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1. Koren-Michowitz M, Rahimi-Levene N, Volcheck Y, Hardan I, Kornberg A: Rituximab monotherapy as interim therapy in precursor B-ALL adults during periods of hepatic toxicity: report of two cases. Am J Hematol; 2006 Dec;81(12):979-80
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  • [Title] Rituximab monotherapy as interim therapy in precursor B-ALL adults during periods of hepatic toxicity: report of two cases.
  • Precursor B-ALL blasts may be positive for CD20 in up to 50% of cases.
  • We report on two adult patients with precursor B-ALL who developed significant hepatic toxicity during induction chemotherapy.
  • Both patients were able to continue further chemotherapy, underwent an Allo BMT and are now 10-12 months after diagnosis in a continuous CR.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Bone Marrow Transplantation. Burkitt Lymphoma / therapy

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  • (PMID = 17019690.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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2. Mårtensson IL, Almqvist N, Grimsholm O, Bernardi AI: The pre-B cell receptor checkpoint. FEBS Lett; 2010 Jun 18;584(12):2572-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pre-B cell receptor checkpoint.
  • During the development of progenitor B cells to mature B cells that express a membrane-bound antibody, the B cell receptor (BCR), the cells undergo selection at several checkpoints, which ensures that a diverse antibody repertoire is generated and that the BCRs recognise foreign-, but not self-, antigens.
  • In this review, we consider the pre-BCR checkpoint.
  • Mutations or alterations that affect this checkpoint underpin the development of pre-B cell leukemias, primary immunodeficiency, and possibly, systemic autoimmunity.
  • [MeSH-major] Pre-B Cell Receptors / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Animals. Autoimmunity / genetics. Cell Differentiation / immunology. Cell Membrane / immunology. Gene Rearrangement, B-Lymphocyte. Humans. Immunologic Deficiency Syndromes / genetics. Immunologic Deficiency Syndromes / immunology. Mice. Models, Immunological. Mutation. Signal Transduction / immunology

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  • [Copyright] Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20420836.001).
  • [ISSN] 1873-3468
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Pre-B Cell Receptors
  • [Number-of-references] 60
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3. Brown VI, Hulitt J, Fish J, Sheen C, Bruno M, Xu Q, Carroll M, Fang J, Teachey D, Grupp SA: Thymic stromal-derived lymphopoietin induces proliferation of pre-B leukemia and antagonizes mTOR inhibitors, suggesting a role for interleukin-7Ralpha signaling. Cancer Res; 2007 Oct 15;67(20):9963-70
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  • [Title] Thymic stromal-derived lymphopoietin induces proliferation of pre-B leukemia and antagonizes mTOR inhibitors, suggesting a role for interleukin-7Ralpha signaling.
  • Understanding the pathogenesis of leukemia in the context of lymphopoiesis may reveal novel therapeutic targets.
  • Previously, we have shown that mTOR inhibitors (MTI) show activity in vitro and in preclinical models of both human and murine precursor B acute lymphoblastic leukemia (pre-B ALL), inhibiting cell proliferation and inducing apoptosis.
  • These MTI-mediated effects can be reversed by interleukin-7 (IL-7), an important regulator of early B-cell development.
  • TSLP is closely related to IL-7 and active in lymphopoiesis, but an effect of TSLP on leukemia cells has not been described.
  • We examined the effect of TSLP on pre-B ALL cells and their response to MTIs.
  • Here, we show that TSLP stimulates proliferation of pre-B ALL cell lines.
  • TSLP also partially reverses the effects of MTI on proliferation, apoptosis, and ribosomal protein S6 and 4E-BP1 phosphorylation in cell lines, with similar biological effects seen in some primary human lymphoblast samples.
  • These data show that TSLP can promote survival of pre-B ALL cells and antagonize the effects of MTIs.
  • These findings suggest that IL-7Ralpha chain is responsible for transducing the survival signal that overcomes MTI-mediated growth inhibition in pre-B ALL.

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  • (PMID = 17942929.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5K08-CA104882; United States / NCI NIH HHS / CA / K08 CA104882-04; United States / NCI NIH HHS / CA / K08 CA104882; United States / NCI NIH HHS / CA / CA104882-04; United States / NCI NIH HHS / CA / R01-CA102646
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Carrier Proteins; 0 / Cytokines; 0 / Eif4ebp1 protein, mouse; 0 / Interleukin-7; 0 / Interleukin-7 Receptor alpha Subunit; 0 / Phosphoproteins; 0 / Protein Kinase Inhibitors; 0 / Recombinant Proteins; 0 / Ribosomal Protein S6; 0 / STAT5 Transcription Factor; 0 / thymic stromal lymphopoietin; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; W36ZG6FT64 / Sirolimus
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4. 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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5. Lovisa F, Mussolin L, Corral L, Pillon M, Cazzaniga G, Biondi A, Rosolen A: IGH and IGK gene rearrangements as PCR targets for pediatric Burkitt's lymphoma and mature B-ALL MRD analysis. Lab Invest; 2009 Oct;89(10):1182-6
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  • [Title] IGH and IGK gene rearrangements as PCR targets for pediatric Burkitt's lymphoma and mature B-ALL MRD analysis.
  • We recently reported that minimal residual disease (MRD) and minimal disseminated disease (MDD), assessed by long-distance PCR (LD-PCR) for t(8;14), are negative prognostic factors in mature B-cell acute lymphoblastic leukemia (B-ALL) and in Burkitt's lymphoma (BL).
  • The aim of our study was to evaluate the characteristics of patient-specific immunoglobulin (Ig) gene rearrangements as RQ-PCR targets for MRD analysis, in order to extend MRD studies to those patients who are not eligible for the LD-PCR assay.
  • In 87% of patients (84% of B-ALLs, 95% of BLs) at least one sensitive target was available.
  • All PCR targets identified at diagnosis were preserved at relapse.
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Immunoglobulin Heavy Chains / genetics. Immunoglobulin kappa-Chains / genetics. Leukemia, B-Cell / genetics

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  • (PMID = 19668242.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin kappa-Chains
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6. Coyaud E, Struski S, Prade N, Familiades J, Eichner R, Quelen C, Bousquet M, Mugneret F, Talmant P, Pages MP, Lefebvre C, Penther D, Lippert E, Nadal N, Taviaux S, Poppe B, Luquet I, Baranger L, Eclache V, Radford I, Barin C, Mozziconacci MJ, Lafage-Pochitaloff M, Antoine-Poirel H, Charrin C, Perot C, Terre C, Brousset P, Dastugue N, Broccardo C: Wide diversity of PAX5 alterations in B-ALL: a Groupe Francophone de Cytogenetique Hematologique study. Blood; 2010 Apr 15;115(15):3089-97
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  • [Title] Wide diversity of PAX5 alterations in B-ALL: a Groupe Francophone de Cytogenetique Hematologique study.
  • PAX5 is the main target of somatic mutations in acute B lymphoblastic leukemia (B-ALL).
  • Contrary to cases with PAX5 fusions, deletions were associated with complex karyotypes and common recurrent translocations.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Cytogenetic Analysis. Mutation / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20160164.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Oncogene Proteins, Fusion; 0 / PAX5 protein, human
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7. Kawano Y, Yoshikawa S, Minegishi Y, Karasuyama H: Pre-B cell receptor assesses the quality of IgH chains and tunes the pre-B cell repertoire by delivering differential signals. J Immunol; 2006 Aug 15;177(4):2242-9
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  • [Title] Pre-B cell receptor assesses the quality of IgH chains and tunes the pre-B cell repertoire by delivering differential signals.
  • It is well understood how a variety of Ig H and L chains, components of BCR, are generated in the DNA level during B cell development.
  • Here we show that muH chains produced by pre-B cells display a wide spectrum of ability to form the pre-BCR, which is composed of muH and surrogate light (SL) chains and is crucial for B cell development.
  • The level of surface pre-BCR expression varies among pre-B cells, depending on the ability of their muH chains to pair with SL chains.
  • The higher the level of pre-BCR expression by pre-B cells, the stronger their pre-BCR signaling, and the better they proliferate and differentiate.
  • Thus, the extent of survival, proliferation, and differentiation of individual pre-B cells is primarily determined by the SL-pairing ability of their muH chains.
  • Furthermore, IgH chains with higher potential to assemble with IgL chains appear to be positively selected and amplified through the assessment of their ability to pair with SL chains at the pre-BCR checkpoint before the assembly into the BCR.
  • These results indicate that the pre-BCR assesses the quality of muH chains and tunes the pre-B cell repertoire by driving the preferential expansion and differentiation of cells with the higher quality of muH chains.
  • [MeSH-minor] Animals. Cell Line. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Mice. Mice, Mutant Strains. Pre-B Cell Receptors. Receptors, Antigen, B-Cell

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  • (PMID = 16887984.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Membrane Glycoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell
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8. Miao K, Li J, Qiu H, Zhang R, Chen L, Wu H, Wang R, Zhang J: The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia. Onkologie; 2010;33(7):385-7
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  • [Title] The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia.
  • BACKGROUND: Cytogenetic abnormalities are the most important independent prognostic factors of acute leukemia and imply the potential molecular mechanism of the disease.
  • Translocation (11;14)(p13;q11) has been predominantly found in T-cell acute lymphocytic leukemia (ALL) but is rare in B-cell ALL.
  • CONCLUSIONS: Translocation (11;14) (p13;q11) in B-cell ALL is rare, but it is worth exploring the molecular mechanisms and discovering the prognostic value in more B-cell ALL patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Leukemia, B-Cell / genetics. Translocation, Genetic / genetics

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20631486.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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9. Lv L, Wu C, Sun H, Zhu S, Yang Y, Chen X, Fu H, Bao L: Combined 677CC/1298AC genotypes of methylenetetrahydrofolate reductase (MTHFR ) reduce susceptibility to precursor B lymphoblastic leukemia in a Chinese population. Eur J Haematol; 2010 Jun;84(6):506-12
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  • [Title] Combined 677CC/1298AC genotypes of methylenetetrahydrofolate reductase (MTHFR ) reduce susceptibility to precursor B lymphoblastic leukemia in a Chinese population.
  • It has been suggested that two MTHFR polymorphisms, 677C>T and 1298A>C, influence risk of acute lymphoblastic leukemia (ALL).
  • Here, we report a case-control study of 127 Chinese patients with adult precursor B lymphoblastic leukemia (B-ALL) to examine correlation between the MTHFR polymorphisms and B-ALL susceptibility in adults.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Single Nucleotide. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20374270.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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10. Kong Y, Yoshida S, Saito Y, Doi T, Nagatoshi Y, Fukata M, Saito N, Yang SM, Iwamoto C, Okamura J, Liu KY, Huang XJ, Lu DP, Shultz LD, Harada M, Ishikawa F: CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL. Leukemia; 2008 Jun;22(6):1207-13
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  • [Title] CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL.
  • In human acute myelogenous leukemia (AML), the leukemia stem cells (LSCs) have been phenotypically restricted within the CD34+CD38- fraction.
  • To understand the origin of malignant cells in primary human B-precursor acute lymphocytic leukemia (B-ALL), we established a novel in vivo xenotransplantation model.
  • In each of the three cases studied, transplantation of CD34+CD38+CD19+ cells resulted in the development of B-ALL in secondary recipients, demonstrating self-renewal capacity.
  • The identification of CD34+CD38+CD19+ self-renewing B-ALL cells proposes a hierarchy of leukemia-initiating cells (LICs) distinct from that of AML.
  • [MeSH-major] Antigens, CD19 / metabolism. Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Hematopoietic Stem Cells / pathology. Neoplastic Stem Cells / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Animals. Animals, Newborn. Cell Differentiation. Cell Lineage. Child. Flow Cytometry. Graft Survival. Humans. Immunophenotyping. Infant. Mice. Mice, Inbred NOD. Mice, SCID. Transplantation, Heterologous. Tumor Cells, Cultured. Whole-Body Irradiation

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  • (PMID = 18418410.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; EC 3.2.2.5 / Antigens, CD38
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11. Cobaleda C, Sánchez-García I: B-cell acute lymphoblastic leukaemia: towards understanding its cellular origin. Bioessays; 2009 Jun;31(6):600-9
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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 leukaemia: towards understanding its cellular origin.
  • B-cell acute lymphoblastic leukaemia (B-ALL) is a clonal malignant disease originated in a single cell and characterized by the accumulation of blast cells that are phenotypically reminiscent of normal stages of B-cell differentiation.
  • B-ALL origin has been a subject of continuing discussion, given the fact that human disease is diagnosed at late stages and cannot be monitored during its natural evolution from its cell of origin, although most B-ALLs probably start off with chromosomal changes in haematopoietic stem cells.
  • However, the cells responsible for maintaining the disease appear to differ between the different types of B-ALLs and this remains an intriguing and exciting topic of research, since these cells have been posited to be responsible for resistance to conventional therapies, recurrence and dissemination.
  • The results from these different reconstitution experiments and their interpretations are compared in this review in the context of normal B-cell developmental plasticity.
  • [MeSH-major] B-Lymphocytes / physiology. Leukemia, B-Cell / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Differentiation / physiology. Humans. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / physiology. Phenotype

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  • (PMID = 19444834.001).
  • [ISSN] 1521-1878
  • [Journal-full-title] BioEssays : news and reviews in molecular, cellular and developmental biology
  • [ISO-abbreviation] Bioessays
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 63
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12. Marin V, Dander E, Biagi E, Introna M, Fazio G, Biondi A, D'Amico G: Characterization of in vitro migratory properties of anti-CD19 chimeric receptor-redirected CIK cells for their potential use in B-ALL immunotherapy. Exp Hematol; 2006 Sep;34(9):1219-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Cytokine-induced killer (CIK) cells are ex vivo expanded cells enriched in CD3(+)CD56(+) natural killer T (NKT) cells with major histocompatibility-unrestricted cytotoxicity against several tumoral targets, except B-lineage acute lymphoblastic leukemia (B-ALL).
  • We redirected CIK cells cytotoxicity toward B-ALL with a chimeric receptor specific for the CD19 antigen and then explored if modified-CIK cells maintain the same chemotactic properties of freshly isolated NKT cells, whose trafficking machinery reflects their preferential localization into the sites of B-ALL infiltration.
  • MATERIAL AND METHODS: CIK cells were expanded ex vivo for 21 days and analyzed for expression of adhesion molecules and chemokine receptors regulating adhesion and homing toward leukemia-infiltrated tissues.
  • Anti-CD19 chimeric receptor-modified CIK cells became cytotoxic against B-ALL cells (mean lysis, 60%) and showed, after exposure to a CXCL12 gradient, high capacity to adhere and transmigrate through endothelial cells and to invade Matrigel.
  • CONCLUSION: The potential capacity to localize into leukemia-infiltrated tissues of anti-CD19 chimeric receptor-redirected CIK cells, together with their ability to efficiently kill B-ALL cells, suggests that modified-CIK cells represent a valuable tool for leukemia immunotherapy.
  • [MeSH-major] Antigens, CD19 / immunology. Burkitt Lymphoma / immunology. Cell Movement / immunology. Cytotoxicity, Immunologic. Killer Cells, Lymphokine-Activated / immunology. Recombinant Fusion Proteins / immunology. T-Lymphocytes / immunology

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  • (PMID = 16939815.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Receptors, Chemokine; 0 / Recombinant Fusion Proteins
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13. Li S: Src kinases as targets for B cell acute lymphoblastic leukaemia therapy. Expert Opin Ther Targets; 2005 Apr;9(2):329-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.
  • The participation of Src kinases in the induction of BCR-ABL-induced B cell acute lymphoblastic leukaemia (B-ALL), but not chronic myeloid leukaemia (CML), demonstrates cell type-specific signalling in Philadelphia chromosome-positive (Ph+) leukaemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / enzymology. Drug Delivery Systems / methods. Protein Kinase Inhibitors / therapeutic use. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 15934919.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 114
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14. 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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15. 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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16. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • METHODS: Stromal cells from marrow core biopsies of 13 CLL patients and 5 normal control subjects were isolated, cultured and confirmed as MSC based on their immunophenotype and capacity to differentiate into three lineages.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.
  • For each CLL patient, interphase FISH analysis to detect the common CLL-associated abnormalities was performed on freshly isolated peripheral blood mononuclear cells (PBMC).

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  • (PMID = 27963169.001).
  • [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. 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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18. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • Bisulfite sequencing of CD 10 type 1 and 2 promoters identified more than 84% of methylated CpG dinucleotides in all three CD10-negative infant ALL cases with MLL/AF4.

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  • (PMID = 27962471.001).
  • [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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19. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • METHODS: In an ongoing phase 1 dose escalation study in sequential cohorts of 3 patients with relapsed/refractory CLL or select B-cell non-Hodgkin's lymphoma, CAL-101 is administered orally twice daily for 28 days per cycle.
  • Partial responses were observed after 2 cycles of 50 mg in a patient with mantle cell lymphoma with 6 prior therapies, and after 1 cycle of 100 mg in a patient with follicular lymphoma with 6 prior therapies, including autologous stem cell transplant.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.
  • CONCLUSIONS: Early results from a phase 1 study of the oral PI3K p110δ inhibitor CAL-101 show that it is well tolerated and has preliminary clinical activity in patients with B-cell malignancies.

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  • (PMID = 27961357.001).
  • [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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20. 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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21. 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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22. 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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23. Krumbholz M, Meinl I, Kümpfel T, Hohlfeld R, Meinl E: Natalizumab disproportionately increases circulating pre-B and B cells in multiple sclerosis. Neurology; 2008 Oct 21;71(17):1350-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natalizumab disproportionately increases circulating pre-B and B cells in multiple sclerosis.
  • Whereas its presumed mode of action is inhibition of T cell/monocyte entry into the brain, little is known about its specific effect on B cells, which are increasingly recognized to participate in MS pathogenesis.
  • We determined numbers of mature and immature lymphocyte subsets by flow cytometry for CD3, CD4, CD8, CD19, CD138, and CD10 in 111 samples.
  • We analyzed marker transcripts for immature hematopoietic cells by quantitative PCR for CD34, Vprebeta1 (pre-B lymphocyte gene 1), and DNTT (terminal deoxynucleotidyltransferase) in 65 samples.
  • RESULTS: Natalizumab therapy increased CD19(+) mature B cells more than other lymphocytes/monocytes in blood (2.8-fold versus 1.3-1.8-fold increase in cells/microL; p < 0.01).
  • Even greater was the increase of immature CD19(+)CD10(+) pre-B cells (7.4-fold; p < 0.01).
  • CONCLUSIONS: Circulating B cells and especially pre-B cells are most prominently elevated among the studied immune cell subsets, raising the possibility that the effects and side effects of natalizumab are partly mediated by actions on B cells.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. B-Lymphocytes / pathology. Multiple Sclerosis, Relapsing-Remitting / immunology. Multiple Sclerosis, Relapsing-Remitting / therapy. Precursor Cells, B-Lymphoid / metabolism. Precursor Cells, B-Lymphoid / pathology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Migration Inhibition / immunology. Humans. Lymphocyte Count. Natalizumab. Prospective Studies. Time Factors

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  • (PMID = 18936427.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Natalizumab
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24. Bankovich AJ, Raunser S, Juo ZS, Walz T, Davis MM, Garcia KC: Structural insight into pre-B cell receptor function. Science; 2007 Apr 13;316(5822):291-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural insight into pre-B cell receptor function.
  • The pre-B cell receptor (pre-BCR) serves as a checkpoint in B cell development.
  • In the 2.7 angstrom structure of a human pre-BCR Fab-like fragment, consisting of an antibody heavy chain (HC) paired with the surrogate light chain, the "unique regions" of VpreB and lambda5 replace the complementarity-determining region 3 (CDR3) loop of an antibody light chain and appear to "probe" the HC CDR3, potentially influencing the selection of the antibody repertoire.
  • Biochemical analysis indicates that the pre-BCR is impaired in its ability to recognize antigen, which, together with electron microscopic visualization of a pre-BCR dimer, suggests ligand-independent oligomerization as the likely signaling mechanism.
  • [MeSH-major] Membrane Glycoproteins / chemistry. Receptors, Antigen, B-Cell / chemistry
  • [MeSH-minor] Animals. Complementarity Determining Regions / chemistry. Complementarity Determining Regions / physiology. Crystallography, X-Ray. Humans. Immunoglobulin Heavy Chains / chemistry. Immunoglobulin Heavy Chains / physiology. Immunoglobulin Light Chains / chemistry. Immunoglobulin Light Chains / physiology. Immunoglobulin Light Chains, Surrogate. Mice. Models, Molecular. Pre-B Cell Receptors. Protein Conformation. Recombinant Proteins. Structure-Activity Relationship

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  • (PMID = 17431183.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2H32/ 2H3N
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI007290
  • [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 / Complementarity Determining Regions; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Light Chains; 0 / Immunoglobulin Light Chains, Surrogate; 0 / Membrane Glycoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell; 0 / Recombinant Proteins
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25. Hendriks RW, Kersseboom R: Involvement of SLP-65 and Btk in tumor suppression and malignant transformation of pre-B cells. Semin Immunol; 2006 Feb;18(1):67-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involvement of SLP-65 and Btk in tumor suppression and malignant transformation of pre-B cells.
  • Signals from the precursor-B cell receptor (pre-BCR) are essential for selection and clonal expansion of pre-B cells that have performed productive immunoglobulin heavy chain V(D)J recombination.
  • In the mouse, the downstream signaling molecules SLP-65 and Btk cooperate to limit proliferation and induce differentiation of pre-B cells, thereby acting as tumor suppressors to prevent pre-B cell leukemia.
  • In contrast, recent observations in human BCR-ABL1(+) pre-B lymphoblastic leukemia cells demonstrate that Btk is constitutively phosphorylated and activated by the BCR-ABL1 fusion protein.
  • [MeSH-major] B-Lymphocytes / metabolism. Carrier Proteins / physiology. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Hematopoietic Stem Cells / metabolism. Phosphoproteins / physiology. Protein-Tyrosine Kinases / physiology. Tumor Suppressor Proteins / physiology

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  • (PMID = 16300960.001).
  • [ISSN] 1044-5323
  • [Journal-full-title] Seminars in immunology
  • [ISO-abbreviation] Semin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Carrier Proteins; 0 / Phosphoproteins; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Agammaglobulinaemia tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 104
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26. Karnowski A, Cao C, Matthias G, Carotta S, Corcoran LM, Martensson IL, Skok JA, Matthias P: Silencing and nuclear repositioning of the lambda5 gene locus at the pre-B cell stage requires Aiolos and OBF-1. PLoS One; 2008;3(10):e3568
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silencing and nuclear repositioning of the lambda5 gene locus at the pre-B cell stage requires Aiolos and OBF-1.
  • The chromatin regulator Aiolos and the transcriptional coactivator OBF-1 have been implicated in regulating aspects of B cell maturation and activation.
  • Mice lacking either of these factors have a largely normal early B cell development.
  • However, when both factors are eliminated simultaneously a block is uncovered at the transition between pre-B and immature B cells, indicating that these proteins exert a critical function in developing B lymphocytes.
  • In mice deficient for Aiolos and OBF-1, the numbers of immature B cells are reduced, small pre-BII cells are increased and a significant impairment in immunoglobulin light chain DNA rearrangement is observed.
  • We identified genes whose expression is deregulated in the pre-B cell compartment of these mice.
  • In particular, we found that components of the pre-BCR, such as the surrogate light chain genes lambda5 and VpreB, fail to be efficiently silenced in double-mutant mice.
  • Strikingly, developmentally regulated nuclear repositioning of the lambda5 gene is impaired in pre-B cells lacking OBF-1 and Aiolos.
  • These studies uncover a novel role for OBF-1 and Aiolos in controlling the transcription and nuclear organization of genes involved in pre-BCR function.

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  • (PMID = 18974788.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ikzf3 protein, mouse; 0 / Immunoglobulin lambda-Chains; 0 / Pou2af1 protein, mouse; 0 / Trans-Activators
  • [Other-IDs] NLM/ PMC2571989
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27. Keenan RA, De Riva A, Corleis B, Hepburn L, Licence S, Winkler TH, Mårtensson IL: Censoring of autoreactive B cell development by the pre-B cell receptor. Science; 2008 Aug 1;321(5889):696-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Censoring of autoreactive B cell development by the pre-B cell receptor.
  • We report here a role for the pre-B cell receptor, composed of Ig heavy and surrogate light chains, in the negative selection of cells expressing Ig heavy chains with the potential to generate autoantibodies.
  • Surrogate light-chain-deficient (SLC-/-) mice harbored elevated levels of antinuclear antibodies (ANAs) in their serum and showed evidence of escape of pre-B cells expressing prototypic autoantibody heavy chains from negative selection, leading to mature autoantibody secreting CD21-CD23- B cells in the periphery.
  • Thus, the pre-B cell receptor appears to censor the development of certain autoantibody-secreting cells and may represent an important factor in multifactorial autoimmune diseases.
  • [MeSH-major] Autoantibodies / blood. Autoimmunity. B-Lymphocytes / immunology. Pre-B Cell Receptors / immunology. Precursor Cells, B-Lymphoid / immunology. Self Tolerance
  • [MeSH-minor] Animals. Antibodies, Antinuclear / biosynthesis. Antibodies, Antinuclear / blood. B-Lymphocyte Subsets / immunology. Complementarity Determining Regions / genetics. Complementarity Determining Regions / immunology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Heavy Chains / immunology. Immunoglobulin Light Chains, Surrogate / genetics. Immunoglobulin Light Chains, Surrogate / immunology. Lymphopoiesis. Mice. Spleen / immunology

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  • (PMID = 18566249.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Autoantibodies; 0 / Complementarity Determining Regions; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Light Chains, Surrogate; 0 / Pre-B Cell Receptors
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28. Klein F, Feldhahn N, Herzog S, Sprangers M, Mooster JL, Jumaa H, Müschen M: BCR-ABL1 induces aberrant splicing of IKAROS and lineage infidelity in pre-B lymphoblastic leukemia cells. Oncogene; 2006 Feb 16;25(7):1118-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCR-ABL1 induces aberrant splicing of IKAROS and lineage infidelity in pre-B lymphoblastic leukemia cells.
  • Pre-B lymphoblastic leukemia cells carrying a BCR-ABL1 gene rearrangement exhibit an undifferentiated phenotype.
  • Comparing the genome-wide gene expression profiles of normal B-cell subsets and BCR-ABL1+ pre-B lymphoblastic leukemia cells by SAGE, the leukemia cells show loss of B lymphoid identity and aberrant expression of myeloid lineage-specific molecules.
  • Consistent with this, BCR-ABL1+ pre-B lymphoblastic leukemia cells exhibit defective expression of IKAROS, a transcription factor needed for early lymphoid lineage commitment.
  • As shown by inducible expression of BCR-ABL1 in human and murine B-cell precursor cell lines, BCR-ABL1 induces the expression of a dominant-negative IKAROS splice variant, termed IK6.
  • Comparing matched leukemia sample pairs from patients before and during therapy with the BCR-ABL1 kinase inhibitor STI571 (Imatinib), inhibition of BCR-ABL1 partially corrected aberrant expression of IK6 and lineage infidelity of the leukemia cells.
  • To elucidate the contribution of IK6 to lineage infidelity in BCR-ABL1+ cell lines, IK6 expression was silenced by RNA interference.
  • Upon inhibition of IK6, BCR-ABL1+ leukemia cells partially restored B lymphoid lineage commitment.
  • Therefore, we propose that BCR-ABL1 induces aberrant splicing of IKAROS, which interferes with lineage identity and differentiation of pre-B lymphoblastic leukemia cells.
  • [MeSH-major] Alternative Splicing. Ikaros Transcription Factor / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Benzamides. Cell Line, Tumor. Cell Lineage / genetics. Cell Nucleus / chemistry. Fusion Proteins, bcr-abl. Gene Expression Profiling. Gene Silencing. Humans. Imatinib Mesylate. Mice. Piperazines / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / pharmacology

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  • (PMID = 16205638.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / IKZF1 protein, human; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 148971-36-2 / Ikaros Transcription Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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29. Melchers F: B cell development and its deregulation to transformed states at the pre-B cell receptor-expressing pre-BII cell stage. Curr Top Microbiol Immunol; 2005;294:1-17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B cell development and its deregulation to transformed states at the pre-B cell receptor-expressing pre-BII cell stage.
  • This chapter will review the scenario of normal B cell development--from the decision of a lymphoid progenitor to enter the B-lineage, over the stages of the generation of the repertoires of antigen-receptor (immunoglobulin)-expressing cells, to the response of mature B cells to develop memory and plasma cells--highlighting some of the cellular stages and the molecular mechanisms that can generate and select transformed states of cells.
  • The scenarios for pre-B lymphoma (lymphocytic leukaemia) development are discussed in more detail.
  • [MeSH-major] B-Lymphocytes / cytology. B-Lymphocytes / immunology. Receptors, Antigen, B-Cell / metabolism
  • [MeSH-minor] Animals. Apoptosis. B-Cell-Specific Activator Protein / metabolism. Cell Differentiation. Cell Proliferation. Cell Transformation, Neoplastic. Gene Rearrangement, B-Lymphocyte. Humans. Interleukin-7 / metabolism. Lymphoma, B-Cell / etiology. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / immunology. Mice. Mutation. Receptors, Interleukin-7 / metabolism. Signal Transduction

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  • (PMID = 16323425.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Interleukin-7; 0 / Pax5 protein, mouse; 0 / Receptors, Antigen, B-Cell; 0 / Receptors, Interleukin-7
  • [Number-of-references] 40
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30. Vettermann C, Jäck HM: The pre-B cell receptor: turning autoreactivity into self-defense. Trends Immunol; 2010 May;31(5):176-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pre-B cell receptor: turning autoreactivity into self-defense.
  • These cells then assemble microHCs with surrogate light chains (SLC) into a pre-B cell receptor (pre-BCR).
  • We propose that the pre-BCR has evolved from an ancient autoreactive BCR, since the SLC is an autoreactive entity that binds to the pre-BCR itself and to other self-antigens.
  • Abrogation of autoreactivity in the SLC diminishes pre-BCR signaling and impairs the clonal expansion of pre-B cells producing functional microHCs.
  • Since SLC expression is restricted to pre-B cells, the autoreactivity encoded by the pre-BCR can be utilized to pre-select the antibody repertoire, while simultaneously avoiding the formation of autoreactive B lymphocytes.
  • [MeSH-major] Autoimmunity. Pre-B Cell Receptors / immunology

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20356792.001).
  • [ISSN] 1471-4981
  • [Journal-full-title] Trends in immunology
  • [ISO-abbreviation] Trends Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Pre-B Cell Receptors
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31. Boag JM, Beesley AH, Firth MJ, Freitas JR, Ford J, Brigstock DR, de Klerk NH, Kees UR: High expression of connective tissue growth factor in pre-B acute lymphoblastic leukaemia. Br J Haematol; 2007 Sep;138(6):740-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of connective tissue growth factor in pre-B acute lymphoblastic leukaemia.
  • In recent years microarrays have been used extensively to characterize gene expression in acute lymphoblastic leukaemia (ALL).
  • Few studies, however, have analysed normal haematopoietic cell populations to identify altered gene expression in ALL.
  • We used oligonucleotide microarrays to compare the gene expression profile of paediatric precursor-B (pre-B) ALL specimens with two control cell populations, normal CD34(+) and CD19(+)IgM(-) cells, to focus on genes linked to leukemogenesis.
  • One gene, connective tissue growth factor (CTGF, also known as CCN2), had exceptionally high expression, which was confirmed in three independent leukaemia studies.
  • Protein studies using Western blot analysis demonstrated the presence of CTGF in ALL cell-conditioned media.
  • These findings indicate that CTGF is secreted by pre-B ALL cells and may play a role in the pathophysiology of this disease.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Immediate-Early Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17760805.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTGF protein, human; 0 / Culture Media, Conditioned; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 139568-91-5 / Connective Tissue Growth Factor
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32. Clark MR, Cooper AB, Wang LD, Aifantis I: The pre-B cell receptor in B cell development: recent advances, persistent questions and conserved mechanisms. Curr Top Microbiol Immunol; 2005;290:87-103
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pre-B cell receptor in B cell development: recent advances, persistent questions and conserved mechanisms.
  • B cell development is a process tightly regulated by the orchestrated signaling of cytokine receptors, the pre-B cell receptor (BCR) and the B cell receptor (BCR).
  • It commences with common lymphoid progenitors (CLP) up-regulating the expression of B cell-related genes and committing to the B cell lineage.
  • Cytokine signaling (IL-7, stem cell factor, FLT3-L) is essential at this stage of development as it suppresses cell death, sustains proliferation and facilitates heavy chain rearrangements.
  • As a result of heavy chain recombination, the pre-BCR is expressed, which then becomes the primary determiner of survival, cell cycle entry and allelic exclusion.
  • In this review, we discuss the mechanisms of B cell lineage commitment and describe the signaling pathways that are initiated by the pre-BCR.
  • Finally, we compare pre-BCR and pre-TCR structure, signal transduction and function, drawing parallels between early pre-B and pre-T cell development.
  • [MeSH-minor] Animals. Cell Differentiation. Cell Lineage. Gene Expression Regulation. Humans. Mice. Pre-B Cell Receptors. Receptors, Antigen, B-Cell. Signal Transduction

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  • (PMID = 16480040.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell
  • [Number-of-references] 90
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33. Bernard N, Devevey L, Jacquemont C, Chrétien P, Helissey P, Guillosson JJ, Arock M, Nafziger J: A new model of pre-B acute lymphoblastic leukemia chemically induced in rats. Exp Hematol; 2005 Oct;33(10):1130-9
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  • [Title] A new model of pre-B acute lymphoblastic leukemia chemically induced in rats.
  • OBJECTIVE: Although B acute lymphoblastic leukemia (B-ALL) is the most common leukemia among children, no chemically inducible model of this leukemia has yet been described in vivo.
  • METHODS: Leukemia was chemically induced in male WKAH/Hkm rats by a nitrosourea derivative, N-butylnitrosourea (BNU), an alkylating agent, administered orally 5 days a week for 24 weeks.
  • Development of leukemia was monitored by clinical observation, follow-up of blood parameters, and appearance of blast cells in peripheral blood samples.
  • The phenotype of the leukemia was determined by cytological examination, cytochemical reactions, and by immunophenotyping of bone marrow cells using various markers.
  • The feasibility of leukemia transplantation was investigated.
  • RESULTS: We observed the appearance of acute leukemia in 60% of the rats treated with BNU.
  • Of these, 65% developed pre-B-ALL, which was serially transplantable to healthy WKAH/Hkm male rats.
  • Clonality determined by immunoglobulin gene rearrangement sequencing disclosed that the pre-B-ALL were mostly oligoclonal.
  • CONCLUSION: This new in vivo model of inducible pre-B-ALL might be useful for investigating the effects of co-initiating or promoting agents suspected to be involved in leukemia development, and for disclosing new molecular events leading to leukemogenic processes.
  • [MeSH-major] Carcinogens / toxicity. Leukemia, Experimental / pathology. Nitrosourea Compounds / toxicity. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16219535.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosourea Compounds; 869-01-2 / N-nitrosobutylurea
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34. Rossi B, Espeli M, Schiff C, Gauthier L: Clustering of pre-B cell integrins induces galectin-1-dependent pre-B cell receptor relocalization and activation. J Immunol; 2006 Jul 15;177(2):796-803
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clustering of pre-B cell integrins induces galectin-1-dependent pre-B cell receptor relocalization and activation.
  • Interactions between B cell progenitors and bone marrow stromal cells are essential for normal B cell differentiation.
  • We have previously shown that an immune developmental synapse is formed between human pre-B and stromal cells in vitro, leading to the initiation of signal transduction from the pre-BCR.
  • This process relies on the direct interaction between the pre-BCR and the stromal cell-derived galectin-1 (GAL1) and is dependent on GAL1 anchoring to cell surface glycosylated counterreceptors, present on stromal and pre-B cells.
  • Pre-B cell integrins and their stromal cell ligands (ADAM15/fibronectin), together with the pre-BCR and GAL1, form a homogeneous lattice at the contact area between pre-B and stromal cells.
  • Moreover, integrin and pre-BCR relocalizations into the synapse are synchronized and require actin polymerization.
  • Finally, cross-linking of pre-B cell integrins in the presence of GAL1 is sufficient for driving pre-BCR recruitment into the synapse, leading to the initiation of pre-BCR signaling.
  • These results suggest that during pre-B/stromal cell synapse formation, relocalization of pre-B cell integrins mediated by their stromal cell ligands drives pre-BCR clustering and activation, in a GAL1-dependent manner.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Aggregation. Galectin 1 / physiology. Hematopoietic Stem Cells / metabolism. Integrins / metabolism. Membrane Glycoproteins / metabolism. Receptor Aggregation
  • [MeSH-minor] Actins / metabolism. Antibodies, Monoclonal / metabolism. Cell Communication / immunology. Cell Line, Tumor. Coculture Techniques. Cross-Linking Reagents / metabolism. Humans. Ligands. Pre-B Cell Receptors. Receptors, Antigen, B-Cell. Stromal Cells / metabolism

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  • (PMID = 16818733.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Antibodies, Monoclonal; 0 / Cross-Linking Reagents; 0 / Galectin 1; 0 / Integrins; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell
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35. Espeli M, Rossi B, Mancini SJ, Roche P, Gauthier L, Schiff C: Initiation of pre-B cell receptor signaling: common and distinctive features in human and mouse. Semin Immunol; 2006 Feb;18(1):56-66
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  • [Title] Initiation of pre-B cell receptor signaling: common and distinctive features in human and mouse.
  • B cell development in the bone marrow is a highly regulated process and expression of a functional pre-BCR represents a crucial checkpoint, common to human and mouse.
  • In this review, we discuss pre-BCR analogies and differences between the two species leading to pre-B cell differentiation and proliferation.
  • In addition, the mechanisms triggering pre-BCR activation are reviewed, taking into account the recent report of heparan sulfates and galectin 1 as stromal cell-derived pre-BCR ligands.
  • Finally, ligand-induced pre-BCR activation models are proposed on the bases of the differences reported for pre-BCR and IL7 dependencies in the two species.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Differentiation / physiology. Membrane Glycoproteins / physiology. Signal Transduction / physiology
  • [MeSH-minor] Amino Acid Sequence. Animals. Humans. Mice. Molecular Sequence Data. Pre-B Cell Receptors. Receptors, Antigen, B-Cell

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  • (PMID = 16337808.001).
  • [ISSN] 1044-5323
  • [Journal-full-title] Seminars in immunology
  • [ISO-abbreviation] Semin. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell
  • [Number-of-references] 102
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36. Correa-González LC, Mandeville PB, Manrique-Dueñas J, Alejo-González F, Salazar-Martínez A, de Pérez-Ramírez OJ, Hernández-Sierra JF: [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients]. Gac Med Mex; 2005 Nov-Dec;141(6):477-82
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  • [Title] [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients].
  • [Transliterated title] Valor pronóstico del inmunofenotipo en la respuesta temprana de la leucemia aguda linfoblástica pre-B en niños.
  • OBJECTIVE: To determine the prognostic value of preB immunophenotype and its variants on early treatment response among of acute pediatric lymphoblast leukemia.
  • PATIENTS AND METHODS: A case-control study nested in a cohort was carried out with male and female patients 15 years and younger with recently diagnosed pre-B lymphoblast leukemia.
  • A panel of B, T, monoclonal antibodies of the myelo-monocytic and megakaryocytic cell type was used.
  • We identified 29 cases with late pre-B immune phenotype, 19 cases with common pre B and 6 cases with early preB immunophenotype.
  • No association was found between the pre-B immunophenotype, age and leukocyte count with early treatment response (p=0.264).
  • CONCLUSIONS: We need to pay special emphasis on early treatment response in children with lymphoblast leukemia as our study did not corroborate the common finding that clinical factors and immune phenotype can be predictive factors.
  • [MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 16381501.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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37. Schuh W, Meister S, Herrmann K, Bradl H, Jäck HM: Transcriptome analysis in primary B lymphoid precursors following induction of the pre-B cell receptor. Mol Immunol; 2008 Jan;45(2):362-75
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  • [Title] Transcriptome analysis in primary B lymphoid precursors following induction of the pre-B cell receptor.
  • Pre-BCR signals are part of a checkpoint where early precursor (pre-) B cells with a pairing Ig muH chain (muHC) are clonally expanded before they differentiate into IgL-rearranging, resting pre-B cells.
  • A pre-BCR consists of two muHCs, two surrogate L chains and the signal transducer Igalpha/Igbeta.
  • The molecular circuits by which the pre-BCR controls proliferation and differentiation of pre-B cells are poorly characterized.
  • Therefore, we identified the differential transcriptome by genome-wide expression profiling in progenitor (pro-) B cells from a Rag2-deficient mouse, in which the expression of a transgenic muHC and thus a pre-BCR as well as pre-BCR-mediated clonal expansion can be controlled by tetracycline (muHC-inducible mouse).
  • This analysis revealed that pre-BCR signals upregulate components of the BCR signalosome, open the IgL chain (LC) locus and induce the krüppel-like transcription factor KLF2, a key regulator of quiescence and lymphocyte migration.
  • Hence, pre-BCR signals establish the molecular network for BCR signaling even before the production of an IgLC and induce the expression of KLF2, a candidate for controlling clonal expansion and migration of functional pre-B cells.
  • [MeSH-major] B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Gene Expression Regulation. Pre-B Cell Receptors / genetics. Stem Cells / immunology. Stem Cells / metabolism. Transcription, Genetic


38. Bao L, Gross SA, Ryder J, Wang X, Ji M, Chen Y, Yang Y, Zhu S, Irons RD: Adult precursor B lymphoblastic leukemia in Shanghai, China: characterization of phenotype, cytogenetics and outcome for 137 consecutive cases. Int J Hematol; 2009 May;89(4):431-7
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  • [Title] Adult precursor B lymphoblastic leukemia in Shanghai, China: characterization of phenotype, cytogenetics and outcome for 137 consecutive cases.
  • Acute lymphoblastic leukemia (ALL) accounts for 20-30% of adult leukemia in the West.
  • However, detailed studies of B-cell-specific ALL in adult Asian populations are lacking.
  • We diagnosed and characterized 137 consecutive cases of precursor B lymphoblastic leukemia (precursor B-cell ALL) presented to our laboratory in Shanghai using the WHO 2001 classification system.
  • In contrast to Western studies, females (71) outnumbered males (66) partly due to an increased prevalence of the CD10- pro B-cell phenotype.
  • Females with a CD10- pro B-cell phenotype exhibited significantly better overall survival than males.
  • The most common cytogenetic abnormality was the Philadelphia chromosome (PH/BCR/ABL) which was found in approximately 37% of the cases.
  • Cases of precursor B cell ALL lacking the PH/BCR/ABL genotype exhibited a pronounced age-dependent, gender prevalence with a modal age in the sixth decade for females compared to the second decade for males.
  • These findings suggest significant geographic heterogeneity in precursor B-cell ALL which may be of both etiological and therapeutic significance.
  • [MeSH-major] Chromosome Aberrations. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19322628.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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39. Wossning T, Herzog S, Köhler F, Meixlsperger S, Kulathu Y, Mittler G, Abe A, Fuchs U, Borkhardt A, Jumaa H: Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells. J Exp Med; 2006 Dec 25;203(13):2829-40
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  • [Title] Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells.
  • The nonreceptor protein spleen tyrosine kinase (Syk) is a key mediator of signal transduction in a variety of cell types, including B lymphocytes.
  • We show that deregulated Syk activity allows growth factor-independent proliferation and transforms bone marrow-derived pre-B cells that are then able to induce leukemia in mice.
  • Syk-transformed pre-B cells show a characteristic pattern of tyrosine phosphorylation, increased c-Myc expression, and defective differentiation.
  • Treatment of Syk-transformed pre-B cells with a novel Syk-specific inhibitor (R406) reduces tyrosine phosphorylation and c-Myc expression.
  • In addition, R406 treatment removes the developmental block and allows the differentiation of the Syk-transformed pre-B cells into immature B cells.
  • Because R406 treatment also prevents the proliferation of c-Myc-transformed pre-B cells, our data indicate that endogenous Syk kinase activity may be required for the survival of pre-B cells transformed by other oncogenes.
  • Collectively, our data suggest that Syk is a protooncogene involved in the transformation of lymphocytes, thus making Syk a potential target for the treatment of leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Differentiation / physiology. Intracellular Signaling Peptides and Proteins / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Adoptive Transfer. Animals. Benzamides. Cell Line. Cell Proliferation / drug effects. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Intercellular Signaling Peptides and Proteins / pharmacology. Intercellular Signaling Peptides and Proteins / physiology. Leukemia / genetics. Leukemia / pathology. Leukemia / therapy. Mice. Mice, Inbred BALB C. Mice, Knockout. Oxazines / pharmacology. Phospholipase C gamma / genetics. Phospholipase C gamma / metabolism. Phosphorylation / drug effects. Piperazines / pharmacology. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-myc / genetics. Proto-Oncogene Proteins c-myc / metabolism. Pyridines / pharmacology. Pyrimidines / pharmacology. Receptors, Antigen, B-Cell / genetics. Spleen / drug effects. Spleen / metabolism. Spleen / pathology. Transfection

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  • (PMID = 17130299.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / N4-(2,2-dimethyl-3-oxo-4H-pyrid(1,4)oxazin-6-yl)-5-fluoro-N2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamine; 0 / Oxazines; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyridines; 0 / Pyrimidines; 0 / Rag2 protein, mouse; 0 / Receptors, Antigen, B-Cell; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.4.3 / Phospholipase C gamma
  • [Other-IDs] NLM/ PMC2118175
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40. van Loo PF, Dingjan GM, Maas A, Hendriks RW: Surrogate-light-chain silencing is not critical for the limitation of pre-B cell expansion but is for the termination of constitutive signaling. Immunity; 2007 Sep;27(3):468-80
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  • [Title] Surrogate-light-chain silencing is not critical for the limitation of pre-B cell expansion but is for the termination of constitutive signaling.
  • The pre-B cell receptor (pre-BCR), composed of immunoglobulin mu heavy chain and the surrogate light chain (SLC) proteins lambda5 and Vpreb, signals for proliferation and maturation of developing pre-B cells.
  • It has been assumed that pre-B cells stop cycling by the pre-BCR-mediated downregulation of SLC transcription.
  • We generated transgenic mice expressing SLC throughout B cell development and, remarkably, found that enforced SLC expression had no effect on pre-B cell proliferation or differentiation.
  • However, in the presence of conventional immunoglobulin light chains, SLC components had the capacity to induce constitutive BCR internalization, secondary immunoglobulin light-chain rearrangement, and a severe developmental arrest of immature B cells, dependent on the adaptor protein Slp65.
  • Thus, the silencing of SLC genes is not essential for the limitation of pre-B cell proliferation, but is required for the prevention of constitutive activation of B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Cell Differentiation / immunology. Gene Silencing. Hematopoietic Stem Cells / immunology. Immunoglobulin Light Chains / genetics. Immunoglobulin Light Chains / immunology. Membrane Glycoproteins / genetics. Membrane Glycoproteins / immunology
  • [MeSH-minor] Animals. Cell Proliferation. Flow Cytometry. Gene Rearrangement, B-Lymphocyte, Light Chain / immunology. Immunoglobulin Light Chains, Surrogate. Lymphocyte Activation / immunology. Mice. Mice, Transgenic. Signal Transduction / immunology

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  • (PMID = 17869135.001).
  • [ISSN] 1074-7613
  • [Journal-full-title] Immunity
  • [ISO-abbreviation] Immunity
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Light Chains; 0 / Immunoglobulin Light Chains, Surrogate; 0 / Membrane Glycoproteins
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41. Herzog S, Storch B, Jumaa H: Dual role of the adaptor protein SLP-65: organizer of signal transduction and tumor suppressor of pre-B cell leukemia. Immunol Res; 2006;34(2):143-55

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dual role of the adaptor protein SLP-65: organizer of signal transduction and tumor suppressor of pre-B cell leukemia.
  • B cell development is characterized by a coordinated progression through defined stages that are controlled at several checkpoints.
  • Signals from the pre-B cell receptor (pre-BCR) are essential for regulated transition from the pre-B cell stage.
  • Recent findings indicate an additional function of SLP-65 as a tumor suppressor that regulates pre-B cell proliferation.
  • We will discuss here the potential mechanisms by which SLP-65 controls the pre-B cell checkpoint.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / physiology. B-Lymphocytes / cytology. Carrier Proteins / physiology. Phosphoproteins / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Signal Transduction. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Proliferation. Humans. Membrane Glycoproteins / metabolism. Pre-B Cell Receptors. Protein-Tyrosine Kinases. Receptors, Antigen, B-Cell

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  • (PMID = 16760574.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Carrier Proteins; 0 / Membrane Glycoproteins; 0 / Phosphoproteins; 0 / Pre-B Cell Receptors; 0 / Receptors, Antigen, B-Cell; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Agammaglobulinaemia tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 71
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42. Kim JY, Park SK, Kim HG, Cho SJ, Kim J, Kang CJ: The HSS3/4 enhancer of Crlz1-IgJ locus is another target of EBF in the pre-B cell stage of B cell development. Immunol Lett; 2006 Sep 15;107(1):63-70
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  • [Title] The HSS3/4 enhancer of Crlz1-IgJ locus is another target of EBF in the pre-B cell stage of B cell development.
  • Unexpectedly, the HSS3/4 enhancer was also found to be opened in the pre-B cells.
  • However, this opening of HSS3/4 enhancer in the pre-B cells could not be related to the IgJ gene expression, because neither the IgJ promoter was opened nor its gene was expressed at the pre-B cell stage of B cell development.
  • Instead, it was postulated that the opened HSS3/4 enhancer might act on some other nearby promoter in pre-B cells, which is now guessed to be the Crlz1 promoter located at 22.5 kb from it.
  • In consistence with this pre-B cell-specific opening of the HSS3/4 enhancer, a pre-B cell-specific in vivo footprint on a sequence similar to the EBF-binding consensus was detected within the enhancer.
  • In this paper, we show that the protein causing the pre-B cell-specific in vivo footprint on a sequence similar to the EBF-binding consensus is truly EBF as judged by EMSA using various oligo-DNA competitors and anti-EBF antibodies.
  • Also, as expected from other previous reports, EBF was shown to be expressed highly in pre-B cells, but very little or not in immature B, mature B and plasma cells using both the cell lines and FACS-sorted normal primary cells.
  • Convincingly, mutations within the EBF site of HSS3/4 enhancer were shown to significantly impair the HSS3/4 enhancer activity in the pre-B cells, but not in the plasma cells.
  • [MeSH-major] B-Lymphocytes / cytology. Cell Differentiation / physiology. DNA-Binding Proteins / genetics. Enhancer Elements, Genetic / genetics. Nerve Tissue Proteins / genetics. Promoter Regions, Genetic / genetics. Trans-Activators / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Base Sequence. Blotting, Western. Cell Line. Electrophoretic Mobility Shift Assay. Flow Cytometry. Immunoglobulin J-Chains / genetics. Immunoglobulin J-Chains / immunology. Mice. Molecular Sequence Data

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  • (PMID = 16962668.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Crlz1protein, mouse; 0 / DNA-Binding Proteins; 0 / Ebf1 protein, mouse; 0 / Immunoglobulin J-Chains; 0 / Nerve Tissue Proteins; 0 / Trans-Activators; 0 / Transcription Factors
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43. Yuroff AS, Jefcoate CR, Czuprynski CJ: Close proximity, but not VLA-4-dependent adherence between pre-B cells and bone marrow stromal cells, is required for DMBA-induced apoptosis of pre-B cells in vitro. Toxicol Lett; 2005 Apr 10;156(2):253-60
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  • [Title] Close proximity, but not VLA-4-dependent adherence between pre-B cells and bone marrow stromal cells, is required for DMBA-induced apoptosis of pre-B cells in vitro.
  • We have previously reported that 7,12-dimethylbenz[a]anthracene (DMBA) induced apoptosis in precursor B lymphocytes (pre-B cells) only when they were co-cultured with bone marrow stromal (BMS) cells.
  • The goal of this research was to determine whether this process was dependent on the adherence of the pre-B cells and stromal cells.
  • Conditioned media from DMBA-treated BMS cells induced apoptosis in pre-B cells, but only when the pre-B cells were co-cultured with stromal cells.
  • When the stromal cells and pre-B cells were separated with a membrane filter insert, DMBA-induced apoptosis of the pre-B cells was blocked suggesting that contact with or close proximity to stromal cells was required for apoptosis.
  • The addition of an anti-VLA-4 Mab disrupted adherence of pre-B cells to the stromal cell monolayer, but did not diminish the numbers of apoptotic pre-B cells.
  • The results of this study support the hypothesis stromal cells and pre-B cells must be in close proximity for apoptosis to occur, but direct interaction via VLA-4 and VCAM-1 is unlikely to be required for this response.
  • [MeSH-minor] Animals. Cell Adhesion. Cell Line. Environmental Pollutants / toxicity. Mice. Rats. Stromal Cells / physiology. Vascular Cell Adhesion Molecule-1 / physiology

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  • (PMID = 15737488.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA81493
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benz(a)Anthracenes; 0 / Environmental Pollutants; 0 / Integrin alpha4beta1; 0 / Vascular Cell Adhesion Molecule-1; 2564-65-0 / 7,12-dihydroxymethylbenz(a)anthracene
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44. Storch B, Meixlsperger S, Jumaa H: The Ig-alpha ITAM is required for efficient differentiation but not proliferation of pre-B cells. Eur J Immunol; 2007 Jan;37(1):252-60
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  • [Title] The Ig-alpha ITAM is required for efficient differentiation but not proliferation of pre-B cells.
  • Signals from the pre-B cell receptor (pre-BCR) mediated by the cytoplasmic tails of Ig-alpha/Ig-beta are essential for developing B cells.
  • To analyze the role of Ig-alpha ITAM and non-ITAM tyrosines in pre-BCR signaling, we reconstituted individual tyrosine mutants of Ig-alpha in src homology 2 domain-containing leukocyte protein of 65 kDa (SLP-65)/Ig-alpha double-deficient pre-B cells.
  • We show that the Ig-alpha mutants led to comparable pre-BCR expression on the cell surface, while the pre-BCR-induced tyrosine phosphorylation was different.
  • We further show that the reconstitution of Ig-alpha and the resulting pre-BCR expression led to enrichment of the pre-BCR-expressing cells in vitro irrespective of the introduced Ig-alpha mutation.
  • Our results indicate that surface IL-7 receptor expression is modulated by the pre-BCR, thereby increasing the IL-7 sensitivity of the respective cells.
  • In contrast to the comparable pre-B cell proliferation, however, the Ig-alpha mutants differed in their capacity to induce calcium flux and activate efficient pre-B cell differentiation.
  • Together, our data suggest that ITAM tyrosines and Y204 are required for efficient pre-B cell differentiation but not proliferation.
  • [MeSH-major] Antigens, CD79 / physiology. B-Lymphocyte Subsets / cytology. Cell Differentiation / immunology. Cell Proliferation. Stem Cells / cytology. Stem Cells / immunology. Tyrosine
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / biosynthesis. Adaptor Proteins, Signal Transducing / genetics. Amino Acid Motifs / genetics. Animals. Cells, Cultured. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / genetics. Membrane Glycoproteins / physiology. Mice. Mice, Inbred BALB C. Mutagenesis, Site-Directed. Phosphorylation. Pre-B Cell Receptors. Receptors, Antigen, B-Cell / biosynthesis. Receptors, Antigen, B-Cell / genetics. Receptors, Antigen, B-Cell / physiology. Signal Transduction / genetics. Signal Transduction / immunology


45. Wang X, Yuling H, Yanping J, Xinti T, Yaofang Y, Feng Y, Ruijin X, Li W, Lang C, Jingyi L, Zhiqing T, Jingping O, Bing X, Li Q, Chang AE, Sun Z, Youxin J, Jinquan T: CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells. J Immunol; 2007 Sep 1;179(5):2880-8

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  • [Title] CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells.
  • In a previous study, we have reported that ligation of CCL19-CCR7 and CXCL13-CXCR5 activates paternally expressed gene 10 (PEG10), resulting in an enhancement of apoptotic resistance in B-cell acute lymphocytic leukemia (B-ALL) CD23+CD5+ B cells.
  • CCL19/CXCL13-activated B-ALL CD23+CD5+ B cells, in turn, increase IL-10 expression in syngeneic CD8+ T cells in a B cell-derived IL-10-dependent manner and requiring a cell-cell contact.
  • IL-10 secreted from B-ALL CD23+CD5+ B cells in vitro impairs tumor-specific CTL responses of syngeneic CD8+ T cells.
  • Moreover, using a short hairpin RNA to knockdown PEG10, we provide direct evidence that increased expression of PEG10 in B-ALL CD23+CD5+ B cells is involved in malignant B-T cell interaction, contributing to the up-regulation of IL-10 expression, as well as to the impairment of cytotoxicity of syngeneic CD8+ T cells.
  • [MeSH-major] B-Lymphocytes / immunology. Burkitt Lymphoma / immunology. CD8-Positive T-Lymphocytes / immunology. Chemokine CCL19 / physiology. Chemokine CXCL13 / physiology. Immunologic Surveillance / immunology

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  • [ErratumIn] J Immunol. 2007 Nov 15;179(10):7184
  • (PMID = 17709502.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CXCL13 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / PEG10 protein, human; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Receptors, IgE; 130068-27-8 / Interleukin-10
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46. Chiaretti S, Guarini A, De Propris MS, Tavolaro S, Intoppa S, Vitale A, Iacobelli S, Elia L, Ariola C, Ritz J, Foà R: ZAP-70 expression in acute lymphoblastic leukemia: association with the E2A/PBX1 rearrangement and the pre-B stage of differentiation and prognostic implications. Blood; 2006 Jan 1;107(1):197-204
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  • [Title] ZAP-70 expression in acute lymphoblastic leukemia: association with the E2A/PBX1 rearrangement and the pre-B stage of differentiation and prognostic implications.
  • We evaluated the expression of 2 members of the Syk family, ZAP-70 and Syk, in acute lymphoblastic leukemia (ALL) samples, using data derived from a series of 33 T-ALL and 95 B-lineage adult ALL patients analyzed by oligonucleotide arrays.
  • Of the B-lineage ALL cases, 37 were BCR/ABL+, 10 were ALL1/AF4+, 5 were E2A/PBX1+, and 43 carried no known molecular abnormality.
  • A higher ZAP-70 expression was also observed in the pre-B group (P < .001).
  • In ALL, ZAP-70 expression is associated with the E2A/PBX1 rearrangement and pre-B stage and may have a prognostic role and be a candidate molecule for targeted therapies.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] Adult. Cell Differentiation. Child. Enzyme Precursors / genetics. Follow-Up Studies. Gene Expression Profiling. Gene Rearrangement. Humans. Immunoglobulin mu-Chains. Intracellular Signaling Peptides and Proteins. Prognosis. Protein-Tyrosine Kinases / genetics. Recurrence

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  • (PMID = 16160012.001).
  • [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 / Enzyme Precursors; 0 / Homeodomain Proteins; 0 / Immunoglobulin mu-Chains; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins, Fusion; 146150-85-8 / E2A-Pbx1 fusion protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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47. Herzog S, Jumaa H: The N terminus of the non-T cell activation linker (NTAL) confers inhibitory effects on pre-B cell differentiation. J Immunol; 2007 Feb 15;178(4):2336-43
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  • [Title] The N terminus of the non-T cell activation linker (NTAL) confers inhibitory effects on pre-B cell differentiation.
  • SLP-65 and the linker for activation of T cells (LAT) are central adaptor proteins that link the activated pre-BCR to downstream events in pre-B cells.
  • Recently, a new transmembrane adaptor called NTAL/LAB/LAT2 (hereafter called NTAL for non-T cell activation linker) with striking functional and structural similarity to LAT has been identified in B cells.
  • In this study, we compare the function of NTAL and LAT in pre-BCR signaling and show that, in contrast to LAT, NTAL does not induce pre-BCR down-regulation, calcium flux, or pre-B cell differentiation.
  • This insertion rendered NTAL capable of activating pre-BCR down-regulation and calcium flux.
  • Unexpectedly however, the ability of NTAL to induce calcium flux was not sufficient to promote pre-B cell differentiation, suggesting that the PLC-gamma binding motif has only partial effects on NTAL-mediated pre-BCR signaling.
  • By generating chimeric swap mutants, we identified the N terminus of NTAL as an inhibitory domain that prevents pre-B cell differentiation while allowing pre-BCR down-regulation and receptor-mediated calcium flux.
  • Our data suggest that, in addition to the missing PLC-gamma1/2 binding motif, the N terminus is responsible for the functional differences between NTAL and LAT in pre-B cells.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / immunology. Adaptor Proteins, Vesicular Transport / immunology. B-Lymphocytes / immunology. Calcium Signaling / immunology. Cell Differentiation / immunology. Membrane Proteins / immunology. Phosphoproteins / immunology. Proto-Oncogene Proteins c-bcr / immunology
  • [MeSH-minor] Amino Acid Motifs / genetics. Amino Acid Motifs / immunology. Animals. Down-Regulation / immunology. Mice. Mutation. Protein Binding / immunology. Type C Phospholipases / genetics. Type C Phospholipases / immunology

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  • (PMID = 17277139.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adaptor Proteins, Vesicular Transport; 0 / LAB protein, mouse; 0 / Lat protein, mouse; 0 / Membrane Proteins; 0 / Phosphoproteins; EC 2.7.11.1 / Bcr protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr; EC 3.1.4.- / Type C Phospholipases
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48. 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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49. Welner R, Swett DJ, Pelsue SC: Age-related loss of bone marrow pre-B- and immature B-lymphocytes in the autoimmune-prone flaky skin mutant mice. Autoimmunity; 2005 Sep;38(6):399-408
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  • [Title] Age-related loss of bone marrow pre-B- and immature B-lymphocytes in the autoimmune-prone flaky skin mutant mice.
  • We observed a rapid age-related loss of the pre-B and immature B cells.
  • It was also noted that an accumulation of early precursor populations occurs coincident with the loss of Fr.D and Fr.E bone marrow B cell populations indicating a developmental block or accumulation of pro-B cells in 7 and 10 week old fsn/fsn mice.
  • Our data suggests changes in the fsn/fsn bone-marrow microenvironment that results in senescence of B cell development.
  • [MeSH-minor] Age Factors. Animals. Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. Cell Differentiation / genetics. Cell Differentiation / immunology. Cells, Cultured. Kinetics. Mice

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  • (PMID = 16278144.001).
  • [ISSN] 0891-6934
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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50. Hewitt SL, Farmer D, Marszalek K, Cadera E, Liang HE, Xu Y, Schlissel MS, Skok JA: Association between the Igk and Igh immunoglobulin loci mediated by the 3' Igk enhancer induces 'decontraction' of the Igh locus in pre-B cells. Nat Immunol; 2008 Apr;9(4):396-404
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  • [Title] Association between the Igk and Igh immunoglobulin loci mediated by the 3' Igk enhancer induces 'decontraction' of the Igh locus in pre-B cells.
  • Variable-(diversity)-joining (V(D)J) recombination at loci encoding the immunoglobulin heavy chain (Igh) and immunoglobulin light chain (Igk) takes place sequentially during successive stages in B cell development.
  • Using three-dimensional DNA fluorescence in situ hybridization, here we identify a lineage-specific and stage-specific interchromosomal association between these two loci that marks the transition between Igh and Igk recombination.
  • Colocalization occurred between pericentromerically located alleles in pre-B cells and was mediated by the 3' Igk enhancer.

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  • (PMID = 18297074.001).
  • [ISSN] 1529-2916
  • [Journal-full-title] Nature immunology
  • [ISO-abbreviation] Nat. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL48702; United States / NIAID NIH HHS / AI / R01 AI040227; United States / NHLBI NIH HHS / HL / R01 HL048702; United States / NIAID NIH HHS / AI / R01 AI40227; United States / NIAID NIH HHS / AI / R37 AI040227-12; United States / NHLBI NIH HHS / HL / R01 HL048702-16; United States / NIAID NIH HHS / AI / R37 AI040227; United States / NHLBI NIH HHS / HL / HL048702-16; United States / NIAID NIH HHS / AI / AI040227-12; United Kingdom / Wellcome Trust / /
  • [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 / IgK; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulins
  • [Other-IDs] NLM/ NIHMS74977; NLM/ PMC2583163
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51. Qiu Y, Morii E, Tomita Y, Zhang B, Matsumura A, Kitaichi M, Okumura M, Aozasa K: Prognostic significance of pre B cell leukemia transcription factor 2 (PBX2) expression in non-small cell lung carcinoma. Cancer Sci; 2009 Jul;100(7):1198-209
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  • [Title] Prognostic significance of pre B cell leukemia transcription factor 2 (PBX2) expression in non-small cell lung carcinoma.
  • Previous studies on the mammary carcinoma cell line have shown that the pre B cell leukemia transcription factor 1 (PBX1) was a transcription factor for valosin-containing protein (VCP), which is involved in invasion and metastasis of cancers.
  • The roles of PBX1 and PBX2, a highly homologous transcription factor to PBX1, for expression of VCP were examined in the cell lines from non-small cell lung cancer (NSCLC).
  • The effects of PBX1 and PBX2 on VCP expression were examined with siRNA in A549 and PC14 NSCLC cell lines.
  • Expression levels of VCP mRNA significantly decreased when PBX2 but not PBX1 expression was knocked down in NSCLC cell lines.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Homeodomain Proteins / metabolism. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Adenosine Triphosphatases / genetics. Adenosine Triphosphatases / metabolism. Adult. Aged. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. RNA, Small Interfering / metabolism. Transfection

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  • (PMID = 19356220.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Homeodomain Proteins; 0 / PBX2 protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / CDC48 protein
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52. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
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  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Thus, the presence of aberrant antigen expression detectable by flow cytometry may be critical for diagnosis of B-ALL and detection of minimal residual disease.
  • Of 200 cases, 9.0% aberrantly expressed T cell-associated antigens.
  • Specific aberrancies correlate with recurrent cytogenetic abnormalities in B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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53. Troeger A, Gudowius S, Escherich G, den Boer ML, Glouchkova L, Ackermann B, Meisel R, Laws HJ, Groeger M, Wessalowski R, Willers R, Harbott J, Pieters R, Goebel U, Janka-Schaub GE, Hanenberg H, Dilloo D: High nerve growth factor receptor (p75NTR) expression is a favourable prognostic factor in paediatric B cell precursor-acute lymphoblastic leukaemia. Br J Haematol; 2007 Nov;139(3):450-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High nerve growth factor receptor (p75NTR) expression is a favourable prognostic factor in paediatric B cell precursor-acute lymphoblastic leukaemia.
  • In spite of its established role in B-cell function and identification as a prognostically favourable marker in a number of malignancies, little is known about the expression pattern and prognostic significance of p75NTR in B cell precursor-acute lymphoblastic leukaemia (BCP-ALL).
  • p75NTR expression was prospectively studied on primary ALL-blasts in a cohort of paediatric patients with common ALL (n = 86) and preB-ALL (n = 34) treated within the Co-operative study group for childhood acute lymphoblastic leukaemia (CoALL) protocol, CoALL06-97.
  • In patients classified as low-risk at diagnosis, p75NTR expression was significantly higher than in high-risk patients (P = 0.001).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Nerve Tissue Proteins / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Receptors, Nerve Growth Factor / blood

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  • (PMID = 17910636.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NGFR protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Receptors, Nerve Growth Factor
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54. Klein F, Feldhahn N, Mooster JL, Sprangers M, Hofmann WK, Wernet P, Wartenberg M, Müschen M: Tracing the pre-B to immature B cell transition in human leukemia cells reveals a coordinated sequence of primary and secondary IGK gene rearrangement, IGK deletion, and IGL gene rearrangement. J Immunol; 2005 Jan 1;174(1):367-75
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  • [Title] Tracing the pre-B to immature B cell transition in human leukemia cells reveals a coordinated sequence of primary and secondary IGK gene rearrangement, IGK deletion, and IGL gene rearrangement.
  • The BCR-ABL1 kinase expressed in acute lymphoblastic leukemia (ALL) drives malignant transformation of pre-B cells and prevents further development.
  • STI571 treatment of leukemia patients induced expression of the Ig L chain-associated transcription factors IRF4 and SPIB, up-regulation of RAG1 and RAG2, Ckappa and Clambda germline transcription, and rearrangement of Ig kappa L chain (IGK) and Ig lambda L chain (IGL) genes.
  • However, STI571-treated pre-B ALL cells expressed lambda L, but almost no kappa L chains.
  • Thus, inhibition of BCR-ABL1 in pre-B ALL cells 1) recapitulates early B cell development, 2) directly shows that IGK, KDE, and IGL genes are rearranged in sequential order, and 3) provides a model for Ig L chain gene regulation in the human.
  • [MeSH-major] B-Lymphocytes / drug effects. Gene Rearrangement, B-Lymphocyte, Light Chain / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Kinase Inhibitors / therapeutic use. Stem Cells / drug effects

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  • (PMID = 15611260.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / DEF6 protein, human; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Guanine Nucleotide Exchange Factors; 0 / Homeodomain Proteins; 0 / IgK; 0 / Immunoglobulins; 0 / Nuclear Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RAG2 protein, human; 0 / Transcription Factors; 0 / V(D)J recombination activating protein 2; 128559-51-3 / RAG-1 protein; 148350-00-9 / SPIB protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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55. Hinman RM, Nichols WA, Diaz TM, Gallardo TD, Castrillon DH, Satterthwaite AB: Foxo3-/- mice demonstrate reduced numbers of pre-B and recirculating B cells but normal splenic B cell sub-population distribution. Int Immunol; 2009 Jul;21(7):831-42
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Foxo3-/- mice demonstrate reduced numbers of pre-B and recirculating B cells but normal splenic B cell sub-population distribution.
  • B cell antigen receptor (BCR) cross-linking promotes proliferation and survival of mature B cells.
  • Phosphoinositide-3-kinase-mediated down-regulation of pro-apoptotic and anti-mitogenic genes such as the Foxo family of transcription factors is an important component of this process.
  • While Foxo1, Foxo3 and Foxo4 bind the same DNA sequence, the differential control of their expression upon B cell activation suggests that they may have unique functions in the B lineage.
  • To begin to address this issue, we evaluated B cell development and function in Foxo3-/- mice.
  • No effect of Foxo3 deficiency was observed with respect to the following parameters in the splenic B cell compartment: sub-population distribution, proliferation, in vitro differentiation and expression of the Foxo target genes cyclin G2 and B cell translocation gene 1.
  • A significant reduction in pre-B cell numbers was also observed in Foxo3-/- bone marrow.
  • Thus, Foxo3 makes a unique contribution to B cell development, B cell localization and control of Ig levels.

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  • (PMID = 19502585.001).
  • [ISSN] 1460-2377
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR024196-04; United States / NCRR NIH HHS / RR / 1K26RR024196; United States / NCRR NIH HHS / RR / K26 RR024196-04; United States / NIAID NIH HHS / AI / AI049248; United States / NCRR NIH HHS / RR / K26 RR024196; United States / NIAID NIH HHS / AI / T32 AI 005284-28
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Butadienes; 0 / Ccng2 protein, mouse; 0 / Chromones; 0 / Cyclin G2; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Forkhead Transcription Factors; 0 / FoxO3 protein, mouse; 0 / FoxO4 protein, mouse; 0 / Foxo1 protein, mouse; 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Interleukin-7; 0 / Morpholines; 0 / Nitriles; 0 / Receptors, Antigen, B-Cell; 0 / U 0126; 0 / anti-IgM; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 83HN0GTJ6D / Cyclosporine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ PMC2699488
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56. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Specific blockers of angiogenesis are now being introduced into early clinical trials with encouraging results.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Bone Marrow Cells / metabolism. Child. Child, Preschool. Female. Fibroblast Growth Factor 2 / biosynthesis. Fibroblast Growth Factor 2 / genetics. Humans. Infant. Male. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Nitric Oxide Synthase Type II / biosynthesis. Nitric Oxide Synthase Type II / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transforming Growth Factor beta / biosynthesis. Transforming Growth Factor beta / genetics. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor C / biosynthesis. Vascular Endothelial Growth Factor C / genetics

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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57. Nygren MK, Døsen G, Hystad ME, Stubberud H, Funderud S, Rian E: Wnt3A activates canonical Wnt signalling in acute lymphoblastic leukaemia (ALL) cells and inhibits the proliferation of B-ALL cell lines. Br J Haematol; 2007 Feb;136(3):400-13
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt3A activates canonical Wnt signalling in acute lymphoblastic leukaemia (ALL) cells and inhibits the proliferation of B-ALL cell lines.
  • Acute lymphoblastic leukaemia (ALL) is the most common malignancy in children.
  • This study found that Wnt3A induced beta-catenin accumulation in both primary B-ALL cells and B-ALL leukaemia cell lines.
  • Further, Wnt3A was shown to induce nuclear translocation of beta-catenin and TCF/Lef-1 dependent transcriptions in the B-ALL cell line Nalm-6.
  • Functional analyses showed that Wnt3A inhibited the proliferation of several, but not all, B-ALL cell lines studied.
  • [MeSH-major] Burkitt Lymphoma / metabolism. Signal Transduction / physiology. Wnt Proteins / pharmacology
  • [MeSH-minor] Blotting, Western / methods. Cell Line, Tumor. Cell Proliferation. Gene Expression Profiling. Humans. Microscopy, Confocal. Oligonucleotide Array Sequence Analysis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Transcription Factors / genetics. Transcription Factors / metabolism. Tumor Cells, Cultured. Wnt3 Protein. Wnt3A Protein. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17156404.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / WNT3A protein, human; 0 / WNT5A protein, human; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / Wnt3A Protein; 0 / beta Catenin
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58. Sabaawy HE, Azuma M, Embree LJ, Tsai HJ, Starost MF, Hickstein DD: TEL-AML1 transgenic zebrafish model of precursor B cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2006 Oct 10;103(41):15166-71
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TEL-AML1 transgenic zebrafish model of precursor B cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a clonal disease that evolves through the accrual of genetic rearrangements and/or mutations within the dominant clone.
  • The TEL-AML1 (ETV6-RUNX1) fusion in precursor-B (pre-B) ALL is the most common genetic rearrangement in childhood cancer; however, the cellular origin and the molecular pathogenesis of TEL-AML1-induced leukemia have not been identified.
  • TEL-AML1 expression in all lineages, but not lymphoid-restricted expression, led to progenitor cell expansion that evolved into oligoclonal B-lineage ALL in 3% of the transgenic zebrafish.
  • This leukemia was transplantable to conditioned wild-type recipients.
  • We demonstrate that TEL-AML1 induces a B cell differentiation arrest, and that leukemia development is associated with loss of TEL expression and elevated Bcl2/Bax ratio.
  • The TEL-AML1 transgenic zebrafish models human pre-B ALL, identifies the molecular pathways associated with leukemia development, and serves as the foundation for subsequent genetic screens to identify modifiers and leukemia therapeutic targets.

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  • (PMID = 17015828.001).
  • [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 / K22 CA120626; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TEL-AML1 fusion protein; 0 / bcl-2-Associated X Protein
  • [Other-IDs] NLM/ PMC1622794
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59. Tröger A, Siepermann M, Mahotka C, Wethkamp N, Bülle H, Laws HJ, Escherich G, Janka-Schaub G, Göbel U, Dilloo D: Role of survivin splice variants in pediatric acute precursor B lymphoblastic leukemia. Klin Padiatr; 2007 May-Jun;219(3):127-33
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of survivin splice variants in pediatric acute precursor B lymphoblastic leukemia.
  • BACKGROUND: Survivin, a member of the inhibitor of apoptosis protein (IAP) family is transiently expressed at low levels during normal hematopoesis but profoundly overexpressed in adult leukemia potentially contributing to leukemogenesis due to deregulated apoptosis and defective cell cycle control.
  • PATIENTS AND METHODS: We therefore determined the expression of the functional survivin splice variants performing RT- and real-time PCR in a purely pediatric cohort of 20 patients suffering from precursor B-ALL (BCP-ALL).
  • RESULTS: Here, we demonstrate for the first time in pediatric patients with precursor B-ALL an association between lower survivin-2B expression and affiliation to the high risk group.
  • [MeSH-major] Apoptosis / genetics. Genetic Variation / genetics. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Isoforms / genetics

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  • (PMID = 17525905.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Coumarins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 41806-51-3 / W10294A
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60. Jiang JG, Roman E, Nandula SV, Murty VV, Bhagat G, Alobeid B: Congenital MLL-positive B-cell acute lymphoblastic leukemia (B-ALL) switched lineage at relapse to acute myelocytic leukemia (AML) with persistent t(4;11) and t(1;6) translocations and JH gene rearrangement. Leuk Lymphoma; 2005 Aug;46(8):1223-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Congenital MLL-positive B-cell acute lymphoblastic leukemia (B-ALL) switched lineage at relapse to acute myelocytic leukemia (AML) with persistent t(4;11) and t(1;6) translocations and JH gene rearrangement.
  • Congenital acute leukemia is a rare form of childhood leukemia, in which lineage conversion at relapse is very rarely reported.
  • Here we describe a case of congenital B-cell acute lymphoblastic leukemia (B-ALL) with t(4;11) and t(1;6) translocations, which at relapse underwent a switch to monocytic lineage with persistence of the original cytogenetic translocations and clonal rearrangement of the JH gene.
  • Similar to the other described cases of congenital acute leukemia with lineage conversion, our case had a MLL gene rearrangement and followed an aggressive clinical course.
  • [MeSH-major] Burkitt Lymphoma / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Lineage. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 6 / genetics. Cytogenetic Analysis. Disease Progression. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin J-Chains / genetics. Immunophenotyping. Infant, Newborn. Prognosis. Recurrence

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  • (PMID = 16085566.001).
  • [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 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin J-Chains; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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61. Tuğcu A, Yildirimtürk O, Aytekin S: [The diagnostic value of N-terminal B-type natriuretic peptide in diastolic heart failure: comparison with echocardiographic findings]. Turk Kardiyol Dern Ars; 2009 Mar;37(2):112-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The diagnostic value of N-terminal B-type natriuretic peptide in diastolic heart failure: comparison with echocardiographic findings].
  • OBJECTIVES: We investigated the value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) to diagnose diastolic heart failure (DHF) without left ventricular (LV) hypertrophy.
  • STUDY DESIGN: The study included 33 patients (17 males, 16 females) with DHF, who had acute pulmonary congestion and LV ejection fraction (EF) >50% on admission, and were stable for at least six months of follow-up.
  • [MeSH-major] Heart Failure, Diastolic / diagnosis. Natriuretic Peptide, Brain / blood. Peptide Fragments / blood

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  • [CommentIn] Turk Kardiyol Dern Ars. 2009 Sep;37(6):439-40 [20019465.001]
  • (PMID = 19404033.001).
  • [ISSN] 1016-5169
  • [Journal-full-title] Türk Kardiyoloji Derneği arşivi : Türk Kardiyoloji Derneğinin yayın organıdır
  • [ISO-abbreviation] Turk Kardiyol Dern Ars
  • [Language] tur
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Peptide Fragments; 0 / pro-brain natriuretic peptide (1-76); 114471-18-0 / Natriuretic Peptide, Brain
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62. van der Velden VH, de Bie M, van Wering ER, van Dongen JJ: Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease. Haematologica; 2006 May;91(5):679-82
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  • [Title] Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease.
  • We analyzed the frequency and characteristics of Vk-Jk and Vlambda-Jlambda rearrangements inpatients with precursor-B-acute lymphoblastic leukemia (ALL) and evaluated the applicability of these rearrangements as targets for minimal residual disease (MRD) detection.
  • Vk-Jk rearrangements were particularly frequent in common-ALL, children between 5-10 years, and TEL-AML1-positive patients.
  • Vk-Jk and Vlambda-Jlambda rearrangements showed a good stability between diagnosis and relapse and reached good sensitivities in real-time quantitative polymerase chain reaction analysis.
  • Our data show that Vk-Jk and Vlambda-Jlambda rearrangements can be successfully applied for MRD detection in a subset of patients with precursor-B-ALL.
  • [MeSH-major] DNA, Neoplasm / genetics. Gene Rearrangement, B-Lymphocyte, Light Chain. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16627258.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / Immunoglobulin Variable Region
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63. Ma S, Turetsky A, Trinh L, Lu R: IFN regulatory factor 4 and 8 promote Ig light chain kappa locus activation in pre-B cell development. J Immunol; 2006 Dec 1;177(11):7898-904
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  • [Title] IFN regulatory factor 4 and 8 promote Ig light chain kappa locus activation in pre-B cell development.
  • Previous studies have shown that B cell development is blocked at the pre-B cell stage in IFN regulatory factor (IRF)4 (pip) and IRF8 (IFN consensus sequence binding protein) double mutant mice (IRF4,8(-/-)).
  • In this study, the molecular mechanism by which IRF4,8 regulate pre-B cell development was further investigated.
  • We show that IRF4,8 function in a B cell intrinsic manner to control pre-B cell development.
  • IRF4,8(-/-) mice expressing a Bcl-2 transgene fail to rescue pre-B cell development, suggesting that the defect in B cell development in IRF4,8(-/-) mice is not due to a lack of survival signal.
  • IRF4,8(-/-) pre-B cells display a high proliferation index that may indirectly inhibit the L chain rearrangement.
  • However, forced cell cycle exit induced by IL-7 withdrawal fails to rescue the development of IRF4,8(-/-) pre-B cells, suggesting that cell cycle exit by itself is not sufficient to rescue the development of IRF4,8(-/-) pre-B cells and that IRF4,8 may directly regulate the activation of L chain loci.
  • Using retroviral mediated gene transduction, we show that IRF4 and IRF8 function redundantly to promote pre-B cell maturation and the generation of IgM(+) B cells.
  • Molecular analysis indicates that IRF4, when expressed in IRF4,8(-/-) pre-B cells, induces kappa germline transcription, enhances V(D)J rearrangement activity at the kappa locus, and promotes L chain rearrangement and transcription.
  • Thus, IRF4,8 control pre-B cell development, at least in part, by promoting the activation of the kappa locus.
  • [MeSH-major] B-Lymphocytes / cytology. Cell Differentiation / immunology. Immunoglobulin kappa-Chains / metabolism. Interferon Regulatory Factors / metabolism. Stem Cells / cytology

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  • (PMID = 17114461.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI 67891
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin kappa-Chains; 0 / Interferon Regulatory Factors
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64. Safa M, Kazemi A, Zand H, Azarkeivan A, Zaker F, Hayat P: Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues. Apoptosis; 2010 Feb;15(2):196-203
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  • [Title] Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues.
  • Exposure of cells to chemotherapeutic drug doxorubicin, a DNA-damaging agent, induces an increase in the levels and activity of the wild-type p53 protein.
  • Here we show that elevation of cAMP in pre-B acute lymphoblastic leukemia NALM-6 cells significantly attenuated phosphorylation state of p53 at Ser6, Ser9, Ser15, Ser20, Ser37, Ser46 and Ser392 upon exposure to doxorubicin.
  • [MeSH-major] Apoptosis / drug effects. Cyclic AMP / pharmacology. Doxorubicin / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Serine / metabolism
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Caspase 3 / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Checkpoint Kinase 2. DNA Damage. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Okadaic Acid / pharmacology. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Phosphoserine / metabolism. Protein Phosphatase 1 / metabolism. Protein Phosphatase 2 / metabolism. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19882354.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 17885-08-4 / Phosphoserine; 1W21G5Q4N2 / Okadaic Acid; 452VLY9402 / Serine; 80168379AG / Doxorubicin; E0399OZS9N / Cyclic AMP; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.16 / Protein Phosphatase 2; EC 3.1.3.16 / protein phosphatase 2C; EC 3.4.22.- / Caspase 3
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65. Stanciu-Herrera C, Morgan C, Herrera L: Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines. Leuk Res; 2008 Apr;32(4):625-32
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  • [Title] Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines.
  • The monoclonal antibodies (MAbs) HD37 and RFB4 bind to receptors on precursor B acute lymphoblastic leukemia (ALL) cells.
  • HD37 and not RFB4 increased the in vitro cytotoxicity of daunorubicin (DNR) and vincristine (VCR) in three Pre-B ALL cell lines.

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  • (PMID = 17706771.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101897-04; United States / NCI NIH HHS / CA / K01 CA101897-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Antineoplastic Agents, Phytogenic; 0 / Sialic Acid Binding Ig-like Lectin 2; 5J49Q6B70F / Vincristine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS42262; NLM/ PMC2276361
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66. Niizuma H, Fujii K, Sato A, Fujiwara I, Takeyama J, Imaizumi M: PTHrP-independent hypercalcemia with increased proinflammatory cytokines and bone resorption in two children with CD19-negative precursor B acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Dec;49(7):990-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PTHrP-independent hypercalcemia with increased proinflammatory cytokines and bone resorption in two children with CD19-negative precursor B acute lymphoblastic leukemia.
  • Hypercalcemia in childhood acute lymphoblastic leukemia (ALL) is rare and occasionally associated with parathyroid hormone-related protein (PTHrP).
  • We report two children with precursor B ALL who had marked hypercalcemia (15.8 and 16.6 mg/dl, respectively) and disseminated osteolysis.
  • These findings suggest that increased osteoclastic bone resorption via stimulation with TNF-alpha and IL-6 may be mechanism causing PTHrP-independent hypercalcemia in some patients with precursor B ALL lacking CD19 expression.
  • [MeSH-major] Bone Resorption / complications. Cytokines / blood. Diphosphonates / administration & dosage. Hypercalcemia / complications. Parathyroid Hormone-Related Protein / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 16496289.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Bone Density Conservation Agents; 0 / Cytokines; 0 / Diphosphonates; 0 / Parathyroid Hormone-Related Protein; 90032-33-0 / deoxypyridinoline
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67. Poitras JL, Dal Cin P, Aster JC, Deangelo DJ, Morton CC: Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia. Genes Chromosomes Cancer; 2008 Oct;47(10):884-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia.
  • In addition, less common aberrations (particularly gene fusions) involving JAK2 have been described in acute leukemias.
  • In this report, we identify SSBP2 as a new JAK2 fusion partner in a patient with pre-B cell acute lymphocytic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 9 / genetics. DNA-Binding Proteins / genetics. Janus Kinase 2 / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Humans. In Situ Hybridization, Fluorescence. Male. Mutation. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18618714.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA066996-11A1
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / SSBP2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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68. Kuiper RP, Waanders E, van der Velden VH, van Reijmersdal SV, Venkatachalam R, Scheijen B, Sonneveld E, van Dongen JJ, Veerman AJ, van Leeuwen FN, van Kessel AG, Hoogerbrugge PM: IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL. Leukemia; 2010 Jul;24(7):1258-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL.
  • Relapse is the most common cause of treatment failure in pediatric acute lymphoblastic leukemia (ALL) and is often difficult to predict.
  • To explore the prognostic impact of recurrent DNA copy number abnormalities on relapse, we performed high-resolution genomic profiling of 34 paired diagnosis and relapse ALL samples.
  • Recurrent lesions detected at diagnosis, including PAX5, CDKN2A and EBF1, were frequently absent at relapse, indicating that they represent secondary events that may be absent in the relapse-prone therapy-resistant progenitor cell.
  • A targeted copy number screen in an unselected cohort of 131 precursor B-ALL cases, enrolled in the dexamethasone-based Dutch Childhood Oncology Group treatment protocol ALL9, revealed that IKZF1 deletions are significantly associated with poor relapse-free and overall survival rates.
  • Consequently, IKZF1 deletion status allowed the prospective identification of 53% of the relapse-prone NHR-classified patients within this subgroup and, therefore, serves as one of the strongest predictors of relapse at the time of diagnosis with high potential for future risk stratification.
  • [MeSH-major] Gene Deletion. Ikaros Transcription Factor / genetics. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics


69. Mihalcik SA, Tschumper RC, Jelinek DF: Transcriptional and post-transcriptional mechanisms of BAFF-receptor dysregulation in human B lineage malignancies. Cell Cycle; 2010 Dec 15;9(24):4884-92
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  • In this study, we used primary cells and cell lines to interrogate the mechanisms underlying aberrant BAFF-R expression in precursor B acute lymphoblastic leukemia (precursor B-ALL) and mature B chronic lymphocytic leukemia (CLL).
  • Here we demonstrate the aberrant expression of BAFF-R in precursor B-ALL cell lines and reveal that these cells acquire BAFF-R expression through premature transcriptional activation of the BAFF-R promoter in coordination with regulatory transcription factor c-Rel.
  • Investigations using primary CLL cells provide a crucial counterpoint through their paucity of BAFF-R relative to their benign mature B cell counterparts, which we establish as functionally significant in its depletion of the CLL cells' BAFF-binding capacity.

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  • (PMID = 21099364.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA062242; United States / NCI NIH HHS / CA / R01 CA105258; United States / NCI NIH HHS / CA / CA062242; United States / NCI NIH HHS / CA / CA105258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / B-Cell Activation Factor Receptor
  • [Other-IDs] NLM/ PMC3047811
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70. Nowell MA, Richards PJ, Fielding CA, Ognjanovic S, Topley N, Williams AS, Bryant-Greenwood G, Jones SA: Regulation of pre-B cell colony-enhancing factor by STAT-3-dependent interleukin-6 trans-signaling: implications in the pathogenesis of rheumatoid arthritis. Arthritis Rheum; 2006 Jul;54(7):2084-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of pre-B cell colony-enhancing factor by STAT-3-dependent interleukin-6 trans-signaling: implications in the pathogenesis of rheumatoid arthritis.
  • OBJECTIVE: To determine whether interleukin-6 (IL-6) trans-signaling directs the expression of pre-B cell colony-enhancing factor (PBEF) in vitro and in vivo.
  • METHODS: Complementary DNA from rheumatoid arthritis (RA) synovial fibroblasts treated with IL-6 and soluble IL-6 receptor (sIL-6R) was used to probe a cytokine microarray.
  • PBEF regulation by the IL-6-related cytokines, IL-6, sIL-6R, oncostatin M (OSM), IL-11, and leukemia inhibitory factor (LIF) was determined by reverse transcription-polymerase chain reaction analysis.
  • IL-6-mediated STAT-3 regulation of PBEF was determined using a cell-permeable STAT-3 inhibitor peptide.
  • Antigen-induced arthritis (AIA) was induced in wild-type (IL-6(+/+)) and IL-6-deficient (IL-6(-/-)) mice.
  • [MeSH-minor] Animals. Cells, Cultured. Disease Progression. Gene Expression Regulation / drug effects. Humans. Interleukin-11 / pharmacology. Leukemia Inhibitory Factor. Mice. Mice, Knockout. Nicotinamide Phosphoribosyltransferase. Oligonucleotide Array Sequence Analysis. Oncostatin M. Receptors, Interleukin-6 / genetics. Receptors, Interleukin-6 / physiology. Synovial Fluid / drug effects. Synovial Fluid / metabolism. Synovial Membrane / drug effects. Synovial Membrane / metabolism. Synovial Membrane / pathology

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  • (PMID = 16802343.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-11; 0 / Interleukin-6; 0 / LIF protein, human; 0 / Leukemia Inhibitory Factor; 0 / Lif protein, mouse; 0 / OSM protein, human; 0 / Osm protein, mouse; 0 / Receptors, Interleukin-6; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 106956-32-5 / Oncostatin M; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
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71. Aiglová K, Ehrmann J Jr, Ehrmann J: [Non-invasive detection of liver fibrosis in patients with chronic hepatitis C]. Cas Lek Cesk; 2007;146(6):542-5
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  • [MeSH-major] Hepatitis C, Chronic / complications. Liver Cirrhosis / diagnosis. Liver Cirrhosis / virology

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  • (PMID = 17650594.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Biomarkers; 0 / alpha-Macroglobulins; EC 2.6.1.1 / Aspartate Aminotransferases
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72. Mowafi F, Cagigi A, Matskova L, Björk O, Chiodi F, Nilsson A: Chemokine CXCL12 enhances proliferation in pre-B-ALL via STAT5 activation. Pediatr Blood Cancer; 2008 Apr;50(4):812-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemokine CXCL12 enhances proliferation in pre-B-ALL via STAT5 activation.
  • BACKGROUND: CXCL12 (SDF-1alpha) is a chemokine, which plays an important role in normal B-cell lymphopoesis, migration and homing to the bone marrow (BM) and previous studies have suggested a role for CXCL12 and its receptor CXCR4 in the pathogenesis of ALL.
  • Signalling via the CXCL12/CXCR4 axis was further characterized in an in vitro model using the pre-B leukaemic cell line Nalm-6.
  • RESULTS: The serum level of CXCL12 in children at diagnosis of pre-B-ALL is significantly higher than in healthy children (4.8 (0-32) ng/ml vs. 0 (0-3.2) ng/ml, P < 0.001).
  • In addition, we found that recombinant CXCL12 enhances pre-B leukaemic cell proliferation in vitro.
  • The CXCL12/CXCR4 axis is able to initiate functional signalling and we show that STAT5 is activated in CD19+ leukaemic cells from BM of ALL patients and in the leukaemic cell line Nalm-6.
  • CONCLUSION: Our findings suggest that CXCL12 may have a role in leukaemic cell proliferation and survival during childhood ALL.
  • [MeSH-major] Cell Proliferation. Chemokine CXCL12 / blood. Chemokine CXCL12 / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Enzyme Activation / physiology. Enzyme-Linked Immunosorbent Assay. Female. Flow Cytometry. Humans. Immunohistochemistry. Infant. Male. Precursor Cells, B-Lymphoid / pathology. Receptors, CXCR4 / metabolism. Recombinant Proteins / metabolism

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17914737.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor
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73. Gudowius S, Recker K, Laws HJ, Dirksen U, Tröger A, Wieczorek U, Furlan S, Göbel U, Hanenberg H: Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL. Klin Padiatr; 2006 Nov-Dec;218(6):327-33
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  • [Title] Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL.
  • BACKGROUND: Contemporary risk adapted treatment protocols for childhood acute lymphoblastic leukemia (ALL) rely on accurate risk assessment strategies for disease re-occurrence by incorporating clinical parameters as well as immunological, molecular and cytogenetic features of the blasts at initial manifestation.
  • PATIENTS AND METHODS: In order to identify target antigen structures, we analyzed the immunological expression profiles of blasts from 181 patients with B-cell precursor ALL treated at our institution in 11 years according to the CoALL-92/97/03 protocols.
  • Blasts were classified according to the EGIL guidelines as 9 proB-, 110 common (c-) and 62 preB-ALL.
  • CD10 was expressed on all c-/preB-ALL and absent on proB-ALL cells.
  • CD20 was expressed on 11-37 % of B-cell precursor ALL samples.
  • CD34 positive blasts were found in 89, 83 and 68 % of patients with proB-, c- and preB-ALL, respectively.
  • < 20 % CD45(+) blasts were found in 11, 19 and 18 % of patients with proB-, c- and preB-ALL.
  • CD33(+) was expressed on 33, 29 and 21 % of patients samples with proB-, c- and preB-ALL.
  • Analyses of the immunological profile of blasts in 9 consecutive children with relapse revealed that the antigen expression profile varied little compared to the initial diagnosis for CD10, CD19, CD22 and HLA-DR.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD19 / analysis. Burkitt Lymphoma / immunology. HLA-DR Antigens / analysis. Immunotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sialic Acid Binding Ig-like Lectin 2 / analysis

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  • (PMID = 17080335.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 2
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74. 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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75. Adam RL, Silva RC, Pereira FG, Leite NJ, Lorand-Metze I, Metze K: The fractal dimension of nuclear chromatin as a prognostic factor in acute precursor B lymphoblastic leukemia. Cell Oncol; 2006;28(1-2):55-9
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  • [Title] The fractal dimension of nuclear chromatin as a prognostic factor in acute precursor B lymphoblastic leukemia.
  • The fractal nature of the DNA arrangement has been postulated to be a common feature of all cell nuclei.
  • We investigated the prognostic importance of the fractal dimension (FD) of chromatin in blasts of patients with acute precursor B lymphoblastic leukemia (B-ALL).
  • White blood cell count (WBC), age and mean fluorescence intensity of CD45 (MFICD45) were all unfavorable prognostic factors in univariate analyses.
  • [MeSH-major] Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / pathology. Cell Nucleus / pathology. Chromatin / pathology. Fractals

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  • (PMID = 16675881.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Azure Stains; 0 / Chromatin
  • [Other-IDs] NLM/ PMC4615964
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76. Reiser M: [Viral hepatitis B und C]. Med Klin (Munich); 2009 May 15;104(5):356-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Viral hepatitis B und C].
  • [Transliterated title] Virushepatitis B und C.
  • Chronic hepatitis B (HBV) and C virus (HCV) infection can lead to liver cirrhosis, hepatocellular carcinoma and death.
  • Treatment of these worldwide prevalent infectious diseases is subject to intensive research efforts with development of new antiviral substances and optimization of treatment strategies using molecular markers.
  • The goal of HBV and HCV treatment is control and elimination of viral replication, respectively, thereby preventing hepatitis-associated complications.
  • While interferon alpha is used less frequently to treat hepatitis B today, it is still (in the pegylated or albumin-fused form) an essential component of hepatitis C therapy.
  • The growing number of targeted therapies such as new nucleus(t)ide analogs, HCV protease and RNA polymerase inhibitors and other new compounds has added complexity to the treatment of viral hepatitis.
  • This update summarizes the current standard of care as well as new developments in chronic hepatitis B and C therapy.
  • [MeSH-major] Antiviral Agents / therapeutic use. Hepatitis B, Chronic / drug therapy. Hepatitis C, Chronic / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Cross-Sectional Studies. Drug Resistance, Viral. Humans. Virus Replication / drug effects

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  • (PMID = 19444416.001).
  • [ISSN] 1615-6722
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiviral Agents
  • [Number-of-references] 35
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77. 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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  • [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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78. Reid AG, Seppa L, von der Weid N, Niggli FK, Betts DR: A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Feb;165(1):64-9
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  • [Title] A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia.
  • Structural rearrangements involving the short arm of chromosome 12 are common in acute lymphoblastic leukemia (ALL) and often involve the TEL locus at 12p13.
  • We identified a t(12;17) in 2 of 398 childhood ALL patients karyotyped at presentation in our institute.
  • Both cases had a precursor-B immunophenotype and were CD10 negative and CD33 positive.
  • Comparison of these and previously published cases demonstrates that the translocation predominately occurs in children and young adults with precursor B-ALL and is typically characterized by low CD10 expression and high CD33 expression.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 17. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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  • (PMID = 16490598.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
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79. Reid GS, She K, Terrett L, Food MR, Trudeau JD, Schultz KR: CpG stimulation of precursor B-lineage acute lymphoblastic leukemia induces a distinct change in costimulatory molecule expression and shifts allogeneic T cells toward a Th1 response. Blood; 2005 May 1;105(9):3641-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CpG stimulation of precursor B-lineage acute lymphoblastic leukemia induces a distinct change in costimulatory molecule expression and shifts allogeneic T cells toward a Th1 response.
  • Pediatric precursor B acute lymphoblastic leukemia (B-ALL) cells express low levels of costimulatory molecules and are generally poor stimulators of T-cell responses.
  • In this study, we evaluated the impact of CpG stimulation on precursor B-ALL cell lines and pediatric patient-derived samples.
  • In contrast to both nonleukemic B-cell precursors and mature B cells, the response of precursor B-ALL cells was characterized by increased CD40 expression but only small changes in CD86 levels and no induction of CD80 expression.
  • These results demonstrate the functional relevance of CpG stimulation of precursor B-ALL cells and provide a rational basis for study of these agents for use in treatment of this disease.
  • [MeSH-major] Dinucleoside Phosphates / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Th1 Cells / immunology
  • [MeSH-minor] Animals. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Line, Tumor. DNA-Binding Proteins / physiology. Humans. Interleukins / biosynthesis. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Oligodeoxyribonucleotides / pharmacology. Receptors, Cell Surface / physiology. T-Lymphocyte Subsets / immunology. Toll-Like Receptor 9. Transplantation, Heterologous

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  • (PMID = 15650062.001).
  • [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 / DNA-Binding Proteins; 0 / Dinucleoside Phosphates; 0 / Interleukins; 0 / Oligodeoxyribonucleotides; 0 / Receptors, Cell Surface; 0 / TLR9 protein, human; 0 / Tlr9 protein, mouse; 0 / Toll-Like Receptor 9; 2382-65-2 / cytidylyl-3'-5'-guanosine
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80. 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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  • [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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81. Morović M, Troselj-Vukić B, Klarin I, Hrstić I, Ostojić R: [Chronic hepatitis B therapy]. Acta Med Croatica; 2009 Dec;63(5):391-5
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  • [Title] [Chronic hepatitis B therapy].
  • [Transliterated title] Terapija kronicnog hepatitisa B.
  • Chronic hepatitis B is associated with the development of cirrhosis in more than one third of patients and in a large proportion of patients with hepatocellular carcinoma.
  • Current standard treatment includes pegylated interferon alfa-2a and five oral nucleoside/nucleotide analogues: entecavir, tenofovir, adefovir, telbivudine and lamivudine (listed according to antiviral efficacy).
  • The advantage of interferon treatment is the possibility of long-term remission in one third of carefully selected HbeAg+ patients without development of resistance.
  • However, interferon treatment is not efficient in the majority of patients.
  • The advantage of treatment with nucleoside and nucleotide analogues is the possibility to suppress HBV DNA to undetectable levels in 70%-90% of patients.
  • However, analogue treatment is a long-term treatment (possibly life-long) and is associated with the development of resistance.
  • [MeSH-major] Hepatitis B, Chronic / drug therapy
  • [MeSH-minor] Antiviral Agents / therapeutic use. Humans. Interferon-alpha / therapeutic use. Polyethylene Glycols / therapeutic use. Recombinant Proteins

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  • (PMID = 20198897.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2a; 30IQX730WE / Polyethylene Glycols; 76543-88-9 / interferon alfa-2a
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82. Catusse J, Wollner S, Leick M, Schröttner P, Schraufstätter I, Burger M: Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells. J Cell Physiol; 2010 Nov;225(3):792-800
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells.
  • Elevated levels of CCL18 have been described in various diseases including childhood acute lymphocytic leukemia (ALL) but its functions remain poorly characterized.
  • CXCL12 is a pivotal chemokine for hematopoiesis and B cell homing processes.
  • We demonstrate that CCL18 interferes with CXCL12-mediated pre-B ALL cell activation.
  • CXCL12-induced calcium mobilization, chemotaxis, pseudo-emperipolesis and cellular proliferation could be significantly reduced by CCL18 in pre-B ALL cell lines.
  • The results could be observed in primary cells from patients suffering from pre-B ALL, but not in cells from patients suffering from common ALL.
  • We therefore suggest that CCL18 is an important modulator of CXCR4-dependent responses in pre-B ALL cells via interactions with GPR30.
  • [MeSH-major] Chemokines, CC / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology. Receptors, CXCR4 / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Apoptosis. COS Cells. Calcium Signaling. Cell Line, Tumor. Cell Proliferation. Cercopithecus aethiops. Chemokine CXCL12 / metabolism. Chemotaxis, Leukocyte. Estradiol / metabolism. Estrogen Antagonists / pharmacology. Humans. Ligands. Lymphocyte Activation. Receptors, Estrogen. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Recombinant Proteins / metabolism. Transfection

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20568229.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL18 protein, human; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Estrogen Antagonists; 0 / GPER protein, human; 0 / Ligands; 0 / Receptors, CXCR4; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol
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83. Morović M: [Treatment of chronic hepatitis B]. Acta Med Croatica; 2005;59(5):429-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Antiviral Agents / therapeutic use. Humans. Interferon Type I / therapeutic use. Lamivudine / therapeutic use. Recombinant Proteins

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  • (PMID = 16381239.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon Type I; 0 / Recombinant Proteins; 2T8Q726O95 / Lamivudine
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84. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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85. Hurford MT, Altman AJ, DiGiuseppe JA, Sherburne BJ, Rezuke WN: Unique pattern of nuclear TdT immunofluorescence distinguishes normal precursor B cells (Hematogones) from lymphoblasts of precursor B-lymphoblastic leukemia. Am J Clin Pathol; 2008 May;129(5):700-5
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  • [Title] Unique pattern of nuclear TdT immunofluorescence distinguishes normal precursor B cells (Hematogones) from lymphoblasts of precursor B-lymphoblastic leukemia.
  • Normal precursor B cells or hematogones share morphologic and immunophenotypic similarities with lymphoblasts of precursor B-lymphoblastic leukemia.
  • The numbers are often increased and difficult to distinguish in many patients following chemotherapy for precursor B-lymphoblastic leukemia.
  • The purpose of this study was to establish a unique method for differentiating hematogones from lymphoblasts by evaluating the immunofluorescence pattern of nuclear terminal deoxynucleotidyl transferase (TdT) staining in 29 cases of TdT+ acute leukemia and 20 cases with increased numbers of hematogones.
  • All 29 cases of TdT+ acute leukemia demonstrated a finely granular pattern of TdT immunofluorescence that was uniformly distributed in the nucleus, whereas all 20 cases with increased hematogones demonstrated a coarsely granular or speckled pattern of TdT immunofluorescence, which often intensely aligns the nuclear membrane.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Nucleus / metabolism. DNA Nucleotidylexotransferase / metabolism. Neoplastic Stem Cells / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Stem Cells / metabolism

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  • (PMID = 18426728.001).
  • [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] EC 2.7.7.31 / DNA Nucleotidylexotransferase
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86. Novoa V, Nuñez N, Cervellini M, Starosta A, Carballo OG: [Presence of B cell clones in acute myelomonocytic leukemia]. Medicina (B Aires); 2010;70(2):163-5
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  • [Title] [Presence of B cell clones in acute myelomonocytic leukemia].
  • [Transliterated title] Hallazgo de células clonales B en leucemia mielomonocítica aguda.
  • The coexistence of acute myeloid leukemia and chronic lymphocytic leukemia in the same patient is rare.
  • The majority of the cases correspond to patients that developed acute leukemia during the evolutionary course of a chronic lymphatic leukemia following treatment with chemotherapy drugs.
  • We report a case of acute myelomonocytic leukemia concurrent with untreated B-cell chronic lymphocytic leukemia in which the use of flow cytometry analysis with a large panel of monoclonal antibodies, allowed the demonstration of different pathological populations and determine immunophenotyping patterns.
  • Published cases of simultaneous chronic lymphocytic leukemia and acute leukemia are reviewed.
  • The use of multiparametric flow cytometry to differentiate the populations demonstrates the utility of this technology in the diagnosis of these hematological malignancies.
  • [MeSH-major] Antibodies, Monoclonal / analysis. B-Lymphocytes / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myelomonocytic, Acute / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 20447900.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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87. Cannizzo E, Carulli G, Buda G, Zucca A, Azzarà A, Orciuolo E, Petrini M: Meningeal relapse in a case of B acute lymphoblastic leukemia: the role of CD56 expression. Med Sci Monit; 2009 Feb;15(2):CS27-29
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  • [Title] Meningeal relapse in a case of B acute lymphoblastic leukemia: the role of CD56 expression.
  • BACKGROUND: Blasts from B acute lymphoblastic leukemia (B-ALL) may express CD56 in about 10% of cases.
  • The presence of this marker at diagnosis is associated with an increased risk of meningeal relapse.
  • A case is described of B-ALL which was CD56 negative at diagnosis, and expressed this marker when isolated meningeal relapse was diagnosed.
  • The latter was carried out by a wide routine panel of MoAbs which was the same as the one at diagnosis and included CD56.
  • Isolated meningeal relapse was diagnosed since blast cell infiltration was detected in the CSF, but not in the peripheral blood and bone marrow samples.
  • Blast cells showed an immunological phenotype similar to that at diagnosis (cyCD79a+, CD79b+, CD19+, CD22+, CD34+, CD10+, CD20+), but characterized by the acquisition of CD56 on the surfaces of more than 90% of cells.
  • CONCLUSIONS: This case shows that CD56 can be expressed at relapse of B-ALL and that its presence likely enables leukemic cell binding to the central nervous system (CNS).
  • [MeSH-major] Antigens, CD56 / metabolism. B-Lymphocytes / pathology. Meninges / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19179973.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD56
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88. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • However, the incidence and type of MLL rearrangements have not been determined in common ALL (cALL) and CD10+ or CD10- pre-B ALL.
  • EXPERIMENTAL DESIGN: To address this question, we analyzed 29 patients with pro-B ALL, 11 patients with CD10- pre-B ALL, 23 pre-B, and 26 cALL patients with CD10 on 20% to 80%, as well as 136 pre-B and 143 cALL patients with CD10 > or = 80% of blasts.
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • However, no 11q23/MLL translocation was identified among the CD10+ pre-B and cALL patients.
  • MLL-rearranged pro-B and CD10- pre-B ALL cases had similar clinical and immunophenotypic (coexpression of CDw65 and CD15) features at initial diagnosis.
  • CONCLUSIONS: The striking similarities between the two CD10- ALL subsets imply that CD10- pre-B ALL variants may represent pro-B ALL cases that maintained the propensity to rearrange and express their immunoglobulin heavy chain rather than actual pre-B ALL forms transformed at this later stage of B-cell differentiation.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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89. Jónsdóttir G, Briem H, Blöndal T, Pálsson G, Olafsson S, Gudnason T: [Viral hepatitis B and C among immigrants in Iceland]. Laeknabladid; 2006 Oct;92(10):669-73
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  • [Title] [Viral hepatitis B and C among immigrants in Iceland].
  • [Transliterated title] Lifrarbólga af vökdum lifrarbólguveira B og C hjá innflytjendum á Islandi.
  • BACKGROUND: Viral hepatitis B and C are a major health problem worldwide.
  • The prevalence of these diseases varies throughout the world.
  • In Iceland, the incidence of hepatitis B and C has increased in recent years.
  • At the same time, the number of immigrants from countries where viral hepatitis is endemic, has also increased.
  • The aim of this study was to investigate the epidemiology of hepatitis B and C among immigrants in Iceland.
  • MATERIAL AND METHODS: Immigrants from outside the European Economic Area (EEA) were screened for hepatitis B and C.
  • Medical records for the years 2000-2002 were reviewed for country of origin, viral serology and liver transaminases.
  • Information was gathered from the State Epidemiologist's central registry of notifiable diseases and from the Icelandic Directorate of Immigration on the number of residence permits issued.
  • RESULTS: 70% of all immigrants from countries outside the EEA during the study period were included in the study.
  • Blood samples were obtained from 2946 immigrants.
  • 83 (2.8%) had hepatitis B and 24 (0.8%) had hepatitis C.
  • Prevalence of hepatitis B was highest among immigrants from Africa,11/171 (6.4%; 95% CI: 3.3-11.2%) and hepatitis C among immigrants from Eastern Europe, 16/1502 (1.1%; 95% CI: 0.6-1.7%).
  • 482 (16%) had serological markers of previous hepatitis B infection.
  • Of all registered cases of hepatitis B, immigrants were 56% and of hepatitis C 10%.
  • CONCLUSIONS: 1.
  • Majority of those diagnosed with hepatitis B during the study period were immigrants.
  • 2. Among immigrants, hepatitis B was more prevalent than hepatitis C.
  • 3) The high prevalence of hepatitis B justifies screening for the disease in this population.
  • [MeSH-major] Emigration and Immigration / statistics & numerical data. Endemic Diseases / statistics & numerical data. Hepatitis B / epidemiology. Hepatitis C / epidemiology. Mass Screening
  • [MeSH-minor] Adolescent. Adult. Africa / ethnology. Age Distribution. Aged. Aged, 80 and over. Asia / ethnology. Child. Child, Preschool. Europe, Eastern / ethnology. Hepatitis Antibodies / blood. Humans. Iceland / epidemiology. Infant. Infant, Newborn. Middle Aged. Prevalence. Registries / statistics & numerical data. Seroepidemiologic Studies. Time Factors. Transaminases / blood

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  • [CommentIn] Laeknabladid. 2006 Oct;92(10):667 [17062899.001]
  • (PMID = 17062900.001).
  • [ISSN] 0023-7213
  • [Journal-full-title] Læknablađiđ
  • [ISO-abbreviation] Laeknabladid
  • [Language] ice
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Iceland
  • [Chemical-registry-number] 0 / Hepatitis Antibodies; EC 2.6.1.- / Transaminases
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90. Troeger A, Schmitz I, Siepermann M, Glouchkova L, Gerdemann U, Janka-Schaub GE, Schulze-Osthoff K, Dilloo D: Up-regulation of c-FLIPS+R upon CD40 stimulation is associated with inhibition of CD95-induced apoptosis in primary precursor B-ALL. Blood; 2007 Jul 1;110(1):384-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Up-regulation of c-FLIPS+R upon CD40 stimulation is associated with inhibition of CD95-induced apoptosis in primary precursor B-ALL.
  • Previous studies on apoptosis defects in acute lymphoblastic leukemia (ALL) have focused on chemotherapy-induced, primarily mitochondrial death pathways.
  • Here, we show that primary B-cell precursor ALL cells from children escape from receptor-dependent cell death in 2 ways: Resting ALL blasts are protected from receptor-mediated apoptosis due to the absence of CD95 surface expression.
  • [MeSH-major] Antigens, CD40 / physiology. Antigens, CD95 / physiology. Apoptosis. CASP8 and FADD-Like Apoptosis Regulating Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 17376892.001).
  • [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, CD40; 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Protein Isoforms
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91. Chung HY, Kim KH, Jun KR, Jang S, Park CJ, Chi HS, Im HJ, Seo JJ, Seo EJ: [Prognostic significance of TEL/AML1 rearrangement and its additional genetic changes in Korean childhood precursor B-acute lymphoblastic leukemia]. Korean J Lab Med; 2010 Feb;30(1):1-8
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  • [Title] [Prognostic significance of TEL/AML1 rearrangement and its additional genetic changes in Korean childhood precursor B-acute lymphoblastic leukemia].
  • BACKGROUND: TEL (ETV6)/AML1 (RUNX1) rearrangement is observed in approximately 20-25% of childhood precursor B-ALL and is associated with a favorable outcome.
  • We evaluated the prevalence and prognostic significance of TEL/AML1 rearrangement and additional genetic changes in the TEL and AML1 genes in Korean childhood precursor B-ALL.
  • METHODS: We performed FISH using LSITEL/AML1 ES probe (Vysis, USA) in 123 children diagnosed as having precursor B-ALL and assessed clinical relevance of the TEL/AML1 rearrangement and additional genetic abnormalities.
  • RESULTS: The frequency of TEL/AML1 was 17.1% (21/123) in patients with precursor B-ALL.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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  • (PMID = 20197715.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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92. Greve J, Bas M, Schipper J, Hoffmann TK: [Primary cutane manifestation of a precursor-B-lymphoblastic lymphoma in the external ear]. Laryngorhinootologie; 2008 Oct;87(10):728-30
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  • [Title] [Primary cutane manifestation of a precursor-B-lymphoblastic lymphoma in the external ear].
  • [Transliterated title] Primäre kutane Manifestation eines Vorläufer-B-lymphoblastischen Lymphoms im Bereich des äusseren Ohres.
  • We report on an extranodal B-cell-lymphoma of the ear in a young woman.
  • Histologic examination resulted in the final diagnosis.
  • [MeSH-major] Ear Neoplasms / diagnosis. Ear, External. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Neoplasms / diagnosis

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  • (PMID = 18633860.001).
  • [ISSN] 0935-8943
  • [Journal-full-title] Laryngo- rhino- otologie
  • [ISO-abbreviation] Laryngorhinootologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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93. Ajana F: [Hepatitis B virus still under debate]. Arch Pediatr; 2006 Sep;13(9):1269-74
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  • [Title] [Hepatitis B virus still under debate].
  • [Transliterated title] L'hépatite virale B, encore et toujours d'actualité.
  • Hepatitis B is the most known viral hepatitis, and often turns into a media event in France.
  • Its prevalence and incidence depend on countries, regions, and their inhabitants.
  • The virus is highly infectious with a high genomic variability.
  • Its immune reaction and pathology seem complex, but the latest consensus conferences gave a practical management.
  • If Papillomavirus vaccine is ready and coming soon as the second STD vaccine, hepatitis B vaccine is available since 1982, and used with a real success.
  • Fighting hepatitis B is to continue all together to immunize children and babies born from infected mothers, to adopt universal health workers precautions, to educate and modify high risk behaviours, to treat and prevent hepatitis B complications and superinfections, and finally to monitor and detect any resistant hepatitis B strain.
  • [MeSH-major] Hepatitis B / prevention & control. Hepatitis B / transmission
  • [MeSH-minor] Hepatitis B Vaccines / administration & dosage. Humans

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  • (PMID = 16920340.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hepatitis B Vaccines
  • [Number-of-references] 12
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94. Moradpour D, Blum HE: [Diagnosis of hepatitis B and C]. Praxis (Bern 1994); 2005 Jan 19;94(3):66-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis of hepatitis B and C].
  • Diagnosis of hepatitis B and C is based on sensitive and specific serological assays.
  • Molecular assays for the detection of HBV DNA or HCV RNA are in some instances needed to confirm the diagnosis.
  • [MeSH-major] Hepatitis B / diagnosis. Hepatitis C / diagnosis

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  • (PMID = 15719800.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Antibodies; 0 / Hepatitis B Surface Antigens; 0 / Hepatitis B e Antigens; 0 / Hepatitis C Antibodies
  • [Number-of-references] 52
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95. Xu C, Zhao HJ, Jiang LM, Yuan XJ, Li L, Tang JY, Shen LS: [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):717-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia].

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  • (PMID = 16928307.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD58; 0 / Biomarkers, Tumor
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96. Rosińska M, Czarkowski MP: [Hepatitis B in Poland in 2007]. Przegl Epidemiol; 2009;63(2):245-50
MedlinePlus Health Information. consumer health - Hepatitis B.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In Poland in 2007 there were registered 1,454 cases of hepatitis B (incidence 3.81 per 100,000 population), including 364 acute cases (incidence 0.95 per 100,000).
  • Acute cases are registered separately beginning in 2005 and since then a decrease of acute hepatitis B incidence of more then 20% per year was observed in contrast to stable epidemiological situation regarding chronic hepatitis B.
  • Total hepatitis B incidence varied across the regions form 1.12 in warminsko-mazurskie to 7.26 per 100,000 in lodzkie and acute hepatitis B incidence from 0.30 in zachodniopomorskie to 1.51 in podlaskie.
  • Chronic hepatitis B was the most common in the age group 15-24, born before the implementation of routine newborn vaccination in 1993-1995 (incidence in the age groups 15-19 and 20-24 respectively 4.55 and 4.35 per 100,000).
  • In contrast acute hepatitis B incidence demonstrated two peaks: at the age 25-29 (1.46) and at the age 65 and over (in the age groups 65-74 and 75+ respectively 1.64 and 1.77).
  • Acute hepatitis B was over two times as frequent among men then women (incidence 1.30 and 0.63 respectively) and more frequent in the urban then in the rural areas (incidence 1.01 and 0.87 respectively).
  • However, age distribution differed in relation to sex (incidence had two peaks in men--age groups 25-29 and 75+ and increased constantly with age in women) and to the type of residence (incidence was the highest among people aged 25--49 in cities and among people aged 60 or more in rural areas).
  • In 2007 97,8% of acute hepatitis B and 67,8% of chronic cases were hospitalized.
  • 72 people died of hepatitis B, including 15 people of acute hepatitis B.

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  • (PMID = 19799254.001).
  • [ISSN] 0033-2100
  • [Journal-full-title] Przegla̧d epidemiologiczny
  • [ISO-abbreviation] Przegl Epidemiol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Hepatitis B Vaccines
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97. Zarski JP: [Epidemiology of chronic hepatitis B]. Presse Med; 2006 Feb;35(2 Pt 2):304-7
Genetic Alliance. consumer health - Hepatitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Epidémiologie de l'hépatite chronique B.

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  • (PMID = 16493334.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Surface Antigens; EC 2.6.1.- / Transaminases
  • [Number-of-references] 12
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98. Wiegand J, Mössner J, Tillmann HL: [Diagnostics and therapy of chronic hepatitis B and C]. Internist (Berl); 2008 Jul;49(7):817-29; quiz 830-1
Genetic Alliance. consumer health - Hepatitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Antiviral Agents / administration & dosage. Hepatitis B, Chronic / diagnosis. Hepatitis B, Chronic / therapy. Hepatitis C, Chronic / diagnosis. Hepatitis C, Chronic / therapy

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  • (PMID = 18548220.001).
  • [ISSN] 0020-9554
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiviral Agents
  • [Number-of-references] 54
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99. Zidovec Lepej S, Dusek D, Budimir J, Vince A: [Molecular diagnosis of hepatitis C and hepatitis B infection]. Acta Med Croatica; 2009 Dec;63(5):361-9
MedlinePlus Health Information. consumer health - Hepatitis C.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Molecular diagnosis of hepatitis C and hepatitis B infection].
  • Molecular diagnosis of HCV and HBV infections in clinical laboratories should be limited to certified standardized assays.
  • [MeSH-major] Hepatitis B / diagnosis. Hepatitis C / diagnosis. Molecular Diagnostic Techniques

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  • MedlinePlus Health Information. consumer health - Hepatitis B.
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  • (PMID = 20198893.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / RNA, Viral
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100. Airoldi I, Cocco C, Di Carlo E, Disarò S, Ognio E, Basso G, Pistoia V: Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells. Cancer Res; 2006 Apr 15;66(8):3978-80
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells.
  • The aim of this study was to investigate (i) whether the IL-12Rbeta2 gene is silenced in B-cell acute lymphoblastic leukemia (B-ALL) cells, and (ii) what the functional implications of such silencing for tumor growth are.
  • Here, we show that although mature B cells expressed both chains of the IL-12R, normal pro-B and pre-B cells failed to express the IL-12Rbeta2 chain.
  • Similarly, primary tumor cells from pediatric pro-B, early pre-B, and pre-B ALL (30 cases) did not express the IL-12Rbeta2 chain.
  • Such methylation was not detected in normal early B cells that when differentiated into mature B cells expressed the IL-12Rbeta2 gene.
  • Detection of IL-12Rbeta2 mRNA and protein in the tumorigenic 697 pre-B-ALL cell line allowed to perform functional experiments in severe combined immunodeficient/nonobese diabetic mice receiving 697 cells with or without human recombinant IL-12 (hrIL-12).
  • [MeSH-major] Burkitt Lymphoma / genetics. DNA Methylation. Receptors, Interleukin / genetics

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  • (PMID = 16618714.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / IL12RB2 protein, human; 0 / Il12rb2 protein, mouse; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-12
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