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1. Hassan R, White LR, Stefanoff CG, de Oliveira DE, Felisbino FE, Klumb CE, Bacchi CE, Seuánez HN, Zalcberg IR: Epstein-Barr virus (EBV) detection and typing by PCR: a contribution to diagnostic screening of EBV-positive Burkitt's lymphoma. Diagn Pathol; 2006 Aug 07;1:17
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  • We performed a systematic comparison between RISH and PCR for EBV detection, in a group of childhood B-cell Non-Hodgkin lymphomas (NHL), aiming to validate PCR as a first, rapid method for the diagnosis of EBV-associated B-cell NHL.
  • METHODS: EBV infection was investigated in formalin fixed paraffin-embedded tumor samples of 41 children with B-cell NHL, including 35 Burkitt's lymphoma (BL), from Rio de Janeiro, Brazil, by in situ hybridization of EBV-encoded small RNA (EBER-RISH) and PCR assays based on EBNA2 amplification.

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  • (PMID = 16893464.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA082274
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1559641
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2. Koklu E, Gunes T, Patiroglu T, Ozturk MA, Kontas O, Arsav V: Leukemia cutis following biphenotypic congenital leukemia. Pediatr Dermatol; 2007 Sep-Oct;24(5):587-8
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  • [Title] Leukemia cutis following biphenotypic congenital leukemia.
  • [MeSH-major] Leukemia, Lymphoid / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Skin / pathology

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  • (PMID = 17958830.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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3. Kawamura M, Kaku H, Taketani T, Taki T, Shimada A, Hayashi Y: Mutations of GATA1, FLT3, MLL-partial tandem duplication, NRAS, and RUNX1 genes are not found in a 7-year-old Down syndrome patient with acute myeloid leukemia (FAB-M2) having a good prognosis. Cancer Genet Cytogenet; 2008 Jan 1;180(1):74-8
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  • [Title] Mutations of GATA1, FLT3, MLL-partial tandem duplication, NRAS, and RUNX1 genes are not found in a 7-year-old Down syndrome patient with acute myeloid leukemia (FAB-M2) having a good prognosis.
  • The prognosis of leukemia developed in Down syndrome (DS) patients has improved markedly.
  • Most DS leukemia occurs before 3 years of age and is classified as acute megakaryocytic leukemia (AMKL).
  • In contrast, it has been shown that occurrence of DS acute myeloid leukemia (DS-AML) after 3 years of age may indicate a higher risk for a poor prognosis, but its frequency is very low.
  • We here describe the case of a 7-year-old DS boy with AML-M2, who had no history of transient abnormal myelopoiesis or any clinical poor prognostic factors, such as high white blood cell counts or extramedullary infiltration.
  • Accumulation of more data on older pediatric DS-AML patients is needed.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Down Syndrome / complications. GATA1 Transcription Factor / genetics. Leukemia, Promyelocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18068539.001).
  • [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] 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / MLL protein, human; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 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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4. Fujita N, Mori T, Mitsui T, Inada H, Horibe K, Tsurusawa M, Lymphoma Committee of the Japanese Pediatric Leukemia/Lymphoma Study Group: The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan. Pediatr Blood Cancer; 2008 Aug;51(2):188-92
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  • [Title] The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan.
  • BACKGROUND: There have been excellent treatment results for children with B-cell non-Hodgkin lymphoma (B-NHL) and mature B-cell leukemia (B-ALL) in the last few decades.
  • Among 18 patients who had a chemotherapy-sensitive disease, 4 of 5 patients who underwent hematopoietic stem cell transplantation (HSCT) during remission survived without progression, while 3 of 12 patients who did not receive HSCT were alive without disease progression.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, B-Cell / therapy. Lymphoma, B-Cell / therapy


5. Langebrake C, Brinkmann I, Teigler-Schlegel A, Creutzig U, Griesinger F, Puhlmann U, Reinhardt D: Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring. Cytometry B Clin Cytom; 2005 Jan;63(1):1-9
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  • [Title] Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring.
  • BACKGROUND: Determination of antigen expression patterns is, in addition to morphologic analysis, essential to the diagnosis of acute myeloid leukemia (AML).
  • The present study was performed to determine (a) the degree of changes in immunophenotype and their consequences on the monitoring of minimal residual disease (MRD) in childhood AML and (b) whether certain clusters of changes in antigen expression patterns exist between diagnosis and relapse.
  • METHODS: Bone marrow specimens of 48 children enrolled in the German AML-BFM-93/98 (Acute Myeloid Leukemia-Berlin-Frankfurt-Munster) studies were analyzed immunologically, morphologically, and genetically at diagnosis and at first relapse.
  • We did not observe significant changes for lineage specific markers, with comparable occurrences of loss or gain of myeloid and lymphoid antigens in the sample pairs.
  • The antibody panels used for MRD monitoring in childhood AML should therefore not be restricted to the immunophenotype detected at presentation but should include in particular markers of lineage immaturity.
  • The clinical observation of a shift toward a more immature phenotype of the myeloblasts is consistent with the model of a clonal evolution of a leukemic stem cell.
  • [MeSH-major] Antigens, Neoplasm / immunology. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Bone Marrow / immunology. Bone Marrow / pathology. Child. Child, Preschool. Clone Cells. Flow Cytometry. Humans. Infant. Karyotyping. Recurrence

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15624201.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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6. Berretta R, Barone A, Rolla M, Bertolini P, Nardelli GB: Isolated ovarian relapse of pre-B acute lymphoblastic leukemia: a case report. J Pediatr Adolesc Gynecol; 2009 Aug;22(4):e65-8
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  • [Title] Isolated ovarian relapse of pre-B acute lymphoblastic leukemia: a case report.
  • BACKGROUND: Acute lymphoblastic leukemia is a malignant disease of the bone marrow in which early lymphoid precursors proliferate and replace normal marrow hematopoietic cells, resulting in a marked decrease in the production of normal blood cells.
  • CONCLUSION: In contrast to testicular relapse, ovarian relapses in acute lymphoblastic leukemia are rarely reported.
  • [MeSH-major] Ovarian Neoplasms / secondary. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19493520.001).
  • [ISSN] 1873-4332
  • [Journal-full-title] Journal of pediatric and adolescent gynecology
  • [ISO-abbreviation] J Pediatr Adolesc Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Mueller D, García-Cuéllar MP, Bach C, Buhl S, Maethner E, Slany RK: Misguided transcriptional elongation causes mixed lineage leukemia. PLoS Biol; 2009 Nov;7(11):e1000249
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  • [Title] Misguided transcriptional elongation causes mixed lineage leukemia.
  • Fusion proteins composed of the histone methyltransferase mixed-lineage leukemia (MLL) and a variety of unrelated fusion partners are highly leukemogenic.
  • Despite their prevalence, particularly in pediatric acute leukemia, many molecular details of their transforming mechanism are unknown.
  • Here, we provide mechanistic insight into the function of MLL fusions, demonstrating that they capture a transcriptional elongation complex that has been previously found associated with the eleven-nineteen leukemia protein (ENL).
  • [MeSH-major] Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Transcriptional Elongation Factors / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Chromatin Assembly and Disassembly. Cyclin-Dependent Kinase 9 / antagonists & inhibitors. Flavonoids. Histone-Lysine N-Methyltransferase. Humans. Mice. Mice, Inbred BALB C. Piperidines

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  • (PMID = 19956800.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ELL protein, human; 0 / Flavonoids; 0 / MLL protein, human; 0 / Piperidines; 0 / Transcriptional Elongation Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 45AD6X575G / alvocidib; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.11.22 / Cyclin-Dependent Kinase 9
  • [Other-IDs] NLM/ PMC2774266
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8. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • This review considers recent advances in our understanding of the role of MLL gene rearrangements in pediatric clinical practice.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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9. Mullighan CG, Zhang J, Harvey RC, Collins-Underwood JR, Schulman BA, Phillips LA, Tasian SK, Loh ML, Su X, Liu W, Devidas M, Atlas SR, Chen IM, Clifford RJ, Gerhard DS, Carroll WL, Reaman GH, Smith M, Downing JR, Hunger SP, Willman CL: JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2009 Jun 9;106(23):9414-8
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  • [Title] JAK mutations in high-risk childhood acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) is a heterogeneous disease consisting of distinct clinical and biological subtypes that are characterized by specific chromosomal abnormalities or gene mutations.
  • We recently identified a poor prognostic subgroup of pediatric BCR-ABL1-negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1-positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype.
  • Here, we report activating mutations in the Janus kinases JAK1 (n = 3), JAK2 (n = 16), and JAK3 (n = 1) in 20 (10.7%) of 187 BCR-ABL1-negative, high-risk pediatric ALL cases.
  • The JAK-mutated cases had a gene expression signature similar to BCR-ABL1 pediatric ALL, and they had a poor outcome.

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  • (PMID = 19470474.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA118100; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / L40 CA142226; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / Howard Hughes Medical Institute / / ; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2695045
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10. Lanciotti M, Dufour C, Corral L, Di Michele P, Pigullo S, De Rossi G, Basso G, Leszl A, Luciani M, Lo Nigro L, Micalizzi C, Valsecchi MG, Biondi A, Haupt R: Genetic polymorphism of NAD(P)H:quinone oxidoreductase is associated with an increased risk of infant acute lymphoblastic leukemia without MLL gene rearrangements. Leukemia; 2005 Feb;19(2):214-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphism of NAD(P)H:quinone oxidoreductase is associated with an increased risk of infant acute lymphoblastic leukemia without MLL gene rearrangements.
  • To assess whether NQO1 inactivating polymorphism (CT/TT) was a possible risk factor for infant acute lymphoblastic leukemia (iALL), we investigated the distribution of NQO1 genotype in 50 iALL patients, 32 with MLL gene rearrangements (MLL+) and 18 without (MLL-).
  • As controls, 106 cases of pediatric ALL (pALL), and 147 healthy subjects were also studied.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Rearrangement. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Gene Expression Regulation, Neoplastic / genetics. Genotype. Histone-Lysine N-Methyltransferase. Humans. Infant. Myeloid-Lymphoid Leukemia Protein. Reference Values

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  • (PMID = 15618957.001).
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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11. Cowan SA: Denmark decides not to introduce hepatitis B into the childhood vaccination programme. Euro Surveill; 2005;10(11):E051103.3
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  • [Title] Denmark decides not to introduce hepatitis B into the childhood vaccination programme.

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  • (PMID = 16794274.001).
  • [ISSN] 1560-7917
  • [Journal-full-title] Euro surveillance : bulletin Européen sur les maladies transmissibles = European communicable disease bulletin
  • [ISO-abbreviation] Euro Surveill.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hepatitis B Vaccines
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12. Dorantes-Acosta E, Arreguin-Gonzalez F, Rodriguez-Osorio CA, Sadowinski S, Pelayo R, Medina-Sanson A: Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report. Cases J; 2009;2:154
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  • [Title] Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report.
  • Acute leukemia, the most common form of cancer in children, accounts for approximately 30% of all childhood malignancies, with acute lymphoblastic leukemia being five times more frequent than acute myeloid leukemia.
  • Lineage switch is the term that has been used to describe the phenomenon of acute leukemias that meet the standard French-American-British system criteria for a particular lineage (either lymphoid or myeloid) upon initial diagnosis, but meet the criteria for the opposite lineage at relapse.
  • Many reports have documented conversions of acute lymphoblastic leukemia to acute myeloid leukemia.
  • Here, we report the case of a 4-year-old child with acute myeloid leukemia, which upon relapse switched to acute lymphoblastic leukemia.

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  • (PMID = 19946525.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2783110
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13. Xie XT, Jiang SY, Li BS, Yang LL: [Relationship between the expression of the genes encoding the key enzymes for cytarabine metabolism and the pharmacokinetics of cytarabine in the treatment of childhood acute leukemia with high-dose cytarabine]. Zhonghua Er Ke Za Zhi; 2008 Apr;46(4):276-80
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  • [Title] [Relationship between the expression of the genes encoding the key enzymes for cytarabine metabolism and the pharmacokinetics of cytarabine in the treatment of childhood acute leukemia with high-dose cytarabine].
  • OBJECTIVE: It has been reported that high-dose cytarabine (HD-AraC) was very effective for childhood hematological malignancies, especially for improving the long-term survival of high-risk acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), and T-cell lymphoid malignancies (T-ALL, T-cell non-Hodgkin's lymphoma).
  • This study aimed to evaluate the pharmacokinetics of HD-AraC for childhood hematological malignancies, and the relationship between the expression of the genes coding the key enzymes for Ara-C metabolism with the outcome of the patients.
  • METHODS: The drug levels of Ara-C in plasma and cerebrospinal fluid were detected with HPLC while HD-AraC was used, the expression of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA in human leukemia cell lines and the bone marrow cells were investigated in 48 cases of childhood hematological malignancies with RT-PCR methods, and the relationship between the expression of these enzymes mRNA and the outcome of the patients was analyzed. RESULTS:.
  • (1) When HD-AraC was used, the plasma levels of Ara-C and Ara-U could be respectively about 50 times and 25 times higher than those obtained when the patients were treated with regular dose of Ara-C treatment, and the level of Ara-C in cerebrospinal fluid could reach about 10% of plasma level of Ara-C. (2) There were significantly different expressions of dCK mRNA in different childhood acute leukemia (AL) patients, which were markedly related to the chemotherapy results.
  • There were no significant differences in expressions of dCK in T-ALL and B lineage ALL. (3) In vitro study found that the expressions of dCK and CDA mRNA did not change in leukemia cell lines incubated at different doses and times of Ara-C.
  • CONCLUSIONS: HD-AraC was a very effective protocol for childhood hematological malignancies for it could significantly elevate the plasma and cerebrospinal fluid drug levels.
  • Good long-term outcomes of the childhood T-ALL could be achieved as the B lineage ALL had been treated with HD-AraC regimen.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Cytarabine / pharmacokinetics. Leukemia / genetics. Leukemia / metabolism
  • [MeSH-minor] Child. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Gene Expression. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19099730.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.5.4.5 / Cytidine Deaminase
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14. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
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  • [Title] CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
  • Acute lymphoblastic leukemia (ALL) is the most frequent malignancy of childhood.
  • We investigated CD1d expression in 80 pediatric B-cell precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
  • CD1d+ ALLs were significantly associated with infant leukemia, pro-B phenotype and mixed-lineage leukemia (MLL)/AF4 gene rearrangement.
  • [MeSH-major] Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism. Cell Communication. Cell Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate

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  • (PMID = 15744356.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
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15. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • The majority of the patients (58.3%) had a B-lymphoid/myeloid phenotype, followed by the T-lymphoid/myeloid phenotype.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Other-IDs] NLM/ PMC2791935
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16. Crews KR, Zhou Y, Pauley JL, Howard SC, Jeha S, Relling MV, Pui CH: Effect of allopurinol versus urate oxidase on methotrexate pharmacokinetics in children with newly diagnosed acute lymphoblastic leukemia. Cancer; 2010 Jan 1;116(1):227-32
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  • [Title] Effect of allopurinol versus urate oxidase on methotrexate pharmacokinetics in children with newly diagnosed acute lymphoblastic leukemia.
  • BACKGROUND: Allopurinol and urate oxidase are both effective in preventing or treating hyperuricemia during remission induction therapy for lymphoid malignancies, but to the authors' knowledge, their effects on concomitant anticancer drug therapy have not been compared.
  • METHODS: The authors compared plasma methotrexate pharmacokinetics in pediatric patients with newly diagnosed acute lymphoblastic leukemia who received concomitant allopurinol (n = 20) versus those treated with nonrecombinant or recombinant urate oxidase (n = 96) during high-dose methotrexate administration before conventional remission induction therapy.
  • Hence, during remission induction therapy for lymphoid malignancies, the authors concluded that renally excreted drugs should be monitored closely, especially in patients who are receiving allopurinol.

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  • [Copyright] Copyright 2010 American Cancer Society.
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  • (PMID = 19834958.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA023099-299002; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA23099; None / None / / R01 CA051001-15; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / U10 CA031566-21; United States / NCI NIH HHS / CA / P01 CA023099; United States / NCI NIH HHS / CA / U10 CA031566; United States / NCI NIH HHS / CA / R01 CA051001-15; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA31566; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA023099-299002; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / CA32053; United States / NCI NIH HHS / CA / CA031566-21
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 268B43MJ25 / Uric Acid; 63CZ7GJN5I / Allopurinol; EC 1.7.3.3 / Urate Oxidase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS149924; NLM/ PMC2846832
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17. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Such translocations result in gain of function fusion proteins that drive cell proliferation.
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [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] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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18. Boatsman EE, Fu CH, Song SX, Moore TB: Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Mar;32(2):e57-60
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  • [Title] Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
  • INTRODUCTION: Infant acute lymphoblastic leukemia (ALL) is considered a high-risk entity.
  • By morphology, infant ALL is classified as a lymphoid lineage leukemia; however, its physiologic behavior has brought many to consider it a pathologic hybrid between lymphoid leukemia and myeloid leukemias.
  • The role of hematopoietic stem cell transplantation and graft-versus-leukemia effect in these patients has not been well studied.
  • CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-cell lymphoblastic leukemia was treated with protocol P9407 and matched sibling hematopoietic stem cell transplantation.
  • CONCLUSION: Traditionally, graft-versus-leukemia effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem cell transplantation (HSCT).
  • The effects of graft-versus-leukemia immunologic phenomenon in our patient with infant acute lymphoblastic leukemia underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
  • Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-leukemia effect may play a role in disease control in infant ALL after HSCT.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20168246.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
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  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Of 200 cases, 9.0% aberrantly expressed T cell-associated antigens.
  • There were significant differences in antigen-expression patterns between adult and pediatric B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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20. Schnakenberg E, Mehles A, Cario G, Rehe K, Seidemann K, Schlegelberger B, Elsner HA, Welte KH, Schrappe M, Stanulla M: Polymorphisms of methylenetetrahydrofolate reductase (MTHFR) and susceptibility to pediatric acute lymphoblastic leukemia in a German study population. BMC Med Genet; 2005 May 27;6:23
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  • [Title] Polymorphisms of methylenetetrahydrofolate reductase (MTHFR) and susceptibility to pediatric acute lymphoblastic leukemia in a German study population.
  • Two common polymorphisms (677C>T and 1298A>C) in the gene coding for MTHFR have been shown to reduce MTHFR enzyme activity and were associated with the susceptibility to different disorders, including vascular disease, neural tube defects and lymphoid malignancies.
  • Studies on the role of these polymorphisms in the susceptibility to acute lymphoblastic leukemia (ALL) led to discrepant results.
  • METHODS: We retrospectively evaluated the association of the MTHFR 677C>T and 1298A>C polymorphisms with pediatric ALL by genotyping a study sample of 443 ALL patients consecutively enrolled onto the German multicenter trial ALL-BFM 2000 and 379 healthy controls.
  • We calculated odds ratios of MTHFR genotypes based on the MTHFR 677C>T and 1298A>C polymorphisms to examine if one or both of these polymorphisms are associated with pediatric ALL.
  • CONCLUSION: Our findings suggest that the MTHFR 677C>T and 1298A>C gene variants do not have a major influence on the susceptibility to pediatric ALL in the German population.
  • [MeSH-major] Genetic Predisposition to Disease / epidemiology. Genetic Predisposition to Disease / genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15921520.001).
  • [ISSN] 1471-2350
  • [Journal-full-title] BMC medical genetics
  • [ISO-abbreviation] BMC Med. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
  • [Other-IDs] NLM/ PMC1164414
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21. Torelli GF, Guarini A, Maggio R, Alfieri C, Vitale A, Foà R: Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission. Haematologica; 2005 Jun;90(6):785-92
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  • [Title] Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission.
  • The anti-leukemic activity of NK cells against acute myeloid leukemia (AML) blasts has been described, but very few data are available for acute lymphoid leukemia (ALL).
  • The present study was designed to investigate whether: (i) NK effectors could be expanded from adult and pediatric ALL patients in complete remission;.
  • (v) any differences in cytotoxic activity could be found between expanded effectors from adult and pediatric patients.
  • DESIGN AND METHODS: We co-cultured patients' peripheral blood mononuclear cells (PBMC) with the feeder cell line RPMI 8866 and analyzed the NK cells' expansion capacity by cell count and cytofluorimetric analyses.
  • 51Cr release assays, before and after stimulation with activating cytokines, were performed to analyze the cytotoxic potential of effector cells against tumor cell lines and autologous blast cells.
  • Patients' expanded cells showed cytotoxic activity against target cell lines comparable to that of normal donors.
  • No differences in expansion and cytotoxic activity were found between pediatric and adult patients.
  • [MeSH-major] Immunotherapy / methods. Killer Cells, Natural / cytology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 15951291.001).
  • [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 / Cytokines; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Receptors, IgG
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22. Hill A, Short MA, Varghese C, Kusumakumary P, Kumari P, Morgan GJ: The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India. Haematologica; 2005 Mar;90(3):414-6
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  • [Title] The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India.
  • t(12;21) (TEL/AML1) is the most common genetic event in childhood B-cell acute lymphoblastic leukemia (B-ALL) in Western countries.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Child. Humans. Incidence. India / epidemiology. Leukemia, B-Cell. Molecular Epidemiology


23. Akiyama S, Dhavan D, Yi T: PRL-2 increases Epo and IL-3 responses in hematopoietic cells. Blood Cells Mol Dis; 2010 Apr 15;44(4):209-14
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  • Dual specificity protein tyrosine phosphatase PRL-2 is overexpressed in pediatric acute myeloid leukemia (AML) and is located at human chromosome 1p35, a region often rearranged or amplified in malignant lymphoma and B-cell chronic lymphocytic leukemia (B-CLL).
  • Herein we demonstrated that ectopic expression of PRL-2 in murine pre-B-cell line Baf3ER and mouse bone marrow cells induced key features associated with malignant progression and metastasis.
  • PRL-2-transfected Baf3ER cells had augmented growth responses to hematopoietic growth factors Epo or IL-3 with shortened cell cycle, reduced requirement (5x) for Epo in cell survival, increased cell migration (3x), reduced cell adhesion (5x), and conversion to an immature cell morphology in association with increased expression (3x) of stem cell marker Bmi-1.

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  • (PMID = 20226699.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102481-03; United States / NCI NIH HHS / CA / R01 CA096636; United States / NCI NIH HHS / CA / R01 CA102481; United States / NCI NIH HHS / CA / R01 CA096636-05; United States / NCI NIH HHS / CA / CA102481-03; United States / NCI NIH HHS / CA / CA096636-05
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-3; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa; EC 3.1.3.48 / PTP4A2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ NIHMS182540; NLM/ PMC2847026
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24. Jetsrisuparb A, Wiangnon S, Komvilaisak P, Kularbkaew C, Yutanawiboonchai W, Mairieng E: Rituximab combined with CHOP for successful treatment of aggressive recurrent, pediatric B-cell large cell non-Hodgkin's lymphoma. J Pediatr Hematol Oncol; 2005 Apr;27(4):223-6
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  • [Title] Rituximab combined with CHOP for successful treatment of aggressive recurrent, pediatric B-cell large cell non-Hodgkin's lymphoma.
  • This report is the first to describe the successful treatment of a 14-year-old boy with aggressive recurrent, CD20-positive, B-cell large cell non-Hodgkin's lymphoma.
  • Rituximab and CHOP in addition to chemotherapy may be an alternative treatment for aggressive recurrent, pediatric CD20-positive B-cell large cell non-Hodgkin's lymphoma if highly intensive chemotherapy and stem cell transplantation are not available.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 15838396.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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25. Li YQ, Wu XL, Yang LJ, Chen SH, Geng SX, Przybylski G, Schmidt CA: [Thymic recent output function in patients with B-cell lymphocytic malignancies]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):1023-7
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  • [Title] [Thymic recent output function in patients with B-cell lymphocytic malignancies].
  • The aim of the study was to analyze the naive T cell level of thymic recent output in patients with B-cell malignancies, thereby to evaluate the potential T-cell function.
  • Quantitative analysis of T-cell receptor rearrangement excision circles (TRECs) in DNA of peripheral blood mononuclear cells from 61 cases of B-cell lymphocytic malignancy (including 20 cases of adult B-ALL, 6 case of childhood B-ALL, 4 cases of B-CLL, 17 cases of B-NHL and 14 cases of MM) were preformed by real-time PCR (TaqMan), and TREC-level was detected according to the number of CD3-positive cells.
  • The mean value of TRECs was 0.53 +/- 1.52 copies/1000 PBMNC and 2.01 +/- 3.93 copies/1000 CD3+ cells in adult B-ALL (p = 0.0005, p = 0.0123), 0.11 +/- 0.15 copies/1000 PBMNC and 0.23 +/- 0.27 copies/1000 CD3+ cells in B-CLL (p = 0.0015, p = 0.0381), 0.71 +/- 1.34 copies/1000 PBMNC in B-NHL (p = 0.0017), 0.53 +/- 0.90 copies/1000 PBMNC in MM patients (p = 0.0018), as compared with 3.76 +/- 3.42 copies/1000 PBMNC and 5.87 +/- 4.96 copies/1000 CD3+ cells in normal individuals, the TREC level was significantly decreased in all groups of B-cell lymphocytic malignancy, as well as in ALL-CR group.
  • However, the TREC level in childhood B-ALL was significant higher than those in adult B-ALL group.
  • It is concluded that the function of thymic recent outputting naive T cells in B-cell malignancies significantly decreases, however, the individual difference of thymic output function is obvious.
  • The thymic recent output function can not be recovered during CR phase in patients with B-cell malignancies, so that dynamic analysis of TREC level is necessary.

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  • (PMID = 17956683.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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26. Burmeister T, Gökbuget N, Schwartz S, Fischer L, Hubert D, Sindram A, Hoelzer D, Thiel E: Clinical features and prognostic implications of TCF3-PBX1 and ETV6-RUNX1 in adult acute lymphoblastic leukemia. Haematologica; 2010 Feb;95(2):241-6
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  • [Title] Clinical features and prognostic implications of TCF3-PBX1 and ETV6-RUNX1 in adult acute lymphoblastic leukemia.
  • BACKGROUND: The t(9;22) and t(4;11) chromosomal translocations, which generate the BCR-ABL and MLL-AF4 fusion genes, define high-risk subtypes of acute lymphoblastic leukemia in adults.
  • However, the prognostic impact of other rarer fusion genes is less well established in adult acute lymphoblastic leukemia than in the childhood form.
  • DESIGN AND METHODS: In the context of the German Multicenter Therapy Study Group for Adult Acute Lymphoblastic Leukemia (GMALL) we used reverse transcriptase polymerase chain reaction to investigate 441 cases of BCR-ABL- and MLL-AF4-negative B-precursor acute lymphoblastic leukemia for the TCF3-PBX1 (E2A-PBX1) and ETV6-RUNX1 (TEL-AML1) fusion transcripts generated by the t(1;19)(q23;p13.3) and t(12;21)(p13;q22) translocations.
  • Both are well-known molecular alterations in pediatric acute lymphoblastic leukemia in which they have favorable prognostic implications.
  • CONCLUSIONS: In contrast to previous suggestions, adult patients with TCF3-PBX1-positive acute lymphoblastic leukemia do not appear to have a worse outcome than their negative counterparts.
  • [MeSH-major] Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Cell Line. Core Binding Factor Alpha 2 Subunit. Female. Fusion Proteins, bcr-abl. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19713226.001).
  • [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 / 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; 0 / abl-bcr fusion protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2817026
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27. Schoumans J, Johansson B, Corcoran M, Kuchinskaya E, Golovleva I, Grandér D, Forestier E, Staaf J, Borg A, Gustafsson B, Blennow E, Nordgren A: Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2. Br J Haematol; 2006 Nov;135(4):492-9
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  • [Title] Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2.
  • Although the dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in paediatric B-cell precursor acute lymphoblastic leukaemia (BCP ALL), occurring in approximately 2% of the cases, its molecular genetic consequences have not been elucidated.
  • In the present study, high-resolution genome-wide array-based comparative genomic hybridisation (array-CGH) and fluorescence in situ hybridisation (FISH) were used to characterise the 9p and 20q breakpoints (BPs) in seven childhood BCP ALLs with dic(9;20), which was shown to be unbalanced in all of them, resulting in loss of 9p13.2-pter.
  • One of the ALLs, shown to have a complex dic(9;20), was further investigated by FISH, revealing a rearrangement of the haemapoietic cell kinase isoform p61 (HCK) gene at 20q11.

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  • (PMID = 16999846.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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28. Mantadakis E, Danilatou V, Stiakaki E, Paterakis G, Papadhimitriou S, Kalmanti M: T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):354-7
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  • [Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.
  • We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.
  • Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.
  • This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16206214.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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29. Steiner M, Attarbaschi A, König M, Nebral K, Gadner H, Haas OA, Mann G, Austrian Berlin-Frankfurt-Münster Group: Equal frequency of TEL/AML1 rearrangements in children with acute lymphoblastic leukemia with and without Down syndrome. Pediatr Hematol Oncol; 2005 Apr-May;22(3):229-34
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  • [Title] Equal frequency of TEL/AML1 rearrangements in children with acute lymphoblastic leukemia with and without Down syndrome.
  • Constitutional trisomy 21 is the most prominent predisposing factor to childhood leukemia, whereas the t(12;21)(p13;q22) with its molecular genetic counterpart, the TEL/AML1 fusion gene, is the most common acquired chromosomal rearrangement in childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL).
  • Accordingly, they were able to analyze 8 of 10 individuals with DS and a BCP ALL, two of whom who suffered from a TEL/AML1+ leukemia.
  • Based on this observation they concluded that individuals with BCP leukemia and a constitutional trisomy 21 may have similar likelihood to have a TEL/AML1 rearrangement as BCP ALL patients without this specific predisposing factor.
  • [MeSH-major] Down Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [RepublishedFrom] Pediatr Hematol Oncol. 2005 Jan-Feb;22(1):11-6 [15770827.001]
  • (PMID = 16020107.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Corrected and Republished Article; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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30. Stefan DC, Stones D: How much does it cost to treat children with Hodgkin lymphoma in Africa? Leuk Lymphoma; 2009 Feb;50(2):196-9
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  • Hodgkin lymphoma (HL) is a common B-cell childhood neoplasm and it has a higher incidence in the 0-14 year age group in developing countries compared to developed countries.

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  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):152-3 [19235011.001]
  • (PMID = 19197725.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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31. Ahmad N, Zaidi A, Badar F, Maaz AU, Akram MS: Clinical characteristics and outcome analysis of pediatric B-cell non-Hodgkin's lymphoma. Experience with FAB-LMB 96 and UKCCSG B-cell NHL guidelines in a developing country. Asia Pac J Clin Oncol; 2010 Mar;6(1):49-56
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  • [Title] Clinical characteristics and outcome analysis of pediatric B-cell non-Hodgkin's lymphoma. Experience with FAB-LMB 96 and UKCCSG B-cell NHL guidelines in a developing country.
  • AIM: To analyze the clinical characteristics of B-cell non-Hodgkin's lymphoma (NHL) patients and the therapeutic efficacy of French-American-British Lymphoma Malins de Burkitt 96 and the recent United Kingdom Children's Cancer Study Group B-cell NHL guidelines in the tertiary care hospital of a developing country.
  • METHODS: Patients aged < or =18 years registered at our hospital between January 1995 and December 2006 with histologically proved B-Cell NHL were selected for retrospective analysis.
  • Of these 95 had Burkitt's lymphoma, 22 diffuse large B-cell lymphoma and five had B-cell NHL not otherwise specified.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / mortality. Practice Guidelines as Topic

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  • (PMID = 20398038.001).
  • [ISSN] 1743-7563
  • [Journal-full-title] Asia-Pacific journal of clinical oncology
  • [ISO-abbreviation] Asia Pac J Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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32. Liu Y, Li ZG, Zhao W, Li B, Gong WY, Wu MY: [Immunophenotypic characteristics of children with acute lymphoblastic leukemia carrying TEL-AML1 fusion gene]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):714-6
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  • [Title] [Immunophenotypic characteristics of children with acute lymphoblastic leukemia carrying TEL-AML1 fusion gene].
  • To investigate the immunological and other clinical characteristics in TEL/AML1+ childhood B-acute lymphoblastic leukemia (B-ALL), immunophenotyping was performed with three-color flow cytometry, and the expression of TEL-AML1 fusion gene was detected with nested RT-PCR.
  • (2) compared with TEL-AML1- group, no significant difference was found in age, gender, white cell count and blasts count in peripheral blood of TEL-AML1+;.
  • It is concluded that TEL-AML1 rearrangement is a frequent molecular abnormality in childhood ALL.
  • These characteristics may be useful in detection of minimal residual leukemia.

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  • (PMID = 16928306.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 3.4.11.2 / Antigens, CD13
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33. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20920256.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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34. 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 addition, it is uncertain whether cancer stem cells arise from malignant transformation of a tissue-specific stem cell, or from committed progenitors or differentiated cells that re-acquire a stem cell-like program.
  • 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

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  • (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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35. Sudhakar N, Nancy NK, Rajalekshmy KR, Rajkumar T: Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia. Iran J Immunol; 2009 Sep;6(3):141-6
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  • [Title] Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia.
  • BACKGROUND: Precursor B-Acute Lymphoblastic Leukemia (precursor B-ALL) occurs due to the uncontrolled proliferation of B-lymphoid precursors arrested at a particular stage of B-cell development.
  • Precursor-B-ALL is classified mainly into pro-B-ALL, common-ALL and pre-B-ALL.
  • The Common Acute Lymphoblastic Antigen CD10 is the marker for common-ALL.
  • OBJECTIVE: This study was aimed to examine the diversity of T-cell receptor Gamma (TCRG) and T-cell receptor Delta (TCRD) gene rearrangements in South Indian Common-ALL patients.
  • METHODS: Clonality of TCRG and TCRD was studied in 52 cases (pediatric=41 and adolescents and young adults=11) of common-ALL.
  • RESULTS: In pediatric common-ALL, clonal TCRG and TCRD gene rearrangements were detected in 19 (46.3%) and 18 (43.9%) cases respectively.
  • In the present study of common-ALL, the frequency of a TCRG rearrangement VII-J1.3/2.3 was significantly high in AYA compared to pediatric (36.3% vs 4.8%; p<0.025).
  • Thus, VII-J1.3/2.3 was highly diverse in AYA compared to pediatric.
  • That shows the difference in biology of the disease between pediatric and AYA in South Indian population.
  • [MeSH-major] Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 19801787.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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36. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
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  • [Title] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Forty cases were B-lineage, four were T-lineage, and one was double-lymphoid lineage.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


37. Trentin L, Giordan M, Dingermann T, Basso G, Te Kronnie G, Marschalek R: Two independent gene signatures in pediatric t(4;11) acute lymphoblastic leukemia patients. Eur J Haematol; 2009 Nov;83(5):406-19
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  • [Title] Two independent gene signatures in pediatric t(4;11) acute lymphoblastic leukemia patients.
  • METHOD: In our study we sought to overcome these limitations and for proof of principle, we analyzed the rare t(4;11) leukemia disease entity.
  • First, gene expression data of each t(4;11) leukemia patient were normalized by pairwise subtraction against normal bone marrow (n = 3) to identify significantly deregulated gene sets for each patient.
  • RESULT: A 'core signature' of 186 commonly deregulated genes present in each investigated t(4;11) leukemia patient was defined.
  • CONCLUSION: A yet homogeneous leukemia entity was further subdivided, based on distinct genetic properties.
  • [MeSH-major] Chromosomes, Human, Pair 11 / metabolism. Chromosomes, Human, Pair 4 / metabolism. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Translocation, Genetic
  • [MeSH-minor] Female. Gene Expression Profiling / methods. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Humans. Male. Myeloid-Lymphoid Leukemia Protein / biosynthesis. Myeloid-Lymphoid Leukemia Protein / genetics. Oligonucleotide Array Sequence Analysis / methods. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics

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  • (PMID = 19558506.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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38. Husak Z, Printz D, Schumich A, Pötschger U, Dworzak MN: Death induction by CD99 ligation in TEL/AML1-positive acute lymphoblastic leukemia and normal B cell precursors. J Leukoc Biol; 2010 Aug;88(2):405-12
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  • [Title] Death induction by CD99 ligation in TEL/AML1-positive acute lymphoblastic leukemia and normal B cell precursors.
  • Our study was performed to examine the role of CD99 in normal and leukemia BCPs.
  • CD99 is strongly expressed by certain pediatric cancers including BCP-ALL.
  • We investigated BCP-ALL cases and normal BCP cells from pediatric BM for CD99 protein and RNA expression as well as for effects of CD99 modulation by mAb.
  • An association of CD99 expression levels with the cytogenetic background of pediatric BCP-ALLs was found.
  • CD99 ligation moderately induced cell death only in TEL/AML1 cases.
  • Stroma cell contact mitigated this effect.
  • We consider our results as an indication that CD99 may play a physiologic role in the clonal deletion processes necessary for B-lymphoid selection.
  • [MeSH-major] Antigens, CD / physiology. Cell Adhesion Molecules / physiology. Core Binding Factor Alpha 2 Subunit. Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, CD99. Apoptosis. B-Lymphocytes / cytology. Cell Death. Child. Humans. Lymphopoiesis. RNA, Messenger / analysis

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  • (PMID = 20453109.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 18196
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD99; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein
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39. Brown VI, Seif AE, Reid GS, Teachey DT, Grupp SA: Novel molecular and cellular therapeutic targets in acute lymphoblastic leukemia and lymphoproliferative disease. Immunol Res; 2008;42(1-3):84-105
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  • [Title] Novel molecular and cellular therapeutic targets in acute lymphoblastic leukemia and lymphoproliferative disease.
  • While the outcome for pediatric patients with lymphoproliferative disorders (LPD) or lymphoid malignancies, such as acute lymphoblastic leukemia (ALL), has improved dramatically, patients often suffer from therapeutic sequelae.
  • (ii) block the interaction of ALL cells with stromal cells or lymphoid growth factors secreted by the bone marrow microenvironment; or (iii) stimulate innate and adaptive immune responses.

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  • (PMID = 18716718.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / NIH 1 K08 CA104882-01A1; United States / NCI NIH HHS / CA / K08 CA104882; United States / NCI NIH HHS / CA / NIH CA102646; United States / NCI NIH HHS / CA / K08 CA104882-05; United States / NCI NIH HHS / CA / R01 CA102646; United States / NCI NIH HHS / CA / NIH R03 CA123554; United States / NCI NIH HHS / CA / CA104882-05; United States / NCI NIH HHS / CA / R03 CA123554; United States / NCI NIH HHS / CA / CA1116660
  • [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 / Adjuvants, Immunologic; 0 / Enzyme Inhibitors; 0 / Receptor, Notch1; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
  • [Number-of-references] 158
  • [Other-IDs] NLM/ NIHMS209775; NLM/ PMC2890314
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40. Moorman AV, Ensor HM, Richards SM, Chilton L, Schwab C, Kinsey SE, Vora A, Mitchell CD, Harrison CJ: Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial. Lancet Oncol; 2010 May;11(5):429-38
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  • [Title] Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial.
  • BACKGROUND: Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease markers and indicators of outcomes.
  • METHODS: We analysed cytogenetic data from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medical Research Council ALL97/99 study and followed up for a median time of 8.2 years.
  • Multivariate analysis incorporating age, white-cell count, and treatment parameters showed that six cytogenetic abnormalities (ETV6-RUNX1, high hyperdiploidy, iAMP21, t(9;22), loss of 13q, and abnormal 17p) retained their significance for effect on relapse risk.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [CommentIn] Lancet Oncol. 2010 May;11(5):403-4 [20409755.001]
  • [ErratumIn] Lancet Oncol. 2010 Jun;11(6):516
  • (PMID = 20409752.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300130; United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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41. Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB: Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids. Cancer Cell Int; 2007 Nov 28;7:18
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  • Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
  • GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.
  • Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).
  • To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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  • (PMID = 18045478.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041407
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2228275
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42. Baris S, Celkan T, Batar B, Guven M, Ozdil M, Ozkan A, Apak H, Yildiz I: Association between genetic polymorphism in DNA repair genes and risk of B-cell lymphoma. Pediatr Hematol Oncol; 2009 Sep;26(6):467-72
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  • [Title] Association between genetic polymorphism in DNA repair genes and risk of B-cell lymphoma.
  • OBJECTIVES: The authors evaluated the possible effect of DNA repair genes, XPD (Xeroderma pigmentosum group D) codon (312 and 751) and XRCC1 (X-ray repair cross-complementing group 1) codon (194 and 399) SNPs (single-nucleotide polymorphisms) on the risk of childhood B-cell lymphoma.
  • RESULTS: The authors observed no association between variation in the XPD codon Asp312Asn, Lys751Gln, and XRCC1 codon Arg399Gln polymorphisms and B-cell lymphoma for any parameter.
  • The frequency of XRCC1 194Arg/Trp genotype in B-cell lymphoma was significantly lower than that in controls (p = .005).
  • CONCLUSIONS: XRCC1 194Trp allele may be associated with a protective effect against development of childhood B-cell lymphoma.
  • [MeSH-major] DNA Repair / genetics. DNA-Binding Proteins / genetics. Lymphoma, B-Cell / genetics. Polymorphism, Single Nucleotide / genetics. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 19657998.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein
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43. Xu JW, Jin RM, Li EQ, Wang YR, Bai Y: Signal pathways in ouabain-induced proliferation of leukemia cells. World J Pediatr; 2009 May;5(2):140-5
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  • [Title] Signal pathways in ouabain-induced proliferation of leukemia cells.
  • BACKGROUND: Cardiotonic steroids (CTSs) can bind to Na(+)/K(+)-ATPase and activate protein kinase cascades, resulting in changes in cell proliferation, differentiation or apoptosis in a cell-specific manner.
  • We explored the participation of ouabain-activated signaling pathways in growth regulation of leukemia cells.
  • METHODS: Lymphocytic leukemia Jhhan cells and megakaryocytic leukemia M07e cells were incubated at different concentrations of ouabain (0, 1 and 10 nmol) for 24 hours.
  • Cell proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay.
  • To probe the role of ouabain-induced signaling in control of cell growth, we employed Src kinase inhibitor PP2 and the MEK inhibitor PD98059, respectively.
  • The expression of Na(+)/K(+)-ATPase alpha1 subunit of leukemia cells was evaluated by RT-PCR and Western blotting.
  • Addition of either PP2 or PD98059 blocked the effects of ouabain on cell proliferation.
  • CONCLUSION: Ouabain activates Src and ERK1/2 pathways and regulates the proliferation of leukemia cells.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Leukemia, Lymphoid / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. Ouabain / pharmacology. Signal Transduction / drug effects. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. In Vitro Techniques. Sodium-Potassium-Exchanging ATPase / metabolism

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  • (PMID = 19718538.001).
  • [ISSN] 1708-8569
  • [Journal-full-title] World journal of pediatrics : WJP
  • [ISO-abbreviation] World J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 5ACL011P69 / Ouabain; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase
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44. Hanna-Wakim R, Yasukawa LL, Sung P, Fang M, Sullivan B, Rinki M, DeHovitz R, Arvin AM, Gans HA: Age-related increase in the frequency of CD4(+) T cells that produce interferon-gamma in response to staphylococcal enterotoxin B during childhood. J Infect Dis; 2009 Dec 15;200(12):1921-7
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  • [Title] Age-related increase in the frequency of CD4(+) T cells that produce interferon-gamma in response to staphylococcal enterotoxin B during childhood.
  • Immune maturation is complex, however, and the interval during which changes occur during childhood has not been identified.
  • METHODS: To assess age-related differences in the CD4(+) T cell responses, we evaluated the frequency of CD4(+) T cells that produced interferon (IFN) gamma in response to staphylococcal enterotoxin B (SEB) stimulation in 382 healthy infants and children (2 months to 11 years of age) and 66 adults.
  • Observed differences in CD45RO(+)CD4(+) T cell function indicate that CD4(+) T cells with the same phenotypes do not possess equivalent functional capabilities.

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  • (PMID = 19909079.001).
  • [ISSN] 1537-6613
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI37127
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD69 antigen; 0 / Enterotoxins; 0 / Lectins, C-Type; 147205-72-9 / CD40 Ligand; 39424-53-8 / enterotoxin B, staphylococcal; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
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45. Kouros CD, Cummings EM, Davies PT: Early trajectories of interparental conflict and externalizing problems as predictors of social competence in preadolescence. Dev Psychopathol; 2010 Aug;22(3):527-37
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  • Consistent with developmental cascade notions, the present study investigated (a) associations between trajectories of interparental conflict and early externalizing problems during childhood and (b) early trajectories of externalizing problems as a pathway by which interparental conflict impacts children's social competence in preadolescence.
  • Results from parallel process models indicated that changes in interparental conflict were positively associated with changes in externalizing problems during childhood.

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  • (PMID = 20576176.001).
  • [ISSN] 1469-2198
  • [Journal-full-title] Development and psychopathology
  • [ISO-abbreviation] Dev. Psychopathol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / T32-MH18921; United States / NIMH NIH HHS / MH / T32 MH018921; United States / NIMH NIH HHS / MH / T32 MH018921-20S1; United States / NIMH NIH HHS / MH / MH057318-01A2; United States / NIMH NIH HHS / MH / R01 MH057318-01A2; United States / NIMH NIH HHS / MH / MH018921-20S1; United States / NIMH NIH HHS / MH / R01 MH057318-06; United States / NIMH NIH HHS / MH / R01 MH057318; United States / NIMH NIH HHS / MH / R01 MH57318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS220333; NLM/ PMC2911621
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46. Olsen M, Madsen HO, Hjalgrim H, Gregers J, Rostgaard K, Schmiegelow K: Preleukemic TEL-AML1-positive clones at cell level of 10(-3) to 10(-4) do not persist into adulthood. J Pediatr Hematol Oncol; 2006 Nov;28(11):734-40
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  • [Title] Preleukemic TEL-AML1-positive clones at cell level of 10(-3) to 10(-4) do not persist into adulthood.
  • The TEL-AML1 translocation, t(12;21)(p13;q22), is one of the most frequent genetic aberrations in childhood B-cell precursor acute lymphoblastic leukemia (ALL), where it occurs in 25% of all cases.
  • Evidence suggests that the TEL-AML1 translocation occurs in utero in 1% of all newborn children at cell levels of 10 to 10.
  • The observed prevalence of TEL-AML1-positive cells in healthy adults is of the same order of magnitude as the prevalence reported in healthy newborns, but the observed cell level of 10 to 10 is much lower.
  • These data indicates that prenatal TEL-AML1 subclones does not persist throughout adult life at cell levels of 10 to 10.
  • The findings are compatible with the risk of t(12;21)(p13;q22) ALL correlating with the total number of TEL-AML1-positive cells in peripheral blood in both childhood and adulthood.
  • [MeSH-minor] Adult. Blood Donors. Child. Female. Humans. Male. Middle Aged. Nucleic Acid Hybridization / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17114960.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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47. Liu Y, Tang JY, Xu C, Gu LJ, Xue HL, Chen J, Pan C, Dong L, Zhou M: [Application of effective antigen combinations in childhood B lineage acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2009 May;47(5):366-70
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  • [Title] [Application of effective antigen combinations in childhood B lineage acute lymphoblastic leukemia].
  • OBJECTIVE: To probe into the occurrence rates of the effective antigen combinations which were used to detect the minimal residual disease (MRD) by flow cytometry in childhood B-lineage acute lymphoblastic leukemia (B-ALL), as well as the relationship between clinical-biologic factors and different combinations.
  • (1) Totally 327 cases of childhood B-ALL were screened for antibody combinations of interest and 88.4 percent of them (289 cases) were identified with effective antibody combinations. (2) The occurrence frequencies of antigen combinations were different.
  • [MeSH-major] Leukemia, B-Cell / immunology. Leukemia, B-Cell / therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy


48. Ozgen IT, Dagdemir A, Elli M, Saraymen R, Pinarli FG, Fisgin T, Albayrak D, Acar S: Hair selenium status in children with leukemia and lymphoma. J Pediatr Hematol Oncol; 2007 Aug;29(8):519-22
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  • [Title] Hair selenium status in children with leukemia and lymphoma.
  • Low serum Se levels have been reported in pediatric and adult patients with cancers.
  • The aim of the study was to investigate the hair Se status in children with newly diagnosed lymphoid malignancies and the relation between malnutrition and Se deficiency.
  • Thirty patients with leukemia (n=17) and lymphoma (n=13), and 25 healthy controls were enrolled to the study.
  • Children with lymphoma had lower Se than the children with acute lymphoblastic leukemia but not statistically significant [547.03+/-283.67 ng/g vs. 758.67+/-361.05 ng/g (P>0.05)].
  • In this study, we found that hair Se levels of the children with leukemia and lymphoma, especially those of malnourished patients, were lower than those of controls.
  • [MeSH-major] Child Nutrition Disorders / complications. Hodgkin Disease / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Selenium / deficiency

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  • (PMID = 17762491.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] H6241UJ22B / Selenium
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49. Wei G, Twomey D, Lamb J, Schlis K, Agarwal J, Stam RW, Opferman JT, Sallan SE, den Boer ML, Pieters R, Golub TR, Armstrong SA: Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL1 and glucocorticoid resistance. Cancer Cell; 2006 Oct;10(4):331-42
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  • A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in acute lymphoblastic leukemia (ALL) cells.
  • We tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells and found that it sensitized to GC-induced apoptosis via modulation of antiapoptotic MCL1.
  • These data indicate that MCL1 is an important regulator of GC-induced apoptosis and that the combination of rapamycin and glucocorticoids has potential utility in lymphoid malignancies.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Databases, Genetic. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Drug Combinations. Drug Resistance, Neoplasm. Green Fluorescent Proteins / metabolism. Humans. Mice. Myeloid Cell Leukemia Sequence 1 Protein. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [CommentIn] Cancer Cell. 2006 Nov;10(5):349-51 [17097556.001]
  • (PMID = 17010674.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE5258/ GSE5820/ GSE5821/ GSE5822
  • [Grant] United States / NCI NIH HHS / CA / K08 CA92551; United States / NCI NIH HHS / CA / P01 CA068484
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Glucocorticoids; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 147336-22-9 / Green Fluorescent Proteins; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
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50. Pichler H, Möricke A, Mann G, Teigler-Schlegel A, Niggli F, Nebral K, König M, Inthal A, Krehan D, Dworzak MN, Janousek D, Harbott J, Schrappe M, Gadner H, Strehl S, Haas OA, Panzer-Grümayer R, Attarbaschi A, Berlin-Frankfurt-Münster (BFM) Study Group: Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy. Br J Haematol; 2010 Apr;149(1):93-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy.
  • The presence of a dicentric chromosome dic(9;20) has been reported to have an unfavourable prognosis in children with B-cell precursor acute lymphoblastic leukaemia (BCP-ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20067563.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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51. Zámecníkova A, Al Bahar S: Simultaneous occurrence of MLL and RARA rearrangements in a pediatric acute lymphoblastic leukemia patient. Pediatr Blood Cancer; 2009 May;52(5):671-4
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  • [Title] Simultaneous occurrence of MLL and RARA rearrangements in a pediatric acute lymphoblastic leukemia patient.
  • We report a case of concurrent translocations of MLL gene, associated with a highly distinct leukemia subtype and RARA gene, which is pathogenomic in acute promyelocytic leukemia.
  • [MeSH-major] Gene Rearrangement / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19142993.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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52. Onda K, Iijima K, Katagiri YU, Okita H, Saito M, Shimizu T, Kiyokawa N: Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma. Int J Hematol; 2010 Jun;91(5):808-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma.
  • B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear.
  • We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells.
  • Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL.
  • BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells.
  • The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.
  • [MeSH-major] B-Cell Activating Factor / immunology. B-Cell Activation Factor Receptor / genetics. Burkitt Lymphoma / immunology. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / pathology
  • [MeSH-minor] Antigens, CD40 / immunology. Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans

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  • (PMID = 20428981.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / B-Cell Activating Factor; 0 / B-Cell Activation Factor Receptor
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53. Krivtsov AV, Feng Z, Armstrong SA: Transformation from committed progenitor to leukemia stem cells. Ann N Y Acad Sci; 2009 Sep;1176:144-9
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  • [Title] Transformation from committed progenitor to leukemia stem cells.
  • Leukemias are composed of a hierarchy of cells, only a fraction of which have stem cell-like properties and are capable of self-renewal.
  • Mixed lineage leukemia (MLL) fusion proteins produced by translocations involving the MLL gene on chromosome 11q23 confer stem cell-like properties on committed hematopoietic progenitors.
  • This provides an opportunity to assess changes in immunophenotype, gene expression, and epigenetic programs during the transition from a hematopoietic cell with minimal inherent self-renewal capability to cells capable of leukemic self-renewal.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Histones / metabolism. Humans. Methylation. Mice. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 19796242.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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54. Linger RM, DeRyckere D, Brandão L, Sawczyn KK, Jacobsen KM, Liang X, Keating AK, Graham DK: Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia. Blood; 2009 Sep 24;114(13):2678-87
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  • [Title] Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is currently treated with an intense regimen of chemotherapy yielding cure rates near 80%.
  • Here, we report ectopic expression of the receptor tyrosine kinase Mer in pediatric B-cell ALL.
  • Inhibition of Mer prevented Erk 1/2 activation, increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and delayed disease onset in a mouse model of leukemia.

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  • (PMID = 19643988.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / F32 HL096416; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U24 CA114766; United States / NHLBI NIH HHS / HL / F32HL096416; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC2927045
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55. Volbrecht MM, Goldsmith HH: Early temperamental and family predictors of shyness and anxiety. Dev Psychol; 2010 Sep;46(5):1192-205
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  • Using hierarchical linear modeling with restricted maximum likelihood estimation to adjust for twin dependency, early BI (b = 0.37, p < .01), IC (b = 0.14, p < .05), and concurrent lower family stress (b = -0.22, p < .05) predicted shyness during middle childhood.
  • Anxiety symptoms were predicted by BI (b = 0.14, p < .05), early negative family affect (b = 0.20, p < .05), and family stress in middle childhood (b = 0.26, p < .05).
  • These findings clarify the relative importance of temperament and family factors in the development of both shyness and anxiety symptoms during childhood.

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  • (PMID = 20822232.001).
  • [ISSN] 1939-0599
  • [Journal-full-title] Developmental psychology
  • [ISO-abbreviation] Dev Psychol
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / MH050560-08; United States / NIMH NIH HHS / MH / P50 MH084051; United States / NIMH NIH HHS / MH / R37 MH050560-08; United States / NIMH NIH HHS / MH / R01 MH059785-01A1; United States / NIMH NIH HHS / MH / P50 MH069315-01; None / None / / P50 MH069315-01; United States / NIMH NIH HHS / MH / R01 MH059785; United States / NIMH NIH HHS / MH / R37 MH050560; United States / NIMH NIH HHS / MH / P50 MH069315; United States / NIMH NIH HHS / MH / MH059785-01A1
  • [Publication-type] Journal Article; Twin Study
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS283658; NLM/ PMC3086562
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56. Lawce H, Olson S: FISH testing for deletions of chromosome 6q21 and 6q23 in hematologic neoplastic disorders. J Assoc Genet Technol; 2009;35(4):167-9
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  • Chromosome 6q deletions are also commonly found in lymphoid malignancies such as acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), multiple myeloma (MM), mantle zone lymphoma (MZL), and Waldenström's macroglobulinemia (WM).
  • In childhood B- and T-cell ALL a deletion of 6q is the hallmark of a neutral prognosis; however, it may be cytogenetically obscure or cryptic, requiring interphase FISH analysis.
  • In adult ALL it indicates a favorable prognosis, but in CLL, B-cell small lymphocytic lymphoma (SLL), WM, and MM it has a poor prognosis.
  • We report the results of the first three patients in our laboratory with deletions of 6q in lymphoid malignancies using this cocktail.

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  • (PMID = 19952391.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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57. Tanyeli A, Erbey F, Bayram I, Kömür M: Myeloid antigen positivity in Turkish children with acute lymphoblastic leukemia lacks influence on prognosis. Asian Pac J Cancer Prev; 2010;11(6):1823-6
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  • [Title] Myeloid antigen positivity in Turkish children with acute lymphoblastic leukemia lacks influence on prognosis.
  • INTRODUCTION: Several studies have suggested that the presence of myeloid antigens is a poor prognostic factor in patients with acute lymphoid leukemia (ALL).
  • [MeSH-major] Antigens, Differentiation, Myelomonocytic / metabolism. Antigens, Surface / metabolism. Biomarkers, Tumor / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 21338240.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Surface; 0 / Biomarkers, Tumor
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58. He GS, Zhang XH, Yao L, Zhang R, Chen ZX, Wu DP, Sun AN, Jin ZM, Qiu HY, Hu XH: [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2009 Oct;30(10):675-7
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  • [Title] [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review].
  • OBJECTIVE: To report a case of T cell acute lymphoblastic leukemia (ALL) with t(1;19)(q23;pl3) and E2A-PBX1 fusion gene, which is a characteristic translocation of childhood B cell ALL (B-ALL).
  • The leukemic cells expressed T cell markers.
  • CONCLUSION: t(1;19)E2A-PBX1(+) can be implicated in adult T-ALL, besides childhood B-ALL.
  • [MeSH-major] Homeodomain Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19954663.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 146150-85-8 / E2A-Pbx1 fusion protein
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59. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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60. Boublikova L, Kalinova M, Ryan J, Quinn F, O'Marcaigh A, Smith O, Browne P, Stary J, McCann SR, Trka J, Lawler M: Wilms' tumor gene 1 (WT1) expression in childhood acute lymphoblastic leukemia: a wide range of WT1 expression levels, its impact on prognosis and minimal residual disease monitoring. Leukemia; 2006 Feb;20(2):254-63
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  • [Title] Wilms' tumor gene 1 (WT1) expression in childhood acute lymphoblastic leukemia: a wide range of WT1 expression levels, its impact on prognosis and minimal residual disease monitoring.
  • Wilms' tumor gene 1 (WT1) is overexpressed in the majority (70-90%) of acute leukemias and has been identified as an independent adverse prognostic factor, a convenient minimal residual disease (MRD) marker and potential therapeutic target in acute leukemia.
  • We examined WT1 expression patterns in childhood acute lymphoblastic leukemia (ALL), where its clinical implication remains unclear.
  • Using a real-time quantitative PCR designed according to Europe Against Cancer Program recommendations, we evaluated WT1 expression in 125 consecutively enrolled patients with childhood ALL (106 BCP-ALL, 19 T-ALL) and compared it with physiologic WT1 expression in normal and regenerating bone marrow (BM).
  • In childhood B-cell precursor (BCP)-ALL, we detected a wide range of WT1 levels (5 logs) with a median WT1 expression close to that of normal BM.
  • WT1 expression in childhood T-ALL was significantly higher than in BCP-ALL (P<0.001).
  • In summary, our study suggests that WT1 expression in childhood ALL is very variable and much lower than in AML or adult ALL.
  • WT1, thus, will not be a useful marker for MRD detection in childhood ALL, however, it does represent a potential independent risk factor in childhood ALL.
  • Interestingly, a proportion of childhood ALL patients express WT1 at levels below the normal physiological BM WT1 expression, and this reduced WT1 expression appears to be associated with a higher risk of relapse.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Molecular Diagnostic Techniques / methods. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics


61. Xu C, Zhao HJ, Jiang LM, Yuan XJ, Li L, Tang JY, Shen LS: [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):717-21
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  • [Title] [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia].
  • This study was aimed to investigate the value of CD58 in evaluation of early therapeutic effect on childhood B-ALL.
  • The expression features of CD58 in 135 cases of childhood B-ALL were analyzed by four-color flow cytometry; MRD detection protocol for B-ALL using CD58/CD10/CD34/CD19 combination was established; the correlation between the expression features of CD58 and MRD detection was analyzed for the early therapeutic response in childhood B-ALL.
  • The CD58 over expression may be considered as a marker of a favorable prognosis in childhood B-ALL.

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  • (PMID = 16928307.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD58; 0 / Biomarkers, Tumor
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62. 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.
  • Ikaros is a zinc-finger transcriptional factor playing an essential role in lymphoid lineage commitment and differentiation.
  • 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.
  • 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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63. Correa-González LC, Mandeville PB, Manrique-Dueñas J, Alejo-González F, Salazar-Martínez A, de Pérez-Ramírez OJ, Hernández-Sierra JF: [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients]. Gac Med Mex; 2005 Nov-Dec;141(6):477-82
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  • [Title] [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients].
  • OBJECTIVE: To determine the prognostic value of preB immunophenotype and its variants on early treatment response among of acute pediatric lymphoblast leukemia.
  • PATIENTS AND METHODS: A case-control study nested in a cohort was carried out with male and female patients 15 years and younger with recently diagnosed pre-B lymphoblast leukemia.
  • A panel of B, T, monoclonal antibodies of the myelo-monocytic and megakaryocytic cell type was used.
  • CONCLUSIONS: We need to pay special emphasis on early treatment response in children with lymphoblast leukemia as our study did not corroborate the common finding that clinical factors and immune phenotype can be predictive factors.
  • [MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 16381501.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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64. Mullighan CG, Su X, Zhang J, Radtke I, Phillips LA, Miller CB, Ma J, Liu W, Cheng C, Schulman BA, Harvey RC, Chen IM, Clifford RJ, Carroll WL, Reaman G, Bowman WP, Devidas M, Gerhard DS, Yang W, Relling MV, Shurtleff SA, Campana D, Borowitz MJ, Pui CH, Smith M, Hunger SP, Willman CL, Downing JR, Children's Oncology Group: Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N Engl J Med; 2009 Jan 29;360(5):470-80
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  • [Title] Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia.
  • BACKGROUND: Despite best current therapy, up to 20% of pediatric patients with acute lymphoblastic leukemia (ALL) have a relapse.
  • METHODS: We studied a cohort of 221 children with high-risk B-cell-progenitor ALL with the use of single-nucleotide-polymorphism microarrays, transcriptional profiling, and resequencing of samples obtained at diagnosis.
  • A copy-number abnormality was identified as a predictor of poor outcome, and it was then tested in an independent validation cohort of 258 patients with B-cell-progenitor ALL.
  • RESULTS: More than 50 recurring copy-number abnormalities were identified, most commonly involving genes that encode regulators of B-cell development (in 66.8% of patients in the original cohort); PAX5 was involved in 31.7% and IKZF1 in 28.6% of patients.
  • This predictor was strongly associated with alteration of IKZF1, a gene that encodes the lymphoid transcription factor IKAROS.
  • The gene-expression signature of the group of patients with a poor outcome revealed increased expression of hematopoietic stem-cell genes and reduced expression of B-cell-lineage genes, and it was similar to the signature of BCR-ABL1-positive ALL, another high-risk subtype of ALL with a high frequency of IKZF1 deletion.
  • CONCLUSIONS: Genetic alteration of IKZF1 is associated with a very poor outcome in B-cell-progenitor ALL.

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  • [Copyright] 2009 Massachusetts Medical Society
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  • (PMID = 19129520.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413-07; None / None / / U10 CA098413-07; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA86011; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / NIGMS NIH HHS / GM / U01GM61374; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / PHS HHS / / 21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061374; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / R01 CA086011
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / EBF1 protein, human; 0 / IKZF1 protein, human; 0 / PAX5 protein, human; 0 / Trans-Activators; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ NIHMS93692; NLM/ PMC2674612
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65. Li ZY, Liu DP, Liang CC: New insight into the molecular mechanisms of MLL-associated leukemia. Leukemia; 2005 Feb;19(2):183-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insight into the molecular mechanisms of MLL-associated leukemia.
  • Rearrangements of the MLL gene (ALL1, HRX, and Hrtx) located at chromosome band 11q23 are commonly involved in adult and pediatric cases of primary acute leukemias and also found in cases of therapy-related secondary leukemias.
  • Studies on mouse models of MLL translocation and cell lines containing MLL rearrangements showed that the MLL gene linked chromosomal rearrangements to cellular differentiation and tumor tropism.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Mutation. Myeloid-Lymphoid Leukemia Protein. Zinc Fingers / genetics

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  • (PMID = 15618964.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 89
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66. Handrup MM, Møller JK, Frydenberg M, Schrøder H: Placing of tunneled central venous catheters prior to induction chemotherapy in children with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2010 Aug;55(2):309-13
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  • [Title] Placing of tunneled central venous catheters prior to induction chemotherapy in children with acute lymphoblastic leukemia.
  • BACKGROUND: Tunneled central venous catheters (CVCs) are inevitable in children with acute lymphoid leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter-Related Infections / etiology. Catheterization, Central Venous / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20582964.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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67. Haltrich I, Csóka M, Kovács G, Fekete G: [Intrachromosomal amplification of AML1 gene in childhood acute lymphoblastic leukemia]. Orv Hetil; 2008 Jun 15;149(24):1143-6
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  • [Title] [Intrachromosomal amplification of AML1 gene in childhood acute lymphoblastic leukemia].
  • [Transliterated title] AML1-gén intrakromoszomális amplifikációja gyermekkori acut lymphoid leukaemiában.
  • The introduction of routine molecular cytogenetic assays enabled us to reveal hitherto unknown genetic disorders of childhood acute leukemias.
  • In our present study we review a novel cytogenetic mutation typical for childhood B-cell ALL, the intrachromosomal amplification of chromosome 21, which requires high-risk therapy irrespective of other risk factors, and which is associated with a cryptic 12;21 translocation of good prognostic value.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Amplification. Genetic Markers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18539581.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Genetic Markers; 0 / RUNX1 protein, human
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68. Yoda A, Yoda Y, Chiaretti S, Bar-Natan M, Mani K, Rodig SJ, West N, Xiao Y, Brown JR, Mitsiades C, Sattler M, Kutok JL, DeAngelo DJ, Wadleigh M, Piciocchi A, Dal Cin P, Bradner JE, Griffin JD, Anderson KC, Stone RM, Ritz J, Foà R, Aster JC, Frank DA, Weinstock DM: Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Jan 5;107(1):252-7
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  • [Title] Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia.
  • The prognosis for adults with precursor B-cell acute lymphoblastic leukemia (B-ALL) remains poor, in part from a lack of therapeutic targets.
  • We demonstrate that CRLF2 is overexpressed in approximately 15% of adult and high-risk pediatric B-ALL that lack MLL, TCF3, TEL, and BCR/ABL rearrangements, but not in B-ALL with these rearrangements or other lymphoid malignancies.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics. Signal Transduction / physiology


69. Kubicka M, Soszynska K, Mucha B, Rafinska B, Kolodziej B, Haus O, Styczynski J: Unusual profiles of pediatric acute lymphoblastic leukemia with MLL gene rearrangement. Leuk Lymphoma; 2007 Oct;48(10):2083-6
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  • [Title] Unusual profiles of pediatric acute lymphoblastic leukemia with MLL gene rearrangement.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17917979.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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70. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
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  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • On the basis of the conventional cytogenetic analysis, molecular methods have improved pediatric hematologists/oncologist's ability to accurately and rapidly perform risk-stratification on patients with childhood ALL during the last few years.
  • The aim of the present study was to assess the demography of cytogenetic abnormalities in childhood ALL.
  • METHOD: The study subjects consisted of 124 newly diagnosed ALL patients younger than 16 years of age, who were diagnosed at the Department of Pediatric Hematology/Oncology, Soochow University Children's Hospital.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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71. Iqbal Z, Iqbal M, Akhter T: Frequency of BCR-ABL fusion oncogene in Pakistani childhood acute lymphoid leukemia (ALL) patients reflects ethnic differences in molecular genetics of ALL. J Pediatr Hematol Oncol; 2007 Aug;29(8):585
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  • [Title] Frequency of BCR-ABL fusion oncogene in Pakistani childhood acute lymphoid leukemia (ALL) patients reflects ethnic differences in molecular genetics of ALL.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ethnology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentOn] J Pediatr Hematol Oncol. 2007 Jan;29(1):27-31 [17230064.001]
  • (PMID = 17762503.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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72. Shalapour S, Eckert C, Seeger K, Pfau M, Prada J, Henze G, Blankenstein T, Kammertoens T: Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia. J Mol Med (Berl); 2010 Mar;88(3):249-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.
  • Even though childhood ALL can be cured in a large number of patients, around 20% of the patients suffer a relapse after chemotherapy.
  • Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.
  • MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).
  • Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.
  • The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.
  • [MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [CommentIn] J Mol Med (Berl). 2010 Mar;88(3):219-22 [20135087.001]
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  • (PMID = 20155409.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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73. Ek T, Pinkava M, Abrahamsson J: Ara-C fever and infections after high-dose ara-C treatment in pediatric lymphoid malignancies. J Pediatr Hematol Oncol; 2005 Jul;27(7):364-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ara-C fever and infections after high-dose ara-C treatment in pediatric lymphoid malignancies.
  • The objective of this study was to examine the incidence and characteristics of Ara-C-related fever and the frequency and severity of infections after single-drug, high-dose Ara-C treatment (HDAC) in children treated for acute lymphoblastic leukemia (ALL) or non-Hodgkin lymphoma (NHL).
  • Profound neutropenia and lymphopenia are causative factors for the high incidence of infections, but the risk of life-threatening complications after HDAC in children in remission of lymphoid malignancies is low, even without prophylactic use of colony-stimulating factors.
  • [MeSH-minor] Adolescent. Biomarkers / blood. C-Reactive Protein / analysis. Child. Child, Preschool. Fever / chemically induced. Humans. Infant. Leukocyte Count. Platelet Count. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Retrospective Studies

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  • (PMID = 16012325.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers; 04079A1RDZ / Cytarabine; 9007-41-4 / C-Reactive Protein
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74. Jiang H, Gu LJ, Xue HL, Tang JY, Chen J, Pan C, Chen J: [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Aug;8(4):272-4
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  • [Title] [Asparagine synthetase activity in pediatric acute lymphoblastic leukemia].
  • OBJECTIVE: To study the cellular activity of asparagine synthetase in different types of childhood acute lymphoblastic leukemia (ALL).
  • METHODS: The cellular activity of asparagine synthetase was detected by HPLC-FLD and Protein measurement in 28 ALL children (7 cases of T-ALL and 21 cases of B-lymphoid lineage ALL) before chemotherapy.
  • RESULTS: The asparagines synthetase activity levels in T-ALL children were significantly higher than those of the B-lymphoid lineage ALL patients, with the median activity level of 9.3 nM Asn/mg protein/hr vs 5.2 nM Asn/mg protein/hr (P < 0.05).
  • The distribution of the asparagine synthetase activity demonstrated a polymorphism in either T-ALL or B-lymphoid lineage ALL patients.
  • The asparagines synthetase activity levels in T-ALL are significantly higher than in B-lymphoid lineage ALL.
  • [MeSH-major] Aspartate-Ammonia Ligase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 16923354.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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75. Wang Y, Lin D, Wang DH, Ku ZF, Liu JZ, Liu XR, Wang JX, Wang M: [The expression of midkine in acute leukemia and its significance]. Zhonghua Xue Ye Xue Za Zhi; 2008 Aug;29(8):544-8
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  • [Title] [The expression of midkine in acute leukemia and its significance].
  • OBJECTIVE: To analyze the expression of midkine (MK) gene in acute leukemia patients, and explore the relationship between the gene and leukemia.
  • METHODS: The MK gene expression levels were detected by real-time quantitative RT-PCR (RQ-RT-PCR) in bone marrow (BM) of 181 acute leukemia (AL) patients and 31 normal controls.
  • The expression of MK showed a notable increase in all B-ALL subtypes (including pro-B-ALL, common-B-ALL and pre-B-ALL) as well as in adult and childhood B-ALL patients (P < 0.01).
  • CONCLUSION: MK gene expression is increased with different levels in B-ALL, M2 and M3 patients, which provides novel insights into the leukemogenesis of acute leukemia.
  • [MeSH-major] Cytokines / metabolism. Leukemia / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Case-Control Studies. Child. Child, Preschool. Female. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19112919.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 137497-38-2 / midkine
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76. Azevedo-Silva F, Camargo Bd, Pombo-de-Oliveira MS: Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia. Braz J Med Biol Res; 2010 Mar;43(3):226-9
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  • [Title] Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia.
  • Acute leukemia is the most frequent cancer in children.
  • Recently, a new hypothesis was proposed for the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The so-called 'adrenal hypothesis' emphasized the role of endogenous cortisol in the etiology of B-cell precursor ALL.
  • The adrenal hypothesis proposes that the risk of childhood B-cell precursor ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis.


77. Germano G, Pigazzi M, del Giudice L, Campo Dell'Orto M, Spinelli M, Zangrando A, Paolucci P, Ladogana S, Basso G: Two consecutive immunophenotypic switches in a child with MLL-rearranged acute lymphoblastic leukemia. Haematologica; 2006 May;91(5 Suppl):ECR09
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  • [Title] Two consecutive immunophenotypic switches in a child with MLL-rearranged acute lymphoblastic leukemia.
  • An 18-month-old girl was diagnosed with pre-pre-B ALL/t(4;11) leukemia, which during the treatment and after matched bone marrow transplantation (BMT), underwent two consecutive switches from lymphoid to myeloid lineage and vice versa.
  • The high expression of HOXA9 and FLT3 genes remaining genotypically stable in a leukemia throughout phenotypic switches, suggests that this leukemia may have originated as a common B/myeloid progenitors.
  • [MeSH-major] Antigens, CD / analysis. Antigens, Neoplasm / analysis. B-Lymphocytes / pathology. Gene Rearrangement. Immunophenotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 4 / ultrastructure. Clone Cells / pathology. Combined Modality Therapy. Fatal Outcome. Female. Gene Expression Regulation, Leukemic. Gene Rearrangement, B-Lymphocyte. Genes, Immunoglobulin. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Humans. Infant. Models, Biological. Neoplasm Proteins / genetics. Recurrence. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16709517.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / MLL-AF4 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 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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78. Chuk MK, McIntyre E, Small D, Brown P: Discordance of MLL-rearranged (MLL-R) infant acute lymphoblastic leukemia in monozygotic twins with spontaneous clearance of preleukemic clone in unaffected twin. Blood; 2009 Jun 25;113(26):6691-4
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  • [Title] Discordance of MLL-rearranged (MLL-R) infant acute lymphoblastic leukemia in monozygotic twins with spontaneous clearance of preleukemic clone in unaffected twin.
  • Concordance of MLL-rearranged acute leukemia in infant monozygotic twins is thought to be 100% with a very short latency period, suggesting that either the MLL fusion itself is sufficient to cause leukemia or that it promotes the rapid acquisition of additional oncogenic events that result in overt disease.
  • Twin A presented at age 9 months with MLL-ENL(+) acute lymphoblastic leukemia and twin B remains healthy 3 years later.
  • Clearance of this clone was temporally associated with viral-induced cytopenias, suggesting an immune-mediated clearance of the clone before the development of leukemia.
  • Thus, concordance of MLL-rearranged acute leukemia in infant monozygotic twins is not universal.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / analysis. Oncogene Proteins, Fusion / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics. Respiratory Tract Infections / immunology. Twins, Monozygotic. Virus Diseases / immunology

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  • (PMID = 19411627.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / R01 CA090668
  • [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 / Biomarkers, Tumor; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2943757
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79. Chatzidakis K, Goulas A, Athanassiadou-Piperopoulou F, Fidani L, Koliouskas D, Mirtsou V: Methylenetetrahydrofolate reductase C677T polymorphism: association with risk for childhood acute lymphoblastic leukemia and response during the initial phase of chemotherapy in greek patients. Pediatr Blood Cancer; 2006 Aug;47(2):147-51
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  • [Title] Methylenetetrahydrofolate reductase C677T polymorphism: association with risk for childhood acute lymphoblastic leukemia and response during the initial phase of chemotherapy in greek patients.
  • BACKGROUND: As of late, a number of studies have focused on the association of the gene for methyletetrahydrofolate reductase (MTHFR) with risk for acute lymphoblastic leukemia (ALL) in children and in adults, as well as with response to chemotherapy.
  • PROCEDURE: We have analyzed the MTHFR C677T polymorphism in 52 patients and 88 control individuals, all ethnic Greek residents of northern Greece, and examined the association of this polymorphism with (a) susceptibility to childhood ALL and (b) the distribution of average plasma alanine aminotransferase (ALT) levels, white blood cell counts (WBC), and hemoglobin levels (Hb) during the induction and consolidation phases of treatment.
  • In addition, we observed a general tendency towards lower values in all three parameters studied, associated with the MTHFR 677CC genotype, which was more evident in the transition from the induction to the consolidation phase, indicating that MTHFR genotyping may be of prognostic value in the early phase of treatment for childhood ALL, in our population.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16123993.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.6.1.2 / Alanine Transaminase
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80. Ju X, Li D, Shi Q, Hou H, Sun N, Shen B: Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2009 Jan;26(1):1-10
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  • [Title] Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • The analysis of differential microRNA expression profiles may be a powerful tool to allow us insight on the mechanisms of childhood B-cell precursor acute lymphoblastic leukemia (pre-B-ALL).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Computational Biology. Gene Expression Profiling. Hematopoiesis / genetics. Humans. Infant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


81. Taylor M, Harrison C, Eden T, Birch J, Greaves M, Lightfoot T, Hussain A, UKCCS Investigators: HLA-DPB1 supertype-associated protection from childhood leukaemia: relationship to leukaemia karyotype and implications for prevention. Cancer Immunol Immunother; 2008 Jan;57(1):53-61
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  • [Title] HLA-DPB1 supertype-associated protection from childhood leukaemia: relationship to leukaemia karyotype and implications for prevention.
  • Most childhood B cell precursor (BCP) acute lymphoblastic leukaemia (ALL) cases carry the reciprocal translocation t(12;21)(p13;q22) ( approximately 25%), or a high hyperdiploid (HeH) karyotype (30%).
  • Based on our previous analysis of HLA-DP in childhood ALL, and evidence from in vitro studies that TEL-AML1 can activate HLA-DP-restricted T cell responses, we hypothesised that the development of TEL-AML1+ ALL might be influenced by the child's DPB1 genotype.
  • To test this, we analysed the frequency of six HLA-DPB1 supertypes in a population-based series of childhood leukaemias (n = 776) classified by their karyotype (TEL-AML1+, HeH and others), in comparison with newborn controls (n = 864).
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genetic Predisposition to Disease. HLA-DP Antigens / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control

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  • (PMID = 17622527.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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82. László R, Alpár D, Kajtár B, Lacza A, Ottóffy G, Kiss C, Bartyik K, Nagy K, Pajor L: Detection of early precursors of t(12;21) positive pediatric acute lymphoblastic leukemia during follow-up. Pediatr Blood Cancer; 2010 Jan;54(1):158-60
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  • [Title] Detection of early precursors of t(12;21) positive pediatric acute lymphoblastic leukemia during follow-up.
  • DNA-, RNA-, and cell-based methods provide different biologic information for determining the presence of minimal residual disease (MRD).
  • We monitored the responses of patients with pediatric acute lymphoblastic leukemia (pALL) using DNA markers, TEL/AML1 expression, and scanning fluorescence microscopy (SFM).
  • CD10+ ancestor cells with germline antigen receptors, but silent TEL/AML1 expression, may reside in the lymphoid stem cell compartment of treated t(12;21)-positive patients and might act as a potential source of cells for late relapses.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 21 / genetics. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19813247.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / TEL-AML1 fusion protein
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83. Jeon IS, Yi DY: Acute lymphoblastic leukemia secondary to chemoradiotherapy for perivascular epithelioid cell tumor of uterus. Pediatr Hematol Oncol; 2009 Mar;26(2):85-8
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  • [Title] Acute lymphoblastic leukemia secondary to chemoradiotherapy for perivascular epithelioid cell tumor of uterus.
  • Acute lymphoblastic leukemia (ALL), a primary hematologic malignancy that is especially common in childhood, occurs relatively rarely as a secondary malignant neoplasm.
  • [MeSH-major] Neoplasms, Second Primary / etiology. Perivascular Epithelioid Cell Neoplasms / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Uterine Neoplasms / complications
  • [MeSH-minor] Anthracyclines / adverse effects. Child. Cytogenetic Analysis. Female. Humans. Precursor Cells, B-Lymphoid / pathology. Topoisomerase II Inhibitors. Translocation, Genetic

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  • (PMID = 19322738.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Topoisomerase II Inhibitors
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84. Reichmann-Decker A, DePrince AP, McIntosh DN: Affective responsiveness, betrayal, and childhood abuse. J Trauma Dissociation; 2009;10(3):276-96
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  • [Title] Affective responsiveness, betrayal, and childhood abuse.
  • We predicted that women who reported childhood abuse by close others would show alterations in affective responsiveness relative to their peers.
  • We tested 100 undergraduate women who reported histories of (a) childhood sexual or physical abuse by someone close, such as a parent (high-betrayal);.
  • (b) childhood abuse by someone not close (low-betrayal); or (c) no abuse in childhood (no-abuse).

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  • (PMID = 19585337.001).
  • [ISSN] 1529-9740
  • [Journal-full-title] Journal of trauma & dissociation : the official journal of the International Society for the Study of Dissociation (ISSD)
  • [ISO-abbreviation] J Trauma Dissociation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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85. Forestier E, Gauffin F, Andersen MK, Autio K, Borgström G, Golovleva I, Gustafsson B, Heim S, Heinonen K, Heyman M, Hovland R, Johannsson JH, Kerndrup G, Rosenquist R, Schoumans J, Swolin B, Johansson B, Nordgren A, Nordic Society of Pediatric Hematology and Oncology, Swedish Cytogenetic Leukemia Study Group, NOPHO Leukemia Cytogenetic Study Group: Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukemias: a Nordic series of 24 cases and review of the literature. Genes Chromosomes Cancer; 2008 Feb;47(2):149-58
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  • [Title] Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukemias: a Nordic series of 24 cases and review of the literature.
  • Although dic(9;20)(p13.2;q11.2) is a characteristic abnormality in childhood B-cell precursor acute lymphoblastic leukemias (BCP ALL), little is known about its clinical impact or the type and frequency of additional aberrations it may occur together with.
  • We here review the clinical and cytogenetic features of a Nordic pediatric series of 24 patients with dic(9;20)-positive BCP ALL diagnosed 1996-2006, constituting 1.3% of the BCP ALL, as well as 47 childhood cases from the literature.
  • Consistent immunophenotypic features of the Nordic cases included positivity for HLA-DR, CD10, CD19, CD20, and CD22 and negativity for T-cell and myeloid markers; no detailed immunophenotypes were reported for the previously published cases.
  • The median patient age was 3 years, the female/male ratio was 2.0, the median white blood cell count was 24 x 10(9)/l, 11% had central nervous system involvement, and 5% had a mediastinal mass at diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Cytogenetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17990329.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 38
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86. Hadziselimovic F: Early successful orchidopexy does not prevent from developing azoospermia. Int Braz J Urol; 2006 Sep-Oct;32(5):570-3
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  • INTRODUCTION: The incidence of Ad spermatogonia (stem cells for fertility) was assessed in 20 cryptorchid patients, all of whom had a successful orchidopexy in childhood but developed azoospermia following puberty.
  • The patients were classified into 2 groups according to the time of surgery: A = < 21 months of age (n = 5, mean = 10.7 +/- 8.6 months) and B = during childhood (n = 15, mean = 10.1 +/- 3 years).

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  • (PMID = 17081328.001).
  • [ISSN] 1677-5538
  • [Journal-full-title] International braz j urol : official journal of the Brazilian Society of Urology
  • [ISO-abbreviation] Int Braz J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 9002-68-0 / Follicle Stimulating Hormone
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87. Kivivuori SM, Siitonen S, Porkka K, Vettenranta K, Alitalo R, Saarinen-Pihkala U: Expression of vascular endothelial growth factor receptor 3 and Tie1 tyrosine kinase receptor on acute leukemia cells. Pediatr Blood Cancer; 2007 Apr;48(4):387-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of vascular endothelial growth factor receptor 3 and Tie1 tyrosine kinase receptor on acute leukemia cells.
  • Activation of vascular endothelial growth factor receptor 3 (VEGFR-3) and Tie1 tyrosine kinase receptor are known to promote leukemia cell survival.
  • PROCEDURE: We studied bone marrow samples from 73 patients with acute lymphoblastic (ALL) or myelogenous (AML) leukemia by using immunological methods.
  • RESULTS: Vascular endothelial growth factor receptor 3 expression was found in 15% of the samples, particularly in samples with pediatric lymphoblastic leukemias and monocytic AMLs.
  • CONCLUSIONS: Our findings suggest that there are angiogenesis-related differences between pediatric and adult lymphoblastic leukemias as well as between lymphoid and myeloid leukemias.
  • [MeSH-major] Hematopoietic Stem Cells / enzymology. Leukemia, Myeloid / enzymology. Neoplastic Stem Cells / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Receptor, TIE-1 / analysis. Vascular Endothelial Growth Factor Receptor-3 / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Antigens, CD / analysis. Antigens, CD34 / analysis. Bone Marrow / pathology. Child. Child, Preschool. Female. Glycoproteins / analysis. Humans. Immunophenotyping. Infant. Leukemia, Monocytic, Acute / enzymology. Leukemia, Monocytic, Acute / pathology. Male. Neovascularization, Pathologic / enzymology. Neovascularization, Pathologic / pathology. Peptides / analysis

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  • (PMID = 16685739.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides; EC 2.7.10.1 / Receptor, TIE-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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88. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


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

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  • (PMID = 20460642.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2930966
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90. Paulsson K, Johansson B: High hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):637-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy (51-67 chromosomes) is the most common cytogenetic abnormality pattern in childhood B-cell precursor acute lymphoblastic leukemia (ALL), occurring in 25-30% of such cases.
  • Despite the high frequency of this karyotypic subgroup, many questions remain regarding the epidemiology, etiology, presence of other genetic changes, the time and cell of origin, and the formation and pathogenetic consequences of high hyperdiploidy.
  • However, during the last few years, several studies have addressed some of these important issues, and these, as well as previous reports on high hyperdiploid childhood ALL, are reviewed herein.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma


91. Lee DS, Kim YR, Cho HK, Lee CK, Lee JH, Cho HI: The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL). Cancer Genet Cytogenet; 2005 Oct 15;162(2):176-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL).
  • TEL/AML1 (also known as ETV6/RUNX1) rearrangement is the most frequent genetic change in childhood B-acute lymphoblastic leukemia (ALL) and is associated with a favorable prognosis.
  • TEL/AML1 rearrangement is not unique in childhood ALL, and cryptic TEL deletion without TEL/AML1 rearrangement was more frequent than the TEL/AML1 rearrangement in adult ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 16213368.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
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92. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • In comparison with that of B cell ALL (B-ALL), the percentages of age older than 10 years, initial WBC count more than 50 x 10(9)/ L, prednisone poor response (PPR), and fa