficacy of an mTOR inhibitor, RAD001 (Everolimus), to induce autophagy in an in vivo model of childhood ALL.
  • The discovery of alternative pathways involved in cell death execution and the role that it plays in leukemia suggest mTOR inhibitors should be included in future chemotherapy protocols of ALL.
  • [MeSH-major] Autophagy / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Sirolimus / analogs & derivatives


35. da Costa Moraes CA, Trompieri NM, Cavalcante Felix FH: Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital. J Pediatr Hematol Oncol; 2008 May;30(5):387-90
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  • [Title] Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital.
  • Acute promyelocytic leukemia (APL) is an uncommon form of pediatric acute nonlymphocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Brazil. Female. Hospitals, Pediatric. Humans. Male. Retrospective Studies

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  • (PMID = 18458575.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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36. Paulsson K, Forestier E, Lilljebjörn H, Heldrup J, Behrendtz M, Young BD, Johansson B: Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Dec 14;107(50):21719-24
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  • [Title] Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploid acute lymphoblastic leukemia (ALL) is one of the most common malignancies in children.
  • Other frequent abnormalities included whole-chromosome uniparental isodisomies (wUPIDs) 9 and 11, gain of 17q not associated with isochromosome formation, extra gain of part of 21q, deletions of ETS variant 6 (ETV6), cyclin-dependent kinase inhibitor 2A (CKDN2A) and paired box 5 (PAX5), and PAN3 poly(A) specific ribonuclease subunit homolog (PAN3) microdeletions.
  • Finally, two cases had partial deletions of AT rich interactive domain 5B (ARID5B), indicating that acquired as well as constitutional variants in this locus may be associated with pediatric ALL.
  • Here we provide a comprehensive characterization of the genetic landscape of high hyperdiploid childhood ALL, including the heterogeneous pattern of secondary genetic events.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


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

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  • (PMID = 15902295.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61393; United States / NIGMS NIH HHS / GM / GM61374
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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38. Novara F, Beri S, Bernardo ME, Bellazzi R, Malovini A, Ciccone R, Cometa AM, Locatelli F, Giorda R, Zuffardi O: Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood. Hum Genet; 2009 Oct;126(4):511-20
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  • [Title] Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
  • Deletion of chromosome 9p21 is a crucial event for the development of several cancers including acute lymphoblastic leukemia (ALL).
  • We have cloned 23 breakpoint junctions for a total of 46 breakpoints in 17 childhood ALL (9 B- and 8 T-lineages) showing different size deletions at one or both homologous chromosomes 9 to investigate which particular sequences make the region susceptible to interstitial deletion.
  • We found that half of 9p21 deletion breakpoints were mediated by ectopic V(D)J recombination mechanisms whereas the remaining half were associated to repeated sequences, including some with potential for non-B DNA structure formation.
  • Other mechanisms, such as microhomology-mediated repair, that are common in other cancers, play only a very minor role in ALL.
  • Nucleotide insertions at breakpoint junctions and microinversions flanking the breakpoints have been detected at 20/23 and 2/23 breakpoint junctions, respectively, both in the presence of recombination signal sequence (RSS)-like sequences and of other unspecific sequences.
  • Four of the 46 breakpoints coincide with those reported in other cases, thus confirming the presence of recurrent deletion hotspots.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion / genetics

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  • (PMID = 19484265.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2762534
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39. Holm C, Ora I, Brunhoff C, Anagnostaki L, Landberg G, Persson JL: Cyclin A1 expression and associations with disease characteristics in childhood acute lymphoblastic leukemia. Leuk Res; 2006 Mar;30(3):254-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclin A1 expression and associations with disease characteristics in childhood acute lymphoblastic leukemia.
  • A critical cell cycle regulatory protein, cyclin A1, has been implicated in the development of acute myeloid leukemia (AML).
  • Here, we have examined the expression and clinical significance of cyclin A1 in childhood acute lymphoblastic leukemia (ALL).
  • Cyclin A1 was highly expressed in lymphoblastic leukemic cell lines and in 22 of 30 ALL patients (73%).
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Cyclin A / biosynthesis. Gene Expression Regulation, Leukemic. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism


40. Mostert S, Sitaresmi MN, Gundy CM, Sutaryo, Veerman AJ: Influence of socioeconomic status on childhood acute lymphoblastic leukemia treatment in Indonesia. Pediatrics; 2006 Dec;118(6):e1600-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of socioeconomic status on childhood acute lymphoblastic leukemia treatment in Indonesia.
  • OBJECTIVE: A major reason for poor survival of childhood acute lymphoblastic leukemia in developing countries is treatment refusal or abandonment.
  • METHODS: Medical charts of 164 patients who received a diagnosis of acute lymphoblastic leukemia between 1997 and 2002 were abstracted retrospectively.
  • RESULTS: Of all patients, 35% refused or abandoned treatment, 23% experienced treatment-related death, 22% had progressive or relapsed leukemia, and 20% had an overall event-free survival.
  • CONCLUSIONS: Children's survival of acute lymphoblastic leukemia in developing countries could improve if problems that are associated with parental financial and educational background and medical teams' attitudes to treatment and follow-up could be addressed better.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17074838.001).
  • [ISSN] 1098-4275
  • [Journal-full-title] Pediatrics
  • [ISO-abbreviation] Pediatrics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. Diffner E, Gauffin F, Anagnostaki L, Nordgren A, Gustafsson B, Sander B, Gustafsson B, Persson JL: Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry. J Pediatr Hematol Oncol; 2009 Sep;31(9):696-701
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry.
  • Perturbation in the expression and signaling pathways of vascular endothelial growth factor (VEGF) has been linked to pathogenesis of hematologic malignancies.
  • We investigated the expression and clinical importance of VEGF and two of its receptors, VEGFR-1 and VEGFR-2, in childhood precursor B-cell acute lymphoblastic leukemia (pre-B ALL) by using immunohistochemistry.
  • These novel findings suggest that VEGFR-1 may have clinical importance in childhood pre-B ALL.
  • [MeSH-major] Immunoenzyme Techniques. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

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  • (PMID = 19707156.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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42. Azevedo-Silva F, Camargo Bd, Pombo-de-Oliveira MS: Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia. Braz J Med Biol Res; 2010 Mar;43(3):226-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia.
  • Acute leukemia is the most frequent cancer in children.
  • Recently, a new hypothesis was proposed for the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The adrenal hypothesis proposes that the risk of childhood B-cell precursor ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis.
  • Because Brazil is a continental and tropical country, the exposure to infections is diversified with endemic viral and regionally non-viral infections, with some characteristics that support the recent adrenal hypothesis.


43. Lightfoot T: Aetiology of childhood leukemia. Bioelectromagnetics; 2005;Suppl 7:S5-S11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aetiology of childhood leukemia.
  • Leukemia is the most common cancer to affect children, accounting for approximately a third of all childhood cancers.
  • The major morphological subtypes of leukemia, acute lymphoblastic leukemia (ALL), and acute myeloblastic leukemia (AML), are characterized by chromosomal translocations involving over 200 genes including mixed lineage leukemia (MLL), TEL, and AML1.
  • Chromosomal translocations involving the MLL gene at 11q23 are a common feature of infant acute leukemia, found in up to 80% of all cases, and there is strong evidence that rearrangements involving the MLL gene or the TEL-AML1 gene fusion can originate in utero.
  • As with most other cancers, the mechanism by which leukemia arises is likely to involve gene-environment interactions.
  • Exposures acting before birth and early in life has long been thought to be important determinants of leukemia, and the list of suspected chemical, physical, and biological agents continues to increase.
  • Unfortunately, the evidence regarding the majority of suggested exposures is limited and often contradictory, and there are areas, which clearly warrant further investigation in order to further our understanding of the aetiology of childhood leukemia.
  • [MeSH-major] Electromagnetic Fields / adverse effects. Environmental Exposure / adverse effects. Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / physiopathology. Prenatal Exposure Delayed Effects / etiology. Prenatal Exposure Delayed Effects / physiopathology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16059922.001).
  • [ISSN] 0197-8462
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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44. 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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  • [ISSN] 1592-8721
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  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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  • [Other-IDs] NLM/ PMC2930966
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45. Pui CH, Campana D, Pei D, Bowman WP, Sandlund JT, Kaste SC, Ribeiro RC, Rubnitz JE, Raimondi SC, Onciu M, Coustan-Smith E, Kun LE, Jeha S, Cheng C, Howard SC, Simmons V, Bayles A, Metzger ML, Boyett JM, Leung W, Handgretinger R, Downing JR, Evans WE, Relling MV: Treating childhood acute lymphoblastic leukemia without cranial irradiation. N Engl J Med; 2009 Jun 25;360(26):2730-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treating childhood acute lymphoblastic leukemia without cranial irradiation.
  • BACKGROUND: Prophylactic cranial irradiation has been a standard treatment in children with acute lymphoblastic leukemia (ALL) who are at high risk for central nervous system (CNS) relapse.
  • CNS leukemia (CNS-3 status) or a traumatic lumbar puncture with blast cells at diagnosis and a high level of minimal residual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with poorer event-free survival.
  • CONCLUSIONS: With effective risk-adjusted chemotherapy, prophylactic cranial irradiation can be safely omitted from the treatment of childhood ALL. (ClinicalTrials.gov number, NCT00137111. )
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] 2009 Massachusetts Medical Society
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  • (PMID = 19553647.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00137111
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / R01 CA051001-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA78224; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NIGMS NIH HHS / GM / GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061393-090007; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS118392; NLM/ PMC2754320
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46. Schotte D, Chau JC, Sylvester G, Liu G, Chen C, van der Velden VH, Broekhuis MJ, Peters TC, Pieters R, den Boer ML: Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):313-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia.
  • To identify miRNAs relevant to pediatric acute lymphoblastic leukemia (ALL), we cloned 105 known and 8 new miRNA genes expressed in patients' leukemia cells.
  • Eight miRNAs were differentially expressed between MLL and non-MLL precursor B-ALL cases (P<0.05).
  • Most remarkably, miR-708 was 250- up to 6500-fold higher expressed in 57 TEL-AML1, BCR-ABL, E2A-PBX1, hyperdiploid and B-other cases than in 20 MLL-rearranged and 15 T-ALL cases (0.0001<P<0.01), whereas the expression of miR-196b was 500-fold higher in MLL-rearranged and 800-fold higher in 5 of 15 T-ALL cases as compared with the expression level in the remaining precursor B-ALL cases (P<0.001).
  • The expression did not correlate with the maturation status of leukemia cells based on immunoglobulin and T-cell receptor rearrangements, immunophenotype or MLL-fusion partner.
  • [MeSH-major] MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Cloning, Molecular. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Myeloid-Lymphoid Leukemia Protein / genetics


47. Bhojwani D, Moskowitz N, Raetz EA, Carroll WL: Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia. Paediatr Drugs; 2007;9(3):149-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease.
  • Childhood ALL has served as an example for demonstrating the feasibility and potential of high-throughput technologies such as global gene expression or transcript profiling.
  • As the methodology undergoes refinement and validation, it is plausible that microarrays may be used in the routine management of childhood ALL in the next few years.
  • This article discusses the numerous applications to date of gene expression profiling in childhood ALL.
  • Identification of patients who are predicted to have an unfavorable outcome may allow for early intervention such as intensification of therapy or avoidance of drugs that are associated with specific secondary effects such as therapy-related acute myelogenous leukemia.
  • These newer methods of genome analyses complemented by studies involving the proteome as well as host polymorphisms will have a profound impact on the diagnosis and management of childhood ALL.
  • [MeSH-major] Gene Expression Profiling. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 17523695.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114762
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Oncogene Proteins
  • [Number-of-references] 36
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48. Sitaresmi MN, Mostert S, Purwanto I, Gundy CM, Sutaryo, Veerman AJ: Chemotherapy-related side effects in childhood acute lymphoblastic leukemia in Indonesia: parental perceptions. J Pediatr Oncol Nurs; 2009 Jul-Aug;26(4):198-207
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy-related side effects in childhood acute lymphoblastic leukemia in Indonesia: parental perceptions.
  • Fifty-one parents of children with acute lymphoblastic leukemia in a tertiary care hospital in Indonesia were interviewed about their perception of side effects and their impact on treatment noncompliance and daily activities.
  • During chemotherapy, childhood acute lymphoblastic leukemia patients suffered from psychological as well as physical side effects.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Parents / psychology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19726791.001).
  • [ISSN] 1043-4542
  • [Journal-full-title] Journal of pediatric oncology nursing : official journal of the Association of Pediatric Oncology Nurses
  • [ISO-abbreviation] J Pediatr Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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49. Sitaresmi MN, Mostert S, Gundy CM, Sutaryo, Veerman AJ: Health-care providers' compliance with childhood acute lymphoblastic leukemia protocol in Indonesia. Pediatr Blood Cancer; 2008 Dec;51(6):732-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Health-care providers' compliance with childhood acute lymphoblastic leukemia protocol in Indonesia.
  • BACKGROUND: Non-compliance with childhood acute lymphoblastic leukemia (ALL) protocol is an important determinant of poor treatment outcome.
  • Non-compliance with protocol may not only concern parents or patients, but may also concern health-care providers (HCP).
  • Our study examines the accuracy of leukemia risk classification and attitude of HCP toward protocol compliance in Indonesia.
  • CONCLUSIONS: Our study shows that HCP should improve their knowledge and assessment of childhood ALL risk classification, especially lymphoblast count on day 8 of chemotherapy.
  • Proper risk classification and subsequent correct treatment may enable more children to be cured of leukemia.
  • [MeSH-major] Delivery of Health Care / standards. Guideline Adherence / standards. Health Personnel / standards. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


50. Chatterton Z, Morenos L, Saffery R, Craig JM, Ashley D, Wong NC: DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia. Epigenomics; 2010 Oct;2(5):697-708
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common cancer in children in the modern world.
  • This suggests that either further genetic contributions to ALL have yet to be characterized or other factors, such as epigenetic aberrations are involved.
  • A number of DNA methylation and miRNA profiling studies have investigated the role of both in childhood ALL.
  • [MeSH-major] DNA Methylation / physiology. Epigenesis, Genetic / physiology. High-Throughput Screening Assays / methods. MicroRNAs / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 22122053.001).
  • [ISSN] 1750-192X
  • [Journal-full-title] Epigenomics
  • [ISO-abbreviation] Epigenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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51. Buizer AI, De Sonneville LM, van den Heuvel-Eibrink MM, Njiokiktjien C, Veerman AJ: Visuomotor control in survivors of childhood acute lymphoblastic leukemia treated with chemotherapy only. J Int Neuropsychol Soc; 2005 Sep;11(5):554-65
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  • [Title] Visuomotor control in survivors of childhood acute lymphoblastic leukemia treated with chemotherapy only.
  • Treatment for childhood acute lymphoblastic leukemia (ALL), which includes CNS prophylaxis, is associated with central and peripheral neurotoxicity.
  • The purpose of the present study was to analyze the effects of chemotherapy on various levels of visuomotor control in survivors of childhood ALL treated without cranial irradiation, and to identify risk factors for possible deficits.
  • Visuomotor function was compared between children after treatment for ALL (n = 34), children after treatment for Wilms tumor, which consists of non-CNS directed chemotherapy (n = 38), and healthy controls (n = 151).
  • Three tasks were administered: a simple visual reaction time task and two tasks measuring visuomotor control with one requiring a higher level of cognitive control than the other.
  • The results indicate that chemotherapy-induced central neurotoxicity in childhood ALL treatment is associated with higher order visuomotor control deficits.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology. Psychomotor Performance / physiology

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  • (PMID = 16212682.001).
  • [ISSN] 1355-6177
  • [Journal-full-title] Journal of the International Neuropsychological Society : JINS
  • [ISO-abbreviation] J Int Neuropsychol Soc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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52. Juarez J, Dela Pena A, Baraz R, Hewson J, Khoo M, Cisterne A, Fricker S, Fujii N, Bradstock KF, Bendall LJ: CXCR4 antagonists mobilize childhood acute lymphoblastic leukemia cells into the peripheral blood and inhibit engraftment. Leukemia; 2007 Jun;21(6):1249-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CXCR4 antagonists mobilize childhood acute lymphoblastic leukemia cells into the peripheral blood and inhibit engraftment.
  • The role of CXCL12 in the bone marrow (BM) homing and growth of B-cell progenitor acute lymphoblastic leukemia (ALL) has been established.
  • We used mouse models of human childhood and murine leukemia and specific peptide and small molecule CXCR4 antagonists to examine the importance of CXCL12/CXCR4 in the development of leukemia in vivo.
  • Extended administration of CXCR4 antagonists to mice with leukemia resulted in a reduction in the number of leukemic cells in the PB and spleens of animals compared to control treated animals in three of the five cases tested.
  • [MeSH-major] Chemotaxis / drug effects. Neoplastic Cells, Circulating / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Blood. Chemokine CXCL12. Chemokines, CXC / antagonists & inhibitors. Child. Child, Preschool. Disease Models, Animal. Drug Interactions. Female. Graft Survival / drug effects. Humans. Infant. Male. Mice. Neoplasm Transplantation. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Spleen. Stromal Cells. Transplantation, Heterologous

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  • (PMID = 17410186.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Receptors, CXCR4
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53. Do TN, Ucisik-Akkaya E, Davis CF, Morrison BA, Dorak MT: TP53 R72P and MDM2 SNP309 polymorphisms in modification of childhood acute lymphoblastic leukemia susceptibility. Cancer Genet Cytogenet; 2009 Nov;195(1):31-6
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  • [Title] TP53 R72P and MDM2 SNP309 polymorphisms in modification of childhood acute lymphoblastic leukemia susceptibility.
  • To investigate its relevance in childhood acute lymphoblastic leukemia (ALL) susceptibility, we genotyped 114 cases and 414 newborn controls from Wales (UK) for polymorphisms in TP53 (R72P), its negative regulator MDM2 (single-nucleotide polymorphism SNP309, rs2279744), and selected HLA complex genes whose products interact with TP53.
  • SNP309 did not show any association with primary susceptibility to childhood ALL, even after stratification by sex.
  • However, females with SNP309 minor allele had earlier onset of childhood ALL (median age at diagnosis was 36 months in females, but 60 months in males; P=0.002).
  • We have therefore identified TP53 R72P as a possible risk modifier for childhood ALL and the association of MDM2 with age at onset with sex effect suggests prenatal hormonal programming of childhood ALL susceptibility.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-mdm2 / genetics. Tumor Suppressor Protein p53 / genetics


54. Paananen P, Arola MO, Pelliniemi TT, Salmi TT, Lähteenmäki PM: Evaluation of the effects of different transfusion trigger levels during the treatment of childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Oct;31(10):745-9
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  • [Title] Evaluation of the effects of different transfusion trigger levels during the treatment of childhood acute lymphoblastic leukemia.
  • Differences in the triggering levels for red blood cell (RBC) and platelet (PLT) transfusions were analyzed in association to the amount and total costs of transfusions and the number of febrile episodes during childhood acute lymphoblastic leukemia (ALL) treatment.
  • Clinical trials are, however, necessary to determine optimal criteria for supportive blood transfusions in childhood cancer patients.
  • [MeSH-major] Blood Transfusion / standards. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19734805.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins
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55. Czyzewski K, Zaborowska A, Styczyński J: Thalidomide increases in vitro sensitivity of childhood acute lymphoblastic leukemia cells to prednisolone and cytarabine. Arch Immunol Ther Exp (Warsz); 2006 Sep-Oct;54(5):341-5
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  • [Title] Thalidomide increases in vitro sensitivity of childhood acute lymphoblastic leukemia cells to prednisolone and cytarabine.
  • INTRODUCTION: Thalidomide is a derivative of glutamic acid with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that was found to inhibit the production of tumor necrosis factor alpha in vitro, stimulate reactive oxygen species production, and inhibit vascular endothelial growth factor receptor in acute leukemias.
  • The purpose of this study was to determine the in vitro activity of thalidomide as a single agent and in combination with prednisolone or cytarabine in childhood acute lymphoblastic leukemia (ALL).
  • MATERIALS AND METHODS: Bone marrow samples of 40 childhood ALL patients, normal lymphocytes of 9 healthy adults, and 3 lymphoid cell lines were evaluated for cytotoxicity of thalidomide (alone and in combination with prednisolone and cytarabine) using the MTT assay.
  • RESULTS: Thalidomide as a single agent had weak antileukemic activity to the childhood ALL samples.
  • Thalidomide increased apoptosis in lymphoblasts and modulated the cell-cycle arrest caused by prednisolone, but not that by cytarabine, in childhood ALL samples.
  • CONCLUSIONS: Thalidomide increases in vitro the sensitivity of childhood ALL cells to prednisolone and cytarabine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17031469.001).
  • [ISSN] 0004-069X
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 4Z8R6ORS6L / Thalidomide; 9PHQ9Y1OLM / Prednisolone
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56. Hu RH, Lu Y, Li QH, Ma L, Li B, Zhu XF, Wang JX, Pang TX: [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1502-6
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  • [Title] [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells].
  • This study was aimed to investigate the expression of midkine gene in childhood acute lymphoblastic leukemia patients (ALL) and to explore the possible effects of midkine gene on the chemotherapeutic drug efflux.
  • The rhodamine 123 efflux test revealed that MFI in the leukemia cells was obviously lower than that in normal cells (p < 0.01), furthermore, there was an evident negative correlation between the MFI and MK mRNA expression (r = -0.869, p < 0.001).
  • It is concluded that there is powerful drug efflux ability in lymphoblastic leukemia cells with high midkine gene expression.

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  • (PMID = 20030935.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MDK protein, human; 0 / Nerve Growth Factors; 0 / RNA, Messenger
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57. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • CONCLUSION: There were statistic differences between T-cell and B-cell childhood ALLs in age, initial WBC count, early response to therapy, and eight-year EFS and RFS.
  • Childhood T-ALL was associated with a worse prognosis than other sub-types of childhood ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Karyotyping. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis

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  • (PMID = 19563031.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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58. Yamamoto T, Isomura M, Xu Y, Liang J, Yagasaki H, Kamachi Y, Kudo K, Kiyoi H, Naoe T, Kojma S: PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia. Leuk Res; 2006 Sep;30(9):1085-9
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  • [Title] PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia.
  • Germline mutations in PTPN11 were first observed in Noonan syndrome, while somatic mutations were identified in hematological myeloid malignancies.
  • Recently, PTPN11 mutations have been reported in children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Burkitt Lymphoma / genetics. Intracellular Signaling Peptides and Proteins / genetics. Mutation, Missense. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Tyrosine Phosphatases / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Down Syndrome / complications. Down Syndrome / genetics. Female. Humans. Infant. Japan. Male. Noonan Syndrome / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 11

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  • (PMID = 16533526.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.6.5.2 / ras Proteins
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59. Lin PC, Chang TT, Lin SR, Chiou SS, Jang RC, Sheen JM: TEL/AML1 fusion gene in childhood acute lymphoblastic leukemia in southern Taiwan. Kaohsiung J Med Sci; 2008 Jun;24(6):289-96
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  • [Title] TEL/AML1 fusion gene in childhood acute lymphoblastic leukemia in southern Taiwan.
  • Chromosomal abnormalities are found in 80-90% of childhood cases of acute lymphoblastic leukemia (ALL).
  • Leukemia-specific chromosome aberrations not only have prognostic value, but also provide important clues for further investigation into leukogenesis, leukemic cell transformation, and proliferation.
  • This study used reverse transcriptase-polymerase chain reaction techniques to detect transcripts of the leukemia-specific chromosome fusion gene, TEL/AML1, and to monitor the expression levels of the TEL-AML1 fusion transcript in ALL patients at sequential intervals during their treatment course.
  • The clinical features of our eight TEL/AML1-positive ALL cases were similar to those in other studies.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18635414.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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60. Yang YL, Lin SR, Chen JS, Lin SW, Yu SL, Chen HY, Yen CT, Lin CY, Lin JF, Lin KH, Jou ST, Hu CY, Chang SK, Lu MY, Chang HH, Chang WH, Lin KS, Lin DT: Expression and prognostic significance of the apoptotic genes BCL2L13, Livin, and CASP8AP2 in childhood acute lymphoblastic leukemia. Leuk Res; 2010 Jan;34(1):18-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and prognostic significance of the apoptotic genes BCL2L13, Livin, and CASP8AP2 in childhood acute lymphoblastic leukemia.
  • Improved treatment of childhood acute lymphoblastic leukemia (ALL) depends on the identification of new molecular markers that are able to predict treatment response and clinical outcome.
  • We investigated the expression of three apoptosis related genes, BCL2L13, CASP8AP2, and Livin, as well as their prognostic significance, in a retrospective study of 90 pediatric ALL patients diagnosed between 1996 and 2007 in Taiwan.
  • Multivariate analysis for EFS and OS demonstrated that high expression of BCL2L13 was an independent prognostic factor for childhood ALL in this ethnic group.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Calcium-Binding Proteins / genetics. Inhibitor of Apoptosis Proteins / genetics. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20109966.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / BCL2L13 protein, human; 0 / BIRC7 protein, human; 0 / CASP8AP2 protein, human; 0 / Calcium-Binding Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2
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61. Brozek J, Bryl E, Płoszyńska A, Balcerska A, Witkowski JM: P-glycoprotein activity predicts outcome in childhood acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Jul;31(7):493-9
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  • [Title] P-glycoprotein activity predicts outcome in childhood acute lymphoblastic leukemia.
  • Treatment of children with acute lymphoblastic leukemia (ALL) is based on P-glycoprotein (P-gp)-dependent cytostatics.
  • [MeSH-major] P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19564743.001).
  • [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 / Antineoplastic Agents; 0 / P-Glycoprotein
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62. Oliveira E, Alves S, Quental S, Ferreira F, Norton L, Costa V, Amorim A, Prata MJ: The MTHFR C677T and A1298C polymorphisms and susceptibility to childhood acute lymphoblastic leukemia in Portugal. J Pediatr Hematol Oncol; 2005 Aug;27(8):425-9
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  • [Title] The MTHFR C677T and A1298C polymorphisms and susceptibility to childhood acute lymphoblastic leukemia in Portugal.
  • The role of two common polymorphisms at the MTHFR gene, C677T and A1298C, in the etiology of childhood or adult acute lymphoblastic leukemia (ALL) has been previously investigated.
  • None of the variations was found to significantly affect the risk of developing childhood ALL in North Portugal, and this finding per se is of relevance in further studies aimed at assessing the etiology of the pathology in this specific population.
  • Despite the absence of statistical significance, these data revealed that the frequency of MTHFR*677T was lower in patients than in controls, a result that is congruent with other reports and with the functional model usually invoked to explain its ALL protective effect.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16096524.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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63. Brennan BM, Mughal Z, Roberts SA, Ward K, Shalet SM, Eden TO, Will AM, Stevens RF, Adams JE: Bone mineral density in childhood survivors of acute lymphoblastic leukemia treated without cranial irradiation. J Clin Endocrinol Metab; 2005 Feb;90(2):689-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone mineral density in childhood survivors of acute lymphoblastic leukemia treated without cranial irradiation.
  • Adult survivors of childhood acute lymphoblastic leukemia (ALL) whose treatment included cranial irradiation (XRT) have reduced bone mineral density (BMD).
  • In conclusion, BMD, except at the radius, is normal in childhood survivors of ALL treated without XRT.
  • [MeSH-major] Bone Density. Brain Neoplasms / prevention & control. Cranial Irradiation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy


64. Tie LJ, Gu LJ, Chen J, Dong L, Chen J, Pan C, Ye H, Xue HL, Tang JY, Wang YP: [Correlation between karyotypic characteristics and treatment outcome in childhood acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):339-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Correlation between karyotypic characteristics and treatment outcome in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the relationship between karyotypic characteristics and treatment outcome of childhood acute lymphoblastic leukemia (ALL) and compare the difference in karyotypic aberration between ALL patients in China and in western countries.
  • The patients were classified into 4 groups according to the karyotype of the leukemia cells: normal karyotype, hypodiploid, hyperdiploid and pseudodiploid.
  • The probability of 5-year EFS for the four subgroups were (78.28 +/- 6.34)%, (86.07 +/- 6.47)%, (53.85 +/- 13.83)% and (40.10 +/- 12.17)%, respectively (P = 0.0041). (2) The clinical presentation and early response to treatment had no difference among the four groups, but the events are significantly different. (3) The probability of 5-year EFS for the combined hypodiploid group and the non-hypodiploid group was (53.85 +/- 13.83)% and (69.98 +/- 5.94)%, respectively (P = 0.1281). (4) The probability of 4-year EFS was significantly worse for patients with Philadelphia chromosome than for no Philadelphia chromosome patients [(28.57 +/- 17.07)% vs (70.85 +/- 5.60)%, P = 0.0009]. (5) Multivariate analysis suggested that the karyotypic characteristics, Philadelphia chromosome, age < 1-year or > 12-year, and white blood cell counts were independent prognostic factors.
  • CONCLUSIONS: The cytogenetic pattern of Chinese childhood ALL patients was similar to that of western countries.
  • [MeSH-major] Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16875587.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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65. Luo XQ, Ke ZY, Guan XQ, Zhang YC, Huang LB, Zhu J: The comparison of outcome and cost of three protocols for childhood non-high risk acute lymphoblastic leukemia in China. Pediatr Blood Cancer; 2008 Aug;51(2):204-9
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  • [Title] The comparison of outcome and cost of three protocols for childhood non-high risk acute lymphoblastic leukemia in China.
  • OBJECTIVE: To compare the outcome and treatment cost of three protocols for childhood non-high risk acute lymphoblastic leukemia (ALL), and evaluate the feasibility of less intensive treatment protocol for low income families.
  • RESULTS: Among 243 patients, 19 abandoned treatment, 3 transferred to other hospitals, 48 were high-risk and were treated with the high risk protocol, and 4 had mature B-ALL.
  • A total of 169 cases were enrolled on non-high risk protocols: 46 treated on China-98 protocol, 73 on modified ALLIC BFM2002 and 50 from low income families on Economic Protocol.
  • The reduced intensity protocol appears to achieve reasonable EFS (72.8% at 4 years) for non-high risk ALL at a much lower cost.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


66. Gao C, Zhao W, Liu Y, Gong WY, Li WJ, Li ZG, Wu MY: [Characteristics of fusion gene and immunophenotype in MLL gene rearrangement positive childhood acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1283-8
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  • [Title] [Characteristics of fusion gene and immunophenotype in MLL gene rearrangement positive childhood acute lymphoblastic leukemia].
  • The study was aimed to investigate the fusion gene transcript and immunophenotypic characteristics of the mixed linage leukemia (MLL)-rearranged positive childhood acute lymphoblastic leukemia (ALL).

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  • (PMID = 19840468.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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67. Goshen Y, Stark B, Kornreich L, Michowiz S, Feinmesser M, Yaniv I: High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Sep;49(3):294-7
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  • [Title] High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Most survivors of childhood acute lymphoblastic leukemia (ALL) and T-cell lymphoma (T-NHL) treated before 1990 received cranial radiation.
  • This study assessed the occurrence of second tumors in irradiated and non-irradiated survivors.
  • Imaging (MRI, CT) was performed every 3-6 years in 76/88 irradiated and 74/122 non-irradiated patients for the last 20 years.
  • Only one of the 74 non-irradiated patients (median follow-up 14 years) developed meningioma.
  • CONCLUSIONS: Survivors of childhood ALL treated with cranial radiation require prolonged surveillance because of a high incidence of late meningiomas.
  • [MeSH-major] Cranial Irradiation / adverse effects. Meningeal Neoplasms / epidemiology. Meningioma / epidemiology. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy


68. Kim NK, Chong SY, Jang MJ, Hong SH, Kim HS, Cho EK, Lee JA, Ahn MJ, Kim CS, Oh D: Association of the methylenetetrahydrofolate reductase polymorphism in Korean patients with childhood acute lymphoblastic leukemia. Anticancer Res; 2006 Jul-Aug;26(4B):2879-81
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  • [Title] Association of the methylenetetrahydrofolate reductase polymorphism in Korean patients with childhood acute lymphoblastic leukemia.
  • Recently, methylenetetrahydrofolate reductase (MTHFR C677T and A1298C) mutations were discovered to be associated with childhood acute lymphoblastic leukemia (ALL), as well as colon cancer, lymphoma, esophageal and stomach cancer.
  • Therefore, it was hypothesized that the MTHFR polymorphisms are associated with the risk of childhood ALL in the Korean population.
  • CONCLUSION: Although no consistent results on associations between MTHFR A 1298C polymorphism and ALL in the populations studied were obtained, the A1298C polymorphism, at least in Koreans, may be a genetic determinant among childhood ALL patients.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16886608.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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69. Ghosh S, Bandyopadhyay S, Bhattacharya DK, Mandal C: Altered erythrocyte membrane characteristics during anemia in childhood acute lymphoblastic leukemia. Ann Hematol; 2005 Feb;84(2):76-84
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  • [Title] Altered erythrocyte membrane characteristics during anemia in childhood acute lymphoblastic leukemia.
  • Anemia is a prominent feature in children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Anemia / etiology. Erythrocyte Membrane / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood


70. Yang B, Fan L, Fang L, He Q: Hypoxia-mediated fenretinide (4-HPR) resistance in childhood acute lymphoblastic leukemia cells. Cancer Chemother Pharmacol; 2006 Oct;58(4):540-6
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  • [Title] Hypoxia-mediated fenretinide (4-HPR) resistance in childhood acute lymphoblastic leukemia cells.
  • PURPOSES: N-(4-Hydroxyphenyl)-retinamide (4-HPR, Fenretinide) is a synthetic retinoid with cytotoxicity in acute lymphoblastic leukemia (ALL) cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Hypoxia. Fenretinide / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16520989.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 187EJ7QEXL / Fenretinide; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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76. Buizer AI, de Sonneville LM, van den Heuvel-Eibrink MM, Veerman AJ: Behavioral and educational limitations after chemotherapy for childhood acute lymphoblastic leukemia or Wilms tumor. Cancer; 2006 May 1;106(9):2067-75
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  • [Title] Behavioral and educational limitations after chemotherapy for childhood acute lymphoblastic leukemia or Wilms tumor.
  • BACKGROUND: The improved prognosis of childhood cancer makes monitoring of functional outcome important.
  • The purpose of this study was to evaluate behavioral and educational functioning in survivors of childhood acute lymphoblastic leukemia (ALL) or a Wilms tumor.
  • CONCLUSION: Evidence is provided of subtle but significant behavioral and educational problems in survivors of childhood ALL, but no dysfunctions in survivors of a Wilms tumor.
  • [MeSH-major] Child Behavior Disorders / etiology. Learning Disorders / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology


77. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M, Jiang LM: [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):333-6
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  • [Title] [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To study the role of minimal residual disease (MRD) in the evaluation of therapeutic effectiveness of childhood B-cell acute lymphoblastic leukemia (ALL).
  • Multivariate analysis confirmed that the MRD level after induction chemotherapy together with the reaction to prednisone, the bone marrow features on the 19th day of induction, and the fusion gene with BCR-ABL or MLL-AF4 had prognostic significance in childhood B-cell ALL.
  • CONCLUSIONS: The MRD level in the whole course of therapy is an important outcome indicator in childhood B cell ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18554462.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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78. He J, Chen ZX, Xue YQ, Li JQ, He HL, Huang YP, He YX, Chai YH, Zhu LL: [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Oct;22(5):551-3
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  • [Title] [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: To detect the expression of the fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia(ALL) and its conformity to WHO classification.
  • The multiplex RT-PCR in combination with chromosome analysis revealed genetic abnormalities in 69.4%(43/62) of childhood ALL.
  • CONCLUSION: Multiplex RT-PCR combined with chromosome analysis and immunophenotyping can provide reliable and helpful information for the diagnosis, therapy evaluation and prognosis prediction in childhood ALL, which may also serve as a basis on which to implement the criteria of WHO classification.
  • [MeSH-major] Chromosome Aberrations. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Flow Cytometry. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Immunophenotyping. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. RNA-Binding Protein FUS / genetics. RNA-Binding Protein FUS / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16215946.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, human; 0 / Homeodomain Proteins; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA-Binding Protein FUS; 0 / TEL-AML1 fusion protein; 0 / TLS-ERG fusion protein, human; 0 / Transcription Factors; 143275-75-6 / TLX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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79. Pakakasama S, Mukda E, Sasanakul W, Kadegasem P, Udomsubpayakul U, Thithapandha A, Hongeng S: Polymorphisms of drug-metabolizing enzymes and risk of childhood acute lymphoblastic leukemia. Am J Hematol; 2005 Jul;79(3):202-5
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  • [Title] Polymorphisms of drug-metabolizing enzymes and risk of childhood acute lymphoblastic leukemia.
  • We hypothesized that polymorphisms of these enzymes might affect the risk of childhood acute lymphoblastic leukemia (ALL).
  • Our data thus demonstrate that the GSTM1 null genotype might increase the risk of childhood ALL in a Thai population.
  • [MeSH-major] Cytochrome P-450 Enzyme System / genetics. Glutathione Transferase / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15981231.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pharmaceutical Preparations; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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80. Urayama KY, Wiencke JK, Buffler PA, Chokkalingam AP, Metayer C, Wiemels JL: MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2007 Jun;16(6):1172-7
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  • [Title] MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia.
  • Among children enrolled in the Northern California Childhood Leukemia Study, we examined the susceptibility conferred by MDR1 single nucleotide polymorphisms (SNP) and predicted haplotypes and whether they modify the association between indoor insecticide exposure and risk of childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: Allele frequencies in non-Hispanic White and Hispanic controls were similar, and with the exception of T-129C, seemed to be in strong linkage disequilibrium.
  • Overall, the SNPs considered individually or within haplotypes (C1236T-G2677T/A-C3435T) were not significantly associated with childhood ALL.
  • [MeSH-major] Air Pollution, Indoor / adverse effects. Genes, MDR. Insecticides / adverse effects. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17548681.001).
  • [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 / Insecticides; 0 / P-Glycoprotein
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81. Jarfelt M, Kujacic V, Holmgren D, Bjarnason R, Lannering B: Exercise echocardiography reveals subclinical cardiac dysfunction in young adult survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Nov;49(6):835-40
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  • [Title] Exercise echocardiography reveals subclinical cardiac dysfunction in young adult survivors of childhood acute lymphoblastic leukemia.
  • OBJECTIVE: Anthracyclines (AC) have contributed significantly to increased survival rate in acute lymphoblastic leukemia (ALL), although the use of these drugs is limited due to cardiotoxicity.
  • The aim was to evaluate heart muscle function in asymptomatic adult survivors of ALL treated in early childhood in relation to the combined effects of AC and other potential cardiotoxic factors.
  • [MeSH-major] Echocardiography, Stress. Exercise Test. Heart Diseases / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma


82. Addeo R, Caraglia M, Baldi A, D'Angelo V, Casale F, Crisci S, Abbruzzese A, Vincenze B, Campioni M, Di Tullio MT, Indolfi P: Prognostic role of bcl-xL and p53 in childhood acute lymphoblastic leukemia (ALL). Cancer Biol Ther; 2005 Jan;4(1):32-8
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  • [Title] Prognostic role of bcl-xL and p53 in childhood acute lymphoblastic leukemia (ALL).
  • Molecular parameters involved in the prediction of response of childhood acute lymphoblastic leukemia (ALL) are still unclear.
  • [MeSH-major] Gene Expression Profiling. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis


83. Benmiloud S, Steffens M, Beauloye V, de Wandeleer A, Devogelaer JP, Brichard B, Vermylen C, Maiter D: Long-term effects on bone mineral density of different therapeutic schemes for acute lymphoblastic leukemia or non-Hodgkin lymphoma during childhood. Horm Res Paediatr; 2010;74(4):241-50
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  • [Title] Long-term effects on bone mineral density of different therapeutic schemes for acute lymphoblastic leukemia or non-Hodgkin lymphoma during childhood.
  • BACKGROUND: Little is known regarding long-term bone deficit in relationship with the modalities of cancer therapy among survivors of childhood malignancy.
  • METHODS: Bone mineral density (BMD) was evaluated at lumbar spine (LS), total hip and femoral neck in 89 patients (44 men) more than 5 years after remission of childhood acute lymphoblastic leukemia (ALL) or non-Hodgkin lymphoma (NHL).
  • CONCLUSIONS: A low bone mass is frequently observed in adult survivors of childhood ALL and NHL, and is associated with male gender at the LS and with dexamethasone treatment, cranial irradiation and BMT/TBI at the hip.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Bone Density / drug effects. Bone Density / radiation effects. Lymphoma, Non-Hodgkin / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


84. 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.
  • METHODS: All patients with ALL treated at the only cancer pediatric hospital in Nicaragua during 2006 were studied prospectively.
  • [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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85. Ma X, Buffler PA, Wiemels JL, Selvin S, Metayer C, Loh M, Does MB, Wiencke JK: Ethnic difference in daycare attendance, early infections, and risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):1928-34
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  • [Title] Ethnic difference in daycare attendance, early infections, and risk of childhood acute lymphoblastic leukemia.
  • A role for infectious agents has been proposed in the etiology of childhood acute lymphoblastic leukemia (ALL), particularly for common ALL (c-ALL; ALL diagnosed in children ages 2-5 years and expressing CD10 and CD19 surface antigens).
  • We evaluated the possible etiologic role of daycare attendance (a proxy measure for exposure to infectious agents) and infections during infancy in the Northern California Childhood Leukemia Study.
  • In non-Hispanic White children, daycare attendance measured by child-hours was associated with a significantly reduced risk of ALL.
  • In addition, self-reported ear infection during infancy was associated with a significantly reduced risk of c-ALL (OR, 0.32; 95% CI, 0.14-0.74) in non-Hispanic White children.
  • In Hispanic children, no association was observed among daycare attendance, early infections, and risk of childhood ALL or c-ALL.
  • These results offer indirect yet strong support for the infectious disease hypothesis in the etiology of ALL in non-Hispanic White children and highlight an important ethnic difference.
  • [MeSH-major] Child Day Care Centers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 16103439.001).
  • [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 / NCHHSTP CDC HHS / PS / PS42 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; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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86. Noble SL, Sherer E, Hannemann RE, Ramkrishna D, Vik T, Rundell AE: Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia. J Theor Biol; 2010 Jun 7;264(3):990-1002
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  • [Title] Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a common childhood cancer in which nearly one-quarter of patients experience a disease relapse.
  • However, it has been shown that individualizing therapy for childhood ALL patients by adjusting doses based on the blood concentration of active drug metabolite could significantly improve treatment outcome.
  • An adaptive model predictive control (MPC) strategy is presented in which maintenance therapy for childhood ALL is personalized using routine patient measurements of red blood cell mean corpuscular volume as a surrogate for the active drug metabolite concentration.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Dose-Response Relationship, Drug. Models, Biological. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138060.001).
  • [ISSN] 1095-8541
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine
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87. Vormoor HJ: Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited. Cell Cycle; 2009 Apr 1;8(7):996-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited.
  • We have recently shown that in childhood acute lymphoblastic leukemia (ALL) blasts at different stages of immunophenotypic maturation possess stem cell properties.
  • Leukemia-propagating stem cells in ALL may be more frequent than previously thought!
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Neoplastic Stem Cells / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19270513.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34
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88. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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).
  • Clinical testing of CEP-701 as a novel molecularly targeted agent for the treatment of childhood ALL is warranted.
  • [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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89. Case M, Matheson E, Minto L, Hassan R, Harrison CJ, Bown N, Bailey S, Vormoor J, Hall AG, Irving JA: Mutation of genes affecting the RAS pathway is common in childhood acute lymphoblastic leukemia. Cancer Res; 2008 Aug 15;68(16):6803-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation of genes affecting the RAS pathway is common in childhood acute lymphoblastic leukemia.
  • We report the first comprehensive mutational screen of key exons of these genes in a large cohort of unselected acute lymphoblastic leukemia (ALL) cases at diagnosis (n = 86) and in a more selected cohort at disease recurrence (n = 47) using the sensitive method of denaturing high-performance liquid chromatography.
  • We show that somatic mutations that deregulate the pathway constitute one of the most common genetic aberrations in childhood ALL (cALL), being found in 35% of diagnostic and 25% of relapse samples.
  • [MeSH-major] Genes, ras / physiology. Mutation / genetics. Neoplasm Recurrence, Local / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Signal Transduction. ras Proteins / genetics
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Survival. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Enzyme Inhibitors / pharmacology. Exons / genetics. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinase Kinases / metabolism. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Peptide Fragments. Ploidies. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics. Proto-Oncogene Proteins B-raf / genetics. Remission Induction. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3 / genetics


90. Imanishi H, Okamura N, Yagi M, Noro Y, Moriya Y, Nakamura T, Hayakawa A, Takeshima Y, Sakaeda T, Matsuo M, Okumura K: Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma. J Hum Genet; 2007;52(2):166-71
Nature Publishing Group. Nature Publishing Group (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma.
  • Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Liver Diseases / genetics. Lymphoma / genetics. Methotrexate / therapeutic use. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


91. Bailey HD, Armstrong BK, de Klerk NH, Fritschi L, Attia J, Lockwood L, Milne E, Aus-ALL Consortium: Exposure to diagnostic radiological procedures and the risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2010 Nov;19(11):2897-909
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  • [Title] Exposure to diagnostic radiological procedures and the risk of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Diagnostic irradiation of the mother during pregnancy increases the risk of childhood acute lymphoblastic leukemia (ALL).
  • There is inconsistent evidence on associations between ALL and other parental or childhood diagnostic irradiation.
  • The aim of this analysis is to investigate whether diagnostic X-rays of the mother before birth, of the father before conception, or of the child increased the risk of childhood ALL.
  • [MeSH-major] Maternal Exposure / adverse effects. Paternal Exposure / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Pregnancy / radiation effects. Prenatal Exposure Delayed Effects / etiology. Radiography / adverse effects

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  • [Copyright] ©2010 AACR.
  • (PMID = 20861400.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Armstrong BK; Milne E; van Bockxmeer FM; Haber M; Scott RJ; Attia J; Norris MD; Bower C; de Klerk NH; Fritschi L; Kees UR; Miller M; Thompson JR; Bailey HD; Alvaro F; Cole C; Dalla Pozza L; Daubenton J; Downie P; Lockwood L; Kirby M; Marshall G; Smibert E; Suppiah R
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92. le Viseur C, Hotfilder M, Bomken S, Wilson K, Röttgers S, Schrauder A, Rosemann A, Irving J, Stam RW, Shultz LD, Harbott J, Jürgens H, Schrappe M, Pieters R, Vormoor J: In childhood acute lymphoblastic leukemia, blasts at different stages of immunophenotypic maturation have stem cell properties. Cancer Cell; 2008 Jul 8;14(1):47-58
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] In childhood acute lymphoblastic leukemia, blasts at different stages of immunophenotypic maturation have stem cell properties.
  • We examined the leukemic stem cell potential of blasts at different stages of maturation in childhood acute lymphoblastic leukemia (ALL).
  • These observations inform a model for leukemia-propagating stem cells in childhood ALL.

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  • (PMID = 18598943.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA034196-19; United States / NCI NIH HHS / CA / P30 CA034196; United States / NCI NIH HHS / CA / CA34196; United States / NCI NIH HHS / CA / P30 CA034196-19
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34; 0 / Immunoglobulins
  • [Other-IDs] NLM/ NIHMS59246; NLM/ PMC2572185
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93. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
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  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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94. Ariffin H, Chen SP, Kwok CS, Quah TC, Lin HP, Yeoh AE: Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group. J Pediatr Hematol Oncol; 2007 Jan;29(1):27-31
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  • [Title] Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group.
  • Childhood acute lymphoblastic leukemia (ALL) is clinically heterogeneous with prognostically and biologically distinct subtypes.
  • Although racial differences in frequency of different types of childhood ALL have been reported, many are confounded by selected or limited population samples.
  • The Malaysia-Singapore (MA-SPORE) Leukemia Study Group provided a unique platform for the study of the frequency of major subgroups of childhood ALL in a large cohort of unselected multiethnic Asian children.
  • Our study suggests that there are indeed significant and important racial differences in the frequency of subtypes of childhood ALL.
  • Comprehensive subgrouping of childhood ALL may reveal interesting population frequency differences of the various subtypes, their risk factors and hopefully, its etiology.
  • [MeSH-major] Asian Continental Ancestry Group. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ethnology

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  • [CommentIn] J Pediatr Hematol Oncol. 2007 Aug;29(8):585 [17762503.001]
  • (PMID = 17230064.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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95. Liu M, Ge Y, Payton SG, Aboukameel A, Buck S, Flatley RM, Haska C, Mohammad R, Taub JW, Matherly LH: Transcriptional regulation of the human reduced folate carrier in childhood acute lymphoblastic leukemia cells. Clin Cancer Res; 2006 Jan 15;12(2):608-16
Hazardous Substances Data Bank. FOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional regulation of the human reduced folate carrier in childhood acute lymphoblastic leukemia cells.
  • PURPOSE: The transcriptional regulation of the human reduced folate carrier (hRFC), involved in cellular uptake of methotrexate and reduced folates, was studied in childhood acute lymphoblastic leukemia (ALL).
  • In 40 ALL and 17 non-ALL specimens, 2 cosegregating high-frequency polymorphisms (T-1309/C-1217 and C-1309/T-1217; allelic frequencies of 36% and 64%, respectively) were detected in the A1/A2 promoter; none were detected in promoter B.
  • [MeSH-major] DNA Methylation. Gene Expression Regulation. Membrane Transport Proteins / genetics. Membrane Transport Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 16428507.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 76641
  • [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 / GATA1 Transcription Factor; 0 / Membrane Transport Proteins; 0 / Protein Isoforms; 0 / Reduced Folate Carrier Protein; 0 / SLC19A1 protein, human; 0 / Slc19a1 protein, mouse; 0 / Sp1 Transcription Factor; 0 / USF1 protein, human; 0 / Upstream Stimulatory Factors; 148971-36-2 / Ikaros Transcription Factor; 935E97BOY8 / Folic Acid
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96. Flotho C, Coustan-Smith E, Pei D, Iwamoto S, Song G, Cheng C, Pui CH, Downing JR, Campana D: Genes contributing to minimal residual disease in childhood acute lymphoblastic leukemia: prognostic significance of CASP8AP2. Blood; 2006 Aug 1;108(3):1050-7
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • [Title] Genes contributing to minimal residual disease in childhood acute lymphoblastic leukemia: prognostic significance of CASP8AP2.
  • In childhood acute lymphoblastic leukemia (ALL), early response to treatment is a powerful prognostic indicator.
  • In a separate cohort of 99 patients not included in the comparison of gene expression profiles and MRD, low levels of CASP8AP2 expression predicted a lower event-free survival (P = .02) and a higher rate of leukemia relapse (P = .01) and were an independent predictor of outcome.
  • Therefore, this gene is a strong candidate for inclusion in gene expression arrays specifically designed for leukemia diagnosis.

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  • (PMID = 16627760.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA60419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CASP8AP2 protein, human; 0 / Calcium-Binding Proteins
  • [Other-IDs] NLM/ PMC1895863
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97. Mullighan CG, Zhang J, Harvey RC, Collins-Underwood JR, Schulman BA, Phillips LA, Tasian SK, Loh ML, Su X, Liu W, Devidas M, Atlas SR, Chen IM, Clifford RJ, Gerhard DS, Carroll WL, Reaman GH, Smith M, Downing JR, Hunger SP, Willman CL: JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2009 Jun 9;106(23):9414-8
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  • [Title] JAK mutations in high-risk childhood acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) is a heterogeneous disease consisting of distinct clinical and biological subtypes that are characterized by specific chromosomal abnormalities or gene mutations.
  • We recently identified a poor prognostic subgroup of pediatric BCR-ABL1-negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1-positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype.
  • Here, we report activating mutations in the Janus kinases JAK1 (n = 3), JAK2 (n = 16), and JAK3 (n = 1) in 20 (10.7%) of 187 BCR-ABL1-negative, high-risk pediatric ALL cases.
  • The JAK-mutated cases had a gene expression signature similar to BCR-ABL1 pediatric ALL, and they had a poor outcome.

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  • (PMID = 19470474.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA118100; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / L40 CA142226; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / Howard Hughes Medical Institute / / ; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2695045
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98. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • We used standard methods to explore NOTCH1 mutations and other specific molecular markers in 15 early childhood T-ALL cases.
  • Despite being found in a lower frequency than that described for overall pediatric T-ALL, NOTCH1 alterations were the most frequent ones.
  • Other alterations included MLL(+) (n=4), SIL-TAL1(+) (n=3), FLT3 mutation (n=1) and HOX11L2(+) (n=1).
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19631984.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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99. Jones LK, Saha V: Philadelphia positive acute lymphoblastic leukaemia of childhood. Br J Haematol; 2005 Aug;130(4):489-500
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Philadelphia positive acute lymphoblastic leukaemia of childhood.
  • On current chemotherapeutic regimens, children with Philadelphia positive acute lymphoblastic leukaemia show a heterogeneous response to treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16098062.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 123
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100. Gadner H, Masera G, Schrappe M, Eden T, Benoit Y, Harrison C, Nachman J, Pui CH: The Eighth International Childhood Acute Lymphoblastic Leukemia Workshop ('Ponte di legno meeting') report: Vienna, Austria, April 27-28, 2005. Leukemia; 2006 Jan;20(1):9-17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Eighth International Childhood Acute Lymphoblastic Leukemia Workshop ('Ponte di legno meeting') report: Vienna, Austria, April 27-28, 2005.
  • The International Acute Lymphoblastic Leukemia Working Group, the so-called 'Ponte di Legno Workshop' has led to substantial progress in international collaboration in leukemia research.
  • Furthermore, collaborative projects of clinical relevance with special emphasis on rare genetic subtypes of Childhood ALL were established.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16281070.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61374; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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