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Items 1 to 100 of about 717242
1. Tembhare PR, Subramanian PG, Sehgal K, Yajamanam B, Kumar A, Gujral S: Hypergranular precursor B-cell acute lymphoblastic leukemia in a 16-year-old boy. Indian J Pathol Microbiol; 2009 Jul-Sep;52(3):421-3
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  • [Title] Hypergranular precursor B-cell acute lymphoblastic leukemia in a 16-year-old boy.
  • Presence of cytoplasmic granules in the blasts is a well known feature of myeloid leukemia.
  • ALL presenting with the numerous cytoplasmic granules in blasts is a rarity and may be misdiagnosed as acute myeloid leukemia.
  • We describe a rare case of hypergranular precursor B-cell acute lymphoblastic leukemia (ALL) in an adolescent male expressing CD10, CD19, CytoCD22, CD34, as well as CD13 and CD117.
  • The blasts were cytochemically negative for myeloperoxidase (MPO), and acid phosphatase (ACP) but were positive for non-specific esterase (NSE).
  • Hence it is important to be aware of this rare entity and to confirm the lineage of acute leukemia by using a comprehensive panel of antibodies for immunophenotypic analysis.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19679981.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD; EC 1.11.1.7 / Peroxidase; EC 3.1.3.2 / Acid Phosphatase
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2. 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 identified the type I cytokine receptor subunit CRLF2 in a functional screen for B-ALL-derived mRNA transcripts that can substitute for IL3 signaling.
  • CRLF2 overexpressing B-ALLs share a transcriptional signature that significantly overlaps with a BCR/ABL signature, and is enriched for genes involved in cytokine receptor and JAK-STAT signaling.
  • In fact, all 22 B-ALLs with mutant JAK2 that we analyzed overexpress CRLF2, distinguishing CRLF2 as the key scaffold for mutant JAK2 signaling in B-ALL.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics. Signal Transduction / physiology


3. Prasad RB, Hosking FJ, Vijayakrishnan J, Papaemmanuil E, Koehler R, Greaves M, Sheridan E, Gast A, Kinsey SE, Lightfoot T, Roman E, Taylor M, Pritchard-Jones K, Stanulla M, Schrappe M, Bartram CR, Houlston RS, Kumar R, Hemminki K: Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood. Blood; 2010 Mar 4;115(9):1765-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood.
  • Recent genome-wide association data have implicated genetic variation at 7p12.2 (IKZF1), 10q21.2 (ARIDB5), and 14q11.2 (CEBPE) in the etiology of B-cell childhood acute lymphoblastic leukemia (ALL).
  • To verify and further examine the relationship between these variants and ALL risk, we genotyped 1384 cases of precursor B-cell childhood ALL and 1877 controls from Germany and the United Kingdom.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 7 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20042726.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
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4. Breakey VR, Abdelhaleem M, Weitzman S, Abla O: Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Dec;30(12):956-8
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  • [Title] Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia.
  • We report the clinical course of a child with precursor B-cell acute lymphoblastic leukemia who developed fever, hepatosplenomegaly, and refractory thrombocytopenia after initiation of chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphohistiocytosis, Hemophagocytic / chemically induced. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19131791.001).
  • [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
  • [Chemical-registry-number] 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase
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5. Muzzafar T, Medeiros LJ, Wang SA, Brahmandam A, Thomas DA, Jorgensen JL: Aberrant underexpression of CD81 in precursor B-cell acute lymphoblastic leukemia: utility in detection of minimal residual disease by flow cytometry. Am J Clin Pathol; 2009 Nov;132(5):692-8
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  • [Title] Aberrant underexpression of CD81 in precursor B-cell acute lymphoblastic leukemia: utility in detection of minimal residual disease by flow cytometry.
  • We studied CD81 expression by flow cytometry (FC) on benign precursor B cells (hematogones) and leukemic blasts in precursor B-cell acute lymphoblastic leukemia (pre-B-ALL) and established its usefulness in minimal residual disease (MRD) assays.
  • In 98 pre-B-ALLs at diagnosis or overt relapse, 80 (82%) showed aberrantly decreased CD81 intensity.
  • In 133 specimens positive for residual pre-B-ALL, 87.2% showed increased CD81-dim immature B cells (>10%) and/or a discrete cluster of CD81-dim cells in a background of hematogones.
  • Decreased CD81 expression is a sensitive and specific marker for residual pre-B-ALL, even in a background of hematogones, making CD81 a useful addition to a panel for MRD detection by FC.
  • [MeSH-major] Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19846809.001).
  • [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 / Antigens, CD; 0 / Antigens, CD81; 0 / Biomarkers, Tumor; 0 / CD81 protein, human
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6. Shabani M, Asgarian-Omran H, Vossough P, Sharifian RA, Faranoush M, Ghragozlou S, Khoshnoodi J, Roohi A, Jeddi-Tehrani M, Mellstedt H, Rabbani H, Shokri F: Expression profile of orphan receptor tyrosine kinase (ROR1) and Wilms' tumor gene 1 (WT1) in different subsets of B-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2008 Jul;49(7):1360-7
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  • [Title] Expression profile of orphan receptor tyrosine kinase (ROR1) and Wilms' tumor gene 1 (WT1) in different subsets of B-cell acute lymphoblastic leukemia.
  • Over-expression of ROR1 gene, a member of the receptor tyrosine kinase family, has recently been reported in B-cell chronic lymphocytic leukemia.
  • In the present study, the expression profile of ROR1 and WT1 was investigated in different immunophenotypic subsets of B-cell acute lymphoblastic leukemia (B-ALL) patients.
  • Based on immunophenotypic results, our B-ALL patients were classified in four differentiation subsets; Pro-B (n = 7), Pre-B I (n = 29), Pre-B II (n = 13) and Immature/mature B-ALL (n = 2).
  • Although ROR1 was over-expressed in more mature subsets (16.7%, 42.9%, 45.5% and 100%, respectively), WT1 was more represented in immature subsets of B-ALL patients (57.1%, 64.3%, 38.5% and 0%, respectively).
  • Comparison of the frequency of ROR1 and WT1 positive samples at each immunophenotypic subtype revealed statistically significant difference only in Pre B I subtype (p = 0.02).
  • [MeSH-major] Burkitt Lymphoma / pathology. Receptor Protein-Tyrosine Kinases / genetics. WT1 Proteins / genetics

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  • (PMID = 18604725.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Neoplasm; 0 / WT1 Proteins; EC 2.7.10.1 / ROR1 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Tyrosine Kinase-like Orphan Receptors
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7. Panagopoulos I, Lilljebjörn H, Strömbeck B, Hjorth L, Olofsson T, Johansson B: MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia. Haematologica; 2006 Sep;91(9):1287-8
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  • [Title] MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia.
  • MLL/GAS7, resulting from t(11;17)(q23;p13), has been reported in one case of treatment-related acute myeloid leukemia (AML).
  • We present a de novo case of t(11;17)-positive pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Humans. Infant. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 16956839.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / GAS7 protein, human; 0 / MLL-GAS7 fusion protein; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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8. Crespo M, Villamor N, Giné E, Muntañola A, Colomer D, Marafioti T, Jones M, Camós M, Campo E, Montserrat E, Bosch F: ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 Feb 1;12(3 Pt 1):726-34
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  • [Title] ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia.
  • PURPOSE: The ZAP-70 gene is normally expressed in T and natural killer cells, where it is required for the T-cell receptor (TCR) signaling.
  • More recently, it has been described that ZAP-70 contributes to the B-cell development at early stages of B-cell differentiation in mice.
  • The purpose was to investigate the presence of ZAP-70 in normal pro/pre B cells and mature B cells and in tumoral cells from B-acute lymphoblastic leukemias (B-ALL).
  • Analysis of ZAP-70 and other signaling proteins of the pre-TCR/TCR was done by Western blot.
  • RESULTS: ZAP-70 was expressed in pro/pre B cells but not in normal mature B cells derived from bone marrow, peripheral blood, or tonsil.
  • Among tumoral cells, ZAP-70 was expressed in 56% of B-ALLs with pro/pre B-cell phenotype and in 4 of 6 Burkitt/ALL lymphomas.
  • Moreover, other elements of the pre-TCR/TCR signaling pathway, like LAT and Lck, were also found in B-ALL cells.
  • CONCLUSIONS: Among normal B-cell subsets, ZAP-70 was found expressed in normal pro/pre B cells but not in a significant proportion of normal B cells with mature phenotype.
  • Moreover, the presence of ZAP-70 in B-ALLs probably reflects their cellular origin.
  • The lack of ZAP-70 expression in normal mature B cells suggests that its expression in mature-derived neoplasms with different cellular origin, such as Burkitt's lymphoma and chronic lymphocytic leukemia, might be due to an aberrant phenomenon.
  • [MeSH-major] B-Lymphocytes / metabolism. Burkitt Lymphoma / genetics. Gene Expression Regulation. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / metabolism. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA Mutational Analysis. Humans. Middle Aged. Phenotype. Phosphorylation. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 16467082.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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9. Ariffin H, Muthukkumaran T, Stanslas J, Sabariah AR, Veerasekaran N, Lin HP: Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies. Leuk Lymphoma; 2005 Aug;46(8):1233-7
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  • [Title] Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies.
  • We report the clinical features and in vitro chemosensitivity assay findings of a 13-year-old girl who developed secondary B-cell acute lymphoblastic leukemia (ALL) 7 years after a diagnosis of Wilms' tumor.
  • [MeSH-major] Burkitt Lymphoma / complications. Kidney Neoplasms / complications. Neoplasms, Second Primary / complications. Wilms Tumor / complications
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Survival / drug effects. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Fatal Outcome. Female. Humans. In Vitro Techniques. Sepsis / drug therapy

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  • (PMID = 16085568.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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10. Imataki O, Ohnishi H, Yamaoka G, Arai T, Kitanaka A, Kubota Y, Kushida Y, Ishida T, Tanaka T: Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse. Int J Clin Oncol; 2010 Feb;15(1):112-5
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  • [Title] Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.
  • A lineage switch in leukemia, in which the leukemic cell lineage at onset converts to another lineage at a later time, is an uncommon type of hybrid (mixed) leukemia regarded as a variation of bilineage leukemia.
  • We present a case of a 60-year-old female diagnosed with precursor B cell acute lymphoblastic leukemia (ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.
  • This phenotypical conversion from B-ALL to hybrid leukemia featuring monocytoid characteristics is known as a lineage switch.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Monocytic, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Bone Marrow / pathology. Cell Lineage. Female. Humans. Immunophenotyping. Middle Aged. Recurrence

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  • (PMID = 20066454.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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11. De Braekeleer E, Douet-Guilbert N, Le Bris MJ, Berthou C, Morel F, De Braekeleer M: A new partner gene fused to ABL1 in a t(1;9)(q24;q34)-associated B-cell acute lymphoblastic leukemia. Leukemia; 2007 Oct;21(10):2220-1
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  • [Title] A new partner gene fused to ABL1 in a t(1;9)(q24;q34)-associated B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 9. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, B-Cell / genetics. Oncogene Proteins, Fusion / chemistry. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / genetics. Translocation, Genetic

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  • [CommentIn] Leukemia. 2013 Jun;27(6):1422-4 [23168614.001]
  • (PMID = 17541395.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins, Fusion; 0 / RCSD1 protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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12. Sonoki T, Iwanaga E, Mitsuya H, Asou N: Insertion of microRNA-125b-1, a human homologue of lin-4, into a rearranged immunoglobulin heavy chain gene locus in a patient with precursor B-cell acute lymphoblastic leukemia. Leukemia; 2005 Nov;19(11):2009-10
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  • [Title] Insertion of microRNA-125b-1, a human homologue of lin-4, into a rearranged immunoglobulin heavy chain gene locus in a patient with precursor B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Base Sequence. Cell Transformation, Neoplastic / genetics. DNA Transposable Elements. Female. Gene Rearrangement. Humans. Molecular Sequence Data

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  • (PMID = 16151463.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Transposable Elements; 0 / Immunoglobulin Heavy Chains; 0 / MicroRNAs
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13. Vasquez-Jimenez EA, Romo-Martínez EJ, Meza-Espinoza JP, Lopez-Guido B, Magaña-Torres MT, Gonzalez-Garcia JR: A new complex chromosomal translocation t(2;12;21)(q33;p13;q22) in B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Jul 15;168(2):179-80
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  • [Title] A new complex chromosomal translocation t(2;12;21)(q33;p13;q22) in B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 21 / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843113.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [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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14. Coyaud E, Struski S, Dastugue N, Brousset P, Broccardo C, Bradtke J: PAX5-AUTS2 fusion resulting from t(7;9)(q11.2;p13.2) can now be classified as recurrent in B cell acute lymphoblastic leukemia. Leuk Res; 2010 Dec;34(12):e323-5
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  • [Title] PAX5-AUTS2 fusion resulting from t(7;9)(q11.2;p13.2) can now be classified as recurrent in B cell acute lymphoblastic leukemia.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 9 / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteins / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Blood Cell Count. Child, Preschool. Female. Humans

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  • (PMID = 20723977.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AUTS2 protein, human; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / PAX5 protein, human; 0 / PAX5-AUTS2 fusion protein, human; 0 / Proteins
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15. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).
  • OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Iacobucci I, Storlazzi C, Lonetti A, Ferrari A, Messina M, Cilloni D, Papayannidis C, Baccarani M, Foà R, Martinelli G: IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report. J Clin Oncol; 2009 May 20;27(15_suppl):11005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report.
  • : 11005 Expression of BCR-ABL1 in hematopoietic stem cells can alone induce a chronic myeloid leukemia (CML) but cooperating oncogenic lesions are required for the generation of a blastic leukemia.
  • To identify oncogenic sub-microscopic lesions that cooperate with BCR-ABL1 to induce ALL, by high resolution single nucleotide polymorphism (SNP) arrays (250K NspI and SNP 6.0, Affymetrix) we studied 106 patients (pts) with de novo adult BCR-ABL1-positive ALL.
  • A variable number of nucleotides (patient-specific) were inserted at the conjunction and maintained with fidelity at the time of relapse.
  • Gene expression profiling analysis of pts with IKZF1 deletion vs wild-type pts identified a unique signature characterized by a down-regulation of genes involved in pre-B-cell differentiation (e.g.
  • VPREB1, VPREB3, IGLL3, BLK), demonstrating that genomic IKZF1 alterations have a strong impact on trascriptoma and contribute to an impaired B-cell differentiation.
  • Univariate analysis showed that the IKZF1 deletion is a negative prognostic marker influencing the cumulative incidence of relapse (10.1 months for pts with deletion vs 56.1 months for wild-type pts, p=0.0103) and disease-free survival (DFS) (10.1 months vs 32.1 months, respectively, p=0.0229).

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  • (PMID = 27964054.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Mussolin L, Pillon M, Conter V, Piglione M, Lo Nigro L, Pierani P, Micalizzi C, Buffardi S, Basso G, Zanesco L, Rosolen A: Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood. J Clin Oncol; 2007 Nov 20;25(33):5254-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood.
  • PURPOSE: To study the prevalence of t(8;14) at diagnosis and the response kinetics to treatment of minimal residual disease (MRD) in B-cell acute lymphoblastic leukemia (B-ALL) patients and determine its impact on prognosis.
  • PATIENTS AND METHODS: A total of 68 children affected by de novo B-ALL enrolled onto the Berlin-Frankfurt-Muenster-based Italian Association of Pediatric Hematology and Oncology LNH-97 clinical protocol were studied.
  • Bone marrow aspirate from each patient was analyzed for the presence of t(8;14)(q24;q32) by long-distance polymerase chain reaction at diagnosis, after the first chemotherapy cycle, and after subsequent cycles until negative for MRD.
  • Morphologic and immunophenotypic analyses were reviewed centrally.
  • [MeSH-major] Burkitt Lymphoma / mortality. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Translocation, Genetic

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  • (PMID = 18024872.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
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18. O'Brien MM, Lee-Kim Y, George TI, McClain KL, Twist CJ, Jeng M: Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2008 Feb;50(2):381-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis.
  • Hemophagocytic lymphohistiocytosis (HLH) is a hyperinflammatory syndrome which can be an inherited congenital disorder or can develop secondary to malignancy, infection, or autoimmune disease.
  • Secondary HLH due to malignancy occurs most commonly with T or NK-cell lymphoid neoplasms.
  • HLH with B-cell malignancies is less common and HLH has rarely been described in association with precursor B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


19. Peterson MR, Noskoviak KJ, Newbury R: CD5-positive B-cell acute lymphoblastic leukemia. Pediatr Dev Pathol; 2007 Jan-Feb;10(1):41-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD5-positive B-cell acute lymphoblastic leukemia.
  • CD5-positive B-cell acute lymphoblastic leukemia (ALL) is an exceedingly rare entity, with only a single case report in the literature.
  • We report 2 additional cases of CD5-positive B-cell ALL in a 16-year-old male and a 15-year-old female.
  • We conclude that CD5-positive B-cell ALL is a rare, aggressive malignancy with a poor prognosis that presents in adolescence.
  • Pathologists and clinicians should be aware of this entity to avoid confusion with other small blue-cell tumors.
  • [MeSH-major] Antigens, CD5 / metabolism. Biomarkers, Tumor / analysis. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Biopsy. Bone Marrow / pathology. Bone Marrow / surgery. Diagnosis, Differential. Diagnostic Errors. Female. Flow Cytometry. Humans. Immunohistochemistry. Leukemia / pathology. Lymphoma / pathology. Male. Prognosis. Sarcoma / pathology

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  • (PMID = 17378623.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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20. Hanbali A, Kuriakose P, Bansal I, Maeda K: Acute pancreatitis induced by adult precursor B-cell acute lymphoblastic leukemia associated with complex cytogenetics. South Med J; 2007 May;100(5):548-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute pancreatitis induced by adult precursor B-cell acute lymphoblastic leukemia associated with complex cytogenetics.
  • [MeSH-major] Pancreatitis / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Sex Chromosome Aberrations


21. Lo A, Gu G, Liu M, Dev VG: ABL deletion without associated BCR-ABL in precursor B-cell acute lymphoblastic leukemia. Leuk Res; 2009 Aug;33(8):e98-103
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABL deletion without associated BCR-ABL in precursor B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Gene Deletion. Genes, abl. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19282030.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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22. De Braekeleer E, Douet-Guilbert N, Morel F, Le Bris MJ, Berthou C, Férec C, De Braekeleer M: RUNX1 amplification in B-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2010 Feb;51(2):329-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Amplification. Leukemia, B-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 20001241.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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23. Forester CM, Braunreiter CL, Yaish H, Hedlund GL, Afify Z: Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia. Pediatr Radiol; 2009 Nov;39(11):1230-3
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  • [Title] Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia.
  • In children, leukemia is the most common malignancy, and approximately 75% of leukemias are acute lymphoblastic leukemia (ALL).
  • Central nervous system leukemia is found at diagnosis in fewer than 5% of children with ALL.
  • Leukemic intracranial masses have been described with acute myeloid leukemia, but ALL presenting as a mass lesion is rare.
  • We describe a unique case of an intracranial confirmed precursor B cell (pre-B) ALL mass in a 13-year-old girl that was diagnosed by brain CT, MRI and cerebral angiography, and confirmed by biopsy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Cerebral Angiography / methods. Magnetic Resonance Imaging / methods. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Tomography, X-Ray Computed / methods


24. Morrissette JJ, Halligan GE, Punnett HH, McKenzie AS, Guerrero F, de Chadarévian JP: Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Aug;169(1):58-61
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  • [Title] Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia.
  • We describe the rare finding of a 33-month-old child neonatally diagnosed with Down syndrome, who presented with pre-B acute lymphoblastic leukemia (ALL) with a pretreatment bone marrow karyotype in which a low hypodiploid cell line (38 chromosomes) was identified in 17/19 cells studied.
  • The abnormal cell line retained the extra constitutional chromosome 21.
  • Hypodiploidy (loss of one or more chromosomes) is seen in approximately 5% of all childhood pre-B ALL cases and in approximately 2.2% cases of individuals with a constitutional trisomy 21.
  • [MeSH-major] Burkitt Lymphoma / genetics. Diploidy. Down Syndrome / genetics

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  • (PMID = 16875938.001).
  • [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
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25. Kim MJ, Yoon HS, Lim G, Kim SY, Lee HJ, Suh JT, Lee J, Lee WI, Park TS: ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review. Cancer Genet Cytogenet; 2010 Jan 15;196(2):184-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review.
  • Here we describe a fifth case of ABL1 deletion without BCR/ABL1 rearrangement in an adolescent patient with precursor B-cell lymphoblastic leukemia (B-ALL) and review the relevant literature.
  • It is not clear how ABL1 deletion affects leukemogenesis; however, it is plausible that ABL1 deletion without BCR/ABL1 rearrangement is a rare but recurrent genetic abnormality in precursor B-ALL patients.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Gene Deletion. Gene Rearrangement. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20082857.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 24
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26. Liu Y, Zhu P, Hu YM: [Epitopes recognized by cytotoxic T lymphocytes in immunoglobulin heavy chain variable regions expressed by B-cell acute lymphoblastic leukemia]. Zhonghua Zhong Liu Za Zhi; 2005 Feb;27(2):106-10
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  • [Title] [Epitopes recognized by cytotoxic T lymphocytes in immunoglobulin heavy chain variable regions expressed by B-cell acute lymphoblastic leukemia].
  • The frequency of QLVQSGAEV-specific CD8+ T cells in a healthy HLA-A*0201+ donor peripheral blood increased from 1.6% and 82.6% after two-round and 3-round stimulations, respectively.
  • These peptides are capable of inducing specific CD8+ T cells to activate and proliferate.
  • [MeSH-major] Burkitt Lymphoma / immunology. CD8-Positive T-Lymphocytes / immunology. Epitopes, T-Lymphocyte / immunology. Immunoglobulin Heavy Chains / immunology. Immunoglobulin Variable Region / immunology
  • [MeSH-minor] Adolescent. Cell Proliferation. Child. Child, Preschool. Gene Rearrangement. HLA-A Antigens / immunology. HLA-A Antigens / metabolism. HLA-A2 Antigen. Humans. Infant. Oligopeptides / immunology

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  • (PMID = 15946551.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Oligopeptides
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27. Nahi H, Hägglund H, Ahlgren T, Bernell P, Hardling M, Karlsson K, Lazarevic VLj, Linderholm M, Smedmyr B, Aström M, Hallböök H: An investigation into whether deletions in 9p reflect prognosis in adult precursor B-cell acute lymphoblastic leukemia: a multi-center study of 381 patients. Haematologica; 2008 Nov;93(11):1734-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An investigation into whether deletions in 9p reflect prognosis in adult precursor B-cell acute lymphoblastic leukemia: a multi-center study of 381 patients.
  • In acute lymphoblastic leukemia, besides age and white cell count at diagnosis, the cytogenetic abnormalities t(9;22)/BCR-ABL and t(4;11)/MLL-AF4 are important prognostic markers and are often included in the treatment stratification of patients with adult acute lymphoblastic leukemia.
  • Deletions in 9p are seen in about 9% of cases of adult acute lymphoblastic leukemia, but their prognostic impact has been controversial.
  • Cytogenetic data from 381 patients diagnosed with B-precursor acute lymphoblastic leukemia were reviewed.
  • Our data suggest that chromosomal abnormalities involving 9p may have a significant negative impact on survival in adult B-precursor acute lymphoblastic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Chromosomes, Human, Pair 9. Sequence Deletion

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  • (PMID = 18728022.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Genetic Markers
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28. Schwartz JR, Sarvaiya PJ, Vedeckis WV: Glucocorticoid receptor knock down reveals a similar apoptotic threshold but differing gene regulation patterns in T-cell and pre-B-cell acute lymphoblastic leukemia. Mol Cell Endocrinol; 2010 May 14;320(1-2):76-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucocorticoid receptor knock down reveals a similar apoptotic threshold but differing gene regulation patterns in T-cell and pre-B-cell acute lymphoblastic leukemia.
  • Glucocorticoids (GCs) are used in combination therapy for treating acute lymphoblastic leukemia (ALL).
  • In T-cell (CEM-C7) and pre-B-cell (697) ALL cell lines, dexamethasone (Dex) treatment causes an auto-upregulation of glucocorticoid receptor (GR) mRNA transcripts and protein.
  • Titration of the 697 cell GR to equal that of the CEM-C7 T-cell ALL line caused a shift in sensitivity to that seen in CEM-C7 cells.
  • While the same level of GR is required to trigger apoptosis in both T-cell and pre-B-cell ALL lineages, similarities and differences were observed for the regulation of target genes in these lineages.
  • These preliminary gene regulation patterns may lead to the development of a molecular signature for GC-sensitive and GC-resistant leukemia cells.

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  • [Copyright] (c) 2010 Elsevier Ireland Ltd. All rights reserved.
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  • (PMID = 20170710.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA116042-04; United States / NCI NIH HHS / CA / R01 CA116042; United States / NCI NIH HHS / CA / CA116042; United States / NCI NIH HHS / CA / R01 CA116042-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ NIHMS180172; NLM/ PMC2844487
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29. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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30. Moon H, Huh J, Cho MS, Chi H, Chung WS: A case of CD45-, CD19- precursor B cell acute lymphoblastic leukemia with an atypical morphology. Korean J Lab Med; 2007 Aug;27(4):253-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of CD45-, CD19- precursor B cell acute lymphoblastic leukemia with an atypical morphology.
  • The differential diagnosis of acute lymphoblastic leukemia (ALL) from other small round blue cell tumors in children is very important for proper treatment, but sometimes difficult.
  • CD45 is expressed on almost all-human leukocytes and not expressed on other small round blue cell tumors.
  • Moreover, CD19 is expressed on all stages of B lineage cells and loss of this antigen is very rare in precursor B-cell ALL.
  • The cytogenetic study showed normal karyotype but amplification of MLL (myeloid/lymphoid or mixed lineage leukemia) gene was suggestive in the fluorescent in situ hybridization.
  • The patient received the standard chemotherapy for acute lymphoblastic leukemia and reached complete remission.
  • [MeSH-major] Antigens, CD19 / analysis. Antigens, CD45 / analysis. Bone Marrow / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Acute Disease. Child. Female. Humans. In Situ Hybridization

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  • (PMID = 18094585.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD19; EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
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31. Bose P, Thompson CL, Gandhi DG, Ghabach BS, Ozer H: Response of AIDS-related plasmablastic lymphoma (PBL) to bortezomib. J Clin Oncol; 2009 May 20;27(15_suppl):e19562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • They are terminally differentiated B-cell neoplasms, and typically lack common B-cell markers but uniformly express plasma cell markers.
  • Flow cytometry was negative for CD45 and all common epithelial, T-cell and B-cell markers, but was positive for CD138 and p63(VS38c).
  • The diagnosis was stage IVBE PBL.
  • The WHO classifies PBL as a variant of diffuse large B-cell lymphoma.
  • However, studies of their immunophenotype and molecular histogenesis suggest that PBL are more closely related to plasma cell neoplasms.
  • Bortezomib is a proteasome inhibitor widely used in multiple myeloma and mantle cell lymphoma.
  • We chose bortezomib based on our patient's poor performance status and immune function, the desire to avoid combination chemotherapy, and translocations involving the immunoglobulin heavy chain gene locus (8;14) similar to those seen in multiple myeloma(4;14, 14;16) and mantle cell lymphoma(11;14).
  • A shift in the paradigm of treatment of PBL towards agents effective in plasma cell malignancies may be necessary.

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  • (PMID = 27961065.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • The continual reassessment method (CRM) was used to determine the maximum tolerated dose (MTD) from 4 pre-defined dose levels.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.
  • All pts had pre-B ALL.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Furutani A, Imamura T, Ueda I, Takanashi M, Hirashima Y, Nakatani T, Inaba T, Morimoto A: Hemophagocytic lymphohistiocytosis during maintenance treatment of precursor B-cell acute lymphoblastic leukemia. Int J Hematol; 2008 Dec;88(5):610-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemophagocytic lymphohistiocytosis during maintenance treatment of precursor B-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / drug therapy. Lymphohistiocytosis, Hemophagocytic / etiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Asian Continental Ancestry Group. Child, Preschool. Humans. Japan. Male. Time Factors

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  • (PMID = 19043809.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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34. Thakker MM, Rubin PA, Chang E: Pre-B-cell acute lymphoblastic leukemia presenting as an orbital mass in an 8-month-old. Ophthalmology; 2006 Feb;113(2):343-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pre-B-cell acute lymphoblastic leukemia presenting as an orbital mass in an 8-month-old.
  • PURPOSE: To present the case of an 8-month-old girl with undiagnosed pre-B-cell acute lymphoblastic leukemia (ALL) presenting as an orbital mass.
  • Based on these findings, the diagnosis of pre-B-cell acute lymphoblastic leukemia was made, and systemic as well as intrathecal chemotherapy was instituted, which resulted in rapid remission of the leukemia.
  • To the best of the authors' knowledge, this is the earliest reported case of pre-B-cell ALL presenting as an orbital lesion.
  • [MeSH-major] Orbital Neoplasms / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16406546.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, CD
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35. Kikuchi A, Mori T, Fujimoto J, Kumagai M, Sunami S, Okimoto Y, Tsuchida M: Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol. Leuk Lymphoma; 2008 Apr;49(4):757-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol.
  • From June 1996 to January 2001, 91 patients with B-cell non-Hodgkin lymphoma or B-cell acute lymphoblastic leukemia up to 18 years of age were enrolled in Tokyo Children's Cancer Study Group (TCCSG) NHL B9604 protocol study.
  • The TCCSG NHL B9604 protocol achieved an excellent treatment outcome especially in patients with the most advanced disease (Group D: high BM blast cell burden and/or central nervous system involvement).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Lymphoma, B-Cell / drug therapy


36. Kato K, Kobayashi C, Kudo K, Hara T, Masuko K, Koike K, Tsuchida M: Late recurrence of precursor B-cell acute lymphoblastic leukemia 9 years and 7 months after allogeneic hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Oct;32(7):e290-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Late recurrence of precursor B-cell acute lymphoblastic leukemia 9 years and 7 months after allogeneic hematopoietic stem cell transplantation.
  • We present the case of a 15-year-old adolescent boy with recurrent precursor B-cell acute lymphoblastic leukemia, which appeared 9 years and 7 months after a first unrelated allogeneic hematopoietic stem cell transplantation (HSCT).
  • A molecular study revealed the same rearrangement pattern at IGK@ in both the first relapse and the later relapse, confirming the common origin of the leukemic blasts at different time points.
  • [MeSH-major] Gene Rearrangement, B-Lymphocyte. Hematopoietic Stem Cell Transplantation. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20881873.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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37. Lee RV, Braylan RC, Rimsza LM: CD58 expression decreases as nonmalignant B cells mature in bone marrow and is frequently overexpressed in adult and pediatric precursor B-cell acute lymphoblastic leukemia. Am J Clin Pathol; 2005 Jan;123(1):119-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD58 expression decreases as nonmalignant B cells mature in bone marrow and is frequently overexpressed in adult and pediatric precursor B-cell acute lymphoblastic leukemia.
  • We used flow cytometry to determine the CD58 expression on nonmalignant B cells at different stages of maturation in the bone marrow and compared it with that of blasts in adult and pediatric precursor B-cell acute lymphoblastic leukemia (B-ALL).
  • The mean fluorescence intensity (MFI) of CD58 expression decreased significantly as nonmalignant B cells differentiated in the bone marrow from an early to a mature stage.
  • Few nonneoplastic B cells at a mid or mature stage of development expressed CD58 MFI values comparable to those seen in leukemic cases.
  • Early-stage nonneoplastic B-cell precursors expressed relatively higher CD58 levels, which frequently overlapped with the variable level of CD58 expression observed among leukemic blasts.
  • As a group, however, the malignant precursor B-ALL cells showed significantly higher expression of CD58 than nonmalignant B-cell populations at any maturational stage.
  • These findings support the potential usefulness of CD58 expression in the diagnosis and monitoring of precursor B-ALL, but only when blasts express high levels of CD58.
  • [MeSH-major] Antigens, CD58 / analysis. B-Lymphocytes / physiology. Bone Marrow Cells / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 15762287.001).
  • [ISSN] 0002-9173
  • [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 / Antigens, CD34; 0 / Antigens, CD58
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38. Bousquet M, Broccardo C, Quelen C, Meggetto F, Kuhlein E, Delsol G, Dastugue N, Brousset P: A novel PAX5-ELN fusion protein identified in B-cell acute lymphoblastic leukemia acts as a dominant negative on wild-type PAX5. Blood; 2007 Apr 15;109(8):3417-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel PAX5-ELN fusion protein identified in B-cell acute lymphoblastic leukemia acts as a dominant negative on wild-type PAX5.
  • We report a novel t(7;9)(q11;p13) translocation in 2 patients with B-cell acute lymphoblastic leukemia (B-ALL).
  • After cloning the full-length cDNA of the chimeric gene, confocal microscopy of transfected NIH3T3 cells and Burkitt lymphoma cells (DG75) demonstrated that PAX5-ELN was localized in the nucleus.
  • Since PAX5 is essential for B-cell differentiation, this translocation may account for the blockage of leukemic cells at the pre-B-cell stage.
  • The mechanism involved in this process appears to be, at least in part, through a dominant-negative effect of PAX5-ELN on the wild-type PAX5 in a setting ofPAX5 haploinsufficiency.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 9 / genetics. Elastin / genetics. Genes, Dominant. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Animals. Antigens, CD19 / biosynthesis. Antigens, CD19 / genetics. Cell Differentiation / genetics. Cell Nucleus / genetics. Cell Nucleus / metabolism. Cell Nucleus / pathology. HeLa Cells. Humans. Male. Mice. NIH 3T3 Cells. Promoter Regions, Genetic / genetics. Transcription, Genetic / genetics

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  • (PMID = 17179230.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Oncogene Proteins, Fusion; 0 / PAX5 protein, human; 9007-58-3 / Elastin
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39. Malbora B, Avci Z, Alioglu B, Tutar NU, Ozbek N: A case with mature B-cell acute lymphoblastic leukemia and pancreatic involvement at the time of diagnosis. J Pediatr Hematol Oncol; 2008 Jan;30(1):87-9
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  • [Title] A case with mature B-cell acute lymphoblastic leukemia and pancreatic involvement at the time of diagnosis.
  • Pancreatic infiltration with leukemic cells is a rare manifestation of acute lymphoblastic leukemia.
  • We report the clinical and radiologic findings of a 4-year-old boy with mature B-cell acute lymphoblastic leukemia and pancreatic involvement.
  • [MeSH-major] Leukemia, B-Cell / drug therapy. Leukemia, B-Cell / radiography. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / radiography. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiography
  • [MeSH-minor] Acute Disease. Amylases / blood. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child, Preschool. Diagnosis, Differential. Humans. Kidney Neoplasms / blood. Kidney Neoplasms / drug therapy. Kidney Neoplasms / radiography. Kidney Neoplasms / secondary. Lipase / blood. Liver Neoplasms / blood. Liver Neoplasms / drug therapy. Liver Neoplasms / radiography. Liver Neoplasms / secondary. Male. Pancreatitis / blood. Pancreatitis / drug therapy. Pancreatitis / radiography. Tomography, X-Ray Computed

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  • (PMID = 18176191.001).
  • [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] EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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40. Rhein P, Mitlohner R, Basso G, Gaipa G, Dworzak MN, Kirschner-Schwabe R, Hagemeier C, Stanulla M, Schrappe M, Ludwig WD, Karawajew L, Ratei R: CD11b is a therapy resistance- and minimal residual disease-specific marker in precursor B-cell acute lymphoblastic leukemia. Blood; 2010 May 6;115(18):3763-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD11b is a therapy resistance- and minimal residual disease-specific marker in precursor B-cell acute lymphoblastic leukemia.
  • A consistently increased mRNA expression of the adhesion receptor CD11b is a hallmark of the reported genomewide gene expression changes in precursor B-cell acute lymphoblastic leukemia (PBC-ALL) after 1 week of induction therapy.
  • To investigate its clinical relevance, CD11b protein expression in leukemic blasts has been prospectively measured at diagnosis (159 patients) and during therapy (53 patients).
  • In the multivariate analysis CD11b expression was an independent prognostic factor compared with other clinically relevant parameters at diagnosis.
  • In more than 30% of MRD-positive cases, the CD11b expression on blast cells exceeded that of mature memory B cells and improved the discrimination of residual leukemic cells from regenerating bone marrow.
  • [MeSH-major] Antigens, CD11b / metabolism. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / metabolism. Drug Resistance, Neoplasm. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20228269.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / ITGAM protein, human; 0 / RNA, Messenger
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41. Nowak NJ, Sait SN, Zeidan A, Deeb G, Gaile D, Liu S, Ford L, Wallace PK, Wang ES, Wetzler M: Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 May;199(1):15-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia.
  • The prognosis of adult normal karyotype (NK) precursor B-cell acute lymphoblastic leukemia (B-ALL) has not improved over the last decade, mainly because separation into distinct molecular subsets has been lacking and no targeted treatments are available.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20417863.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; None / None / / P30 CA016056-33; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / P30 CA016056-33
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ NIHMS173834; NLM/ PMC2862995
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42. Diffner E, Gauffin F, Anagnostaki L, Nordgren A, Gustafsson B, Sander B, Gustafsson B, Persson JL: Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry. J Pediatr Hematol Oncol; 2009 Sep;31(9):696-701
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry.
  • We investigated the expression and clinical importance of VEGF and two of its receptors, VEGFR-1 and VEGFR-2, in childhood precursor B-cell acute lymphoblastic leukemia (pre-B ALL) by using immunohistochemistry.
  • Notably, pre-B ALL patients had significantly increased expression of VEGFR-1 compared with no expression in the nonmalignant group, indicating a link between VEGFR-1 protein expression and pre-B ALL.
  • These novel findings suggest that VEGFR-1 may have clinical importance in childhood pre-B ALL.
  • [MeSH-major] Immunoenzyme Techniques. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

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  • (PMID = 19707156.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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43. Takenokuchi M, Saigo K, Nakamachi Y, Kawano S, Hashimoto M, Fujioka T, Koizumi T, Tatsumi E, Kumagai S: Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18). Acta Haematol; 2006;116(1):30-40
Cellosaurus - a cell line knowledge resource. culture/stock collections - UTree-O2 (CVCL_W195) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18).
  • Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the nuclear receptor superfamily, has been detected in several human leukemia cells.
  • Recent studies reported that PPARgamma ligands inhibit cell proliferation and induce apoptosis in both normal and malignant B-lineage cells.
  • We investigated the expression of PPARgamma and the effects of PPARgamma ligands on UTree-O2, Bay91 and 380, three B-cell acute lymphoblastic leukemia (B-ALL) cell lines with t(14;18), which show a poor prognosis, accompanying c-myc abnormality.
  • Western blot analysis identified expression of PPARgamma protein and real-time PCR that of PPARgamma mRNA on the three cell lines.
  • Troglitazone (TGZ), a synthetic PPARgamma ligand, inhibited cell growth in these cell lines in a dose-dependent manner, which was associated with G(1) cell cycle arrest and apoptosis.
  • We assessed the expression of c-myc, an apoptosis-regulatory gene, since c-myc abnormality was detected in most B-ALL cells with t(14;18).
  • TGZ was found to dose-dependently downregulate the expression of c-myc mRNA and c-myc protein in the three cell lines.
  • These results suggest that TGZ inhibits cell growth via induction of G(1) cell cycle arrest and apoptosis in these cell lines and that TGZ-induced apoptosis, at least in part, may be related to the downregulation of c-myc expression.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Burkitt Lymphoma / metabolism. Chromans / pharmacology. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. G1 Phase / drug effects. PPAR gamma / biosynthesis. Thiazolidinediones / pharmacology. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Ligands. Male. Prognosis. Proto-Oncogene Proteins c-myc / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16809887.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / Ligands; 0 / MYC protein, human; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-myc; 0 / Thiazolidinediones; I66ZZ0ZN0E / troglitazone
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44. Liu Y, Zhu P, Hu YM: [Induction of anti-B-cell acute lymphoblastic leukemia cytotoxic T lymphocyte response against immunoglobulin heavy chain frame-derived nonapeptide]. Zhonghua Xue Ye Xue Za Zhi; 2005 May;26(5):285-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Induction of anti-B-cell acute lymphoblastic leukemia cytotoxic T lymphocyte response against immunoglobulin heavy chain frame-derived nonapeptide].
  • OBJECTIVE: To induce anti-B-cell acute lymphoblastic leukemia (B-ALL) cytotoxic T lymphocyte response against immunoglobulin heavy chain frame-derived nonapeptide.
  • HLA-A * 0201/IgHV1(3-11) tetramers were used to detect the proliferation of IgHV1(3-11)-specific CD8(+) T cells in the culture.
  • Cytotoxicity of IgHV1(3-11)-specific CD8(+) T cells against HLA-A * 0201-positive IgHV1/IgHV3 family B-ALL cells was measured by MTT assay.
  • RESULTS: The synthesized IgHV1(3-11) up-regulated HLA-A * 0201 expression on T2 cell surface by 1.63-folds.
  • The percentage of IgHV1(3-11)-specific CD8(+) T cells in HLA-A * 0201-positive normal PBMNC was increased from 1.64% after second stimulation to 82.57% after third stimulation.
  • At effector: target ratio of 20:1, the killing rate of IgHV1(3-11)-specific CD8(+) T cells against IgHV1 family B-ALL cells was 18.24%, being 1.8-folds as that against IgHV3 family B-ALL cells (P = 0.01).
  • [MeSH-major] Immunoglobulin Heavy Chains / pharmacology. Leukemia, B-Cell / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 15949291.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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45. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.

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  • (PMID = 27960689.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Liu Y, Zhu P, Hu YM: Generation of cytotoxic T lymphocytes specific for B-cell acute lymphoblastic leukemia family-shared peptides derived from immunoglobulin heavy chain framework region. Chin Med J (Engl); 2007 Apr 20;120(8):652-7
Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Generation of cytotoxic T lymphocytes specific for B-cell acute lymphoblastic leukemia family-shared peptides derived from immunoglobulin heavy chain framework region.
  • BACKGROUND: Immunoglobulin heavy chain variable region (IgHV) is a well-characterized tumor antigen for B-cell malignancies.
  • It can function as a target for T cell-mediated immune response.
  • Clinical trials of IgHV protein vaccines against lymphoma have demonstrated induction of tumor-specific cytotoxic T lymphocyte (CTL) responses.
  • However, complementary determining regions-based individual vaccines have disadvantages for wide clinical application.
  • Although a recent study demonstrated that immunogenic peptides are derived from framework regions (FR) shared among patients with B-cell lymphoma, how to choose the appropriate peptides for each patient is still unsolved.
  • The aim of this study was to investigate whether immunoglobulin heavy chain FR-derived peptides shared in each IgHV family are potential CTL epitopes presented by B-cell acute lymphoblastic leukemia (B-ALL).
  • An antigen-specific T cell expansion system was used to generate peptide-specific CTLs.
  • CTLs specific for the peptide QLVQSGAEV located in FR1 (3 - 11) shared among the IgHV1 family could be successfully generated from peripheral blood mononuclear cells of two HLA-A*0201 + healthy donors in vitro and were capable of killing HLA-matched B-ALL cell clones belonging to the IgHV1 family.
  • CONCLUSION: Anti-B-ALL CTLs against immunoglobulin heavy chain FR-derived peptides have family-specific cytotoxicity.
  • [MeSH-major] Burkitt Lymphoma / immunology. Immunoglobulin Heavy Chains / immunology. Immunoglobulin Variable Region / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 17517179.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Oligopeptides
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47. Lee K, Bang J, Kim K: Proteome analysis of malignant pleural effusion. J Clin Oncol; 2009 May 20;27(15_suppl):e22194

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Twenty microliters of pleural effusions(PEs) from 3 patients with non-small cell lung cancer(NSCLC) and 3 patients with tuberculous pleurisy(TBC) were used for proteome analysis.
  • Among the identified proteins, we found the biomarker candidates that significantly have different expression levels in malignant effusion; apolipoprotein B precursor, vitronectin, complement factor B, histidine-rich glycoprotein precursor, coagulation factor II precursor variant.
  • CONCLUSIONS: We found that several pleural effusion proteins may serve as potential biomarker candidates for differential diagnosis between maligant and tuberculous pleural effusion.

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  • (PMID = 27963631.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Tchinda J, Volpert S, Berdel WE, Büchner T, Horst J: Novel three-break rearrangement and cryptic translocations leading to colocalization of MYC and IGH signals in B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Mar;165(2):180-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel three-break rearrangement and cryptic translocations leading to colocalization of MYC and IGH signals in B-cell acute lymphoblastic leukemia.
  • Reciprocal translocations involving the MYC locus and immunoglobulin heavy chain (IGH) and light chain (IgK and IgL) loci are characteristic for non-Hodgkin lymphomas, especially Burkitt lymphoma, and have been described in B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Rearrangement. Genes, myc. Immunoglobulin Heavy Chains / genetics. Translocation, Genetic

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  • (PMID = 16527615.001).
  • [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 / Immunoglobulin Heavy Chains
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49. Healy J, Richer C, Bourgey M, Kritikou EA, Sinnett D: Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia. Haematologica; 2010 Sep;95(9):1608-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia.
  • Although childhood acute lymphoblastic leukemia is the most common pediatric cancer, its etiology remains poorly understood.
  • In an attempt to replicate the findings of 2 recent genome-wide association studies in a French-Canadian cohort, we confirmed the association of 5 SNPs [rs7073837 (P=4.2 x 10(-4)), rs10994982 (P=3.8 x 10(-4)), rs10740055 (P=1.6 x 10(-5)), rs10821936 (P=1.7 x 10(-7)) and rs7089424 (P=3.6 x 10(-7))] in the ARID5B gene with childhood acute lymphoblastic leukemia.
  • We also confirmed a selective effect for B-cell acute lymphoblastic leukemia with hyperdiploidy and report a putative gender-specific effect of ARID5B SNPs on acute lymphoblastic leukemia risk in males.
  • This study provides a strong rationale for more detailed analysis to identify the causal variants at this locus and to better understand the overall functional contribution of ARID5B to childhood acute lymphoblastic leukemia susceptibility.

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  • (PMID = 20460642.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2930966
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50. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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  • (PMID = 27962472.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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51. Chatterton Z, Morenos L, Saffery R, Craig JM, Ashley D, Wong NC: DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia. Epigenomics; 2010 Oct;2(5):697-708
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common cancer in children in the modern world.
  • [MeSH-major] DNA Methylation / physiology. Epigenesis, Genetic / physiology. High-Throughput Screening Assays / methods. MicroRNAs / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 22122053.001).
  • [ISSN] 1750-192X
  • [Journal-full-title] Epigenomics
  • [ISO-abbreviation] Epigenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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52. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • This analysis confirmed that in addition to t(12;21), AML1 amplification and overexpression existed already at the time the diagnosis was made.
  • While the first course of chemotherapy successfully eradicated the cell line with the t(12;21), the second cell line with AML1 amplification remained latent during the time of complete remission and reappeared with a different immunophenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


53. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • ZAP-70 expression may hold prognostic value for pre-B ALL and raises the prospect of a novel therapeutic target.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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54. Prabhu S, Gottlieb DJ, Varikatt W, St Heaps L, Diaz S, Smith A: Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones. Cancer Genet Cytogenet; 2010 Aug;201(1):24-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones.
  • The presence of two different abnormal cell lines at diagnosis in hematologic malignancies is rare and raises the question of etiology and pathogenesis--two separate malignant lineages occurring together or a common stem cell malignancy?
  • On the basis of the morphology, flow cytometry, and lack of myeloid-associated markers, a diagnosis of precursor B-cell acute lymphoblastic leukemia (B-ALL) was made.
  • The dic(7;9) is a rare but recurrent abnormality in B-ALL, while trisomy 8 as a sole abnormality is most commonly associated with myeloid malignancies.
  • After standard treatment for B-ALL, BM cytogenetic analysis showed disappearance of the dic(7;9) cell line but persistence of cells with trisomy 8.
  • [MeSH-major] Leukemia, B-Cell / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633764.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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55. Tie LJ, Gu LJ, Chen J, Jiang LM, Dong L, Pan C, Ye H, Song DL, Xue HL, Tang JY, Wang YP, Chen J: [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Feb;27(2):120-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To assess the prognostic value of minimal residual disease (MRD) in childhood B-cell acute lymphoblastic leukemia (ALL) after induction chemotherapy.
  • CONCLUSION: The MRD level at achieving CR is one of important prognostic factor in the treatment of childhood B-cell ALL, and might be used to assess the early treatment response.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, B-Cell / drug therapy. Neoplasm, Residual

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  • (PMID = 16732969.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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56. Vey N, Thomas X, Picard C, Kovascovicz T, Charin C, Cayuela JM, Dombret H, Dastugue N, Huguet F, Bastard C, Stamatoulas A, Giollant M, Tournilhac O, Macintyre E, Buzyn A, Bories D, Kuentz M, Dreyfus F, Delannoy A, Raynaud S, Gratecos N, Bordessoule D, de Botton S, Preudhomme C, Reman O, Troussard X, Pigneux A, Bilhou C, Vernant JP, Boucheix C, Gabert J, GET-LALA Group the Swiss Group for Clinical Cancer Research (SAKK): Allogeneic stem cell transplantation improves the outcome of adults with t(1;19)/E2A-PBX1 and t(4;11)/MLL-AF4 positive B-cell acute lymphoblastic leukemia: results of the prospective multicenter LALA-94 study. Leukemia; 2006 Dec;20(12):2155-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic stem cell transplantation improves the outcome of adults with t(1;19)/E2A-PBX1 and t(4;11)/MLL-AF4 positive B-cell acute lymphoblastic leukemia: results of the prospective multicenter LALA-94 study.
  • Adult patients with acute lymphoblastic leukemia (ALL) and t(1;19)/E2A-PBX1 or t(4;11)/MLL-AF4 have a poor outcome.
  • CR rates achieved by MLL and E2A groups were similar to other B-cell ALL (87, 82 and 86% respectively).
  • [MeSH-major] Burkitt Lymphoma / genetics. Burkitt Lymphoma / therapy. Hematopoietic Stem Cell Transplantation. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Basic Helix-Loop-Helix Transcription Factors / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Prospective Studies. Proto-Oncogene Proteins / genetics. Transplantation, Homologous

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  • (PMID = 17039234.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / TCF3 protein, human; 0 / pbx1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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57. Sharma LM, Kashyap R, Gupta S, Bhargava M: B-cell acute lymphoblastic leukemia in a child with ataxia telangiectasia. Pediatr Hematol Oncol; 2008 Jun;25(5):473-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-cell acute lymphoblastic leukemia in a child with ataxia telangiectasia.
  • [MeSH-major] Ataxia Telangiectasia / complications. Burkitt Lymphoma / etiology


58. Wang JD, Huang FL, Chi CS, Chou G, Chang TK: Skull mass as a heralding sign of precursor B-cell acute lymphoblastic leukemia in a toddler. J Pediatr; 2006 Oct;149(4):577
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skull mass as a heralding sign of precursor B-cell acute lymphoblastic leukemia in a toddler.
  • [MeSH-major] Burkitt Lymphoma / diagnosis. Skull Neoplasms / diagnosis

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  • (PMID = 17011339.001).
  • [ISSN] 0022-3476
  • [Journal-full-title] The Journal of pediatrics
  • [ISO-abbreviation] J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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59. Ratei R, Basso G, Dworzak M, Gaipa G, Veltroni M, Rhein P, Biondi A, Schrappe M, Ludwig WD, Karawajew L, AIEOP-BFM-FCM-MRD-Study Group: Monitoring treatment response of childhood precursor B-cell acute lymphoblastic leukemia in the AIEOP-BFM-ALL 2000 protocol with multiparameter flow cytometry: predictive impact of early blast reduction on the remission status after induction. Leukemia; 2009 Mar;23(3):528-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring treatment response of childhood precursor B-cell acute lymphoblastic leukemia in the AIEOP-BFM-ALL 2000 protocol with multiparameter flow cytometry: predictive impact of early blast reduction on the remission status after induction.
  • Treatment response is a strong outcome predictor for childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-minor] Adolescent. Area Under Curve. Blood Cells / pathology. Bone Marrow / pathology. Cell Count. Child. Child, Preschool. Clinical Trials as Topic / statistics & numerical data. Drug Monitoring. Female. Humans. Infant. Male. Neoplasm, Residual. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma. Prognosis. ROC Curve. Remission Induction. Treatment Outcome

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  • (PMID = 19020543.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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60. Sonoki T, Iwanaga E, Mitsuya H, Asou N: Ovarian relapse seven years after bone marrow transplantation for B-cell acute lymphoblastic leukemia: an unusual Krukenberg tumor. Am J Hematol; 2005 Sep;80(1):75-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ovarian relapse seven years after bone marrow transplantation for B-cell acute lymphoblastic leukemia: an unusual Krukenberg tumor.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Burkitt Lymphoma / therapy. Krukenberg Tumor / etiology. Ovarian Neoplasms / etiology


61. Riva G, Luppi M, Potenza L, Morselli M, Ferrari A, Saviola A, Volzone F, Imovilli A, Merighi A, Maiorana A, Torelli G: Cytomegalovirus and Clostridium Difficile co-infection in severe ulcero-hemorrhagic colitis during induction chemotherapy for acute lymphoblastic leukemia. Haematologica; 2005 Jan;90(1):ECR01
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomegalovirus and Clostridium Difficile co-infection in severe ulcero-hemorrhagic colitis during induction chemotherapy for acute lymphoblastic leukemia.
  • Here we describe the first case of a biopsy-proven Cytomegalovirus ulcero-hemorrhagic colitis, associated with Clostridium Difficile co-infection, occurring during standard induction chemotherapy for common B cell acute lymphoblastic leukemia.
  • [MeSH-major] Clostridium difficile. Colitis, Ulcerative / microbiology. Colitis, Ulcerative / virology. Cytomegalovirus Infections / pathology. Enterocolitis, Pseudomembranous / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


62. DiGiuseppe JA, Fuller SG, Borowitz MJ: Overexpression of CD49f in precursor B-cell acute lymphoblastic leukemia: potential usefulness in minimal residual disease detection. Cytometry B Clin Cytom; 2009 Mar;76(2):150-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of CD49f in precursor B-cell acute lymphoblastic leukemia: potential usefulness in minimal residual disease detection.
  • BACKGROUND: The persistence of minimal residual disease (MRD) following therapy is an established prognostic factor in precursor B-cell acute lymphoblastic leukemia (pB-ALL).
  • Detection of MRD in pB-ALL by flow cytometric immunophenotyping requires demonstration of abnormal antigen expression in leukemic B-cell precursors relative to that of normal B-cell precursors.
  • The gene encoding CD49f (integrin alpha-6) is one of several whose overexpression in pB-ALL at diagnosis has been associated with the subsequent detection of MRD.
  • METHODS: We evaluated CD49f expression by 4-color flow cytometry in normal B-cell precursors, and in a series of cases of pB-ALL, both at diagnosis and at intervals following the initiation of therapy.
  • RESULTS: In 10 control marrow samples, CD49f was undetectable or extremely dim in all but a minor subset of normal CD19+ B-lineage cells, whereas in 11 of 15 cases (73%) of pB-ALL, CD49f was moderate or bright at diagnosis, and persisted or became brighter after initiation of therapy.
  • Of the four pB-ALL cases in which CD49f was undetectable or dim at diagnosis, MRD was detected in two; in one of these, CD49f expression was substantially increased in the leukemic cells that persisted following initiation of therapy.
  • [MeSH-major] Flow Cytometry / methods. Integrin alpha6 / analysis. Integrin alpha6 / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Age Factors. B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Biomarkers / analysis. Biomarkers / blood. Child. Child, Preschool. Female. Humans. Immunophenotyping / methods. Infant. Male. Neoplasm Recurrence, Local / blood. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / immunology. Neoplasm, Residual. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Predictive Value of Tests. Prognosis. Young Adult

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  • [Copyright] 2008 Clinical Cytometry Society.
  • (PMID = 18831072.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Integrin alpha6
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63. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M, Jiang LM: [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):333-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To study the role of minimal residual disease (MRD) in the evaluation of therapeutic effectiveness of childhood B-cell acute lymphoblastic leukemia (ALL).
  • METHODS: MRD testing was performed in 124 children with B-cell ALL, who were newly diagnosed and enrolled in the ALL-XH-99 treatment protocol from September 2001 to April 2005MRD was determined by 4-color flow cytometry in the different time points during the treatment period.
  • Multivariate analysis confirmed that the MRD level after induction chemotherapy together with the reaction to prednisone, the bone marrow features on the 19th day of induction, and the fusion gene with BCR-ABL or MLL-AF4 had prognostic significance in childhood B-cell ALL.
  • CONCLUSIONS: The MRD level in the whole course of therapy is an important outcome indicator in childhood B cell ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18554462.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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64. Lonetti A, Iacobucci I, Ferrari A, Messina M, Cilloni D, Soverini S, Papayannidis C, Baccarani M, Foà R, Martinelli G: Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients. J Clin Oncol; 2009 May 20;27(15_suppl):7049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients.
  • : 7049 Since the activation-induced cytidine deaminase (AID) enzyme can target non-immunoglobulin (Ig) genes and may even act as a genome-wide mutator, we investigated AID expression in BCR-ABL1-positive ALL and in chronic myeloid leukemia (CML) at the time of progression to blast crisis.
  • On the 61 de novo adult BCR-ABL1-positive ALL patients (pts), AID mRNA and protein were detected in 36 (59%); their expression correlated with BCR-ABL1 transcript levels and disappeared after treatment with tyrosine kinase inhibitors at the time of remission.
  • Different isoforms of AID were identified: 13/61 (21%) pts expressed the full-length isoform; 19/61 (31%) co-expressed the wild-type and different AID splice variants with deaminase activity (AIDΔE4a, with a 30 bp deletion of exon 4; AIDΔE4, with the exon 4 deletion; AIDins3, with the retention of intron 3-4); 4/61 (7%) expressed the AIDΔE3-E4 isoform without deaminase activity (deletion of exons 2 and 3).
  • Patients who expressed wild-type AID had a higher number of alterations compared to AID-negative (median copy number alteration of 14 versus 4. respectively, p < 0.03).
  • Our findings show that BCR-ABL1-positive ALL cells aberrantly express different isoforms of AID that can act as mutator outside the Ig gene loci in promoting genetic instability in leukemia cells.

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  • (PMID = 27961429.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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65. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.
  • We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.
  • RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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66. Ahmed D, Ahmed TA, Ahmed S, Tipu HN, Wiqar MA: CD5-positive acute lymphoblastic leukemia. J Coll Physicians Surg Pak; 2008 May;18(5):310-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD5-positive acute lymphoblastic leukemia.
  • CD5-positive B-ALL is a rare variant of Acute Lymphoblastic Leukemia (ALL).
  • This fourth case report describes a young lady who was diagnosed as ALL (L-2) on bone marrow examination and was found to be CD5 positive B-cell acute lymphoblastic leukemia on immunophenotyping.
  • [MeSH-major] Antigens, CD5 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Biopsy, Needle. Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans

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  • (PMID = 18541090.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antigens, CD5
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67. Balin J, Parmar H, Kujawski L: Conventional and diffusion-weighted MRI findings of methotrexate related sub-acute neurotoxicity. J Neurol Sci; 2008 Jun 15;269(1-2):169-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conventional and diffusion-weighted MRI findings of methotrexate related sub-acute neurotoxicity.
  • We describe longitudinal diffusion-weighted MRI findings of sub-acute leukoencephalopathy following methotrexate therapy in a 24-year-old man diagnosed with pre-B-cell acute lymphoblastic leukemia (ALL), presenting with right-sided paralysis and aphasia after second consolidation with intrathecal triple-drug therapy given intrathecally.
  • This case demonstrates the value of DWI in evaluation and diagnosis of sub-acute toxic leukoencephalopathy in patients being treated with methotrexate.
  • [MeSH-major] Diffusion Magnetic Resonance Imaging. Immunosuppressive Agents / adverse effects. Methotrexate / adverse effects. Neurotoxicity Syndromes / diagnosis. Neurotoxicity Syndromes / etiology
  • [MeSH-minor] Adult. Brain Diseases / complications. Brain Diseases / drug therapy. Humans. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18191947.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; YL5FZ2Y5U1 / Methotrexate
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68. Karremann M, Schreiner U, Büsing KA, von Komorowski G, Dürken M: [Acute lymphoblastic leukemia presenting without peripheral blasts but with osteolysis and hypercalcemia in an adolescent. Atypical but not rare]. Orthopade; 2009 Aug;38(8):752-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute lymphoblastic leukemia presenting without peripheral blasts but with osteolysis and hypercalcemia in an adolescent. Atypical but not rare].
  • Joint pain is one of the major symptoms in early leukemia.
  • Acute lymphoblastic leukemia was diagnosed, but the laboratory workup and radiologic imaging revealed atypical results.
  • Particularly in early precursor B-cell acute lymphoblastic leukemia, comparable initial symptoms and signs have been reported in adolescents; therefore, we recommend performing a bone marrow aspiration early on in cases of suspected osteolytic bone lesions.
  • [MeSH-major] Hypercalcemia / complications. Hypercalcemia / diagnosis. Osteolysis / complications. Osteolysis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Blast Crisis / complications. Blast Crisis / diagnosis. Diagnosis, Differential. Female. Humans

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  • (PMID = 19533085.001).
  • [ISSN] 1433-0431
  • [Journal-full-title] Der Orthopäde
  • [ISO-abbreviation] Orthopade
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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69. Bakathir AA, Al-Hamdani AS: Relapse of acute lymphoblastic leukemia in the jaw. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2009 May;107(5):e14-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relapse of acute lymphoblastic leukemia in the jaw.
  • This case report describes the clinical case of relapse of precursor B-cell acute lymphoblastic leukemia in the jaw of a 19-year-old female patient who presented with facial swelling, sensory disturbances of the face, and teeth mobility 10 months after a successful allogenic bone marrow transplant.
  • [MeSH-major] Mandibular Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19426901.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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70. Lad EM, Jain A, Lad SP, Lin RC, Alcorn DM, Moshfeghi DM: Orbital recurrence of B-progenitor acute lymphoblastic leukemia in a child. J Pediatr Ophthalmol Strabismus; 2010 Jan-Feb;47(1):46-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Orbital recurrence of B-progenitor acute lymphoblastic leukemia in a child.
  • Orbital mass is an exceedingly rare presentation of acute lymphoblastic leukemia.
  • This report describes a 12-year-old boy with recurrent orbital pre-B-cell acute lymphoblastic leukemia and reviews the literature on the incidence, presentation, prognosis, and management of orbital tumors in acute lymphoblastic leukemia.
  • Early diagnosis and treatment of orbital acute lymphoblastic leukemia with a multidisciplinary approach is essential to minimize or prevent deterioration of vision and optimize clinical outcomes.
  • [MeSH-major] Neoplasm Recurrence, Local / diagnosis. Orbital Neoplasms / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Biopsy. Bone Marrow / pathology. Child. Combined Modality Therapy. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male

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  • [Copyright] Copyright 2010, SLACK Incorporated.
  • (PMID = 20128555.001).
  • [ISSN] 0191-3913
  • [Journal-full-title] Journal of pediatric ophthalmology and strabismus
  • [ISO-abbreviation] J Pediatr Ophthalmol Strabismus
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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71. Czuchlewski DR, Andrews J, Madden R, Clericuzio CL, Zhang QY: Acute lymphoblastic leukemia in a patient with Miller-Dieker syndrome. J Pediatr Hematol Oncol; 2008 Nov;30(11):865-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia in a patient with Miller-Dieker syndrome.
  • A 15-month-old girl with Miller-Dieker syndrome, a contiguous gene deletion syndrome involving chromosome 17p13.3 and resulting in lissencephaly, was diagnosed with precursor B-cell acute lymphoblastic leukemia.
  • This is, to our knowledge, the first report of acute leukemia in the setting of Miller-Dieker syndrome.
  • [MeSH-major] Classical Lissencephalies and Subcortical Band Heterotopias / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


72. Zuo Z, Jones DM, Thomas DA, O'Brien S, Ravandi F, Kantarjian HM, Medeiros LJ, Luthra R, Chen SS: A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL).
  • There was no statistical difference in age, initial peripheral blood white cell and BM blast counts, and initial normalized BCR/ABL1 levels between groups.

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  • (PMID = 27961387.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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73. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Kahwash R, Rugg SS, Smith MD: Relapsing B-cell lymphoblastic leukemia in an adult presenting as an infiltrative cardiac mass with tamponade. J Am Soc Echocardiogr; 2007 Nov;20(11):1319.e1-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relapsing B-cell lymphoblastic leukemia in an adult presenting as an infiltrative cardiac mass with tamponade.
  • We present a case of a 51-year-old man with a history of bone-marrow transplantation for acute lymphoblastic leukemia who returned 4 months later with cardiac tamponade.
  • Surgical biopsy of the mass revealed early relapse with lymphoblasts derived from B-cell precursors.
  • We believe that this is the first description of relapsing B-cell acute lymphoblastic leukemia presenting as an intrathoracic mass with direct invasion of the adjacent cardiac structures causing tamponade physiology.
  • [MeSH-major] Cardiac Tamponade / etiology. Cardiac Tamponade / ultrasonography. Heart Neoplasms / etiology. Heart Neoplasms / ultrasonography. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / ultrasonography

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  • (PMID = 17658241.001).
  • [ISSN] 1097-6795
  • [Journal-full-title] Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
  • [ISO-abbreviation] J Am Soc Echocardiogr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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75. Cobanoglu U, Sonmez M, Ozbas HM, Erkut N, Can G: The expression of LMO2 protein in acute B-cell and myeloid leukemia. Hematology; 2010 Jun;15(3):132-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of LMO2 protein in acute B-cell and myeloid leukemia.
  • LIM domain only-2 (LMO2) is an important regulator of hematopoietic stem cell development.
  • LMO2 is also expressed in blast cells of different types of acute leukemia.
  • Here, we analyzed the LMO2 protein expression in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-ALL) and examined whether the LMO2 protein expression can predict outcomes of patients with acute leukemia.
  • Patients with acute B-ALL (22 cases) and AML (57 cases) were examined using immunohistochemistry for LMO2 on paraffin-embedded bone marrow biopsies.
  • We report that LMO2 protein is expressed in a significant proportion of B-ALL and AML and the staining of LMO2 protein does not predict survival in acute leukemia.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Leukemia, B-Cell / metabolism. Leukemia, Myeloid, Acute / metabolism. Metalloproteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adolescent. Adult. Aged. Cell Differentiation / physiology. Female. Gene Expression Regulation, Leukemic. Humans. LIM Domain Proteins. Male. Middle Aged. Young Adult

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  • (PMID = 20557670.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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76. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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  • (PMID = 15749681.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
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77. Vancura RW, Kepes JJ, Newell KL, Ha TM, Arnold PM: Secondary intracranial neoplasms exhibiting features of astrocytoma and neuroblastoma in 2 children treated for acute lymphoblastic leukemia: report of 2 cases. Surg Neurol; 2006 May;65(5):490-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary intracranial neoplasms exhibiting features of astrocytoma and neuroblastoma in 2 children treated for acute lymphoblastic leukemia: report of 2 cases.
  • We report 2 patients who were diagnosed with pre-B-cell acute lymphoblastic leukemia and later presented with intracranial malignancies.
  • Each patient was in remission for leukemia at the time of diagnosis of the second malignancy.
  • The possible causes of the brain tumors in association with acute lymphoblastic leukemia are discussed.
  • [MeSH-major] Astrocytoma. Brain Neoplasms / secondary. Brain Neoplasms / therapy. Neoplasms, Second Primary. Neuroblastoma. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


78. Chapiro E, Russell L, Radford-Weiss I, Bastard C, Lessard M, Struski S, Cave H, Fert-Ferrer S, Barin C, Maarek O, Della-Valle V, Strefford JC, Berger R, Harrison CJ, Bernard OA, Nguyen-Khac F: Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3560-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia.
  • The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation.
  • In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties.
  • We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13).
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 16873674.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Immunoglobulin Heavy Chains; 0 / RNA, Neoplasm
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79. Marçais A, Jeannet R, Hernandez L, Soulier J, Sigaux F, Chan S, Kastner P: Genetic inactivation of Ikaros is a rare event in human T-ALL. Leuk Res; 2010 Apr;34(4):426-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]
  • (PMID = 19796813.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
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80. Kim IS, Kim HJ, Yoo KH, Sung KW, Kim SH: A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation. J Pediatr Hematol Oncol; 2006 Aug;28(8):540-3
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  • [Title] A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation.
  • An 8-year-old boy was diagnosed with precursor B-cell acute lymphoblastic leukemia.
  • Postcord blood transplantation cytogenetic studies revealed engraftment failure evidenced by switching into the recipient type (XY), and, notably, various complex chromosomal aberrations in the recipient cells.
  • [MeSH-major] Blood Group Incompatibility / pathology. Burkitt Lymphoma / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 7 / genetics. Cord Blood Stem Cell Transplantation / adverse effects

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  • (PMID = 16912597.001).
  • [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
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81. Pound CM, Keene DL, Udjus K, Humphreys P, Johnston DL: Acute encephalopathy and cerebral vasospasm after multiagent chemotherapy including PEG-asparaginase and intrathecal cytarabine for the treatment of acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2007 Mar;29(3):183-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute encephalopathy and cerebral vasospasm after multiagent chemotherapy including PEG-asparaginase and intrathecal cytarabine for the treatment of acute lymphoblastic leukemia.
  • A 7-year-old girl with an unusual reaction to induction chemotherapy for precursor B-cell acute lymphoblastic leukemia (ALL) is described.
  • The patient developed acute encephalopathy evidenced by behavioral changes, aphasia, incontinence, visual hallucinations, and right-sided weakness with diffuse cerebral vasospasm on magnetic resonance angiography after the administration of intrathecal cytarabine.
  • Neurologic status returned to baseline within 10 days of the acute event, and magnetic resonance angiography findings returned to normal 4 months later.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Asparaginase / adverse effects. Brain Diseases / chemically induced. Burkitt Lymphoma / drug therapy. Cytarabine / adverse effects. Polyethylene Glycols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vasospasm, Intracranial / chemically induced
  • [MeSH-minor] Acute Disease. Brain / pathology. Child. Female. Follow-Up Studies. Humans. Injections, Spinal. Magnetic Resonance Angiography / methods. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 17356399.001).
  • [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 / pegaspargase; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; EC 3.5.1.1 / Asparaginase
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82. Layden BT, Joseph M, Tallman MS, Platanias LC: Acute lymphoblastic leukemia in a patient with chronic cyanoacrylate exposure. Acta Haematol; 2007;118(4):242-3
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  • [Title] Acute lymphoblastic leukemia in a patient with chronic cyanoacrylate exposure.
  • We report here the case of a 36-year-old man with pre-B cell acute lymphoblastic leukemia.
  • This case raises the possibility that chronic exposure to cyanoacrylates, the adhesive agents in industrial strength glue, may be associated with the development of acute lymphoblastic leukemia in humans.
  • [MeSH-major] Adhesives / adverse effects. Cyanoacrylates / adverse effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Self Care / adverse effects. Tooth Fractures / therapy

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 18087146.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adhesives; 0 / Cyanoacrylates; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; CVAD protocol
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83. Shoo BA, Shinkai K, McCalmont TH, Fox LP: Xanthogranulomas associated with hematologic malignancy in adulthood. J Am Acad Dermatol; 2008 Sep;59(3):488-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Herein we report a case of XG in a 45-year-old man with B-cell acute lymphoblastic leukemia and review the literature regarding the association of XG and hematologic disorders in adults.
  • [MeSH-major] Hematologic Neoplasms / complications. Histiocytosis, Non-Langerhans-Cell / etiology. Leukemia, B-Cell / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Skin Diseases / etiology

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  • (PMID = 18538449.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.3.2.13 / Factor XIIIa
  • [Number-of-references] 39
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84. Scholz C, Nimmrich I, Burger M, Becker E, Dörken B, Ludwig WD, Maier S: Distinction of acute lymphoblastic leukemia from acute myeloid leukemia through microarray-based DNA methylation analysis. Ann Hematol; 2005 Apr;84(4):236-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinction of acute lymphoblastic leukemia from acute myeloid leukemia through microarray-based DNA methylation analysis.
  • To investigate whether disease-specific methylation profiles exist for different entities of acute leukemia, a microarray-based DNA methylation analysis simultaneously assessing 249 CpG dinucleotides originating from 57 genes was employed.
  • Hereby, samples from precursor B-cell acute lymphoblastic leukemia (ALL) could be distinguished from cases of acute myeloid leukemia by virtue of N33, EGR4, CDC2, CCND2, or MOS hypermethylation in ALL.
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. Classification. Diagnosis, Differential. Dinucleoside Phosphates / metabolism. Humans. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic

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  • (PMID = 15538567.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dinucleoside Phosphates; 0 / Neoplasm Proteins; 2382-65-2 / cytidylyl-3'-5'-guanosine
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85. Andiran N, Alikaşifoğlu A, Küpeli S, Yetgin S: Use of bisphosphonates for resistant hypercalcemia in children with acute lymphoblastic leukemia: report of two cases and review of the literature. Turk J Pediatr; 2006 Jul-Sep;48(3):248-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of bisphosphonates for resistant hypercalcemia in children with acute lymphoblastic leukemia: report of two cases and review of the literature.
  • We present two children, one of whom is the youngest reported, with CALLA+ B-cell acute lymphoblastic leukemia (ALL) who developed hypercalcemia at the time of diagnosis and were treated with relatively low-dose (0.5 mg/kg) intravenous pamidronate successive to conventional therapy.
  • [MeSH-major] Diphosphonates / therapeutic use. Hypercalcemia / drug therapy. Hypercalcemia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [CommentIn] Turk J Pediatr. 2008 May-Jun;50(3):305 [18773683.001]
  • (PMID = 17172070.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Diphosphonates
  • [Number-of-references] 28
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86. Lancioni C, LaBeaud AD, Esper F, Abughali N, Auletta J: Pulmonary tuberculosis presenting as fever without source in a pediatric patient with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Dec 15;53(7):1318-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pulmonary tuberculosis presenting as fever without source in a pediatric patient with acute lymphoblastic leukemia.
  • In this report we describe a case of primary pulmonary tuberculosis (TB) in a boy with precursor B-cell acute lymphoblastic leukemia (ALL) and review the pertinent literature.
  • [MeSH-major] Fever of Unknown Origin / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Tuberculosis, Pulmonary / diagnosis

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19618457.001).
  • [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 / Antitubercular Agents; 04079A1RDZ / Cytarabine; 2KNI5N06TI / Pyrazinamide; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 83905-01-5 / Azithromycin; 8G167061QZ / Ethambutol; 8N3DW7272P / Cyclophosphamide; V83O1VOZ8L / Isoniazid; VJT6J7R4TR / Rifampin
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87. Savelli SL, Klopfenstein KJ, Termuhlen AM: Mucoepidermoid carcinoma of the parotid gland as a second malignant neoplasm. Pediatr Blood Cancer; 2005 Dec;45(7):997-1000
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patient 1 was initially diagnosed with precursor B-cell lymphoblastic lymphoma of the scalp.
  • Eight years after her initial diagnosis she presented with a small, painless mass in the region of her parotid gland.
  • Patient 2 was diagnosed with pre-B-cell acute lymphoblastic leukemia (ALL).
  • Thirteen years after her initial diagnosis she presented with a painless mass in her right cheek.
  • [MeSH-major] Carcinoma, Mucoepidermoid / surgery. Leukemia, B-Cell / drug therapy. Neoplasms, Second Primary / surgery. Parotid Neoplasms / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] 2004 Wiley-Liss, Inc.
  • (PMID = 15602710.001).
  • [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
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88. Bousquet M, Harris MH, Zhou B, Lodish HF: MicroRNA miR-125b causes leukemia. Proc Natl Acad Sci U S A; 2010 Dec 14;107(50):21558-63
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  • [Title] MicroRNA miR-125b causes leukemia.
  • MicroRNA miR-125b has been implicated in several kinds of leukemia.
  • The chromosomal translocation t(2;11)(p21;q23) found in patients with myelodysplasia and acute myeloid leukemia leads to an overexpression of miR-125b of up to 90-fold normal.
  • Moreover, miR-125b is also up-regulated in patients with B-cell acute lymphoblastic leukemia carrying the t(11;14)(q24;q32) translocation.
  • All mice transplanted with fetal liver cells ectopically expressing miR-125b showed an increase in white blood cell count, in particular in neutrophils and monocytes, associated with a macrocytic anemia.
  • Among these mice, half died of B-cell acute lymphoblastic leukemia, T-cell acute lymphoblastic leukemia, or a myeloproliferative neoplasm, suggesting an important role for miR-125b in early hematopoiesis.
  • Furthermore, coexpression of miR-125b and the BCR-ABL fusion gene in transplanted cells accelerated the development of leukemia in mice, compared with control mice expressing only BCR-ABL, suggesting that miR-125b confers a proliferative advantage to the leukemic cells.
  • Thus, we show that overexpression of miR-125b is sufficient both to shorten the latency of BCR-ABL-induced leukemia and to independently induce leukemia in a mouse model.

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  • (PMID = 21118985.001).
  • [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 / NIDDK NIH HHS / DK / DK068348; United States / NIDDK NIH HHS / DK / R56 DK068348; United States / NIDDK NIH HHS / DK / R01 DK068348; United States / NHLBI NIH HHS / HL / 5P01 HL066105; United States / NHLBI NIH HHS / HL / P01 HL066105
  • [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 / MIRN125 microRNA, human; 0 / MicroRNAs; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC3003065
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89. Geng CD, Vedeckis WV: Use of recombinant cell-permeable small peptides to modulate glucocorticoid sensitivity of acute lymphoblastic leukemia cells. Biochemistry; 2010 Oct 19;49(41):8892-901
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  • [Title] Use of recombinant cell-permeable small peptides to modulate glucocorticoid sensitivity of acute lymphoblastic leukemia cells.
  • Glucocorticoid (GC) hormones induce apoptosis in T-cell and pre-B-cell acute lymphoblastic leukemia (ALL) cells.
  • Purified, bacterially expressed Tat-c-Myb DBD and Tat-GR(554-777) exhibited highly efficient transduction into cultured ALL cell lines including 697 (pre-B-ALL) and CEM-C7 (T-ALL) cells.
  • Significantly, transduced Tat-GR(554-777) effectively increased intracellular GR levels in the GC-resistant T-ALL cell line, CEM-C1, and in the pre-B-ALL 697 cell line.
  • The use of Tat-fusion peptide transduction may eventually lead to innovative therapeutic modalities to improve the clinical response of patients suffering from T-cell and pre-B-cell acute lymphoblastic leukemia by increasing steroid responsiveness and perhaps converting steroid-resistant leukemia to a hormone-responsive phenotype.

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  • (PMID = 20831260.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116042; United States / NCI NIH HHS / CA / CA116042
  • [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 / Glucocorticoids; 0 / Peptides; 0 / Proto-Oncogene Proteins c-myb; 0 / Receptors, Glucocorticoid; 0 / Recombinant Fusion Proteins; 0 / tat Gene Products, Human Immunodeficiency Virus
  • [Other-IDs] NLM/ NIHMS238675; NLM/ PMC2953583
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90. Harb JG, Chyla BI, Huettner CS: Loss of Bcl-x in Ph+ B-ALL increases cellular proliferation and does not inhibit leukemogenesis. Blood; 2008 Apr 1;111(7):3760-9
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  • The kinase inhibitors imatinib mesylate and dasatinib are the preferred treatment for Philadelphia chromosome-positive (Ph+) leukemias, and they are highly successful in the chronic phase of chronic myeloid leukemia (CML).
  • However, they are not efficient in Ph+ B-cell acute lymphoblastic leukemia (B-ALL).
  • Ph+ leukemia cells are highly resistant to apoptosis, and evidence from cell lines and primary cells suggest Bcl-xL as a critical mediator of resistance to apoptosis: however, this concept has never been rigorously tested in an animal model.
  • In the first model, Ph+ B-ALL and loss of Bcl-xL expression are coinduced; in the second model, leukemia is induced with expression of Bcl-xL protein well above the levels found in wild-type lymphoblasts.
  • These models reveal an unexpected role for Bcl-xL in cell-cycle entry and the proliferation of tumor cells.

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  • (PMID = 18216295.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007209; United States / NHLBI NIH HHS / HL / HL-07209
  • [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 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / bcl-X Protein
  • [Other-IDs] NLM/ PMC2275032
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91. Atas A, Cakmak A, Soran M, Soker M, Varma M: Severe osteoporosis and high level TSH in a child before the diagnosis of acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Aug;31(8):588-91
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  • [Title] Severe osteoporosis and high level TSH in a child before the diagnosis of acute lymphoblastic leukemia.
  • Diagnosis of IJO was made by excluding other common causes of osteoporosis in this age.
  • We report this case, whose symptoms were disappeared after parenteral pamidronat treatment, and he was reexamined owing to anemia and trombositopenia, and diagnosed as B-cell acute lymphoblastic leukemia, just to emphasis the importance of close follow-ups of IJO patients.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Diphosphonates / administration & dosage. Osteoporosis / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma. Thyrotropin / blood
  • [MeSH-minor] Adolescent. Bone Density Conservation Agents / administration & dosage. Diagnosis, Differential. Humans. Male

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  • (PMID = 19636264.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 9002-71-5 / Thyrotropin; OYY3447OMC / pamidronate
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92. Peng C, Chen Y, Yang Z, Zhang H, Osterby L, Rosmarin AG, Li S: PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice. Blood; 2010 Jan 21;115(3):626-35
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  • [Title] PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice.
  • However, it is unknown whether PTEN functions as a tumor suppressor in human Philadelphia chromosome-positive leukemia that includes chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induced by the BCR-ABL oncogene.
  • By using our mouse model of BCR-ABL-induced leukemias, we show that Pten is down-regulated by BCR-ABL in leukemia stem cells in CML and that PTEN deletion causes acceleration of CML development.
  • In addition, overexpression of PTEN delays the development of CML and B-ALL and prolongs survival of leukemia mice.
  • PTEN suppresses leukemia stem cells and induces cell-cycle arrest of leukemia cells.
  • These results demonstrate a critical role of PTEN in BCR-ABL-induced leukemias and suggest a potential strategy for the treatment of Philadelphia chromosome-positive leukemia.

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  • (PMID = 19965668.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114199; United States / NCI NIH HHS / CA / R01 CA122142; United States / NCI NIH HHS / CA / R01-CA114199; United States / NCI NIH HHS / CA / R01-CA122142
  • [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 / Tumor Suppressor Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2810991
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93. Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia. Leuk Res; 2005 May;29(5):557-64
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  • [Title] p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
  • Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with acute leukemia.
  • To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-cell acute lymphoblastic leukemia (PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
  • Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Lineage. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured

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  • (PMID = 15755508.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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94. Russell LJ, Capasso M, Vater I, Akasaka T, Bernard OA, Calasanz MJ, Chandrasekaran T, Chapiro E, Gesk S, Griffiths M, Guttery DS, Haferlach C, Harder L, Heidenreich O, Irving J, Kearney L, Nguyen-Khac F, Machado L, Minto L, Majid A, Moorman AV, Morrison H, Rand V, Strefford JC, Schwab C, Tönnies H, Dyer MJ, Siebert R, Harrison CJ: Deregulated expression of cytokine receptor gene, CRLF2, is involved in lymphoid transformation in B-cell precursor acute lymphoblastic leukemia. Blood; 2009 Sep 24;114(13):2688-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulated expression of cytokine receptor gene, CRLF2, is involved in lymphoid transformation in B-cell precursor acute lymphoblastic leukemia.
  • We report 2 novel, cryptic chromosomal abnormalities in precursor B-cell acute lymphoblastic leukemia (BCP-ALL): a translocation, either t(X;14)(p22;q32) or t(Y;14)(p11;q32), in 33 patients and an interstitial deletion, either del(X)(p22.33p22.33) or del(Y)(p11.32p11.32), in 64 patients, involving the pseudoautosomal region (PAR1) of the sex chromosomes.
  • Overexpression of CRLF2 was associated with activation of the JAK-STAT pathway in cell lines and transduced primary B-cell progenitors, sustaining their proliferation and indicating a causal role of CRLF2 overexpression in lymphoid transformation.
  • In Down syndrome (DS) ALL and 2 non-DS BCP-ALL cell lines, CRLF2 deregulation was associated with mutations of the JAK2 pseudokinase domain, suggesting oncogenic cooperation as well as highlighting a link between non-DS ALL and JAK2 mutations.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Lymphocytes / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics


95. Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S: Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice. Proc Natl Acad Sci U S A; 2006 Nov 7;103(45):16870-5
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  • [Title] Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.
  • Imatinib is highly effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in chronic phase but not Ph(+) B cell acute lymphoblastic leukemia (B-ALL) and CML blast crisis.
  • Besides BCR-ABL and SRC kinases, stem cell pathways must be targeted for curative therapy of Ph(+) leukemia.

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  • (PMID = 17077147.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114199; United States / NCI NIH HHS / CA / CA 114199
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1629087
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96. Kanazawa T, Ogawa C, Taketani T, Taki T, Hayashi Y, Morikawa A: TLS/FUS-ERG fusion gene in acute lymphoblastic leukemia with t(16;21)(p11;q22) and monitoring of minimal residual disease. Leuk Lymphoma; 2005 Dec;46(12):1833-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TLS/FUS-ERG fusion gene in acute lymphoblastic leukemia with t(16;21)(p11;q22) and monitoring of minimal residual disease.
  • This study reports a 1-year-old boy with precursor B cell acute lymphoblastic leukemia (ALL) carrying t(16;21)(p11;q22).
  • Complete remission (CR) was achieved by chemotherapy oriented for acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Neoplasm, Residual / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

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  • (PMID = 16263589.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
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97. Hong D, Gupta R, Ancliff P, Atzberger A, Brown J, Soneji S, Green J, Colman S, Piacibello W, Buckle V, Tsuzuki S, Greaves M, Enver T: Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia. Science; 2008 Jan 18;319(5861):336-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia.
  • Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations but also the cellular framework in which they arise and function.
  • Here we explore the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is characterized by a chromosomal translocation generating a TEL-AML1 fusion gene.
  • We identify a cell compartment in leukemic children that can propagate leukemia when transplanted in mice.
  • By studying a monochorionic twin pair, one preleukemic and one with frank leukemia, we establish the lineal relationship between these "cancer-propagating" cells and the preleukemic cell in which the TEL-AML1 fusion first arises or has functional impact.
  • Analysis of TEL-AML1-transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Diseases in Twins. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Preleukemia / pathology
  • [MeSH-minor] Acute Disease. Animals. Antigens, CD19 / analysis. Antigens, CD34 / analysis. Antigens, CD38 / analysis. Apoptosis. Bone Marrow Transplantation. Child, Preschool. Female. Fetal Blood / transplantation. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Humans. Male. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Neoplastic Stem Cells / pathology. Precursor Cells, B-Lymphoid / chemistry. Precursor Cells, B-Lymphoid / physiology. Recombination, Genetic. Transplantation, Heterologous. Twins, Monozygotic


98. Alpár D, Nagy G, Hohoff C, Kajtár B, Bartyik K, Hermesz J, Jáksó P, Andrikovics H, Kereskai L, Pajor L: Sex chromosome changes after sex-mismatched allogeneic bone marrow transplantation can mislead the chimerism analysis. Pediatr Blood Cancer; 2010 Dec 1;55(6):1239-42
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  • A 12-year-old male with pre-B-cell acute lymphoblastic leukemia with cryptic BCR/ABL rearrangement underwent sex-mismatched allogeneic bone marrow transplantation (allo-BMT).
  • Y-chromosome-specific quantitative polymerase chain reaction and sex chromosome-specific interphase fluorescence in situ hybridization (i-FISH) showed complete donor chimerism.
  • Metaphase-FISH and combined BCR/ABL and sex chromosome-specific i-FISH patterns revealed loss of the Y-chromosome and duplication of the X-chromosome in the host cells.
  • [MeSH-major] Bone Marrow Transplantation. Chimera. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sex Determination Analysis

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  • (PMID = 20979181.001).
  • [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] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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99. Schiffman JD, Wang Y, McPherson LA, Welch K, Zhang N, Davis R, Lacayo NJ, Dahl GV, Faham M, Ford JM, Ji HP: Molecular inversion probes reveal patterns of 9p21 deletion and copy number aberrations in childhood leukemia. Cancer Genet Cytogenet; 2009 Aug;193(1):9-18
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  • [Title] Molecular inversion probes reveal patterns of 9p21 deletion and copy number aberrations in childhood leukemia.
  • Childhood leukemia, which accounts for >30% of newly diagnosed childhood malignancies, is one of the leading causes of death for children with cancer.
  • Genome-wide studies using microarray chips to identify copy number changes in human cancer are becoming more common.
  • In this pilot study, 45 pediatric leukemia samples were analyzed for gene copy aberrations using novel molecular inversion probe (MIP) technology.
  • Acute leukemia subtypes included precursor B-cell acute lymphoblastic leukemia (ALL) (n=23), precursor T-cell ALL (n=6), and acute myeloid leukemia (n=14).
  • We report unique patterns of copy number loss in samples with 9p21.3 (CDKN2A) deletion in the precursor B-cell ALL patients, compared with the precursor T-cell ALL patients.

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  • (PMID = 19602459.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / P01 HG000205; United States / NHGRI NIH HHS / HG / 2P01HG000205; United States / NCI NIH HHS / CA / CA96879; United States / NHGRI NIH HHS / HG / P01 HG000205-20; United States / NCI NIH HHS / CA / K08 CA096879
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS151549; NLM/ PMC2776674
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100. Zhang JY, Lü T, Yang JC, Pan L, Luo JM, Yang L, Yao L, Dong ZR, Xu SR: Comparative study of expressions of cytoplasmic CD79a and other B-lymphoid immunomarkers in acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):954-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative study of expressions of cytoplasmic CD79a and other B-lymphoid immunomarkers in acute leukemic cells.
  • To evaluate the expression of cytoplasmic CD79a (CyCD79a) and other commonly used B-lymphoid immunomarkers including cytoplasmic CD22 (CyCD22), CD19, CD20 and CD10 in various acute leukemia cells and to define the most sensitive and specific markers in the diagnosis of precursor B-cell acute lymphoblastic leukemia (pB-ALL), the immunophenotypic data from 221 de novo adult and pediatric acute leukemia patients as studied using multi-parameter flow cytometry in addition to routine morphologic and enzyme cytochemical assay, were retrospectively analyzed.
  • Cytogenetic and/or molecular biological data in all 45 cases of acute promyelocytic leukemia (APL) and 13 cases of acute leukemia suspected as AML with the fusion genes such as AML1/ETO and CBFbeta/MYH11 were investigated.
  • The results showed that CyCD79a and CyCD22 were the most sensitive and specific markers respectively for pB-ALL.
  • At the same time, none (0%) of all 147 cases of acute myeloid leukemia (AML) and 15 cases of precursor T-cell acute leukemia (pT-ALL) was positive for CyCD22.
  • The conclusion is made that united detection of CyCD79a and CyCD22 is the optimal immune combination for the diagnosis pB-ALL and the distinguishing pB-ALL with AML and pT-ALL.

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  • (PMID = 16403258.001).
  • [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] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD79; 0 / Biomarkers, Tumor; 0 / Sialic Acid Binding Ig-like Lectin 2
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