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1. von Neuhoff C, Reinhardt D, Sander A, Zimmermann M, Bradtke J, Betts DR, Zemanova Z, Stary J, Bourquin JP, Haas OA, Dworzak MN, Creutzig U: Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98. J Clin Oncol; 2010 Jun 1;28(16):2682-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98.
  • PURPOSE: Because cytogenetic data are essential for risk stratification of childhood acute myeloid leukemia (AML), the impact of chromosomal aberrations is crucial.
  • PATIENTS AND METHODS: Data of a large group of patients younger than 18 years treated according to study AML-Berlin-Frankfurt-Münster (BFM) 98 (n = 454), including their cytogenetics, were analyzed.
  • CONCLUSION: Because the prognostic value of rare recurrent chromosomal aberrations still has to be elucidated, these data will contribute to future risk stratification for the treatment of pediatric AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Combined Modality Therapy. Confidence Intervals. Cytarabine / administration & dosage. Cytogenetic Analysis. Disease-Free Survival. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Idarubicin / administration & dosage. In Situ Hybridization, Fluorescence. Male. Probability. Proportional Hazards Models. Radiotherapy, Adjuvant. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Severity of Illness Index. Statistics, Nonparametric. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 20439630.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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2. Rubnitz JE, Razzouk BI, Lensing S, Pounds S, Pui CH, Ribeiro RC: Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia. Cancer; 2007 Jan 1;109(1):157-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia.
  • BACKGROUND: Outcome after recurrence of childhood acute myeloid leukemia (AML) is poor.
  • We performed this study to identify prognostic factors for recurrence and for survival after recurrence of AML.
  • METHODS: The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo AML who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied.
  • CONCLUSIONS: Survival after recurrence was poor in children with AML.
  • Novel therapies are urgently needed to prevent or to treat recurring AML.
  • [MeSH-major] Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Prognosis. Recurrence. Sex Factors. Stem Cell Transplantation. Survival Rate. Time Factors. Transplantation, Autologous

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17133407.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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3. Sayed HA, El-Mahallawy HA, Kaddah AM, Ismael HT, Talaat SM: Profile of infections in newly diagnosed patients with acute leukemia during the induction phase of treatment. J Egypt Natl Canc Inst; 2009 Dec;21(4):315-22
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  • [Title] Profile of infections in newly diagnosed patients with acute leukemia during the induction phase of treatment.
  • BACKGROUND AND PURPOSE: Acute leukemia is the most common pediatric malignancy.
  • The aim of the present study is to assess the type, frequency, and severity of infectious complications in a cohort of pediatric cancer patients treated at a single medical institution.
  • We also aim to identify factors affecting bloodstream infections in newly diagnosed ALL and AML pediatric patients during the induction phase of treatment.
  • PATIENTS AND METHODS: This study was carried out at the Department of Pediatric Oncology, National Cancer Institute, Cairo University, during the time period from January 1st to June 30th 2007.
  • Inclusion criteria were pediatric age group (from 0-16 years), newly diagnosed acute leukemia, positive blood culture and documented site of infection.
  • RESULTS: This is a retrospective study including 100 newly diagnosed cases of acute leukemia.
  • Fifty-four patients had ALL, and 46 patients had AML.
  • KEY WORDS: Acute leukemia - Blood stream infection - Bacterial infection - Pediatric cancer patients.

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  • (PMID = 21415868.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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4. Armengol G, Canellas A, Alvarez Y, Bastida P, Toledo JS, Pérez-Iribarne Mdel M, Camós M, Tuset E, Estella J, Coll MD, Caballín MR, Knuutila S: Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia. Leuk Lymphoma; 2010 Jan;51(1):114-24
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  • [Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.
  • We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).
  • Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Male. Polymerase Chain Reaction. Prognosis. Translocation, Genetic


5. Burjanivova T, Madzo J, Muzikova K, Meyer C, Schneider B, Votava F, Marschalek R, Stary J, Trka J, Zuna J: Prenatal origin of childhood AML occurs less frequently than in childhood ALL. BMC Cancer; 2006;6:100
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  • [Title] Prenatal origin of childhood AML occurs less frequently than in childhood ALL.
  • BACKGROUND: While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive.
  • Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant childhood AML and ALL patients for the presence of their respective leukemic markers.
  • In AML patients (n = 13, age 1-14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers.
  • We did not find patient-specific molecular markers in any patient with AML.
  • CONCLUSION: In the largest cohort examined so far we used identical approach for the backtracking of non-infant childhood ALL and AML.
  • Our data suggest that either the prenatal origin of AML is less frequent or the load of pre-leukemic cells is significantly lower at birth in AML compared to ALL cases.
  • [MeSH-major] Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Fetal Blood / chemistry. Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte. Leukemia, Myeloid / embryology. Oncogene Proteins, Fusion / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / embryology
  • [MeSH-minor] Bone Marrow Cells / chemistry. Child. Child, Preschool. Clone Cells / chemistry. Cohort Studies. Core Binding Factor Alpha 2 Subunit / blood. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / blood. Myeloid-Lymphoid Leukemia Protein / genetics. Neonatal Screening. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / blood. fms-Like Tyrosine Kinase 3 / genetics

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  • [Cites] Br J Haematol. 2003 Jul;122(1):24-9 [12823342.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):449-54 [15626757.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2000 Jul 1;96(1):264-8 [10891460.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Blood. 2001 Jul 15;98(2):478-82 [11435320.001]
  • [Cites] Blood. 2001 Oct 1;98(7):2272-4 [11568017.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2992-6 [11929791.001]
  • [Cites] Blood. 2002 May 15;99(10):3801-5 [11986239.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6 [12415113.001]
  • [Cites] Br J Cancer. 2002 Oct 21;87(9):994-9 [12434291.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):36-43 [12661004.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4640-1 [12756163.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):406-11 [12800152.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2202-6 [12931229.001]
  • [Cites] Leuk Lymphoma. 2003 Dec;44(12):2099-102 [14959854.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Apr;39(4):335-40 [14978794.001]
  • [Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]
  • [Cites] Nucleic Acids Res. 1995 Sep 25;23(18):3788-9 [7479012.001]
  • [Cites] Blood. 1997 Jan 1;89(1):281-5 [8978302.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 May-Jun;20(3):264-7 [9628441.001]
  • [Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4079-85 [10361104.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1057-62 [10419898.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1667-9 [12886258.001]
  • (PMID = 16630339.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF6 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1463004
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6. Olde Nordkamp L, Mellink C, van der Schoot E, van den Berg H: Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics? J Pediatr Hematol Oncol; 2009 Dec;31(12):930-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics?
  • BACKGROUND: Chromosomal abnormalities, such as t(9;22)(q34;q11) (ABL/BCR), t(12;21)(p13;q22) (TEL/AML1), and t(11q23) (MLL) are independent prognostic indicators in childhood acute lymphoblastic leukemia resulting in risk adapted therapy.
  • All consecutive patients under 18 years with acute lymphoblastic leukaemia were included.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Rearrangement. Humans. Infant. Infant, Newborn. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Retrospective Studies. Translocation, Genetic / genetics

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  • (PMID = 19875970.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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7. Hudson MM: Anthracycline cardiotoxicity in long-term survivors of childhood cancer: The light is not at the end of the tunnel. Pediatr Blood Cancer; 2007 Jun 15;48(7):649-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anthracycline cardiotoxicity in long-term survivors of childhood cancer: The light is not at the end of the tunnel.
  • [MeSH-major] Anthracyclines / adverse effects. Heart / drug effects. Heart Diseases / chemically induced. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Cohort Studies. Drug-Related Side Effects and Adverse Reactions. Follow-Up Studies. Humans. Infant. Multivariate Analysis. Risk Factors. Survivors. Time. Treatment Outcome

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  • [CommentOn] Pediatr Blood Cancer. 2007 Jun 15;48(7):651-62 [17183582.001]
  • (PMID = 17318875.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines
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8. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • LAF4 is the first gene fused with both AML1 and MLL in acute leukemia.
  • Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Child. DNA Mutational Analysis / methods. DNA, Complementary / analysis. Humans. Male. Models, Biological. Molecular Sequence Data

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  • (PMID = 17968322.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AFF3 protein, human; 0 / AML1-LAF4 fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
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9. Stumpel DJ, Schneider P, van Roon EH, Boer JM, de Lorenzo P, Valsecchi MG, de Menezes RX, Pieters R, Stam RW: Specific promoter methylation identifies different subgroups of MLL-rearranged infant acute lymphoblastic leukemia, influences clinical outcome, and provides therapeutic options. Blood; 2009 Dec 24;114(27):5490-8
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  • [Title] Specific promoter methylation identifies different subgroups of MLL-rearranged infant acute lymphoblastic leukemia, influences clinical outcome, and provides therapeutic options.
  • MLL-rearranged infant acute lymphoblastic leukemia (ALL) remains the most aggressive type of childhood leukemia, displaying a unique gene expression profile.
  • [MeSH-major] DNA Methylation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19855078.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE18400
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 5CSZ8459RP / Cytidine
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10. Zwaan CM, den Boer ML, Kazemier KM, Hählen K, Loonen AH, Reinhardt D, Creutzig U, Kaspers GJ, Pieters R: Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia? Blood; 2006 Jun 15;107(12):4975-6; author reply 4976-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia?
  • [MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Antibodies, Monoclonal / chemistry. Child. Child, Preschool. Cyclosporine / pharmacology. Female. Flow Cytometry. Humans. Male. Randomized Controlled Trials as Topic. Remission Induction

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  • [CommentOn] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • (PMID = 16754781.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / P-Glycoprotein; 83HN0GTJ6D / Cyclosporine
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11. Ribeiro RC, Razzouk BI, Pounds S, Hijiya N, Pui CH, Rubnitz JE: Successive clinical trials for childhood acute myeloid leukemia at St Jude Children's Research Hospital, from 1980 to 2000. Leukemia; 2005 Dec;19(12):2125-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successive clinical trials for childhood acute myeloid leukemia at St Jude Children's Research Hospital, from 1980 to 2000.
  • Despite substantial progress in the management of childhood acute myeloid leukemia (AML), only about 50% of patients are cured by intensive chemotherapy.
  • From 1980 to 2000, 251 patients <15 years of age with newly diagnosed AML were enrolled on one of the five consecutive St Jude AML studies.
  • With the exception of one protocol (AML-83), outcomes improved in general over the two decades.
  • The estimated 5-year event-free survival (+/-s.e.) was 30.8+/-5.6% for AML-80; 11.1+/-4.3% for AML-83; 35.9+/-7.4% for AML-87; 43.5+/-6.2% for AML-91; and 45.0+/-11.1% for AML-97.
  • Resistant or relapsed AML caused the great majority of treatment failures.
  • Increasing the intensity of chemotherapy (AML-87) did not improve outcome, partially because of toxicity, nor did prolonging postremission therapy by adding sequential myeloablative (AML-80) or nonmyeloablative (AML-83) chemotherapy cycles.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Survival Analysis. Treatment Failure. Treatment Outcome

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  • (PMID = 16281077.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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12. van Casteren NJ, van der Linden GH, Hakvoort-Cammel FG, Hählen K, Dohle GR, van den Heuvel-Eibrink MM: Effect of childhood cancer treatment on fertility markers in adult male long-term survivors. Pediatr Blood Cancer; 2009 Jan;52(1):108-12
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  • [Title] Effect of childhood cancer treatment on fertility markers in adult male long-term survivors.
  • BACKGROUND: Although it is accepted that pediatric cancer treatment harbors a risk of gonadal damage, large cohort studies using up-to-date fertility markers are lacking.
  • PROCEDURE: The aim of our study was to evaluate the gonadal toxicity of childhood cancer treatment using fertility markers.
  • We included 248 adult male long-term survivors of childhood cancer.
  • Significantly decreased Inhibin B levels and increased FSH levels were found in men treated for Hodgkin and non-Hodgkin lymphoma, acute-myeloid leukemia, neuroblastoma, and sarcoma as compared to other malignancies.
  • CONCLUSIONS: Severe gonadal impairment is a risk in a considerable subgroup of childhood cancer survivors based on current fertility markers like Inhibin B.
  • [MeSH-minor] Biomarkers / analysis. Child, Preschool. Cyclophosphamide / adverse effects. Female. Follicle Stimulating Hormone / analysis. Follow-Up Studies. Gonads / drug effects. Gonads / physiopathology. Humans. Inhibins / analysis. Leukemia, Myeloid, Acute / complications. Lymphoma / complications. Male. Neuroblastoma / complications. Procarbazine / adverse effects. Sarcoma / complications

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  • (PMID = 18819129.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / inhibin B; 35S93Y190K / Procarbazine; 57285-09-3 / Inhibins; 8N3DW7272P / Cyclophosphamide; 9002-68-0 / Follicle Stimulating Hormone
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13. Nebral K, König M, Schmidt HH, Lutz D, Sperr WR, Kalwak K, Brugger S, Dworzak MN, Haas OA, Strehl S: Screening for NUP98 rearrangements in hematopoietic malignancies by fluorescence in situ hybridization. Haematologica; 2005 Jun;90(6):746-52
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  • BACKGROUND AND OBJECTIVES: The aim of this study was to determine the incidence of rearrangements of NUP98 (the gene coding for nucleoporin 98kDa protein) in childhood acute myeloid leukemia (AML) and selected patients with 11p13-15 rearrangements.
  • DESIGN AND METHODS: Screening of 59 consecutive patients enrolled in the Austrian AML-BFM93 clinical trial was performed by dual-color FISH.
  • RESULTS: Among the 59 AML patients, one NUP98-NSD1 positive case (1.7%) was detected.
  • INTERPRETATION AND CONCLUSIONS: The observed frequency of 1.7% confirmed the low incidence of NUP98 rearrangements in childhood AML.
  • [MeSH-major] Chromosome Aberrations. Hematologic Neoplasms / diagnosis. Hematologic Neoplasms / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Chromosome Inversion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Molecular Sequence Data. Translocation, Genetic

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  • (PMID = 15951287.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / nuclear pore complex protein 98
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14. Manola KN: Cytogenetics of pediatric acute myeloid leukemia. Eur J Haematol; 2009 Nov;83(5):391-405
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  • [Title] Cytogenetics of pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a clinically and genetically heterogeneous disease accounting for 15-20% of all childhood acute leukemias, while it is responsible for more than half of the leukemic deaths in these patients.
  • This article focuses on the significance of cytogenetic analysis in pediatric AML supporting the importance of cytogenetic analysis in the pathogenesis, diagnosis, prognosis, follow-up and treatment selection in childhood AML.
  • Furthermore, it discusses the association of specific chromosome rearrangements with prenatal exposure to carcinogenic agents or therapeutic agents and highlights the ongoing and future research on pediatric AML in the evolving field of Cytogenetics.
  • [MeSH-major] Cytogenetics / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 19563518.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens, Environmental
  • [Number-of-references] 123
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15. Barnes E: Cancer coverage: the public face of childhood leukaemia in 1960s Britain. Endeavour; 2008 Mar;32(1):10-5
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  • [Title] Cancer coverage: the public face of childhood leukaemia in 1960s Britain.
  • The Ministry of Health and cancer research organisations struggled to find a fair and honest way to inform the public and affected families about childhood leukaemia without raising or crushing hope.
  • [MeSH-major] Antineoplastic Agents / history. Child Welfare / history. Leukemia, Myeloid, Acute / history. Quackery / history
  • [MeSH-minor] Child. Drug Design. Financing, Organized / history. Great Britain. History, 20th Century. Humans. Public Opinion. State Medicine / history


16. Barnard DR, Woods WG: Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update. Leuk Lymphoma; 2005 May;46(5):651-63
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  • [Title] Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update.
  • Treatment-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/t-AML) is a devastating complication of treatment for childhood cancer.
  • The understanding of the presentation, incidence, predisposing risk factors and pathobiology of t-MDS/t-AML is increasing.
  • This increased understanding has not yet been translated into improved outcomes of therapy for t-MDS/t-AML.
  • [MeSH-major] Leukemia, Myeloid / etiology. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Child. Female. Humans. Male. Neoplasms / therapy. Survivors


17. Gratwohl A: Activity survey and historical perspective of autologous stem cell transplantation in Europe. Semin Hematol; 2007 Oct;44(4):220-6
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  • Initially developed as a tool to restore rapid remission or chronic phase in patients with advanced leukemia without a sibling donor, it evolved over the last three decades to be used as a standard tool in patients with malignancies that are responsive to high-dose chemoradiotherapy.
  • Autologous HSCTs are the standard of care for defined patients with lymphoid malignancies and for certain solid tumors of childhood.
  • They continue to be evaluated in acute myeloid leukemia and are being investigated in phase II and III studies for defined severe autoimmune disorders.

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  • (PMID = 17961720.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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18. Stams WA, den Boer ML, Beverloo HB, Kazemier KM, van Wering ER, Janka-Schaub GE, Pieters R: Effect of the histone deacetylase inhibitor depsipeptide on B-cell differentiation in both TEL-AML1-positive and negative childhood acute lymphoblastic leukemia. Haematologica; 2005 Dec;90(12):1697-9
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  • [Title] Effect of the histone deacetylase inhibitor depsipeptide on B-cell differentiation in both TEL-AML1-positive and negative childhood acute lymphoblastic leukemia.
  • The fusion protein TEL-AML1 in t(12;21)+ acute lymphoblastic leukemia (ALL) recruits co-repressors and histone deacetylases (HDAC), which transrepress AML1 target genes.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. B-Lymphocytes / drug effects. Core Binding Factor Alpha 2 Subunit / analysis. Depsipeptides / pharmacology. Histone Deacetylase Inhibitors. Oncogene Proteins, Fusion / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, Differentiation, B-Lymphocyte / analysis. Antineoplastic Agents / pharmacology. Asparaginase / pharmacology. Bone Marrow Cells / drug effects. Bone Marrow Cells / enzymology. Butyrates / pharmacology. Cell Differentiation / drug effects. Humans. Myeloid Cells / drug effects. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology

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  • (PMID = 16330447.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Antineoplastic Agents; 0 / Butyrates; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Depsipeptides; 0 / Histone Deacetylase Inhibitors; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; CX3T89XQBK / romidepsin; EC 3.5.1.1 / Asparaginase
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19. Menendez P, Catalina P, Rodríguez R, Melen GJ, Bueno C, Arriero M, García-Sánchez F, Lassaletta A, García-Sanz R, García-Castro J: Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene. J Exp Med; 2009 Dec 21;206(13):3131-41
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  • [Title] Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene.
  • MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero.
  • BM mesenchymal stem cells (BM-MSC) from 38 children diagnosed with cytogenetically different acute leukemias were screened for leukemic fusion genes.
  • Fusion genes were absent in BM-MSCs of childhood leukemias carrying TEL-AML1, BCR-ABL, AML1-ETO, MLL-AF9, MLL-AF10, MLL-ENL or hyperdiploidy.
  • [MeSH-major] Mesenchymal Stromal Cells / metabolism. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Cells, Cultured. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / analysis. Gene Rearrangement. Homeostasis. Humans. Infant


20. Woods WG: Curing childhood acute myeloid leukemia (AML) at the half-way point: promises to keep and miles to go before we sleep. Pediatr Blood Cancer; 2006 May 1;46(5):565-9
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  • [Title] Curing childhood acute myeloid leukemia (AML) at the half-way point: promises to keep and miles to go before we sleep.
  • Childhood and adolescent acute myeloid leukemia (AML) is traditionally one of the hardest childhood cancers to successfully treat and had an overall survival well under 10% in the 1960s.
  • Some of the challenges that will lead to ongoing reduction of population-based mortality for AML through young adulthood include:.
  • (1) improving access of adolescents to pediatric AML therapy;.
  • (3) individualized therapy based on individual genetics and leukemia cell biology;.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Disease-Free Survival. Enzyme Inhibitors / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Remission Induction. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


21. Styczynski J, Toporski J, Wysocki M, Debski R, Chybicka A, Boruczkowski D, Wachowiak J, Wojcik B, Kowalczyk J, Gil L, Balwierz W, Matysiak M, Krawczuk-Rybak M, Balcerska A, Sonta-Jakimczyk D: Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia. Anticancer Res; 2007 May-Jun;27(3B):1547-51
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  • [Title] Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia.
  • BACKGROUND: The prognostic role of the ex vivo drug resistance profile has not yet been proved in childhood acute myeloid leukemia (AML).
  • The aim of the study was the analysis of the impact of the ex vivo drug resistance profile in a cohort of 44 children with AML undergoing hematopoietic stem cell transplantation (HSCT).
  • CONCLUSION: The combined drug resistance profile to fludarabine, treosulfan and etoposide may be useful for better stratification of children with AML undergoing stem cell transplantation or to indicate the necessity for additional post-transplant therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Granulocyte Precursor Cells / drug effects. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Busulfan / analogs & derivatives. Busulfan / pharmacology. Child. Child, Preschool. Etoposide / pharmacology. Female. Humans. Infant. Male. Prognosis. Recurrence. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 17595774.001).
  • [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 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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22. Zhang LJ, Wang PP, Lu XL, He J, Li Y, Zhai M: [Identification of chromosome 21 anomalies in patients with acute myeloid leukemia by fluorescence in situ hybridization]. Zhonghua Yi Xue Za Zhi; 2006 Dec 26;86(48):3393-6
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  • [Title] [Identification of chromosome 21 anomalies in patients with acute myeloid leukemia by fluorescence in situ hybridization].
  • OBJECTIVE: To investigate the possible complex anomalies of chromosome 21 in patients with acute myeloid leukemia (AML).
  • METHODS: Fluorescence in situ hybridization (FISH) was performed by using commercially available DNA probes, including whole chromosome painting probes, locus specific probes, and specific and dual color translocation fusion probes, on 50 AML patients, 37 adults and 13 children.
  • Four of the 13 pediatric patients were found to have trisomy of chromosome 21, among which one had an additional chromosome rearrangement: 47-49,XX,der(1)t(1;17)(p36.1;q23), +4, +10, der(11)t(11;17)(q23;q23), -17, -18, +20, +21.
  • CONCLUSION: Rearrangement of chromosome 21 is common in both childhood and adult patients with AML.
  • However, childhood patients tend to have numerical change of chromosome 21, whereas the adult patients are likely to have structural changes of chromosome 21.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Middle Aged

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  • (PMID = 17313849.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi 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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23. Yang YL, Lin SR, Chen JS, Hsiao CC, Lin KH, Sheen JM, Cheng CN, Wu KH, Lin SW, Yu SL, Chen HY, Lu MY, Chang HH, Yen CT, Lin JF, Su YH, Li YP, Lin CY, Jou ST, Lin DT: Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Nov;32(8):e323-30
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  • [Title] Multiplex reverse transcription-polymerase chain reaction as diagnostic molecular screening of 4 common fusion chimeric genes in Taiwanese children with acute lymphoblastic leukemia.
  • BACKGROUND: The classification of B-lineage acute lymphoblastic leukemia (ALL) by specific chromosomal translocations has prognostic implications for risk-directed therapy.
  • The patients received risk-directed protocols of the Taiwan Pediatric Oncology Group-ALL-2002 that consisted of multiple chemotherapeutic agents of different intensities.
  • CONCLUSIONS: The biological factors of leukemia cells are associated with treatment outcomes in childhood ALL.
  • [MeSH-major] Genetic Testing / methods. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Cell Lineage / genetics. Child. Child, Preschool. Chimera. Core Binding Factor Alpha 2 Subunit. Female. Fusion Proteins, bcr-abl / genetics. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction / methods. Prognosis. Risk Factors. Sensitivity and Specificity. Taiwan / epidemiology

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  • (PMID = 20930648.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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24. Trobaugh-Lotrario AD, Kletzel M, Quinones RR, McGavran L, Proytcheva MA, Hunger SP, Malcolm J, Schissel D, Hild E, Giller RH: Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT). Bone Marrow Transplant; 2005 Jan;35(2):143-9
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  • [Title] Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT).
  • Pediatric acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) with monosomy 7 is associated with poor disease-free survival when treated by conventional chemotherapy, immunosuppression or supportive measures.
  • To better understand the curative potential of HSCT in these patients, all cases of AML and MDS with monosomy 7 treated by two transplant programs (1992 to present) were reviewed.
  • Primary diagnoses were MDS (N = 5), therapy-related MDS (N = 3), AML (N = 5) and therapy-related AML (N = 3).
  • Toxicity caused deaths of the five nonsurviving patients, four of whom were transplanted with active leukemia.
  • Allogeneic HSCT is effective therapy for childhood AML and MDS associated with monosomy 7, particularly for patients with AML in complete remission and MDS.
  • [MeSH-major] Chromosomes, Human, Pair 7. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Monosomy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Cause of Death. Child. Child, Preschool. Disease Management. Female. Humans. Male. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous. Treatment Outcome


25. Radhi M, Meshinchi S, Gamis A: Prognostic factors in pediatric acute myeloid leukemia. Curr Hematol Malig Rep; 2010 Oct;5(4):200-6
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  • [Title] Prognostic factors in pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML), a heterogeneous group of diseases with variable responses to the same therapy, comprises nearly a quarter of childhood acute leukemias.
  • Although historically very few prognostic markers have been incorporated into therapeutic decision making in AML, recent advances in technology have enabled identification of numerous factors associated with disease outcome.
  • This review provides a detailed analysis of most clinically relevant factors associated with disease outcome in childhood AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis
  • [MeSH-minor] Age Factors. Biomarkers, Tumor. Body Mass Index. Child. Cytogenetics. Humans. Polymorphism, Genetic. Prognosis. Risk Factors. Sex Factors

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  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):62-7 [15604893.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]
  • [Cites] Leukemia. 2002 May;16(5):776-84 [11986937.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S108-12 [15124698.001]
  • [Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1279-87 [11230469.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Best Pract Res Clin Haematol. 2008 Dec;21(4):621-8 [19041601.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4641-7 [17299091.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]
  • [Cites] Blood. 1985 Feb;65(2):298-304 [3881140.001]
  • [Cites] Cancer. 2008 Jan 15;112(2):407-15 [18058809.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]
  • [Cites] Br J Haematol. 1999 Oct;107(1):69-79 [10520026.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jan;48(1):10-5 [16642489.001]
  • [Cites] Blood. 2009 Sep 17;114(12):2489-96 [19528532.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4172-4 [17909077.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):578-85 [20038731.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4791-7 [18695255.001]
  • [Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Leukemia. 2002 Apr;16(4):601-7 [11960339.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]
  • [Cites] Best Pract Res Clin Haematol. 2009 Dec;22(4):523-8 [19959103.001]
  • [Cites] J Clin Oncol. 2004 Apr 15;22(8):1404-12 [15084614.001]
  • (PMID = 20652454.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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26. Franklin JL, Seibel NL, Krailo M, Fu C, Adamson PC, Reaman G, Children's Oncology Group: Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report. Pediatr Blood Cancer; 2008 Mar;50(3):533-6
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  • [Title] Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report.
  • BACKGROUND: To determine the response rate and toxicity of docetaxel when administered as a 60 mg/m(2) dose by 1 hr intravenous (IV) infusion weekly x 3 weeks in children with relapsed acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML).
  • PROCEDURE: Patients who were under the age of 22-year-old at the time of the original ALL or AML diagnosis and in a second relapse were accrued from August 2002 to May 2005 for this Children's Oncology Group (COG) phase 2 study (ADVL0023).
  • Ten patients with ALL and two patients with AML were enrolled.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Leukemia / drug therapy. Salvage Therapy. Taxoids / therapeutic use
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Bone Marrow Diseases / chemically induced. Child. Child, Preschool. Drug Administration Schedule. Female. Fever / etiology. Humans. Infant. Infusions, Intravenous. Leukemia, Myeloid / drug therapy. Male. Neutropenia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Failure

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17668867.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
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27. Guo Y, Chen YM, Zou Y, Chen XJ, Zhang L, Wang SC, Zhu XF: [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Oct;11(10):793-6
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  • [Title] [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study].
  • OBJECTIVE: To investigate the biologic features of childhood acute leukemia in the northern region of China through a small cohort study in a single center.
  • METHODS: The medical records of 688 children with acute leukemia (age< or =15 years) who were initially diagnosed at Blood Disease Hospital of Chinese Academy of Medical Sciences from October 2003 to June 2006 were retrospectively studied.
  • RESULTS: Four hundred children were diagnosed as acute lymphoblastic leukemia (ALL), with a peak incidence at ages of 1-4 years.
  • Two hundred and twenty-two children were diagnosed as acute myeloid leukemia (AML), with a peak incidence at ages of 10-15 years.
  • AML-M2 was the most common subtype.
  • Acute hybrid leukemia (AHL) was confirmed in 24 children (4.2%), with a median age of 9 years.
  • Seventy-four percent of the children with (AHL) had mainly CD13 and CD33 expression in myeloid antigen integral.
  • CONCLUSIONS: There are differences in the biologic features of childhood acute leukemia between the northern region of China and other regions and races, which suggests that there might be differences in the pathogenesis of childhood acute leukemia in different environmental exposures.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. China / epidemiology. Female. Humans. Infant. Infant, Newborn. Male. Retrospective Studies

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  • (PMID = 19849934.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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28. Haddy TB, Mosher RB, Reaman GH: Late effects in long-term survivors after treatment for childhood acute leukemia. Clin Pediatr (Phila); 2009 Jul;48(6):601-8
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  • [Title] Late effects in long-term survivors after treatment for childhood acute leukemia.
  • BACKGROUND: This is a report of late effects in childhood cancer survivors seen in the follow-up clinic of a single institution.
  • MATERIALS AND METHODS: There were 324 acute leukemia survivors in the database of the Long Term Follow Up Clinic of Children's National Medical Center from January 1, 1997, through June 30, 2005.
  • RESULTS: Of the 324 acute leukemia survivors, 228 were white, 48 black, 20 Hispanic, and 12 other.
  • More black and Hispanic children had acute myeloid leukemia, relapses, cardiac problems, and hypertension than white and other subjects.
  • CONCLUSION: Childhood cancer survivors require lifelong monitoring, with prompt identification and treatment of adverse late effects.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Survivors / statistics & numerical data
  • [MeSH-minor] Adolescent. Adolescent Development / drug effects. Adolescent Development / radiation effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation / adverse effects. Child. Child Development / drug effects. Child Development / radiation effects. Child, Preschool. Cognition Disorders / chemically induced. Continuity of Patient Care. Female. Follow-Up Studies. Health Status. Humans. Infant. Infant, Newborn. Learning Disorders / chemically induced. Male. Neuromuscular Diseases / chemically induced. Obesity / chemically induced. Radiotherapy, Adjuvant / adverse effects. Retrospective Studies. Secondary Prevention. Stress, Psychological / chemically induced. United States / epidemiology

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  • (PMID = 19264722.001).
  • [ISSN] 0009-9228
  • [Journal-full-title] Clinical pediatrics
  • [ISO-abbreviation] Clin Pediatr (Phila)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
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  • [Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics
  • [MeSH-minor] Child. Humans. Male. Molecular Sequence Data

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  • (PMID = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
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30. Gudowius S, Recker K, Laws HJ, Dirksen U, Tröger A, Wieczorek U, Furlan S, Göbel U, Hanenberg H: Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL. Klin Padiatr; 2006 Nov-Dec;218(6):327-33
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  • [Title] Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL.
  • BACKGROUND: Contemporary risk adapted treatment protocols for childhood acute lymphoblastic leukemia (ALL) rely on accurate risk assessment strategies for disease re-occurrence by incorporating clinical parameters as well as immunological, molecular and cytogenetic features of the blasts at initial manifestation.
  • Other myeloid antigens (CD13, CD14, CD15, CD65) were positive on blasts in < 25 % of patients.
  • CONCLUSIONS: These analyses clearly identified the three antigens CD19, CD22 and HLA-DR present on blasts in more than 90 % of patients as potential target structures for targeted therapies with native or toxin-bound monoclonal antibodies in childhood ALL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD19 / analysis. Burkitt Lymphoma / immunology. HLA-DR Antigens / analysis. Immunotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sialic Acid Binding Ig-like Lectin 2 / analysis
  • [MeSH-minor] Adolescent. Child. Female. Flow Cytometry. Humans. Immunophenotyping. Risk Assessment

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  • (PMID = 17080335.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 2
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31. Styczynski J, Wysocki M, Debski R, Czyzewski K, Balwierz W, Juraszewska E, Matysiak M, Malinowska I, Stanczak E, Sońta-Jakimczyk D, Szczepanski T, Wachowiak J, Konatkowska B, Balcerska A, Ploszynska A, Kowalczyk J, Stefaniak J, Badowska W, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M: In vitro sensitivity of leukemic cells to nucleoside derivatives in childhood acute leukemias: good activity in leukemic relapses. Neoplasma; 2005;52(1):74-8
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  • [Title] In vitro sensitivity of leukemic cells to nucleoside derivatives in childhood acute leukemias: good activity in leukemic relapses.
  • Nucleoside analogues such as fludarabine and cladribine are used in therapy of indolent lymphomas and leukemias in adults, while cytarabine is used mainly in protocols for acute leukemias.
  • The objective of the study was the analysis of in vitro cellular drug sensitivity in childhood acute lymphoblastic (ALL) and myeloid (AML) leukemia.
  • Isolated leukemic cells obtained from 264 patients, including 152 initial ALL, 45 relapsed ALL, 54 initial AML and 13 relapsed AML were tested for cytotoxicity for fludarabine, cladribine, and cytarabine by the MTT assay.
  • Samples of relapsed ALL and initial AML were more resistant than ALL de novo ones.
  • Unexpectedly, no differences were observed between initial and relapsed AML samples for all tested drugs, what suggests that nucleoside analogues are active drugs in relapsed AML, which is commonly regarded as a resistant disease.
  • In summary, tested nucleoside analogues presented relatively good activity against childhood leukemias at relapse stage.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cladribine / pharmacology. Cytarabine / pharmacology. Leukemia, Myeloid / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
  • [MeSH-minor] Adolescent. Adult. Cell Death. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Infant, Newborn. Male. Recurrence. Tumor Cells, Cultured

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  • (PMID = 15739031.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 47M74X9YT5 / Cladribine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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32. Olcay L, Aribaş BK, Gökçe M: A patient with acute myeloblastic leukemia who presented with conus medullaris syndrome and review of the literature. J Pediatr Hematol Oncol; 2009 Jun;31(6):440-7
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  • [Title] A patient with acute myeloblastic leukemia who presented with conus medullaris syndrome and review of the literature.
  • In childhood, the conus medullaris syndrome owing to leukemia is rare.
  • Here, a 12-year-old boy with acute myeloblastic leukemia, maxillary mass, and conus medullaris syndrome is reported.
  • A biopsy from the maxillary mass revealed "granulocytic sarcoma."
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Spinal Cord Compression / etiology
  • [MeSH-minor] Antigens, CD / metabolism. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Child. Combined Modality Therapy. Face / pathology. Flow Cytometry. Humans. Magnetic Resonance Imaging. Male. Radiotherapy

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  • (PMID = 19648794.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
  • [Number-of-references] 34
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33. Roman E, Simpson J, Ansell P, Lightfoot T, Mitchell C, Eden TO: Perinatal and reproductive factors: a report on haematological malignancies from the UKCCS. Eur J Cancer; 2005 Mar;41(5):749-59
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  • The United Kingdom Childhood Cancer Study was designed to examine the potential aetiological role of a range of perinatal and reproductive factors.
  • Associations were seen for severe hyperemesis (Odds Ratio=3.6, 95%Confidence Interval=1.3-10.1, for all leukaemias), polyhydramnios (OR=4.0, 95%CI=1.5-10.3, for acute myeloid leukaemia (AML)), anaemia (haemoglobin <10 g, OR=2.6, 95%CI=1.7-4.1, for AML), and pre-eclampsia (OR=1.7, 95%CI=1.1-2.7, for non-Hodgkin's lymphoma).
  • Mothers' whose children developed common B-cell precursor acute lymphoblastic leukaemia (ALL) were more likely to have had a previous molar pregnancy (OR=5.2, 95%CI=1.9-14.7).
  • Gender-specific analysis revealed that findings often differed markedly for boys and girls; and, in common with other reports, strong associations with Down's syndrome were seen for both ALL and AML.
  • [MeSH-minor] Acute Disease. Adolescent. Birth Weight. Case-Control Studies. Child. Child, Preschool. Down Syndrome. Female. Humans. Infant. Infant, Newborn. Leukemia, Myeloid / etiology. Male. Odds Ratio. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Pregnancy

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  • (PMID = 15763652.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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34. Choi HW, Shin MG, Sawyer JR, Cho D, Kee SJ, Baek HJ, Kook H, Kim HJ, Shin JH, Suh SP, Hwang TJ, Ryang DW: Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22). Cancer Genet Cytogenet; 2006 Jun;167(2):172-6
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  • [Title] Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22).
  • We report on a case of pediatric acute myelocytic leukemia showing 47,XX,+10,t(16;21)(p11;q22) that resulted in an unusual TLS/FUS-ERG chimeric transcript.
  • The leukemic cells showed erythrophagocytosis, positive reactions for myeloperoxidase and Sudan black B stains, and negative reactions for periodic acid-Schiff and alpha-naphtyl butyrate esterase stains as well as expression of myeloid antigens.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Marrow Cells / cytology. Child, Preschool. Chromosomes, Human, Pair 10. Female. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Trisomy

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  • (PMID = 16737920.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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35. Bellezza I, Tucci A, Minelli A: 2-Chloroadenosine and human prostate cancer cells. Anticancer Agents Med Chem; 2008 Oct;8(7):783-9
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  • Cladribine, i.e.2-deoxy-Chloroadenosine is currently in use as chemotherapeutic agent in chronic lymphoid malignancies and pediatric acute myelogenous leukemia whereas the structurally related counterpart, 2-Chloroadenosine, has been less studied.

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  • (PMID = 18855579.001).
  • [ISSN] 1871-5206
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-23; 0 / Receptor, PAR-1; 146-77-0 / 2-Chloroadenosine
  • [Number-of-references] 137
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36. Shimada A, Taki T, Kubota C, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y: No nucleophosmin mutations in pediatric acute myeloid leukemia with normal karyotype: a study of the Japanese Childhood AML Cooperative Study Group. Leukemia; 2007 Jun;21(6):1307
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  • [Title] No nucleophosmin mutations in pediatric acute myeloid leukemia with normal karyotype: a study of the Japanese Childhood AML Cooperative Study Group.
  • [MeSH-major] Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. DNA Mutational Analysis. Humans. Infant. Infant, Newborn. Japan. Karyotyping. Mutation


37. Bhushan B, Chauhan PS, Saluja S, Verma S, Mishra AK, Siddiqui S, Kapur S: Aberrant phenotypes in childhood and adult acute leukemia and its association with adverse prognostic factors and clinical outcome. Clin Exp Med; 2010 Mar;10(1):33-40
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  • [Title] Aberrant phenotypes in childhood and adult acute leukemia and its association with adverse prognostic factors and clinical outcome.
  • Occurrence of aberrant phenotypes in childhood and adult acute leukemia (AL) differs considerably in independent studies and their association with prognostic factors is still controversial.
  • In the present study, 214 patients with AL (106 children and 108 adults) were evaluated for the aberrant expression of CD33 in ALL (B cell and T cell) and CD3, CD5, CD7, and CD19 in AML.
  • In AML, aberrant expression of CD19 was expressed in 52 and 32% while CD7 was expressed in 14 and 15% cases of childhood and adult AML, respectively.
  • One adult patient (AML-M5) showed expression of CD3, CD5, and CD19.
  • In summary, aberrant phenotype was commonly seen in adults than childhood B-ALL while in AML, aberrant phenotype was more common in children than adults.
  • CD19 was most commonly expressed antigen followed by CD7 in both childhood and adult AML.
  • Interestingly, aberrant phenotype was not found in childhood T-ALL; however, it was seen in 33% cases of adults.
  • We did not find any association of aberrant phenotype with adverse prognosis factors, CD34 marker, and clinical outcome except the absence of auer rod which was found to be significantly associated with aberrant phenotype of childhood AML (P = 0.01).
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / biosynthesis. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Phenotype. Prognosis. Treatment Outcome. Young Adult

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  • [Cites] Haematologica. 1997 Jan-Feb;82(1):31-7 [9107079.001]
  • [Cites] Pediatr Hematol Oncol. 1995 Sep-Oct;12(5):463-9 [8519631.001]
  • [Cites] Leuk Lymphoma. 2001 Jun;42(1-2):75-82 [11699224.001]
  • [Cites] N Engl J Med. 1991 Mar 21;324(12):800-8 [1997852.001]
  • [Cites] N Engl J Med. 1987 Apr 30;316(18):1111-7 [3494942.001]
  • [Cites] Cytometry B Clin Cytom. 2008 Jan;74(1):25-9 [18061959.001]
  • [Cites] Exp Mol Pathol. 2007 Dec;83(3):462-3 [17927977.001]
  • [Cites] Ann Hematol. 1995 Apr;70(4):189-94 [7748963.001]
  • [Cites] Blood. 1993 May 1;81(9):2399-405 [7683218.001]
  • [Cites] Cancer. 1995 Nov 1;76(9):1564-70 [8635059.001]
  • [Cites] J Trop Pediatr. 2000 Apr;46(2):73-8 [10822932.001]
  • [Cites] Blood. 1993 Jul 15;82(2):343-62 [8329694.001]
  • [Cites] Am J Hematol. 1998 Aug;58(4):278-84 [9692390.001]
  • [Cites] Blood. 1988 Aug;72(2):579-87 [3261183.001]
  • [Cites] J Clin Oncol. 1990 Aug;8(8):1389-98 [1696310.001]
  • [Cites] Blood. 1992 Nov 15;80(10):2471-8 [1421370.001]
  • [Cites] Blood. 1991 Sep 1;78(5):1327-37 [1878594.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]
  • [Cites] Blood. 1991 May 15;77(10):2242-50 [1709379.001]
  • [Cites] Am J Clin Pathol. 1998 Feb;109(2):211-20 [9583894.001]
  • [Cites] Blood. 2000 Aug 1;96(3):870-7 [10910899.001]
  • [Cites] Leukemia. 1994 Mar;8(3):388-94 [7907393.001]
  • [Cites] Haematologica. 2001 Aug;86(8):801-6 [11522535.001]
  • [Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]
  • [Cites] Exp Mol Pathol. 2007 Dec;83(3):471-3 [17963747.001]
  • [Cites] Blood. 1993 Aug 1;82(3):889-94 [7687897.001]
  • [Cites] J Exp Clin Cancer Res. 2007 Sep;26(3):313-21 [17987789.001]
  • [Cites] Leukemia. 1991 Aug;5(8):637-45 [1886419.001]
  • [Cites] Exp Mol Pathol. 2005 Aug;79(1):39-41 [16005710.001]
  • [Cites] Leukemia. 1993 Apr;7(4):489-98 [7681917.001]
  • [Cites] J Egypt Natl Canc Inst. 2006 Sep;18(3):244-9 [17671534.001]
  • [Cites] Ann Hematol. 2002 Sep;81(9):498-503 [12373349.001]
  • [Cites] Blood. 1992 May 1;79(9):2415-22 [1571553.001]
  • [Cites] Br J Haematol. 1989 Dec;73(4):480-5 [2482063.001]
  • [Cites] Zhonghua Er Ke Za Zhi. 2003 May;41(5):334-7 [14751050.001]
  • [Cites] Blood. 1997 Jul 1;90(1):28-35 [9207434.001]
  • [Cites] Leuk Res. 1990;14(1):23-6 [1689436.001]
  • [Cites] Blood. 1991 Sep 1;78(5):1292-300 [1715222.001]
  • [Cites] Blood. 1983 Jun;61(6):1138-45 [6404327.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1419-29 [1517785.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2118-26 [7807999.001]
  • [Cites] Hua Xi Yi Ke Da Xue Xue Bao. 2002 Jan;33(1):118-20 [12599447.001]
  • [Cites] Blood. 1993 Jun 1;81(11):3083-90 [8499643.001]
  • [Cites] Haematologica. 2007 Mar;92(3):342-8 [17339183.001]
  • [Cites] Am J Clin Pathol. 2002 Mar;117(3):380-9 [11888077.001]
  • (PMID = 19779962.001).
  • [ISSN] 1591-9528
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
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38. Stam RW, Den Boer ML, Schneider P, de Boer J, Hagelstein J, Valsecchi MG, de Lorenzo P, Sallan SE, Brady HJ, Armstrong SA, Pieters R: Association of high-level MCL-1 expression with in vitro and in vivo prednisone resistance in MLL-rearranged infant acute lymphoblastic leukemia. Blood; 2010 Feb 4;115(5):1018-25
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  • [Title] Association of high-level MCL-1 expression with in vitro and in vivo prednisone resistance in MLL-rearranged infant acute lymphoblastic leukemia.
  • MLL-rearranged acute lymphoblastic leukemia (ALL) represents an unfavorable type of leukemia that often is highly resistant to glucocorticoids such as prednisone and dexamethasone.
  • Because response to prednisone largely determines clinical outcome of pediatric patients with ALL, overcoming resistance to this drug may be an important step toward improving prognosis.
  • Here, we show how gene expression profiling identifies high-level MCL-1 expression to be associated with prednisolone resistance in MLL-rearranged infant ALL, as well as in more favorable types of childhood ALL.
  • To validate this observation, we determined MCL-1 expression with quantitative reverse transcription-polymerase chain reaction in a cohort of MLL-rearranged infant ALL and pediatric noninfant ALL samples and confirmed that high-level MCL-1 expression is associated with prednisolone resistance in vitro.
  • Finally, down-regulation of MCL-1 in prednisolone-resistant MLL-rearranged leukemia cells by RNA interference, to some extent, led to prednisolone sensitization.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Cell Survival / drug effects. Child. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Gene Rearrangement. Glucocorticoids / pharmacology. Glucocorticoids / therapeutic use. Histone-Lysine N-Methyltransferase. Humans. Immunoblotting. Infant. Myeloid Cell Leukemia Sequence 1 Protein. Oligonucleotide Array Sequence Analysis. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction


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

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  • (PMID = 20672366.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / HOXB2 protein, human; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
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40. Suzuki N, Yumura-Yagi K, Yoshida M, Hara J, Nishimura S, Kudoh T, Tawa A, Usami I, Tanizawa A, Hori H, Ito Y, Miyaji R, Oda M, Kato K, Hamamoto K, Osugi Y, Hashii Y, Nakahata T, Horibe K, Japan Association of Childhood Leukemia Study (JACLS): Outcome of childhood acute lymphoblastic leukemia with induction failure treated by the Japan Association of Childhood Leukemia study (JACLS) ALL F-protocol. Pediatr Blood Cancer; 2010 Jan;54(1):71-8
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  • [Title] Outcome of childhood acute lymphoblastic leukemia with induction failure treated by the Japan Association of Childhood Leukemia study (JACLS) ALL F-protocol.
  • BACKGROUND: Children with acute lymphoblastic leukemia (ALL) who fail to achieve complete remission (CR) after induction therapy (induction failure: IF) have a poor prognosis; however, there have been few prospective studies in patients with IF.
  • Twenty-three of these patients entered the F-protocol study, which mainly consisted of acute-myeloid-leukemia-oriented chemotherapy followed by scheduled hematopoietic cell transplantation (HCT).
  • CONCLUSION: Acute-myeloid-leukemia-oriented chemotherapy followed by scheduled HCT is a promising treatment strategy for non-Ph(+) ALL patients with IF.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Male. Philadelphia Chromosome. Prognosis. Prospective Studies. Remission Induction. Survival Rate. Treatment Outcome


41. Lan ZJ, Tang YM, Shen HQ, Qian BQ, Ning BT, Chen YH: [Evaluation of the P-gp pump function on leukemic cell membrane and proper application of its reversal agents with Calcein-AM and flow cytometry]. Zhonghua Er Ke Za Zhi; 2007 May;45(5):334-8
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  • OBJECTIVE: Leukemia is the most common malignancy in children.
  • During the past decade, very high cure rates of childhood acute lymphoblastic leukemia (ALL) have been reported both at home and abroad.
  • However, the cure rates of children with acute myeloid leukemia (AML) remain low due to the multiple-drug resistance (MDR).
  • P-glycoprotein (P-gp) is one of the most important mechanisms of MDR for leukemia cells.
  • The present study aimed to evaluate the P-gp pump function on leukemia cell membrane and the effects of the combined administration of the reversal agents cyclosporin A (CSA) and verapamil (VER) through the observation of Calcein-AM (C-AM) metabolism in the cell line K562 and its multi-drug resistant subline K562/VCR.
  • [MeSH-minor] Child. Flow Cytometry / methods. Humans. K562 Cells. Tumor Cells, Cultured. Verapamil / pharmacology. Vincristine / pharmacology

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  • (PMID = 17697617.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fluoresceins; 0 / P-Glycoprotein; 148504-34-1 / calcein AM; 5J49Q6B70F / Vincristine; CJ0O37KU29 / Verapamil; V0YM2B16TS / fluorexon
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42. Bresolin S, Zecca M, Flotho C, Trentin L, Zangrando A, Sainati L, Stary J, de Moerloose B, Hasle H, Niemeyer CM, Te Kronnie G, Locatelli F, Basso G: Gene expression-based classification as an independent predictor of clinical outcome in juvenile myelomonocytic leukemia. J Clin Oncol; 2010 Apr 10;28(11):1919-27
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  • [Title] Gene expression-based classification as an independent predictor of clinical outcome in juvenile myelomonocytic leukemia.
  • PURPOSE Juvenile myelomonocytic leukemia (JMML) is a rare early childhood myelodysplastic/myeloproliferative disorder characterized by an aggressive clinical course.
  • A diagnostic classification (DC) model developed for leukemia and myelodysplastic syndrome classification was used to classify the specimens and identify prognostically relevant categories.
  • RESULTS The samples could be divided into two major groups: 20 specimens were classified as acute myeloid leukemia (AML) -like and 20 samples as nonAML-like.
  • The 10-year probability of survival after diagnosis of AML-like and nonAML-like patients was significantly different (7% v 74%; P = .0005).
  • Similarly, the 10-year event-free survival after HSCT was 6% for AML-like and 63% for nonAML-like patients (P = .0010).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia, Myelomonocytic, Juvenile / classification. Leukemia, Myelomonocytic, Juvenile / diagnosis. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Survival Rate. Treatment Outcome

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  • (PMID = 20231685.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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43. 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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  • [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
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Glucocorticoids / therapeutic use. Humans. Infant. Neoplasm, Residual / drug therapy. Polymerase Chain Reaction. Recurrence. Remission Induction. Treatment Outcome

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  • [Cites] Blood. 2008 Mar 15;111(6):2984-90 [18182569.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):447-53 [17968326.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1496-503 [18349402.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Bone Marrow Transplant. 2008 Jun;41 Suppl 2:S71-4 [18545248.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4027-31 [18593977.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4392-9 [18628453.001]
  • [Cites] Haematologica. 2008 Aug;93(8):1155-60 [18519521.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1005-12 [18477770.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4376-84 [18802149.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4318-27 [18723429.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):39-51 [19100367.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):100-6 [19100372.001]
  • [Cites] JAMA. 2009 Jan 28;301(4):393-403 [19176441.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9414-8 [19470474.001]
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] Blood. 2006 Jul 1;108(1):97-102 [16537802.001]
  • [Cites] Blood. 2006 Jul 15;108(2):441-51 [16556894.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1050-7 [16627760.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5329-35 [17000665.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5742-9 [17179108.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):16-24 [17194902.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Feb;13(2):218-27 [17241927.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2327-30 [17095619.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Lancet. 2007 Jun 9;369(9577):1947-54 [17560447.001]
  • [Cites] Blood. 2007 Jul 15;110(2):727-34 [17405907.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1112-5 [17473063.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4813-20 [17947730.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2258-63 [17690691.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1668-72 [12200679.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):445-53 [12406084.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(10):909-18 [12748668.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] Pediatr Blood Cancer. 2004 Jan;42(1):8-23 [14752789.001]
  • [Cites] Leukemia. 2004 Mar;18(3):521-9 [14712291.001]
  • [Cites] Leukemia. 2004 Mar;18(3):499-504 [14981525.001]
  • [Cites] Nat Genet. 2004 May;36(5):453-61 [15098032.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S124-6 [15124703.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Nov;3(11):1513-21 [3863894.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1717-26 [9351539.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):527-35 [9469337.001]
  • [Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]
  • [Cites] Cancer. 1998 Nov 1;83(9):2030-9 [9806664.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1221-6 [10450750.001]
  • [Cites] Blood. 2005 Jan 15;105(2):821-6 [15388585.001]
  • [Cites] JAMA. 2005 Mar 23;293(12):1485-9 [15784872.001]
  • [Cites] Blood. 2005 May 1;105(9):3749-56 [15637143.001]
  • [Cites] Lancet. 2005 Aug 20-26;366(9486):635-42 [16112299.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2484-90 [15956279.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):999-1005 [16338622.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Leukemia. 2006 Feb;20(2):264-71 [16357833.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):283-9 [18182669.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):352-9 [18223208.001]
  • [Cites] Curr Probl Pediatr Adolesc Health Care. 2008 Mar;38(3):78-94 [18279790.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2548-55 [18039957.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • (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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44. Han X, Bueso-Ramos CE: Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias. Am J Clin Pathol; 2007 Apr;127(4):528-44
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  • [Title] Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
  • Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (pre-T ALL/LBL) and acute biphenotypic leukemia.
  • Pre-T ALL represents approximately 15% of childhood and 25% of adult ALL cases.
  • Acute biphenotypic leukemias are characterized by a single population of blasts that express myeloid, T- or B-lineage antigens in various combinations and account for fewer than 4% of all acute leukemias.
  • An accurate diagnosis of pre-T ALL/LBL and acute biphenotypic leukemia requires a multiparametric approach, including examination of morphologic features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Lymphoid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


45. Rubin J, Frost BM, Arvidson J, Wide K, Gustafsson-Jernberg A, Gustafsson B: Intrathecal chemoprophylaxis after HSCT in children. Pediatr Transplant; 2008 Dec;12(8):889-95
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  • We compared 74 patients (56 ALL/18 AML), who received i.t. therapy post-HSCT with 46 patients (36 ALL/10 AML) who did not receive post-HSCT i.t. therapy.
  • Our study did not demonstrate a protective effect of i.t. therapy indicating that post-HSCT i.t. therapy may only be of limited use in the treatment of acute childhood leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adolescent. Central Nervous System / pathology. Chemoprevention. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Injections, Spinal. Male. Recurrence. Treatment Outcome

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  • (PMID = 18822104.001).
  • [ISSN] 1399-3046
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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46. Kadan-Lottick NS, Zeltzer LK, Liu Q, Yasui Y, Ellenberg L, Gioia G, Robison LL, Krull KR: Neurocognitive functioning in adult survivors of childhood non-central nervous system cancers. J Natl Cancer Inst; 2010 Jun 16;102(12):881-93
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  • [Title] Neurocognitive functioning in adult survivors of childhood non-central nervous system cancers.
  • BACKGROUND We sought to measure self-reported neurocognitive functioning among survivors of non-central nervous system (CNS) childhood cancers, overall and compared with a sibling cohort, and to identify factors associated with worse functioning.
  • Impaired task efficiency was most often identified in patients with acute lymphoblastic leukemia who received cranial radiation therapy (18.1% with impairment), myeloid leukemia who received cranial radiation therapy (21.2%), and non-Hodgkin lymphoma (13.9%).

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  • [Cites] N Engl J Med. 2001 Apr 19;344(16):1207-13 [11309635.001]
  • [Cites] Psychosomatics. 2001 May-Jun;42(3):241-6 [11351113.001]
  • [Cites] Neurology. 2001 Jun 12;56(11):1539-45 [11402112.001]
  • [Cites] Child Neuropsychol. 2000 Sep;6(3):235-8 [11419452.001]
  • [Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Feb;24(2):106-14 [11990695.001]
  • [Cites] Med Pediatr Oncol. 2002 May;38(5):320-8 [11979456.001]
  • [Cites] Pediatrics. 2002 Jul;110(1 Pt 1):42-52 [12093945.001]
  • [Cites] Eur J Cancer. 2003 Feb;39(3):359-65 [12565989.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1115-26 [12569614.001]
  • [Cites] Lancet Oncol. 2004 Jul;5(7):399-408 [15231246.001]
  • [Cites] Lancet. 1981 Nov 7;2(8254):1015-8 [6118478.001]
  • [Cites] Pediatrics. 1985 Apr;75(4):745-53 [3838584.001]
  • [Cites] Biometrics. 1986 Mar;42(1):121-30 [3719049.001]
  • [Cites] J Clin Oncol. 1988 Feb;6(2):315-20 [3422262.001]
  • [Cites] J Child Psychol Psychiatry. 1988 Nov;29(6):839-52 [3069852.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1989 Spring;11(1):74-86 [2496615.001]
  • [Cites] Dev Med Child Neurol. 1990 Mar;32(3):238-48 [2311827.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):145-51 [1985164.001]
  • [Cites] J Clin Oncol. 1991 Aug;9(8):1348-56 [2072138.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(1):13-6 [1727109.001]
  • [Cites] J Pediatr. 1992 Dec;121(6):885-9 [1447650.001]
  • [Cites] Lancet. 1994 Jul 23;344(8917):224-7 [7913156.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1712-22 [9586883.001]
  • [Cites] J Pediatr Psychol. 1998 Oct;23(5):333-40 [9782681.001]
  • [Cites] J Pediatr Psychol. 2005 Jan-Feb;30(1):65-78 [15610986.001]
  • [Cites] Pediatr Blood Cancer. 2005 Sep;45(3):281-90 [15806539.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 May-Jun;22(3):206-13 [10864051.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3858-64 [16921038.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 6;98(23):1742-5 [17148777.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4914-21 [17971588.001]
  • [Cites] Pediatrics. 2007 Nov;120(5):e1229-36 [17974716.001]
  • [Cites] Neuropsychol Rev. 2008 Jun;18(2):121-31 [18415683.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3025-30 [18565888.001]
  • [Cites] Cancer. 2008 Oct 15;113(8):2188-97 [18792068.001]
  • [Cites] Pediatr Blood Cancer. 2009 Feb;52(2):159-64 [18680151.001]
  • [Cites] J Int Neuropsychol Soc. 2009 Jan;15(1):31-41 [19128526.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2308-18 [19364948.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2626-35 [19815636.001]
  • [Cites] Neuropsychology. 2009 Nov;23(6):705-17 [19899829.001]
  • [Cites] Eur J Pharmacol. 2010 Jan 10;626(1):83-6 [19835870.001]
  • [CommentIn] J Natl Cancer Inst. 2011 Apr 6;103(7):607; author reply 607-9 [21350219.001]
  • (PMID = 20458059.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / KL2 RR024138; United States / NCI NIH HHS / CA / U24-CA55727
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2886093
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47. Meyer S, White DJ, Will AM, Eden T, Sim A, Brown R, Strathdee G: No evidence of significant silencing of Fanconi genes FANCF and FANCB or Nijmegen breakage syndrome gene NBS1 by DNA hyper-methylation in sporadic childhood leukaemia. Br J Haematol; 2006 Jul;134(1):61-3
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  • [Title] No evidence of significant silencing of Fanconi genes FANCF and FANCB or Nijmegen breakage syndrome gene NBS1 by DNA hyper-methylation in sporadic childhood leukaemia.
  • Combined bisulphite restriction analysis for methylation of FANCF, FANCB and NBS1 was used to investigate 81 sporadic acute childhood leukaemias.
  • This does not exclude very low levels of FANCF, FANCB or NBS1 methylation, but suggests other factors are responsible for chemo-sensitivity and chromosomal instability in sporadic childhood leukaemia.
  • [MeSH-major] Cell Cycle Proteins / genetics. Fanconi Anemia Complementation Group Proteins / genetics. Leukemia / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosomal Instability. CpG Islands. DNA Methylation. Fanconi Anemia Complementation Group F Protein / genetics. Genes, Neoplasm / genetics. Humans. Infant. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16803569.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Fanconi Anemia Complementation Group F Protein; 0 / Fanconi Anemia Complementation Group Proteins; 0 / NBN protein, human; 0 / Nuclear Proteins
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48. Shimada A, Taki T, Kubota C, Itou T, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y, Japanese childhood AML cooperative study group: N822 mutation of KIT gene was frequent in pediatric acute myeloid leukemia patients with t(8;21) in Japan: a study of the Japanese childhood AML cooperative study group. Leukemia; 2007 Oct;21(10):2218-9
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  • [Title] N822 mutation of KIT gene was frequent in pediatric acute myeloid leukemia patients with t(8;21) in Japan: a study of the Japanese childhood AML cooperative study group.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mutation. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / physiology. Translocation, Genetic
  • [MeSH-minor] Bone Marrow Cells / metabolism. Child. Exons. Humans. Japan. Oncogenes. Protein Structure, Tertiary. Remission Induction


49. Sung L, Gamis A, Alonzo TA, Buxton A, Britton K, Deswarte-Wallace J, Woods WG: Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia. Cancer; 2009 Mar 1;115(5):1100-8
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  • [Title] Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia.
  • BACKGROUND: The objectives were to compare infections during different intensities of therapy in children with acute myeloid leukemia (AML).
  • METHODS: Subjects were children enrolled in Children's Cancer Group 2891 with AML.
  • This information sheds insight into the mechanisms behind susceptibility and outcome of infections in pediatric AML.

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  • [Copyright] (c) 2009 American Cancer Society.
  • [Cites] J Clin Oncol. 2000 May;18(9):1845-55 [10784625.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Clin Infect Dis. 2002 Jan 1;34(1):7-14 [11731939.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Nov;24(8):627-35 [12439034.001]
  • [Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4384-93 [15514380.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):1179-87 [9508206.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):436-44 [10460604.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]
  • [Cites] Ann Intern Med. 2005 Jun 21;142(12 Pt 1):979-95 [15968013.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5207-15 [17114653.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3532-9 [17660380.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [ErratumIn] Cancer. 2009 Jun 15;115(12):2807
  • (PMID = 19156894.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-08; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA095861; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-06; United States / NCI NIH HHS / CA / CA095861-06; None / None / / U10 CA098543-06
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS107661; NLM/ PMC2677372
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50. He J, Chen ZX, Xue YQ, Pan JL, He HL, Li JQ, Wu YF, Huang YP, Zhu LL: [Study on clinical and biological characteristics of childhood acute leukemia with MLL gene rearrangements]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):477-80
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  • [Title] [Study on clinical and biological characteristics of childhood acute leukemia with MLL gene rearrangements].
  • OBJECTIVE: To study the clinical and laboratory features of childhood acute leukemia (AL) with MLL gene rearrangements.
  • METHODS: Sixteen of 298 cases of childhood AL with MLL rearrangements were studied by using MLL dual-color FISH, multiplex RT-PCR with 13 pairs of primers in combination with R banding karyotype analysis and cell immunophenotyping by flow cytometry.
  • RESULTS: Sixteen cases of childhood AL with MLL rearrangements accounted for 5.4% of 298 AL patients, and 56.3% of infant ALs.
  • Among these 16 patients, 11 were B-ALL, and 5 AML-M5, 3 of the latter were CD7+ and CD2+.
  • Finding out MLL gene rearrangement is of most importance in guiding therapy and predicting prognosis in childhood AL.
  • [MeSH-major] Gene Rearrangement. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male

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  • (PMID = 16383239.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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51. Tsukimoto I, Tawa A, Horibe K, Tabuchi K, Kigasawa H, Tsuchida M, Yabe H, Nakayama H, Kudo K, Kobayashi R, Hamamoto K, Imaizumi M, Morimoto A, Tsuchiya S, Hanada R: Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia: the AML99 trial from the Japanese Childhood AML Cooperative Study Group. J Clin Oncol; 2009 Aug 20;27(24):4007-13
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  • [Title] Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia: the AML99 trial from the Japanese Childhood AML Cooperative Study Group.
  • PURPOSE: To improve the prognosis in children with newly diagnosed acute myeloid leukemia (AML) by introducing a dose-dense intensive chemotherapy regimen and an appropriate risk stratification system.
  • PATIENTS AND METHODS: Two hundred forty children with de novo AML were treated with continuous cytarabine-based induction therapy and stratified to three risk groups based on the initial treatment response, age, and WBC at diagnosis and cytogenetics.
  • CONCLUSION: A high survival rate, 75.6% at 5 years, was achieved for childhood with de novo AML in the AML99 trial.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Transplantation, Homologous


52. van der Velden VH, van der Sluijs-Geling A, Gibson BE, te Marvelde JG, Hoogeveen PG, Hop WC, Wheatley K, Bierings MB, Schuurhuis GJ, de Graaf SS, van Wering ER, van Dongen JJ: Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol. Leukemia; 2010 Sep;24(9):1599-606
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  • [Title] Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol.
  • Analysis of minimal residual disease (MRD) in childhood acute myeloid leukemia (AML) may predict for clinical outcome.
  • MRD levels were assessed by flowcytometric immunophenotyping in 94 children with AML enrolled into a single trial (United Kingdom Medical Research Council AML12 and similar Dutch Childhood Oncology Group ANLL97).
  • In conclusion, flowcytometric MRD detection is possible in children with AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Child. Clinical Protocols. Flow Cytometry. Humans. Immunophenotyping. Probability. Prognosis. RNA, Messenger / genetics. Recurrence

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  • (PMID = 20668473.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300133
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger
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53. Dorantes-Acosta E, Chávez-González A, Santos JI, Medina-Sanson A, Mayani H: Defective in vitro growth of primitive hematopoietic cells from pediatric patients with acute myeloid leukemia. Pediatr Blood Cancer; 2008 Dec;51(6):741-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defective in vitro growth of primitive hematopoietic cells from pediatric patients with acute myeloid leukemia.
  • BACKGROUND: Acute myeloid leukemia (AML) is a neoplastic hematologic disorder that arises at the level of a primitive stem/progenitor cell.
  • Most studies on the biology of the hematopoietic system in AML have focused on cells from adult patients; much less is known about hematopoietic cells from childhood AML.
  • PROCEDURE: By using a negative immunoselection system, we have obtained a primitive cell population (enriched for CD34(+) Lin(-) cells) from the bone marrow (BM) of 17 pediatric AML patients and characterized its proliferation, expansion, and differentiation potentials in liquid cultures supplemented with a mixture of 8 different recombinant stimulatory cytokines.
  • RESULTS: The proportion of CD34(+) cells in AML patients was extremely heterogeneous, ranging from 0% to 74%.
  • Regardless of their CD34(+) cell content, and in contrast to normal cells, AML cells showed a deficient capacity to proliferate even in the presence of the stimulatory cytokines.
  • AML progenitors were unable to generate new progenitor cells, indicating their inability to expand.
  • Interestingly, AML cells were able to differentiate in culture, giving rise to morphologically recognizable precursors.
  • A major difference, however, as compared to hematopoietic progenitors from normal subjects, was the fact that whereas in cultures of normal cells both myeloid and erythroid precursors were produced, in AML cultures the vast majority of the cells generated corresponded to myeloid cells, mostly mature macrophages.
  • CONCLUSION: As compared to their normal counterparts, primitive hematopoietic cells from pediatric patients with AML possess impaired proliferation, expansion, and differentiation potentials in vitro.
  • [MeSH-major] Bone Marrow Cells / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid, Acute / blood
  • [MeSH-minor] Adolescent. Antigens, CD34 / blood. Cell Differentiation. Cell Proliferation. Cells, Cultured. Child. Child, Preschool. Cytokines / metabolism. Female. Humans. In Vitro Techniques. Male

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  • (PMID = 18680148.001).
  • [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 / Antigens, CD34; 0 / Cytokines
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54. Evrard AS, Hémon D, Morin A, Laurier D, Tirmarche M, Backe JC, Chartier M, Clavel J: Childhood leukaemia incidence around French nuclear installations using geographic zoning based on gaseous discharge dose estimates. Br J Cancer; 2006 May 8;94(9):1342-7
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  • [Title] Childhood leukaemia incidence around French nuclear installations using geographic zoning based on gaseous discharge dose estimates.
  • The present study investigated for the first time the incidence of childhood leukaemia (1990-2001) around French nuclear installations using a geographic zoning based on estimated doses to the red bone marrow due to gaseous radioactive discharges.
  • The observed number of cases of acute leukaemia (O=750) in 40 km2 centred on 23 French nuclear installations between 1990 and 2001 was lower than expected (E=795.01), although not significantly so (standardised incidence ratio SIR=0.94, 95% confidence interval=(0.88-1.01)).
  • This study confirmed that there was no evidence of an increased incidence of childhood leukaemia around the 23 French nuclear sites.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Power Plants. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Epidemiologic Studies. Female. France. Geography. Humans. Incidence. Infant. Infant, Newborn. Male

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  • [Cites] J Radiol Prot. 2000 Dec;20(4):361-80 [11140710.001]
  • [Cites] Epidemiol Rev. 1999;21(2):188-206 [10682257.001]
  • [Cites] Rev Epidemiol Sante Publique. 2000 Aug;48 Suppl 2:2S24-36 [10992107.001]
  • [Cites] J Radiol Prot. 2001 Sep;21(3):209-19 [11594649.001]
  • [Cites] Acta Oncol. 2002;41(1):14-24 [11990512.001]
  • [Cites] Eur J Cancer Prev. 2004 Apr;13(2):97-103 [15100575.001]
  • [Cites] Health Phys. 2006 Jun;90(6):569-79 [16691105.001]
  • [Cites] Stat Med. 1988 Jun;7(6):649-60 [3406597.001]
  • [Cites] BMJ. 1994 Aug 20-27;309(6953):501-5 [8086902.001]
  • [Cites] Stat Med. 1995 Nov 15-30;14(21-22):2309-22 [8711271.001]
  • [Cites] Eur J Cancer Prev. 2005 Apr;14(2):147-57 [15785319.001]
  • [Cites] Radiat Prot Dosimetry. 2005;113(3):314-20 [15713740.001]
  • [Cites] Br J Cancer. 2004 Aug 31;91(5):916-22 [15280917.001]
  • (PMID = 16622448.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ HALMS137976; NLM/ PMC2292746
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55. Chang JS, Selvin S, Metayer C, Crouse V, Golembesky A, Buffler PA: Parental smoking and the risk of childhood leukemia. Am J Epidemiol; 2006 Jun 15;163(12):1091-100
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  • [Title] Parental smoking and the risk of childhood leukemia.
  • Cigarette smoke has been linked to adult myeloid leukemia; however, the association between parental smoking and childhood leukemia remains unclear.
  • Parental smoking and the risk of childhood leukemia were examined in the Northern California Childhood Leukemia Study, a case-control study, between 1995 and 2002.
  • The present analysis included 327 acute childhood leukemia cases (281 acute lymphoblastic leukemia (ALL) and 46 acute myeloid leukemia (AML)) and 416 controls matched on age, sex, maternal race, and Hispanic ethnicity.
  • Maternal smoking was not associated with an increased risk of either ALL or AML.
  • Paternal preconception smoking was significantly associated with an increased risk of AML (odds ratio = 3.84, 95% confidence interval: 1.04, 14.17); an increased risk for ALL was suggestive for paternal preconception smoking (odds ratio = 1.32, 95% confidence interval: 0.86, 2.04).
  • These results strongly suggest that exposure to paternal preconception smoking alone or in combination with postnatal passive smoking may be important in the risk of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Parents. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Prenatal Exposure Delayed Effects. Smoking / adverse effects. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adolescent. Adult. California / epidemiology. Case-Control Studies. Child. Child, Preschool. Female. Humans. Infant. Logistic Models. Male. Pregnancy. Risk Factors


56. Taylor GM, Hussain A, Verhage V, Thompson PD, Fergusson WD, Watkins G, Lightfoot T, Harrison CJ, Birch JM, UKCCS Investigators: Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601. Leukemia; 2009 May;23(5):863-9
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  • [Title] Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601.
  • We previously reported that susceptibility to childhood B cell precursor ALL (BCP ALL) is associated with HLA-DPB1 alleles having glutamic acid (E) rather than lysine (K) in the P4 antigenic peptide-binding pocket.
  • Here, we report that only one of seven alleles with the DP6 supertype (DPB1(*)0601) is associated with childhood leukaemia (leukaemia vs controls: odds ratio, 95% confidence interval [OR, CI]: 4.6, 2.0-10.4; corrected P=0.019), but not with childhood solid tumours or lymphomas.
  • DPB1(*)0601 is also significantly associated with leukaemia subtypes, including BCP ALL, Pro-B ALL, T-ALL and AML.
  • Sequencing the coding region of DPB1(*)0601 revealed an exon 1-4 haplotype [T-DEAV-KIL-RVI] shared with DPB1(*)0301 and 0901, but no evidence of germline mutations in childhood leukaemia.
  • These results suggest that the DPbeta0601 molecule may be functionally involved in childhood leukaemia.
  • Analysis of peptide binding and T-cell activation by DPbeta0601-peptide complexes should help determine its role in childhood leukaemia causation.
  • [MeSH-major] HLA-DP Antigens / genetics. Haplotypes / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Alleles. Amino Acid Sequence. Case-Control Studies. Child. Disease Susceptibility. HLA-DP beta-Chains. Humans. Infant, Newborn. Molecular Sequence Data. Sequence Homology, Amino Acid

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  • (PMID = 19148140.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen
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57. Oliansky DM, Rizzo JD, Aplan PD, Arceci RJ, Leone L, Ravindranath Y, Sanders JE, Smith FO 3rd, Wilmot F, McCarthy PL Jr, Hahn T: The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myeloid leukemia in children: an evidence-based review. Biol Blood Marrow Transplant; 2007 Jan;13(1):1-25
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  • [Title] The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myeloid leukemia in children: an evidence-based review.
  • Clinical research examining the role of hematopoietic stem cell transplantation (SCT) in the therapy of acute myeloid leukemia (AML) in children is presented and critically evaluated in this systematic evidence-based review.
  • Treatment recommendations based on the evidence are presented in the table entitled "Summary of Treatment Recommendations Made by the Expert Panel for Pediatric Acute Myeloid Leukemia" and were reached unanimously by a panel of experts in AML.
  • The identified priority areas of needed future research in pediatric AML include: What is the role of risk group stratification, including the role of cytogenetics, in selection of patients for allogeneic SCT, especially those in first CR?
  • and What is the role of biologically targeted agents (ie, tyrosine kinase inhibitors, farnesyl transferase inhibitors, Flt-3 inhibitors, etc) in the treatment of AML, including induction, consolidation, conditioning regimens, and after SCT?
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Transplantation. Child. Child, Preschool. Evidence-Based Medicine. Humans. Remission Induction / methods. Transplantation Conditioning / methods. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 17222748.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 69
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58. Steiner M, Attarbaschi A, Dworzak M, Strobl H, Pickl W, Kornmüller R, Haas O, Gadner H, Mann G, Austrian Berlin-Frankfurt-Münster Study Group: Cytochemically myeloperoxidase positive childhood acute leukemia with lymphoblastic morphology treated as lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Jan;32(1):e4-7
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  • [Title] Cytochemically myeloperoxidase positive childhood acute leukemia with lymphoblastic morphology treated as lymphoblastic leukemia.
  • SUMMARY: Cytochemical myeloperoxidase (MPO) positivity represents the gold standard for discrimination between lymphatic and myeloid blasts.
  • We present 5 patients with cytochemically MPO-positive acute leukemia classified as lymphoblastic by cytomorphology and lymphoblastic (n=3) or biphenotypic (n=2) by immunophenotyping, who entered first-line treatment for lymphoblastic leukemia.
  • The former 3 are in first remission and both with biphenotypic leukemia relapsed with acute myeloid leukemia.
  • The study primarily shows that cytochemical MPO expression in childhood acute leukemia revealing typical lymphoblastic morphology and phenotype does rarely exist.
  • Although a small number of patients studied, cytochemical MPO expression in acute leukemia does not seem to require myeloid leukemia treatment in case of otherwise lymphoblastic cytomorphology and phenotype.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Peroxidase / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


59. Altieri A, Castro F, Bermejo JL, Hemminki K: Number of siblings and the risk of lymphoma, leukemia, and myeloma by histopathology. Cancer Epidemiol Biomarkers Prev; 2006 Jul;15(7):1281-6
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  • [Title] Number of siblings and the risk of lymphoma, leukemia, and myeloma by histopathology.
  • Epidemiologic evidence indicates that several markers of exposure to childhood infections are inversely associated with the risk of childhood leukemia and lymphomas.
  • Having four or more siblings compared with none was associated with an excess risk of childhood acute lymphoblastic leukemia [ALL; rate ratio (RR), 2.11; P(trend) = 0.001], acute monocytic leukemia (RR, 2.51; P(trend) = 0.002), and multiple myeloma (RR, 1.34; P(trend) = 0.006).
  • Having three or more older siblings compared with none decreased the risk of acute monocytic leukemia (RR, 0.35; P(trend) = 0.001) and childhood ALL (RR, 0.69; P(trend) = 0.01).
  • Acute myeloid leukemia, chronic lymphocytic leukemia, and other lymphoproliferative malignancies were not associated with number of siblings.
  • In conclusion, we found an excess risk of childhood ALL and acute monocytic leukemia in large families.
  • However, for ALL, acute monocytic leukemia, and Hodgkin's lymphoma, younger siblings were strongly protected compared with older siblings.
  • The remarkable protective effect of number of older siblings on acute monocytic leukemia is a novel finding of potential interest.
  • [MeSH-major] Birth Order. Hodgkin Disease / etiology. Leukemia / etiology. Multiple Myeloma / etiology. Siblings
  • [MeSH-minor] Adolescent. Adult. Age of Onset. Aged. Child. Child, Preschool. Family Characteristics. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Registries. Risk Factors. Sweden / epidemiology

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  • (PMID = 16835324.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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60. Tavil B, Cetin M, Tuncer M: CD34/CD117 positivity in assessment of prognosis in children with myelodysplastic syndrome. Leuk Res; 2006 Feb;30(2):222-4
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal stem cell disorders that are characterized by morphology identifying dysplastic changes in one or more cell lineages, peripheral blood cytopenias and a propensity to evolve into secondary acute myeloid leukemia (AML).
  • CD34 is commonly expressed in all types of childhood leukemias, whereas CD117 is a reliable and specific marker to detect leukemia cells committed to myeloid lineage.
  • Co-expression of CD34/CD117 may strongly suggest the diagnosis of AML (Rytting ME.
  • Pediatric myelodysplastic syndromes.
  • May; Uçkan D, Hiçsönmez G, Yetgin S, Gürgey A, Cetin M, Karaağaoğlu E, et al. CD34/CD117 co-expression in childhood acute leukemia.
  • Leukemia Res 2000;24:201-6.).
  • We describe the case of a 22 month-old-girl with MDS and Down syndrome who was presented with severe anemia and thrombocytosis at diagnosis, transformed into AML-M7.
  • As the disease progressed, CD34/117 co-existence was increased and MDS transformed into AML.
  • [MeSH-minor] Bone Marrow Examination. Female. Humans. Infant. Leukemia, Myeloid, Acute / etiology. Prognosis


61. Bakhshi S, Sethuraman G, Singh MK, Arya LS: Atypical pyoderma gangrenosum as a manifestation of childhood acute lymphoblastic leukemia. Pediatr Dermatol; 2005 Nov-Dec;22(6):543-5
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  • [Title] Atypical pyoderma gangrenosum as a manifestation of childhood acute lymphoblastic leukemia.
  • Although the association of this entity with myeloid malignancies is well known, its association with lymphoid malignancy is extremely rare.
  • We describe atypical pyoderma gangrenosum in association with acute lymphoblastic leukemia in a 2-year-old child, an occurrence not reported before.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyoderma Gangrenosum / drug therapy. Pyoderma Gangrenosum / pathology
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Asparaginase / therapeutic use. Biopsy, Needle. Child, Preschool. Daunorubicin / therapeutic use. Diagnosis, Differential. Follow-Up Studies. Humans. Immunohistochemistry. Male. Prednisone / therapeutic use. Risk Assessment. Severity of Illness Index. Treatment Outcome. Vincristine / therapeutic use


62. Hasanbegovic E, Mehadzic S: [Etiology of lymphadenopathy in childhood]. Med Glas (Zenica); 2010 Aug;7(2):132-6
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  • [Title] [Etiology of lymphadenopathy in childhood].
  • METHODS: One hundred and fifteen children aged 0-15 years with diagnosed lymphadenopathy at the Pediatric Clinic in Sarajevo during 2008 were included in the study.
  • Most frequent causes of malignant lymphadenopathy were acute lymphoblastic leukemia in 11 children (55 %) and acute myeloid leukemia in two (10%) children.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 21258308.001).
  • [ISSN] 1840-0132
  • [Journal-full-title] Medicinski glasnik : official publication of the Medical Association of Zenica-Doboj Canton, Bosnia and Herzegovina
  • [ISO-abbreviation] Med Glas (Zenica)
  • [Language] bos
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Bosnia and Herzegovina
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63. Bernt KM, Armstrong SA: Leukemia stem cells and human acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):33-8
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  • [Title] Leukemia stem cells and human acute lymphoblastic leukemia.
  • Leukemia stem cells are fairly well described for acute myeloid leukemia (AML), but their existence and relevance for acute lymphoblastic leukemia (ALL) is less clear.
  • However, it has also been suggested that the majority of leukemic subfractions can propagate leukemia in the appropriate experimental setting, and that their hierarchical organization is less strict than in AML.
  • In common childhood ALL, current evidence points towards the cell of origin being a committed lymphoid progenitor.
  • In this review, we highlight recent findings relating to the question of leukemia stem cells in ALL.
  • [MeSH-major] Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Child. Child, Preschool. Humans

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  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Hepatology. 2006 Jul;44(1):240-51 [16799977.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 29;351(4):820-4 [17097610.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4010-5 [17483311.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10158-63 [17548814.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2542-56 [17570225.001]
  • [Cites] Curr Drug Targets. 2007 Jun;8(6):703-14 [17584026.001]
  • [Cites] Science. 2007 Jul 20;317(5836):337 [17641192.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2240-5 [17657218.001]
  • [Cites] Science. 2007 Dec 14;318(5857):1722; author reply 1722 [18079385.001]
  • [Cites] Cell Mol Immunol. 2007 Dec;4(6):467-72 [18163959.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Ann Surg Oncol. 2008 Feb;15(2):638-48 [17932721.001]
  • [Cites] Br J Cancer. 2008 Feb 26;98(4):756-65 [18268494.001]
  • [Cites] Pigment Cell Melanoma Res. 2008 Feb;21(1):39-55 [18353142.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Jun;47(6):471-80 [18311775.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]
  • [Cites] Cancer Cell. 2008 Jul 8;14(1):47-58 [18598943.001]
  • [Cites] Blood. 2008 Aug 1;112(3):568-75 [18523148.001]
  • [Cites] Blood. 2000 Feb 1;95(3):1007-13 [10648416.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3925-30 [11389036.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8242-7 [12048236.001]
  • [Cites] Blood. 2002 Jul 15;100(2):640-6 [12091359.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Blood. 2004 May 1;103(9):3544-6 [14670924.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14228-33 [15381773.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2919-25 [15242869.001]
  • [Cites] Br J Cancer. 1973 Aug;28(2):123-35 [4730176.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Leukemia. 1996 May;10(5):795-802 [8656674.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1508-15 [9305606.001]
  • [Cites] Leukemia. 1998 May;12(5):666-74 [9593263.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1442-9 [15735032.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • (PMID = 19100366.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / T32 CA009172
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 44
  • [Other-IDs] NLM/ NIHMS89422; NLM/ PMC4031465
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64. Velardi A, Ruggeri L, Mancusi A, Aversa F, Christiansen FT: Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia. Curr Opin Immunol; 2009 Oct;21(5):525-30
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  • [Title] Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia.
  • Donor-versus-recipient natural killer (NK) cell alloreactivity has been established as a key therapeutic element in HLA haplotype mismatched hematopoietic transplants in adult AML and pediatric ALL and as a possible beneficial effector in cord blood transplant for AML.
  • At present NK cell allotherapy for leukemia is deployed through stem cell transplantation (and ensuing NK cell reconstitution) across KIR ligand mismatches.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Adult. Child. Humans. Immunotherapy / methods. Transplantation, Homologous

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  • (PMID = 19717293.001).
  • [ISSN] 1879-0372
  • [Journal-full-title] Current opinion in immunology
  • [ISO-abbreviation] Curr. Opin. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 PO1 CA100265
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 46
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65. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • Blast crisis is characterized by the rapid expansion of a population of differentiation arrested blast cells (myeloid or lymphoid cells population), with secondary chromosomal abnormalities present.
  • We report a case of myeloid blast crisis of CML resistant to imatinib mesylate and chemotherapy.
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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66. Deschler B, Lübbert M: Acute myeloid leukemia: epidemiology and etiology. Cancer; 2006 Nov 1;107(9):2099-107
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  • [Title] Acute myeloid leukemia: epidemiology and etiology.
  • Acute myeloid leukemias (AMLs) are infrequent, yet highly malignant neoplasms responsible for a large number of cancer-related deaths.
  • It continuously shows 2 peaks in occurrence in early childhood and later adulthood.
  • With an incidence of 3.7 per 100,000 persons and an age-dependent mortality of 2.7 to nearly 18 per 100,000 persons, there is a rising awareness in the Western world of AML's special attributes resulting from an ever-aging population.
  • A review of the literature is presented, reflecting highlights of current research with respect to AML etiology.
  • To estimate outcome and discuss informed treatment decisions with AML patients of different age groups and different biologic risk categories, it is mandatory to consider that the outcome results reported in clinical trials were until now heavily biased toward younger patients, whereas the overall dismal prognosis documented in population-based studies most likely reflects the exclusion of older patients from aggressive treatment.
  • The etiology for most cases of AML is unclear, but a growing knowledge concerning leukemogenenic agents within chemotherapy regimens for other malignancies is already available.
  • This includes specific associations of the most frequent balanced translocations in AML, including the "good-risk" abnormalities comprised by the core binding factor leukemias (i.e., AML with the translocation (8;21) and inversion of chromosome 16, and acute promyelocytic leukemia with the translocation (15;17)).
  • In contrast to these genetic alterations, epigenetic lesions, e.g., promoter silencing by hypermethylation of the p15/INK4b and other genes, are increasingly recognized as important in the pathogenesis of AML.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Leukemia, Myeloid / etiology

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17019734.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 89
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67. Children's Oncology Group, Aplenc R, Alonzo TA, Gerbing RB, Smith FO, Meshinchi S, Ross JA, Perentesis J, Woods WG, Lange BJ, Davies SM: Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group. Blood; 2006 Jul 1;108(1):74-80
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  • [Title] Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group.
  • We evaluated differences in outcome by ethnicity among children with acute myeloid leukemia (AML).
  • In conclusion, Hispanic and black children with AML have worse survival than white children.
  • Access to chemotherapy, differences in supportive care or leukemia phenotype, and reduced compliance are unlikely explanations for this difference because therapy was given intravenously according to CCG protocols.


68. Braoudaki M, Papathanassiou C, Katsibardi K, Tourkadoni N, Karamolegou K, Tzortzatou-Stathopoulou F: The frequency of NPM1 mutations in childhood acute myeloid leukemia. J Hematol Oncol; 2010;3:41
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  • [Title] The frequency of NPM1 mutations in childhood acute myeloid leukemia.
  • BACKGROUND: Mutations in the nucleophosmin (NPM1) gene have been solely associated with childhood acute myeloid leukemia (AML).
  • We evaluated the frequency of NPM1 mutations in childhood AML, their relation to clinical and cytogenetic features and the presence of common FLT3 and RAS mutations.
  • The role of different types of NPM1 mutations, either individually or in the presence of other common gene mutations may be essential for childhood AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Gene Frequency. Humans. Infant. Prognosis. Survival Analysis


69. Mizushima Y, Taki T, Shimada A, Yui Y, Hiraumi Y, Matsubara H, Watanabe M, Watanabe K, Kamitsuji Y, Hayashi Y, Tsukimoto I, Kobayashi R, Horibe K, Tawa A, Nakahata T, Adachi S: Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2010 Jun;91(5):831-7
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  • [Title] Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group.
  • High BAALC (brain and acute leukemia, cytoplasmic) gene expression may indicate an adverse prognosis for adults who have acute myeloid leukemia (AML) and a normal karyotype, but its prognostic significance for pediatric AML cases is unclear.
  • Newly diagnosed AML patients with normal karyotype who were treated by the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed in terms of their BAALC expression levels (n = 29), BAALC isoforms (n = 29), and CEBPA mutations (n = 49).
  • Thus, 1-5-6-8 isoform expression may be associated with an adverse prognosis in pediatric AML with normal karyotype.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. CCAAT-Enhancer-Binding Proteins. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Mutation. Neoplasm Proteins
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Prognosis. Protein Isoforms / genetics


70. Maule MM, Zuccolo L, Magnani C, Pastore G, Dalmasso P, Pearce N, Merletti F, Gregori D: Bayesian methods for early detection of changes in childhood cancer incidence: trends for acute lymphoblastic leukaemia are consistent with an infectious aetiology. Eur J Cancer; 2006 Jan;42(1):78-83
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  • [Title] Bayesian methods for early detection of changes in childhood cancer incidence: trends for acute lymphoblastic leukaemia are consistent with an infectious aetiology.
  • Published data on time trends in the incidence of childhood leukaemia show inconsistent patterns, with some studies showing increases and others showing relatively stable incidence rates.
  • Data on time trends in childhood cancer incidence from the Childhood Cancer Registry of Piedmont, Italy were analysed using two different approaches: standard Poisson regression and a Bayesian regression approach including an autoregressive component.
  • Our focus was on acute lymphoblastic leukaemia (ALL), since this is hypothesised to have an infectious aetiology, but for purposes of comparison we also conducted similar analyses for selected other childhood cancer sites (acute non-lymphoblastic leukaemia (AnLL), central nervous system (CNS) tumours and neuroblastoma (NB)).
  • Although sudden changes in time trends should be interpreted with caution, the results of the Bayesian approach are consistent with current knowledge of the natural history of childhood ALL, including a short latency time and the postulated infectious aetiology of the disease.
  • [MeSH-major] Central Nervous System Neoplasms / epidemiology. Infection / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Neuroblastoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Bayes Theorem. Child. Child, Preschool. Humans. Incidence. Infant. Infant, Newborn. Italy / epidemiology


71. Lehrnbecher T, Bernig T, Hanisch M, Koehl U, Behl M, Reinhardt D, Creutzig U, Klingebiel T, Chanock SJ, Schwabe D: Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia. Leukemia; 2005 Oct;19(10):1745-50
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  • [Title] Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia.
  • Infectious complications represent a substantial cause of morbidity and mortality in children undergoing therapy for acute myeloid leukemia (AML).
  • Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes (TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for pediatric AML.
  • The study population consisted of 168 North European Caucasian children enrolled on the clinical trial AML-BFM 93.
  • Our data suggest that variant alleles of both IL6 and CHIT could influence susceptibility to infection with Gram-negative bacteria in children undergoing therapy for AML.
  • [MeSH-major] Gram-Negative Bacterial Infections / etiology. Hexosaminidases / genetics. Interleukin-6 / genetics. Leukemia, Myeloid / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Alleles. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Female. Genetic Variation. Genotype. Gram-Negative Bacteria / isolation & purification. Humans. Infant. Infant, Newborn. Male

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  • (PMID = 16107886.001).
  • [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 / Interleukin-6; EC 3.2.1.- / Hexosaminidases; EC 3.2.1.- / chitotriosidase
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72. Bachas C, Schuurhuis GJ, Hollink IH, Kwidama ZJ, Goemans BF, Zwaan CM, van den Heuvel-Eibrink MM, de Bont ES, Reinhardt D, Creutzig U, de Haas V, Assaraf YG, Kaspers GJ, Cloos J: High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine. Blood; 2010 Oct 14;116(15):2752-8
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  • [Title] High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.
  • Although virtually all pediatric patients with acute myeloid leukemia (AML) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.
  • To determine relevance of established AML type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse pediatric AML specimens.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precision Medicine
  • [MeSH-minor] Adolescent. Base Sequence. Biomarkers, Tumor / genetics. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Genes, Wilms Tumor. Genes, ras. Humans. Infant. Male. Prognosis. Recurrence. Time Factors. Treatment Outcome. fms-Like Tyrosine Kinase 3 / genetics

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  • [CommentIn] Blood. 2010 Oct 14;116(15):2622-3 [20947687.001]
  • (PMID = 20592250.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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73. Kömür M, Erbey F, Bayram I, Tanyeli A: Incidence and prognostic importance of molecular genetic defects in children with acute myeloblastic leukemia. Asian Pac J Cancer Prev; 2010;11(5):1393-5
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  • [Title] Incidence and prognostic importance of molecular genetic defects in children with acute myeloblastic leukemia.
  • INTRODUCTION: Acute myeloblastic leukemia (AML) accounts for 15 to 25 percent of childhood acute leukemias.
  • The most common genetic abnormalities seen in pediatric AML patients are AML1-ETO, PML-RARα and CBFB-MYH11 genes resulting in t(8;21), t(15;17) and inv(16).
  • These genetic defects are seen in approximately 20-25% of AML patients.
  • OBJECTIVE: We investigated in this study, incidence and prognostic significance of the AML1-ETO, PML-RARα and CBFB-MYH11 genes in children with AML.
  • MATERIALS AND METHODS: The authors analyzed 34 children with AML using the real time-polymerase chain reaction for AML1-ETO, PML-RARα and CBFB-MYH11 genes.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction. Prognosis. Survival Rate

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  • (PMID = 21198299.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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74. Krstovski N, Tosic N, Janic D, Dokmanovic L, Kuzmanovic M, Spasovski V, Pavlovic S: Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature. Med Oncol; 2010 Sep;27(3):640-5
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  • [Title] Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature.
  • Mutations in the fms-like tyrosine kinase 3 (FLT3) gene (internal tandem duplication (ITD) and point mutation in the tyrosine kinase domain, FLT3/D835) as well as the nucleophosmin (NPM1) gene are the most common abnormalities in adult acute myeloid leukemia (AML).
  • Their significance in pediatric AML is still unclear.
  • In this study we evaluated the frequency of FLT3 and NPM1 mutations in childhood AML.
  • FLT3 and NPM1 mutations were analysed in 42 and 37 childhood AML patients, respectively, using polymerase chain reaction (PCR) and direct sequencing.
  • Here we report the results of the study of FLT3 and NPM1 gene mutations in childhood AML patients in Serbia.
  • Comparative study of data on NPM1 mutations in childhood AML revealed that various NPM1 gene mutation types are associated with childhood AML.
  • Our findings as well as previously reported data, contributes to a hypothesis of different biology and etiology of adult and childhood AML.
  • More extensive studies of NPM1 and FLT3 mutations in childhood AML are needed to determine their biological and clinical importance.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Female. Humans. Male. Serbia

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  • [Cites] Ann Hematol. 2007 Oct;86(10):741-7 [17579862.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Leukemia. 2003 May;17(5):883-6 [12750701.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Leuk Res. 2005 Jun;29(6):617-23 [15863200.001]
  • [Cites] Leukemia. 1999 Jan;13(1):38-43 [10049058.001]
  • [Cites] Med Pediatr Oncol. 1999 Dec;33(6):525-9 [10573574.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1447-52 [9305596.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Br J Haematol. 2003 Jan;120(1):89-92 [12492581.001]
  • [Cites] Leukemia. 1996 Apr;10(4):588-99 [8618433.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):155-62 [10233379.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3292-8 [12115363.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 1999 Jan 15;93(2):632-42 [9885226.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1552-9 [17940205.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1307 [17315018.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2000-9 [17597811.001]
  • [Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • (PMID = 19557552.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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75. Chen SH, Yang CP, Hung IJ, Jaing TH, Shih LY, Tsai MH: Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan. Pediatr Blood Cancer; 2010 Dec 15;55(7):1264-71
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  • [Title] Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan.
  • BACKGROUND: Infant leukemia is rare and quite distinct from other childhood leukemias.
  • Differentiating between leukemia and transient myeloproliferative disorder (TMD) in phenotypically normal infants is sometimes difficult.
  • The clinical features and molecular analyses for the fusion transcripts of mixed lineage leukemia (MLL) gene rearrangement in infant leukemia have not been well documented in the Chinese population.
  • PROCEDURE: Forty-five consecutive infants diagnosed with leukemia between 1995 and 2007 in a tertiary medical center in Taiwan were studied.
  • Acute lymphoblastic leukemia (ALL) was diagnosed in 23 infants, acute myeloid leukemia (AML) in 21 (including TMD in 4), and juvenile myelomonocytic leukemia (JMML) in 1.
  • RESULTS: The median white count at diagnosis was higher in ALL than in AML (154.4 × 10(9)/l vs. 58.3 × 10(9)/l, P = 0.05).
  • Chromosome 11q23/MLL abnormalities were present in 77% of ALL and 31% of AML.
  • The 5-year event-free survival (EFS) in infant ALL and AML showed no difference (18% vs. 12%, respectively).
  • However, no factor was associated with an adverse outcome for infants with AML.
  • CONCLUSIONS: The molecular assessments and prognostic factors of infant leukemia in Taiwan mirror those in developed Western countries.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Gene Rearrangement. Humans. Infant. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Leukemia, Myelomonocytic, Juvenile / diagnosis. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / therapy. Leukocyte Count. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloproliferative Disorders / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Taiwan. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2010 Dec 15;55(7):1247-9 [20981686.001]
  • (PMID = 20979094.001).
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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76. Gutiérrez MI, Timson G, Siraj AK, Bu R, Barbhaya S, Banavali S, Bhatia K: Single monochrome real-time RT-PCR assay for identification, quantification, and breakpoint cluster region determination of t(9;22) transcripts. J Mol Diagn; 2005 Feb;7(1):40-7
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  • t(9;22) generates the BCR-ABL fusion gene, the hallmark of chronic myeloid leukemia (CML) but also found in acute lymphoblastic leukemia (ALL).
  • We applied this assay to assess the distribution of p190 and p210 in 260 childhood ALL samples from India.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Alternative Splicing. Child. Child, Preschool. Female. Humans. Infant. Male. Multigene Family / genetics. Sensitivity and Specificity. Transcription, Genetic

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  • [Cites] Leukemia. 1999 Nov;13(11):1825-32 [10557058.001]
  • [Cites] Haematologica. 2003 Sep;88(9):1074-6 [12969819.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • [Cites] Haematologica. 2000 Dec;85(12):1248-54 [11114130.001]
  • [Cites] Haematologica. 2001 Mar;86(3):252-9 [11255271.001]
  • [Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]
  • [Cites] Leukemia. 2002 Jan;16(1):53-9 [11840263.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1536-43 [11861265.001]
  • [Cites] Med Sci Monit. 2002 May;8(5):BR193-7 [12011769.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1167-75 [12040449.001]
  • [Cites] Ann Oncol. 2002 May;13(5):781-8 [12075749.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):445-53 [12406084.001]
  • [Cites] Am J Hematol. 2002 Dec;71(4):291-9 [12447959.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1423-32 [14534335.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:132-52 [14633780.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Mod Pathol. 2004 Jan;17(1):96-103 [14657955.001]
  • [Cites] N Engl J Med. 1988 Oct 13;319(15):990-8 [3047582.001]
  • [Cites] Blood. 1990 Nov 1;76(9):1819-24 [2224129.001]
  • [Cites] Blood. 1991 Nov 1;78(9):2411-8 [1932753.001]
  • [Cites] Blood. 1995 Dec 15;86(12):4603-11 [8541551.001]
  • [Cites] Blood. 1996 Jun 15;87(12):5213-7 [8652835.001]
  • [Cites] Leukemia. 1996 Jun;10(6):957-63 [8667652.001]
  • [Cites] Baillieres Clin Haematol. 1997 Jun;10(2):203-22 [9376660.001]
  • [Cites] Cancer Res. 1999 Jul 1;59(13):3171-4 [10397261.001]
  • [Cites] Clin Cancer Res. 2002 Dec;8(12):3832-40 [12473597.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Mar;36(3):211-23 [12557221.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1033-41 [12569603.001]
  • [Cites] Eur J Haematol. 2003 Jan;70(1):1-10 [12631253.001]
  • [Cites] J Mol Diagn. 2003 May;5(2):63-72 [12707370.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1192-3 [12764391.001]
  • [Cites] Am J Clin Pathol. 2003 Jul;120(1):42-8 [12866371.001]
  • [Cites] Curr Oncol Rep. 2003 Sep;5(5):426-35 [12895396.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • (PMID = 15681473.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC1867499
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77. Sung TJ, Lee DH, Kim SK, Jun YH: Congenital acute myeloid leukemia with t(8;16) and t(17;19) double translocation: case presentation and literature review. J Korean Med Sci; 2010 Jun;25(6):945-9
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  • [Title] Congenital acute myeloid leukemia with t(8;16) and t(17;19) double translocation: case presentation and literature review.
  • Congenital leukemia is uncommon and excluding transient myeloproliferation associated with Down syndrome, makes up approximately 1% of childhood leukemias.
  • Bone marrow morphology was consistent with acute myeloid leukemia (M5) and cytogenetic studies revealed t(8;16) and t(17;19) double translocation.
  • Although prognosis of congenital leukemia is known to be dismal, recent reports showed spontaneous remissions.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • [Cites] J Pediatr Hematol Oncol. 2000 May-Jun;22(3):252-5 [10864057.001]
  • [Cites] J Am Acad Dermatol. 2006 Feb;54(2 Suppl):S22-7 [16427986.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Nov;139(1):57-9 [12547160.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 May;25(5):348-61 [12759620.001]
  • [Cites] Pediatr Hematol Oncol. 2004 Mar;21(2):135-44 [15160512.001]
  • [Cites] Clin Lab Haematol. 1980;2(3):243-5 [6933032.001]
  • [Cites] Pediatrics. 1983 Feb;71(2):277-9 [6823435.001]
  • [Cites] Pediatrics. 1983 Dec;72(6):916-7 [6646941.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1985 Winter;7(4):346-51 [3866495.001]
  • [Cites] Blood. 1987 May;69(5):1289-93 [2952182.001]
  • [Cites] Cancer Genet Cytogenet. 1988 Feb;30(2):233-8 [2830011.001]
  • [Cites] Cancer Genet Cytogenet. 1988 Sep;34(2):277-80 [3165702.001]
  • [Cites] J Am Acad Dermatol. 1989 Aug;21(2 Pt 2):347-51 [2754068.001]
  • [Cites] Pediatr Dermatol. 1989 Dec;6(4):306-11 [2694129.001]
  • [Cites] Eur J Pediatr. 1991 Mar;150(5):323-4 [2044602.001]
  • [Cites] Blood. 1991 Aug 1;78(3):748-52 [1859887.001]
  • [Cites] Cancer. 1993 Mar 1;71(5):1928-30 [8448758.001]
  • [Cites] Arch Dermatol. 1993 Oct;129(10):1301-6 [8215495.001]
  • [Cites] Cancer Genet Cytogenet. 1995 May;81(1):38-41 [7773958.001]
  • [Cites] Cytometry. 1995 Jun 15;22(2):89-92 [7587753.001]
  • [Cites] Pediatr Hematol Oncol. 1996 Mar-Apr;13(2):151-7 [8721029.001]
  • [Cites] Pediatr Dermatol. 1996 Nov-Dec;13(6):472-6 [8987056.001]
  • [Cites] Br J Haematol. 1997 Mar;96(4):740-2 [9074415.001]
  • [Cites] J Pediatr. 1997 Aug;131(2):176-7 [9290598.001]
  • [Cites] J Pediatr. 1997 Aug;131(2):300-3 [9290620.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 Mar-Apr;21(2):152-7 [10206463.001]
  • [Cites] Semin Perinatol. 1999 Aug;23(4):274-85 [10475541.001]
  • [Cites] Pediatr Dermatol. 2005 Jan-Feb;22(1):26-30 [15660893.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Nov;163(1):71-3 [16271959.001]
  • [Cites] Br J Haematol. 2000 Nov;111(2):641-3 [11122113.001]
  • (PMID = 20514319.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Number-of-references] 30
  • [Other-IDs] NLM/ PMC2877231
  • [Keywords] NOTNLM ; Drug Therapy / Leukemia / Leukemic Infiltration / Translocation, Genetic
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78. Spanaki A, Perdikogianni C, Linardakis E, Kalmanti M: Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia. Leuk Res; 2007 May;31(5):639-42
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  • [Title] Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia.
  • The purpose of this study was to investigate PRAME expression levels in children with acute leukemia with real-time PCR analysis.
  • Seventeen children with newly diagnosed or relapsed acute leukemia (11 ALL, 4 AML, 1 acute myeloblastic leukemia secondary to MDS, 1 ALL at relapse) and a control group of seven children were studied.
  • Overexpression of PRAME was found in 52.9% (3 AML, 6 ALL) of the patients studied.
  • The above findings indicate that PRAME expression in acute leukemia does not seem to be of prognostic significance, whereas it might represent a candidate marker for the monitoring of minimal residual disease.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Leukemia, Myeloid / genetics. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Humans. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16860864.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
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79. Anak S, Saribeyoglu ET, Bilgen H, Unuvar A, Karakas Z, Devecioglu O, Agaoglu L, Gedikoglu G: Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience. Pediatr Blood Cancer; 2005 Jun 15;44(7):654-9
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  • [Title] Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience.
  • BACKGROUND: Treatment of childhood acute myelocytic leukemia (AML) in first remission, is still evolving.
  • PROCEDURE: Out of 81 pediatric patients with AML in first CR, 67 were biologically randomized for allogeneic (n = 31), autologous (n = 20), or peripheral stem cell transplant (n = 16) after completing consolidation treatment, with the remaining (n = 11) dropping out or receiving chemotherapy.
  • CONCLUSION: In pediatric AML patients without a donor, autologous BMT or autologous PBSCT appears to be an effective treatment option with low transplant related mortality especially in less privileged countries where the chemotherapy only results are still low.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Transplantation, Autologous. Transplantation, Homologous

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15700262.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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80. Rudant J, Menegaux F, Leverger G, Baruchel A, Nelken B, Bertrand Y, Hartmann O, Pacquement H, Vérité C, Robert A, Michel G, Margueritte G, Gandemer V, Hémon D, Clavel J: Family history of cancer in children with acute leukemia, Hodgkin's lymphoma or non-Hodgkin's lymphoma: the ESCALE study (SFCE). Int J Cancer; 2007 Jul 1;121(1):119-26
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  • [Title] Family history of cancer in children with acute leukemia, Hodgkin's lymphoma or non-Hodgkin's lymphoma: the ESCALE study (SFCE).
  • The role of a family history of cancer in the etiology of childhood hematopoietic malignancies was investigated using the data from the ESCALE study.
  • A total of 773 cases of acute leukemia (AL), 130 of Hodgkin's lymphoma (HL), 163 of non-Hodgkin's lymphoma (NHL) and 1,681 population-based controls were included.
  • In conclusion, the study findings support the hypothesis of familial susceptibility to childhood lymphoma, but do not suggest familial susceptibility to childhood AL.
  • [MeSH-major] Hodgkin Disease / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Child. Child, Preschool. Disease Susceptibility / classification. Disease Susceptibility / epidemiology. Disease Susceptibility / pathology. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Odds Ratio

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  • (PMID = 17330239.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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81. Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA: A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood; 2009 Jan 29;113(5):1075-85
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  • NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood.
  • However, evidence suggests that Nf1 loss alone does not cause leukemia.
  • We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause acute leukemia.
  • One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of leukemia of either myeloid or lymphoid lineage in mice when expressed in Nf1-deficient bone marrow.
  • Importantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia samples.
  • A subset of AML patients, who had poor outcomes, of 16 clusters, displayed high levels of BCL11A in leukemic cells.
  • These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis, and a therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of leukemia.

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  • [Cites] Leukemia. 2007 May;21(5):1093-7 [17301810.001]
  • [Cites] Blood. 2007 May 15;109(10):4392-8 [17284535.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] Exp Hematol. 2007 Jun;35(6):908-19 [17533045.001]
  • [Cites] Bioinformatics. 2007 Jul 1;23(13):i133-41 [17646289.001]
  • [Cites] Biotechniques. 2007 Jul;43(1):79-84 [17695256.001]
  • [Cites] Oncogene. 2007 Aug 30;26(40):5840-50 [17369851.001]
  • [Cites] Mol Cell Biol. 2000 May;20(9):3178-86 [10757802.001]
  • [Cites] Leuk Res. 2000 Jul;24(7):601-10 [10867136.001]
  • [Cites] Genomics. 2000 Dec 15;70(3):387-91 [11161790.001]
  • [Cites] Exp Hematol. 2001 Mar;29(3):278-85 [11274754.001]
  • [Cites] Genes Dev. 2001 Apr 1;15(7):859-76 [11297510.001]
  • [Cites] Semin Cancer Biol. 2001 Jun;11(3):191-200 [11407944.001]
  • [Cites] Nature. 2001 Aug 9;412(6847):647-51 [11493923.001]
  • [Cites] J Virol. 2001 Oct;75(19):9427-34 [11533205.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]
  • [Cites] Cell. 2001 Oct 19;107(2):137-48 [11672522.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3274-82 [11719364.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3413-20 [11719382.001]
  • [Cites] Blood. 2002 Jan 15;99(2):627-33 [11781247.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1474-7 [11830502.001]
  • [Cites] EMBO J. 2002 May 15;21(10):2383-96 [12006491.001]
  • [Cites] Oncogene. 2002 Jul 25;21(32):4978-82 [12118376.001]
  • [Cites] Exp Hematol. 2002 Nov;30(11):1263-72 [12423679.001]
  • [Cites] Oncogene. 2002 Dec 5;21(55):8486-97 [12466968.001]
  • [Cites] J Virol. 2003 Jan;77(2):1059-68 [12502821.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(8):2859-70 [12665584.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3188-97 [12515727.001]
  • [Cites] Nat Immunol. 2003 Jun;4(6):525-32 [12717432.001]
  • [Cites] Oncogene. 2003 Jul 17;22(29):4581-5 [12881715.001]
  • [Cites] Curr Opin Neurol. 2004 Apr;17(2):101-5 [15021234.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4243-50 [14982883.001]
  • [Cites] J Virol. 1982 May;42(2):379-88 [6283161.001]
  • [Cites] Nature. 1990 Mar 15;344(6263):251-3 [2179728.001]
  • [Cites] Mol Cell Biol. 1990 Sep;10(9):4658-66 [2167436.001]
  • [Cites] Cell. 1990 Nov 16;63(4):843-9 [2121370.001]
  • [Cites] Cell. 1992 Apr 17;69(2):265-73 [1568246.001]
  • [Cites] Nature. 1992 Apr 23;356(6371):713-5 [1570015.001]
  • [Cites] Mol Cell Biol. 1993 Jan;13(1):351-7 [8093327.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5539-43 [8516298.001]
  • [Cites] Cell. 1993 Sep 10;74(5):833-43 [8104101.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1019-29 [7926784.001]
  • [Cites] Br J Cancer. 1994 Nov;70(5):969-72 [7947106.001]
  • [Cites] J Virol. 1995 Aug;69(8):5095-102 [7609078.001]
  • [Cites] Blood. 1995 Dec 15;86(12):4603-11 [8541551.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Blood. 1996 Nov 15;88(10):3710-9 [8916935.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] Science. 1997 May 2;276(5313):795-8 [9115204.001]
  • [Cites] Brain Res. 1997 Jun 6;759(1):149-52 [9219873.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Arch Biochem Biophys. 2005 Feb 15;434(2):316-25 [15639232.001]
  • [Cites] Int J Cancer. 2005 May 1;114(5):683-95 [15609309.001]
  • [Cites] Fam Cancer. 2005;4(4):323-33 [16341812.001]
  • [Cites] Leukemia. 2006 Jan;20(1):151-4 [16307021.001]
  • [Cites] Exp Hematol. 2006 May;34(5):631-41 [16647569.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2024-9 [16882980.001]
  • [Cites] Nat Rev Cancer. 2006 Sep;6(9):663-73 [16915296.001]
  • [Cites] Leukemia. 2006 Oct;20(10):1880-2 [16871282.001]
  • [Cites] J Immunol. 2007 Feb 15;178(4):2527-34 [17277161.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1687-91 [17090653.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 6;355(2):538-42 [17306224.001]
  • [Cites] Nat Genet. 2007 Apr;39(4):476-85 [17369827.001]
  • [Cites] Br J Haematol. 2007 May;137(3):252-61 [17408467.001]
  • (PMID = 18948576.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221
  • [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 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2635073
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82. Klingebiel T, Reinhardt D, Bader P, EBMT Paediatric Diseases Working Party: Place of HSCT in treatment of childhood AML. Bone Marrow Transplant; 2008 Oct;42 Suppl 2:S7-9
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  • [Title] Place of HSCT in treatment of childhood AML.
  • This short review focuses on the role of hematopoietic SCT (HSCT) in childhood AML.
  • Data on haploidentical HSCT and on cord blood HSCT are still lacking in the case of AML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Living Donors
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Clinical Trials as Topic. Disease-Free Survival. Humans. Infant. Remission Induction. Siblings. Survival Rate. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 18978749.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 15
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83. Hijiya N, Metzger ML, Pounds S, Schmidt JE, Razzouk BI, Rubnitz JE, Howard SC, Nunez CA, Pui CH, Ribeiro RC: Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):63-9
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  • [Title] Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia.
  • BACKGROUND: Life-threatening pulmonary complications that coincide with cell lysis during early chemotherapy and that mimic systemic inflammatory response syndrome (SIRS) have been reported in patients with acute myeloid leukemia (AML).
  • METHODS: We reviewed the records of patients with de novo AML, excluding M3 and Down syndrome, treated at our institution between 1991 and 2002 to determine the prevalence of severe SIRS with grade 3/4 pulmonary complications and to identify AML subtypes associated with severe SIRS.
  • To examine the role of cell lysis, we compared leukocyte reduction in AML subtypes affected by severe SIRS with that in unaffected subtypes.
  • Severe SIRS was significantly more common in myelomonocytic or monocytic AML (M4/M4eo/M5) than in other subtypes (P = 0.010) and significantly more common in M4eo than in M4/M5 (P = 0.008).
  • CONCLUSIONS: Patients with M4/M4eo/M5 AML, especially M4eo, experience life-threatening cardiopulmonary complications of tumor lysis that meet the criteria for severe SIRS.
  • [MeSH-major] Cell Death. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / drug therapy. Systemic Inflammatory Response Syndrome / etiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Humans. Male. Retrospective Studies. Risk Factors

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368547.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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84. Kalina T, Vaskova M, Mejstrikova E, Madzo J, Trka J, Stary J, Hrusak O: Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens. BMC Cancer; 2005;5:38
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  • [Title] Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens.
  • BACKGROUND: Aberrant expression of myeloid antigens (MyAgs) on acute lymphoblastic leukemia (ALL) cells is a well-documented phenomenon, although its regulating mechanisms are unclear.
  • Granulocytic marker CD66c -- Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is aberrantly expressed on ALL with strong correlation to genotype (negative in TEL/AML1 and MLL/AF4, positive in BCR/ABL and hyperdiploid cases).
  • Our data show that different myeloid antigens often differ in biological importance, which may be obscured by combining them into "MyAg positive ALL".
  • CONCLUSION: In contrast to general notion we show that different MyAgs in lymphoblastic leukemia represent different biological circumstances.
  • [MeSH-major] Antigens, CD / biosynthesis. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Antigens, CD13 / biosynthesis. Antigens, CD15 / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Blotting, Western. Cell Membrane / metabolism. Child. Child, Preschool. Cohort Studies. Cytoplasm / metabolism. Czech Republic. Disease-Free Survival. Flow Cytometry. GPI-Linked Proteins. Genotype. Glycosylation. Humans. Immunophenotyping. Infant. Prognosis. RNA / metabolism. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Sialic Acid Binding Ig-like Lectin 3. Time Factors. Transcription, Genetic

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  • [Cites] Crit Rev Oncol Hematol. 1999 Dec;32(3):175-85 [10633847.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1092-4 [15830012.001]
  • [Cites] Cancer Res. 2000 Jul 1;60(13):3419-24 [10910050.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):794-9 [11564065.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1952-8 [11877265.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Mar;15(1):1-19 [11987913.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1233-58 [12094248.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):105-13 [12491511.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3638-46 [14512395.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):465-73 [14724575.001]
  • [Cites] Biochem Biophys Res Commun. 2004 May 7;317(3):837-43 [15081416.001]
  • [Cites] Oncogene. 2004 Jul 29;23(34):5834-42 [15208677.001]
  • [Cites] Cancer Res. 1968 Sep;28(9):1908-14 [5676741.001]
  • [Cites] Science. 1986 Nov 7;234(4777):697-704 [3535067.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3305-14 [8205554.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2127-33 [7808000.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1233-9 [7543176.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] J Leukoc Biol. 1996 Jul;60(1):106-17 [8699114.001]
  • [Cites] Infect Immun. 1996 Nov;64(11):4574-9 [8890209.001]
  • [Cites] Leukemia. 1998 Jul;12(7):1064-70 [9665191.001]
  • [Cites] Blood. 1998 Aug 1;92(3):795-801 [9680347.001]
  • [Cites] Tissue Antigens. 1998 Jul;52(1):1-8 [9714468.001]
  • [Cites] Leukemia. 1999 May;13(5):779-85 [10374883.001]
  • [Cites] Cytometry. 1999 Aug 15;38(4):139-52 [10440852.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):595-605 [10666389.001]
  • (PMID = 15826304.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD65s antigen, human; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 63231-63-0 / RNA; EC 3.4.11.2 / Antigens, CD13
  • [Other-IDs] NLM/ PMC1112585
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85. Vyas P, Roberts I: Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis. Early Hum Dev; 2006 Dec;82(12):767-73
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  • [Title] Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis.
  • Newborns and children with Down Syndrome are predisposed to a range of blood disorders, which include acute lymphoblastic leukaemia and acute megakaryocytic leukaemia (AMKL).
  • Like other childhood leukaemias DS AMKL is initiated in utero and can present in the neonatal period as a clinically overt preleukaemic condition, transient myeloproliferative disorder (TMD).
  • Thus, DS TMD and AMKL provide a unique model of childhood leukaemia where the preleukaemic and leukaemic phases are ascertainable and separable allowing distinct steps in leukaemogenesis to be studied individually.
  • These findings also have implications for the clinical management of DS TMD and AMKL specifically and also of childhood leukaemia more generally.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / physiopathology. Megakaryocytes / physiology. Thrombopoiesis / physiology
  • [MeSH-minor] Child. GATA1 Transcription Factor / genetics. Humans. Myeloproliferative Disorders / genetics. Myeloproliferative Disorders / physiopathology

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  • (PMID = 17064858.001).
  • [ISSN] 0378-3782
  • [Journal-full-title] Early human development
  • [ISO-abbreviation] Early Hum. Dev.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 23
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86. Rubnitz JE, Inaba H, Ribeiro RC, Pounds S, Rooney B, Bell T, Pui CH, Leung W: NKAML: a pilot study to determine the safety and feasibility of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia. J Clin Oncol; 2010 Feb 20;28(6):955-9
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  • [Title] NKAML: a pilot study to determine the safety and feasibility of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.
  • PURPOSE To conduct a pilot study to determine the safety, feasibility, and engraftment of haploidentical natural killer (NK) cell infusions after an immunosuppressive regimen in children with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS Ten patients (0.7 to 21 years old) who had completed chemotherapy and were in first complete remission of AML were enrolled on the Pilot Study of Haploidentical Natural Killer Cell Transplantation for Acute Myeloid Leukemia (NKAML) study.
  • We propose to further investigate the efficacy of KIR-mismatched NK cells in a phase II trial as consolidation therapy to decrease relapse without increasing mortality in children with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotherapy. Killer Cells, Natural / transplantation. Leukemia, Myeloid, Acute / therapy. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Feasibility Studies. Female. Haplotypes. Humans. Infant. Interleukin-2 / administration & dosage. Male. Neoplasm Staging. Pilot Projects. Prognosis. Survival Rate. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult


87. Yang CP, Hung IJ, Jaing TH, Shih LY, Chang WH: Cancer in infants: a review of 82 cases. Pediatr Hematol Oncol; 2005 Sep;22(6):463-81
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  • Acute leukemia was diagnosed in 21 infants (25.6%; acute myeloid leukemia in 12, and acute lymphoblastic leukemia in 9), retinoblastoma in 14 (17.1%), neuroblastoma in 12 (14.6%), brain tumor in 9 (11.0%), germ cell tumor in 8 (9.8%), renal cancer in 8 (Wilms tumor 3, mesoblastic nephroma 1, renal sarcoma 1, rhabdoid tumor 3), hepatoblastoma in 5 (6.1%), and soft tissue sarcoma in 5 (rhabdomyosarcoma 1, fibrosarcoma 3, other sarcoma 1).
  • The 4 most common types of cancer occurring in infants are the same in the present series and in most larger childhood cancer series reported by other countries; but rank differently.
  • In this study there were more infants with acute leukemia and retinoblastoma, and less with neuroblastoma.
  • The prognosis is poor for infant leukemia and rhabdoid tumor, while it is good for embryonal tumors and germ cell tumors occurring in infancy.

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  • (PMID = 16169813.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 31
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88. Smith MT: Advances in understanding benzene health effects and susceptibility. Annu Rev Public Health; 2010;31:133-48 2 p following 148
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  • Benzene is a ubiquitous chemical in our environment that causes acute leukemia and probably other hematological cancers.
  • Evidence for an association with childhood leukemia is growing.

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  • (PMID = 20070208.001).
  • [ISSN] 1545-2093
  • [Journal-full-title] Annual review of public health
  • [ISO-abbreviation] Annu Rev Public Health
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01ES06721; United States / NIEHS NIH HHS / ES / R01 ES006721; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / U54ES01611
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens, Environmental; 0 / Receptors, Aryl Hydrocarbon; J64922108F / Benzene
  • [Number-of-references] 129
  • [Other-IDs] NLM/ NIHMS668017; NLM/ PMC4360999
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89. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6
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  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • We used standard methods to explore NOTCH1 mutations and other specific molecular markers in 15 early childhood T-ALL cases.
  • Despite being found in a lower frequency than that described for overall pediatric T-ALL, NOTCH1 alterations were the most frequent ones.
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Child, Preschool. Chromosome Aberrations. Female. Gene Rearrangement / physiology. Genes, T-Cell Receptor delta. Genes, T-Cell Receptor gamma. Genetic Testing. Histone-Lysine N-Methyltransferase. Humans. Infant. Male

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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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90. Brown P, Levis M, McIntyre E, Griesemer M, Small D: Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner. Leukemia; 2006 Aug;20(8):1368-76
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  • [Title] Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner.
  • Mixed lineage leukemia (MLL) rearrangements occur in 80% of infants and 5% of older children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carbazoles / administration & dosage. Indoles / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • [MeSH-minor] Cell Line, Tumor. Child. Dose-Response Relationship, Drug. Drug Synergism. G1 Phase / drug effects. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant

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  • (PMID = 16761017.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA70970
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; 0 / MLL protein, human; 0 / Protein Kinase Inhibitors; 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 / fms-Like Tyrosine Kinase 3
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91. Meleshko AN, Movchan LV, Belevtsev MV, Savitskaja TV: Relative expression of different Ikaros isoforms in childhood acute leukemia. Blood Cells Mol Dis; 2008 Nov-Dec;41(3):278-83
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  • [Title] Relative expression of different Ikaros isoforms in childhood acute leukemia.
  • We estimate the relative level of Ikaros mRNA transcripts in 80 childhood ALL cases in comparison with AML and healthy donor groups.
  • We detected eight major isoforms and several minor mutant isoforms in most patients with acute lymphoblastic and myeloid leukemia and in healthy donors, but the relative level of expression varied.
  • The ratio was significantly less in AML (p=0.027) and BCR-ABL positive ALL (p=0.0028) than in healthy bone marrow.
  • We found a negative association between the Ikaros ratio and myeloid coexpression in B-cell ALL, the most prominent was for CD15.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Ikaros Transcription Factor / genetics. Leukemia / genetics
  • [MeSH-minor] Adolescent. Cell Line. Child. Child, Preschool. Gene Expression. Humans. Infant. Infant, Newborn. Mutant Proteins. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18675565.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
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92. Jóhannsdóttir IM, Hjermstad MJ, Moum T, Wesenberg F, Hjorth L, Schrøder H, Lähteenmäki P, Jónmundsson G, Loge JH: Social outcomes in young adult survivors of low incidence childhood cancers. J Cancer Surviv; 2010 Jun;4(2):110-8
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  • [Title] Social outcomes in young adult survivors of low incidence childhood cancers.
  • INTRODUCTION: The intensity and duration of childhood cancer treatment may disrupt psychosocial development and thereby cause difficulties in transition into adulthood.
  • The study objective was to assess social outcomes in early adulthood after successful treatment for childhood acute myeloid leukemia (AML), Wilms tumor (WT) and infratentorial astrocytoma (IA).
  • METHODS: Nordic patients treated for AML, WT and IA from 1985 to 2001 identified from a database administered by NOPHO (Nordic Society of Paediatric Haematology and Oncology) were invited to participate in a postal survey.
  • [MeSH-major] Astrocytoma / psychology. Infratentorial Neoplasms / psychology. Leukemia, Myeloid, Acute / psychology. Social Behavior. Survivors / psychology. Wilms Tumor / psychology
  • [MeSH-minor] Adolescent. Adult. Child, Preschool. Female. Follow-Up Studies. Humans. Incidence. Infant. Kidney Neoplasms / mortality. Kidney Neoplasms / psychology. Male. Prognosis. Survival Rate. Young Adult

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  • [Cites] Med Pediatr Oncol. 1999 Jul;33(1):60-3 [10401499.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):104-10 [17554791.001]
  • [Cites] Curr Probl Cancer. 2003 May-Jun;27(3):112-26 [12748581.001]
  • [Cites] Psychooncology. 2003 Apr-May;12(3):213-25 [12673806.001]
  • [Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]
  • [Cites] Int J Cancer Suppl. 1999;12:25-31 [10679867.001]
  • [Cites] Pediatr Blood Cancer. 2009 Sep;53(3):417-23 [19479971.001]
  • [Cites] Cancer. 2005 Oct 15;104(8):1751-60 [16130127.001]
  • [Cites] J Pediatr Hematol Oncol. 2008 Nov;30(11):807-14 [18989157.001]
  • [Cites] Med Pediatr Oncol. 1999 Jul;33(1):29-33 [10401494.001]
  • [Cites] Curr Probl Cancer. 2003 Jul-Aug;27(4):177-97 [12855950.001]
  • [Cites] Psychosomatics. 1997 Jan-Feb;38(1):54-62 [8997117.001]
  • [Cites] J Clin Oncol. 2000 Dec 15;18(24):4060-6 [11118467.001]
  • [Cites] J Cancer Surviv. 2008 Sep;2(3):205-14 [18663582.001]
  • [Cites] J Clin Oncol. 2007 Aug 10;25(23):3518-24 [17687156.001]
  • [Cites] J Cancer Surviv. 2008 Sep;2(3):149-58 [18792789.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2374-81 [19364956.001]
  • [Cites] Pediatr Hematol Oncol. 1997 Nov-Dec;14(6):513-24 [9383804.001]
  • [Cites] Pediatr Hematol Oncol. 1999 Jan-Feb;16(1):9-21 [9932269.001]
  • [Cites] Med Pediatr Oncol. 1991;19(6):459-66 [1961132.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Acta Paediatr Scand. 1989 Sep;78(5):728-35 [2596279.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2390-5 [19224833.001]
  • [Cites] Pediatrics. 2007 Mar;119(3):554-68 [17332209.001]
  • [Cites] Br J Cancer. 2004 Aug 31;91(5):923-8 [15292930.001]
  • [Cites] Hum Reprod. 2008 Jan;23(1):178-86 [18024486.001]
  • [Cites] Lancet. 2000 Apr 15;355(9212):1310-4 [10776743.001]
  • [Cites] Lancet Oncol. 2008 Jun;9(6):569-76 [18510988.001]
  • [Cites] Pediatr Hematol Oncol. 1997 May-Jun;14(3):223-32 [9185207.001]
  • [Cites] Cancer. 1993 May 15;71(10 Suppl):3392-9 [8490888.001]
  • [Cites] Pediatr Blood Cancer. 2007 Oct 15;49(5):704-15 [16830322.001]
  • [Cites] Cancer. 2006 Jul 1;107(1):1-11 [16718655.001]
  • [Cites] Psychooncology. 2007 Oct;16(10):920-7 [17279494.001]
  • [Cites] Cancer. 1986 Jul 15;58(2 Suppl):529-33 [3719547.001]
  • [Cites] J Dev Behav Pediatr. 2007 Dec;28(6):448-55 [18091089.001]
  • [Cites] Ann Oncol. 2003;14 Suppl 5:v119-27 [14684502.001]
  • [Cites] Eur J Cancer. 1996 Jul;32A(8):1354-8 [8869099.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):229-34 [11838795.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Jun;26(6):354-62 [15167348.001]
  • [Cites] Pediatr Hematol Oncol. 1998 Nov-Dec;15(6):479-88 [9842641.001]
  • [Cites] Pediatr Clin North Am. 2008 Feb;55(1):251-73, xiii [18242324.001]
  • [Cites] Support Care Cancer. 2002 Nov;10(8):579-600 [12436217.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jul;47(1):61-70 [16572415.001]
  • [Cites] Psychooncology. 2002 Mar-Apr;11(2):132-41 [11921329.001]
  • [Cites] CA Cancer J Clin. 2004 Jul-Aug;54(4):208-36 [15253918.001]
  • [Cites] Cancer. 2008 May 1;112(9):2071-9 [18327823.001]
  • [Cites] Pediatr Neurosurg. 2005 Jan-Feb;41(1):15-21 [15886508.001]
  • [Cites] Eur J Cancer. 2001 Aug;37(12):1523-7, discussion 1527-30 [11506960.001]
  • (PMID = 20082150.001).
  • [ISSN] 1932-2267
  • [Journal-full-title] Journal of cancer survivorship : research and practice
  • [ISO-abbreviation] J Cancer Surviv
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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93. Silva ML, Pombo-de-Oliveira MS, Raimondi SC, Mkrtchyan H, Abdelhay E, de Figueiredo AF, de Souza MT, Garcia DR, de Ventura EM, de Sousa AM, Liehr T: Unbalanced chromosome 1 abnormalities leading to partial trisomy 1q in four infants with Down syndrome and acute megakaryocytic leukemia. Mol Cytogenet; 2009;2:7
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  • [Title] Unbalanced chromosome 1 abnormalities leading to partial trisomy 1q in four infants with Down syndrome and acute megakaryocytic leukemia.
  • BACKGROUND: Children with Down syndrome (DS) have an increased risk of childhood acute leukemia, especially acute megakaryoblastic leukemia (AMKL) also called acute myeloid leukemia (AML) type M7.

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  • [Cites] Cancer Genet Cytogenet. 2008 Apr 1;182(1):56-60 [18328953.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jan 1;116(1):1-5 [10616523.001]
  • [Cites] Early Hum Dev. 2006 Dec;82(12):767-73 [17064858.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4606-13 [16469874.001]
  • [Cites] Nat Rev Cancer. 2005 Jan;5(1):11-20 [15630411.001]
  • [Cites] Leukemia. 1999 Mar;13(3):491-2 [10086746.001]
  • [Cites] Nucleic Acids Res. 1992 Mar 25;20(6):1433 [1313972.001]
  • [Cites] Ann Intern Med. 1985 Sep;103(3):460-2 [2411180.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2480-9 [14656875.001]
  • [Cites] Cytogenet Genome Res. 2003;103(1-2):34-9 [15004461.001]
  • [Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] Cytogenet Genome Res. 2002;98(2-3):118-25 [12697993.001]
  • [Cites] Leukemia. 2003 Feb;17(2):277-82 [12592323.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Jan;24(1):14-7 [11902731.001]
  • [Cites] Int J Mol Med. 2002 Apr;9(4):335-9 [11891523.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1575-83 [17971484.001]
  • (PMID = 19228396.001).
  • [ISSN] 1755-8166
  • [Journal-full-title] Molecular cytogenetics
  • [ISO-abbreviation] Mol Cytogenet
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2653040
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94. Flotho C, Paulun A, Batz C, Niemeyer CM: AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies. Br J Haematol; 2007 Sep;138(5):644-50
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  • [Title] AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies.
  • We hypothesized that epigenetic repression of the AKAP12 gene might occur in malignant myeloid disorders.
  • AKAP12 hypermethylation was found in one case of refractory anaemia with excess blasts (RAEB) and two cases of acute myeloid leukaemia (AML) in a panel of 21 blood or bone marrow samples from children with malignant myeloid disorders including refractory cytopenia, RAEB, juvenile myelomonocytic leukaemia and AML.
  • While AKAP12 function has not been previously linked to leukaemogenesis, our results raise the possibility that epigenetic silencing of AKAP12 is involved in myeloid malignancies.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA Methylation. DNA, Neoplasm / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] A Kinase Anchor Proteins. Adolescent. Anemia, Refractory, with Excess of Blasts / genetics. Anemia, Refractory, with Excess of Blasts / metabolism. Child. Child, Preschool. Epigenesis, Genetic. Female. Gene Silencing. Humans. Infant. Infant, Newborn. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Male. Neoplasm Proteins / metabolism. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured

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  • (PMID = 17686059.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / A Kinase Anchor Proteins; 0 / AKAP12 protein, human; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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95. Kaspers GJ, Creutzig U: Pediatric acute myeloid leukemia: international progress and future directions. Leukemia; 2005 Dec;19(12):2025-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric acute myeloid leukemia: international progress and future directions.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Child. Forecasting. Humans. Prognosis. Treatment Outcome

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  • (PMID = 16304569.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Number-of-references] 30
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96. Subspecialty Group of Hematology Diseases, Society of Pediatrics, Chinese Medical Association, Editorial Board of Chinese Journal of Pediatrics: [Suggestion of diagnosis and treatment of acute myelocytic leukemia in childhood]. Zhonghua Er Ke Za Zhi; 2006 Nov;44(11):877-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Suggestion of diagnosis and treatment of acute myelocytic leukemia in childhood].
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Child. Humans

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  • (PMID = 17274886.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
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97. Puhlmann U, Ziemann C, Ruedell G, Vorwerk H, Schaefer D, Langebrake C, Schuermann P, Creutzig U, Reinhardt D: Impact of the cyclooxygenase system on doxorubicin-induced functional multidrug resistance 1 overexpression and doxorubicin sensitivity in acute myeloid leukemic HL-60 cells. J Pharmacol Exp Ther; 2005 Jan;312(1):346-54
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  • [Title] Impact of the cyclooxygenase system on doxorubicin-induced functional multidrug resistance 1 overexpression and doxorubicin sensitivity in acute myeloid leukemic HL-60 cells.
  • Multidrug resistance (MDR), a challenge in treating childhood acute myeloid leukemia (AML), is frequently associated with decreased drug accumulation caused by multidrug transporter MDR1.
  • Doxorubicin, an important anti-AML drug, is a known MDR1 substrate and inducer.
  • Our study focused on cyclooxygenase system's impact on drug-induced MDR1 overexpression in AML cells.
  • As a prerequisite, coexpression of MDR1 and cyclooxygenase-2 mRNA in HL-60 cells and primary AML blasts was demonstrated by Northern blot.
  • Interestingly, incubation of AML cells with doxorubicin not only induced functionally active MDR1 overexpression but also mediated increased cyclooxygenase-2 mRNA and protein expressions with subsequent PGE(2) release (determined by flow cytometry, rhodamine123 efflux assay, reverse transcription-polymerase chain reaction, and enzyme-linked immunosorbent assay).
  • After preincubation and subsequent parallel treatment with the cyclooxygenase-2-preferential inhibitor meloxicam, doxorubicin-induced MDR1 overexpression and function were reduced (maximally at 0.1-0.5 microM meloxicam), whereas cytostatic efficacy of doxorubicin in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assays was significantly increased by up to 78 (HL-60) and 30% (AML blasts) after 72 h of doxorubicin treatment.
  • In conclusion, the cyclooxygenase system, especially the cyclooxygenase-2 isoform, might be involved in regulating doxorubicin-induced MDR1 overexpression in AML cells, with PGE(2) seeming to be a mediating factor.
  • Cyclooxygenase inhibitors thus bear promise to overcome MDR in AML and improve therapy.
  • [MeSH-minor] Apoptosis. Biological Transport. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / pharmacology. Dinoprostone / metabolism. Drug Interactions. Drug Resistance, Multiple. Drug Screening Assays, Antitumor. Gene Expression / drug effects. HL-60 Cells. Humans. Leukemia, Myeloid, Acute. Membrane Proteins. Rhodamine 123 / pharmacology. Thiazines / pharmacology. Thiazoles / pharmacology

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  • (PMID = 15501994.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Membrane Proteins; 0 / P-Glycoprotein; 0 / Thiazines; 0 / Thiazoles; 1N3CZ14C5O / Rhodamine 123; 71125-38-7 / meloxicam; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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98. Zhang JB, Sun Y, Dong J, Liu LX, Ning F: [Expression of lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance]. Ai Zheng; 2005 Aug;24(8):1015-7
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  • [Title] [Expression of lung resistance protein and multidrug resistance-associated protein in naive childhood acute leukemia and their clinical significance].
  • BACKGROUND & OBJECTIVE: Previous studies revealed that lung resistance protein (LRP) and multidrug resistance-associated protein (MRP) relate to drug resistance of childhood leukemia, which is not caused by only one mechanism.
  • This study was to evaluate the expression of LRP and MRP genes in childhood leukemia and their correlation.
  • METHODS: The expression of LRP and MRP in 38 children with acute leukemia and 6 healthy children were measured with reverse transcription-polymerase chain reaction (RT-PCR); their clinical significance was analyzed according to complete remission (CR) rate of the patients after chemotherapy.
  • The positive rate of LRP was significantly lower in acute lymphoblastic leukemia (ALL) than in acute nonlymphocytic leukemia (ANLL) [18.5% (5/27) vs. 45.5% (6/11), P < 0.05]; however, the positive rate of MRP was 59.3% (16/27) in ALL, and 45.5% (5/11) in ANLL (P > 0.05).
  • CONCLUSION: Childhood acute leukemia patients with overexpression of LRP and MRP suffer severe disease and achieve low remission rateû lower remission rate of childhood ANLL patients may relate to LRP expression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Male. Remission Induction

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  • (PMID = 16086885.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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99. Walter RB, Alonzo TA, Gerbing RB, Ho PA, Smith FO, Raimondi SC, Hirsch BA, Gamis AS, Franklin JL, Hurwitz CA, Loken MR, Meshinchi S: High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group. J Clin Oncol; 2010 Jun 10;28(17):2831-8
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  • [Title] High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group.
  • PURPOSE: To evaluate the prognostic significance of the integrin cell adhesion molecule very late antigen-4 (VLA-4) in acute myeloid leukemia (AML).
  • Subgroup analyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with standard-risk AML, in whom low VLA-4 expression was associated with inferior DFS (34% +/- 16% v 69% +/- 14% for high expression; P = .011) and higher RR (61% +/- 16% v 26% +/- 14% for high expression; P = .009).
  • CONCLUSION: High VLA-4 expression is associated with better clinical outcome in pediatric AML and is an independent predictor of relapse that may refine our abilities to stratify patients without identifiable cytogenetic or molecular risk factors.

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  • [Cites] Blood. 2001 Apr 1;97(7):2121-9 [11264180.001]
  • [Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):579-89 [12899713.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3125-32 [7693037.001]
  • [Cites] Leukemia. 1996 Apr;10(4):682-6 [8618447.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3008-17 [19636064.001]
  • [Cites] Nat Rev Immunol. 2007 Sep;7(9):678-89 [17717539.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]
  • [Cites] Blood. 2009 Jan 22;113(4):866-74 [18927435.001]
  • [Cites] Annu Rev Immunol. 2009;27:339-62 [19302044.001]
  • [Cites] Leuk Res. 2009 Jun;33(6):764-8 [19042019.001]
  • [Cites] Genome Biol. 2007;8(5):215 [17543136.001]
  • (PMID = 20421533.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha4beta1
  • [Other-IDs] NLM/ PMC2903318
  •  go-up   go-down


100. Palermo CM, Bennett CA, Winters AC, Hemenway CS: The AF4-mimetic peptide, PFWT, induces necrotic cell death in MV4-11 leukemia cells. Leuk Res; 2008 Apr;32(4):633-42
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  • [Title] The AF4-mimetic peptide, PFWT, induces necrotic cell death in MV4-11 leukemia cells.
  • Despite ongoing success in the treatment of childhood acute lymphoblastic leukemia, patients harboring translocations involving the MLL gene at chromosome 11q23 remain resistant to treatment.
  • PFWT induced cell death in leukemia cells expressing MLL-AF4 with little effect on the colony forming potential of hematopoietic progenitor cells, suggesting the AF4-AF9 complex is an important pharmacological target for leukemia therapy and PFWT is a promising chemotherapeutic prototype.

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  • [Cites] Neurobiol Aging. 2000 May-Jun;21(3):383-421 [10858586.001]
  • [Cites] Cell Death Differ. 2005 Sep;12(9):1219-24 [16094402.001]
  • [Cites] Leukemia. 2000 Oct;14(10):1833-49 [11021759.001]
  • [Cites] Mutat Res. 2000 Nov 20;455(1-2):111-27 [11113471.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):439-44 [11212227.001]
  • [Cites] Mol Cell. 2001 Sep;8(3):613-21 [11583623.001]
  • [Cites] J Biol Chem. 2002 Jan 4;277(1):432-8 [11606597.001]
  • [Cites] Anal Biochem. 2002 Apr 15;303(2):153-66 [11950215.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Pharmacol Res. 2003 Apr;47(4):355-62 [12644394.001]
  • [Cites] Prostate. 2003 May 1;55(2):147-57 [12661040.001]
  • [Cites] Cell Death Differ. 2003 Oct;10(10):1204-12 [14502243.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7414-30 [14576849.001]
  • [Cites] Leukemia. 2004 Jan;18(1):92-102 [14603337.001]
  • [Cites] Leukemia. 2004 Feb;18(2):227-32 [14671638.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2299-307 [14645012.001]
  • [Cites] Genes Dev. 2004 May 1;18(9):965-74 [15132992.001]
  • [Cites] Genes Dev. 2004 Jun 1;18(11):1272-82 [15145826.001]
  • [Cites] Cell Death Differ. 2004 Aug;11(8):937-9 [15044964.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Aug;310(2):425-36 [15075382.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1364-72 [15269783.001]
  • [Cites] Pharmacol Rev. 1972 Dec;24(4):583-655 [4565956.001]
  • [Cites] Blood. 1987 Jul;70(1):192-9 [3496132.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3671-5 [2023917.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 May 15;90(10):4631-5 [8506309.001]
  • [Cites] Br J Haematol. 1997 Jul;98(1):157-69 [9233580.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1469-77 [9305600.001]
  • [Cites] Am J Pathol. 1997 Nov;151(5):1205-13 [9358745.001]
  • [Cites] Leukemia. 1998 Oct;12(10):1561-4 [9766500.001]
  • [Cites] Curr Biol. 1999 Sep 9;9(17):967-70 [10508592.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1605-12 [16034464.001]
  • [Cites] Acta Biochim Biophys Sin (Shanghai). 2005 Nov;37(11):719-27 [16270150.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2296-303 [16208414.001]
  • [Cites] Exp Cell Res. 2006 Jan 1;312(1):27-39 [16288739.001]
  • [Cites] Infect Immun. 2007 Apr;75(4):1984-93 [17283090.001]
  • [Cites] Curr Opin Immunol. 2003 Oct;15(5):553-9 [14499264.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1539-47 [10516755.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:80-97 [15561678.001]
  • [Cites] Infect Immun. 2005 Apr;73(4):1907-16 [15784530.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3155-62 [15867207.001]
  • [Cites] Trends Neurosci. 2000 Sep;23(9):410-1 [10941188.001]
  • (PMID = 17875318.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098459-03; United States / NCI NIH HHS / CA / CA098459-03; United States / NCI NIH HHS / CA / CA098459-03S1; United States / NCRR NIH HHS / RR / P20 RR020152; United States / NCI NIH HHS / CA / CA 098459; United States / NCI NIH HHS / CA / R01 CA098459-03S2; United States / NCI NIH HHS / CA / R01 CA098459; United States / NCRR NIH HHS / RR / P20 RR020152-037527; United States / NCI NIH HHS / CA / R01 CA098459-03S1; United States / NCRR NIH HHS / RR / RR 020152; United States / NCI NIH HHS / CA / F32 CA 119474; United States / NCI NIH HHS / CA / F32 CA119474; United States / NCRR NIH HHS / RR / RR020152-037527; United States / NCI NIH HHS / CA / CA098459-03S2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / MLLT3 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Peptide Fragments; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS41852; NLM/ PMC2270790
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