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11. Saxena A, Rai A, Raina V, Seth T, Mitra DK: Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells. Cancer Immunol Immunother; 2010 Jan;59(1):125-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells.
  • Expression of cell surface CD13 in acute B-cell leukemia (ALL-B) is often viewed, as an aberrant expression of a myeloid lineage marker.
  • Here, we attempted to study the stage specific expression of CD13 on ALL-B blasts and understand its role in leukemogenesis as pertaining to stage of B-cell ontogeny.
  • Among 68 cases of early B-cell ALL, 22 cases with distinct immunophenotype was identified as immature B-cell ALL.
  • This strongly indicates leukemogenesis at an early stage of B-cell development.
  • By blocking their cell surface CD13 in leukemic blasts with monoclonal antibody we were able to inhibit their proliferation.
  • CD13 may thus be an important target for novel molecular therapy of early stage acute B-cell leukemia.
  • [MeSH-major] Antigens, CD13 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19562339.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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12. Smal C, Lisart S, Maerevoet M, Ferrant A, Bontemps F, Van Den Neste E: Pharmacological inhibition of the MAPK/ERK pathway increases sensitivity to 2-chloro-2'-deoxyadenosine (CdA) in the B-cell leukemia cell line EHEB. Biochem Pharmacol; 2007 Feb 1;73(3):351-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacological inhibition of the MAPK/ERK pathway increases sensitivity to 2-chloro-2'-deoxyadenosine (CdA) in the B-cell leukemia cell line EHEB.
  • EHEB leukemic cells, which are derived from a patient suffering B-cell chronic lymphocytic leukemia (B-CLL), display intermediate sensitivity to the purine analogue 2-chloro-2'-deoxyadenosine (CdA).
  • This activation required CdA metabolism and de novo protein synthesis, and was independent on caspase activation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cladribine / pharmacology. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. MAP Kinase Signaling System / drug effects. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Drug Interactions. Humans. Phosphorylation

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  • (PMID = 17137556.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 47M74X9YT5 / Cladribine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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13. Smal C, Lisart S, Ferrant A, Bontemps F, van den Neste E: Inhibition of the ERK pathway promotes apoptosis induced by 2-chloro-2'-deoxyadenosine in the B-cell leukemia cell line EHEB. Nucleosides Nucleotides Nucleic Acids; 2006;25(9-11):1009-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of the ERK pathway promotes apoptosis induced by 2-chloro-2'-deoxyadenosine in the B-cell leukemia cell line EHEB.
  • 2-Chloro-2'-deoxyadenosine (CdA) is a nucleoside analogue active in B-cell chronic lymphocytic leukemia (B-CLL).
  • In this study, we show that CdA, at concentrations close to the IC50, activated the ERK pathway in the B-cell line EHEB.
  • [MeSH-major] Apoptosis. Cladribine / pharmacology. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Caspase 3 / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Inhibitory Concentration 50. Phosphorylation

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  • (PMID = 17065055.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 47M74X9YT5 / Cladribine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspase 3
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4. Caligaris-Cappio F, Ghia P: The normal counterpart to the chronic lymphocytic leukemia B cell. Best Pract Res Clin Haematol; 2007 Sep;20(3):385-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The normal counterpart to the chronic lymphocytic leukemia B cell.
  • Chronic lymphocytic leukemia (CLL) is characterized by the monoclonal expansion of small mature-looking B cells that accumulate in the blood, marrow, and lymphoid organs, and have a remarkable phenotypic homogeneity.
  • In recent years the biology of CLL has been enriched by an unprecedented flurry of new observations that are leading to a better understanding of the natural history of the disease.
  • Still CLL cells have so far defied any attempt to satisfactorily answer the simple time-honored question of what their cell of origin is.
  • It is the purpose of this review to discuss the features a cell must possess to be considered with reasonable approximation the normal counterpart of a CLL B cell.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / blood

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  • (PMID = 17707828.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Antigens, CD79; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  • [Number-of-references] 97
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15. Shamaa LA, Hussein Ael-S, Balbaa OA, Farahat NM, Ali MA: Modulation of IL-4 level by fludarabine and its relation to apoptosis in chronic B-cell lymphocytic leukemia. Egypt J Immunol; 2008;15(1):181-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of IL-4 level by fludarabine and its relation to apoptosis in chronic B-cell lymphocytic leukemia.
  • Accumulation of malignant B-lymphocytes in chronic B-cell lymphocytic leukemia (B-CLL) is mainly attributed to reduced apoptosis rather than increased proliferation rate.
  • Fludarabine is one of purine analogs and the current standard treatment for B-CLL, which has been proved to induce apoptosis in normal and malignant lymphocytes.
  • We investigated the effect of ex vivo treatment of peripheral blood lymphocytes (PBLs) with Fludarabine on apoptosis and IL-4 production in untreated patients with B-CLL.


16. Qiu Y, Song B, Zhao G, Deng B, Makino T, Tomita Y, Wang J, Luo W, Doki Y, Aozasa K, Morii E: Expression level of Pre B cell leukemia homeobox 2 correlates with poor prognosis of gastric adenocarcinoma and esophageal squamous cell carcinoma. Int J Oncol; 2010 Mar;36(3):651-63
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  • [Title] Expression level of Pre B cell leukemia homeobox 2 correlates with poor prognosis of gastric adenocarcinoma and esophageal squamous cell carcinoma.
  • Pre B cell leukemia homeobox 2 (PBX2), a member of PBX family, acts as a co-factor of homeobox proteins to regulate proliferation and differentiation of tumor cells.
  • Our recent study revealed prognostic significance of PBX2 expression in non-small cell lung carcinoma.
  • The significance of PBX2 expression was examined in cases with gastric cancer (GC) and esophageal squamous cell carcinoma (ESCC), and the role of PBX2 in tumor behavior was evaluated in GC and ESCC cell lines of knocked-down PBX2 expression.
  • Knocked-down expression of PBX2 in GC and ESCC cell lines resulted in decrease of in vitro colony formation and in vivo tumorigenic activities, but proliferative and invasive activities did not change.
  • Under serum depletion, apoptotic cell proportion was higher in PBX2 knocked-down cells than in control cells.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis. Cell Differentiation. Cell Proliferation. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 20126986.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / PBX2 protein, human; 0 / Proto-Oncogene Proteins
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17. Fujita N, Mori T, Mitsui T, Inada H, Horibe K, Tsurusawa M, Lymphoma Committee of the Japanese Pediatric Leukemia/Lymphoma Study Group: The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan. Pediatr Blood Cancer; 2008 Aug;51(2):188-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan.
  • BACKGROUND: There have been excellent treatment results for children with B-cell non-Hodgkin lymphoma (B-NHL) and mature B-cell leukemia (B-ALL) in the last few decades.
  • Among 18 patients who had a chemotherapy-sensitive disease, 4 of 5 patients who underwent hematopoietic stem cell transplantation (HSCT) during remission survived without progression, while 3 of 12 patients who did not receive HSCT were alive without disease progression.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, B-Cell / therapy. Lymphoma, B-Cell / therapy


18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosome Banding. Disease Progression. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Prognosis. Remission Induction

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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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19. Marinello E, Carlucci F, Rosi F, Floccari F, Raspadori D, Tabucchi A: Purine metabolism in B-cell lymphocytic leukemia: a microarray approach. Nucleosides Nucleotides Nucleic Acids; 2006;25(9-11):1277-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Purine metabolism in B-cell lymphocytic leukemia: a microarray approach.
  • B-cell chronic lymphocytic leukemia (B-CLL) is an adult-onset highly heterogeneous malignancy characterized by a cells resistance to apoptosis rather than to highly proliferative cells.
  • We prepared a microarray chip for the analysis of 50 selected genes that could be of interest in B-CLL: enzymes of purine de-novo, salvage and catabolic pathway, oxidative stress enzymes, and apoptotis-related proteins.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / metabolism. Oligonucleotide Array Sequence Analysis / methods. Purines / metabolism
  • [MeSH-minor] Adenosine / metabolism. Apoptosis. Cell Proliferation. Humans. Oxidative Stress. Signal Transduction

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  • (PMID = 17065106.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Purines; K72T3FS567 / Adenosine
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20. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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21. Kronenberger K, Nössner E, Frankenberger B, Wahl U, Dreyling M, Hallek M, Mocikat R: A polyvalent cellular vaccine induces T-cell responses against specific self-antigens overexpressed in chronic lymphocytic B-cell leukemia. J Immunother; 2008 Oct;31(8):723-30
Genetic Alliance. consumer health - Leukemia, T-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A polyvalent cellular vaccine induces T-cell responses against specific self-antigens overexpressed in chronic lymphocytic B-cell leukemia.
  • B cell-derived chronic lymphocytic leukemia (CLL) is an incurable disease that requires innovative therapeutic regimens.
  • Experimental approaches of immunotherapy aiming at induction of systemic T-cell responses have been developed.
  • Using trioma cell-pulsed dendritic cells (DCs) for T-cell activation in vitro, we asked whether specific Ags overexpressed by CLL can be identified as target structures of such responses and what is the nature of these Ags.
  • T lymphocytes were polyvalently stimulated by trioma-pulsed DCs and specificities were tested by determining cytokine secretion in the presence of target cells transfected with RNA coding for those Ags that were found to be overexpressed.
  • We demonstrate that DCs pulsed with the modified tumor cells efficiently activate T lymphocytes against CLL and that overexpressed Ags related to leukemogenesis, such as BCL-2, MDM2, and ETV5, serve as targets for those T cells.
  • [MeSH-major] Antigens, Neoplasm / immunology. Autoantigens / immunology. B-Lymphocytes / transplantation. Cancer Vaccines / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18779747.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Autoantigens; 0 / Cancer Vaccines; 0 / DNA-Binding Proteins; 0 / ETV5 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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22. Rutten CE, van Luxemburg-Heijs SA, Griffioen M, Marijt EW, Jedema I, Heemskerk MH, Posthuma EF, Willemze R, Falkenburg JH: HLA-DP as specific target for cellular immunotherapy in HLA class II-expressing B-cell leukemia. Leukemia; 2008 Jul;22(7):1387-94
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  • [Title] HLA-DP as specific target for cellular immunotherapy in HLA class II-expressing B-cell leukemia.
  • Mismatching for human leukocyte antigen (HLA)-DPB1 in unrelated donor hematopoietic stem cell transplantation (URD-SCT) has been associated with a decreased risk of disease relapse, indicating that HLA-DP may represent a target for graft-versus-leukemia (GVL) reactivity in HLA class II-expressing hematological malignancies.
  • To investigate whether HLA-DP-specific T cells could mediate GVL reactivity following HLA-DPB1-mismatched URD-SCT and donor lymphocyte infusion (DLI), we analyzed the immune response in a patient with leukemic lymphoplasmacytic lymphoma responding to DLI without graft-versus-host disease.
  • The emergence of leukemia-reactive CD4+ T cells during the clinical immune response was demonstrated by interferon-gamma (IFN-gamma) enzyme-linked immunosorbent spot(ELISPOT)analysis.
  • Following clonal isolation of these leukemia-reactive CD4+ T cells, blocking studies, panel studies and retroviral transduction experiments of both mismatched HLA-DPB1 alleles identified HLA-DPB1(*)0201 and HLA-DPB1(*)0301 as the targets of this immune response.
  • The HLA-DPB1-specific CD4+ T-cell clones were capable of recognizing and lysing several HLA-DP-expressing myeloid and lymphoid hematological malignant cells.
  • Since HLA-DP expression is mainly restricted to hematopoietic cells, HLA-DP may be used as a specific target for immunotherapy following T-cell-depleted URD-SCT.
  • [MeSH-major] HLA-DP Antigens / immunology. Hematopoietic Stem Cell Transplantation. Histocompatibility Antigens Class II / analysis. Immunotherapy, Adoptive. Leukemia, Lymphocytic, Chronic, B-Cell / therapy
  • [MeSH-minor] CD4-Positive T-Lymphocytes / immunology. Female. Graft vs Host Disease / etiology. Graft vs Leukemia Effect. HLA-DP beta-Chains. Histocompatibility Testing. Humans. Middle Aged

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  • (PMID = 18418406.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen; 0 / Histocompatibility Antigens Class II
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23. Hentges KE, Weiser KC, Schountz T, Woodward LS, Morse HC, Justice MJ: Evi3, a zinc-finger protein related to EBFAZ, regulates EBF activity in B-cell leukemia. Oncogene; 2005 Feb 10;24(7):1220-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evi3, a zinc-finger protein related to EBFAZ, regulates EBF activity in B-cell leukemia.
  • The AKXD recombinant inbred mice are predisposed to a variety of leukemias and lymphomas as a result of viral integration.
  • One common insertion site, the ecotropic viral insertion site 3 (Evi3), has been implicated in most B-cell tumors in the AKXD-27 strain.
  • The Evi3 gene encodes a zinc-finger protein with sequence similarity to the Early B-cell Factor-Associated Zinc-finger gene (EBFAZ).
  • We show that the Evi3 gene is overexpressed in several tumors with viral insertions at Evi3, which results in the upregulation of Early B-cell Factor (EBF)-target gene expression, suggesting that Evi3 modulates EBF activity.
  • Reconstitution of primary leukemia cells showed that these tumors express high densities of the B-cell surface proteins CD19 and CD38, which are EBF targets.
  • Further, these data imply that Evi3 misexpression initiates tumorigenesis by perturbing B-cell development via an interaction with EBF.
  • [MeSH-major] Carrier Proteins / physiology. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic / genetics. Leukemia, B-Cell / genetics. Nuclear Proteins / physiology. Trans-Activators / metabolism
  • [MeSH-minor] ADP-ribosyl Cyclase / analysis. ADP-ribosyl Cyclase / biosynthesis. Amino Acid Sequence. Animals. Antigens, CD / analysis. Antigens, CD / biosynthesis. Antigens, CD / genetics. Antigens, CD19 / analysis. Antigens, CD19 / biosynthesis. Antigens, CD38. Antigens, CD79. B-Cell-Specific Activator Protein. Cell Line. Female. Gene Expression. Kidney / cytology. Kidney / metabolism. Male. Membrane Glycoproteins. Mice. Mice, Mutant Strains. Molecular Sequence Data. Receptors, Antigen, B-Cell / genetics. Transcription Factors / genetics. Transcription Factors / physiology. Zinc Fingers / genetics. Zinc Fingers / physiology

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  • (PMID = 15580294.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / F32 HD42436; United States / NCI NIH HHS / CA / R01 CA63229
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD79; 0 / B-Cell-Specific Activator Protein; 0 / Carrier Proteins; 0 / Cd79a protein, mouse; 0 / Cd79b protein, mouse; 0 / DNA-Binding Proteins; 0 / Ebf1 protein, mouse; 0 / Ebfaz protein, mouse; 0 / Evi3 protein, mouse; 0 / Membrane Glycoproteins; 0 / Nuclear Proteins; 0 / Pax5 protein, mouse; 0 / Receptors, Antigen, B-Cell; 0 / Trans-Activators; 0 / Transcription Factors; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / Cd38 protein, mouse
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24. Abrahamsen IW, Stronen E, Wälchli S, Johansen JN, Kjellevoll S, Kumari S, Komada M, Gaudernack G, Tjonnfjord G, Toebes M, Schumacher TN, Lund-Johansen F, Olweus J: Targeting B cell leukemia with highly specific allogeneic T cells with a public recognition motif. Leukemia; 2010 Nov;24(11):1901-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting B cell leukemia with highly specific allogeneic T cells with a public recognition motif.
  • The possibility that allogeneic T cells may be targeted to leukemia has important therapeutic implications.
  • Here, we cocultured HLA-A(*)0201-negative T cells with autologous dendritic cells engineered to present HLA-A(*)0201 complexed with a peptide from the B cell antigen CD20 (CD20p).
  • The polyclonal cells showed exquisite peptide and MHC specificity, and efficiently killed HLA-A(*)0201-positive B cells, including primary chronic lymphocytic leukemia cells.
  • The T cell receptor (TCR) sequences displayed a novel type of conservation, with extensive homology in the TCR β chain complementarity-determining region 3 and in J, but not V, region.
  • The allo-restricted T cells or TCRs could provide graft-versus-leukemia in the absence of graft-versus-host disease.
  • [MeSH-major] Isoantigens / immunology. Leukemia, B-Cell / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Antibody Specificity. Antigens, CD20 / immunology. Autoantigens / immunology. B-Lymphocytes / immunology. Dendritic Cells / immunology. Flow Cytometry. HEK293 Cells / immunology. HLA Antigens / immunology. HLA-A Antigens / immunology. HLA-A2 Antigen. Humans. Receptors, Antigen, T-Cell, alpha-beta / immunology

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  • (PMID = 20844564.001).
  • [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, CD20; 0 / Autoantigens; 0 / HLA Antigens; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Isoantigens; 0 / Receptors, Antigen, T-Cell, alpha-beta
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25. Zhu L, Liao W, Zhu H, Lei P, Wang Z, Shao J, Zhang Y, Shen G: Construction, expression and in vitro biological behaviors of Ig scFv fragment in patients with chronic B cell leukemia. J Huazhong Univ Sci Technolog Med Sci; 2006;26(2):157-60, 171
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

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  • [Title] Construction, expression and in vitro biological behaviors of Ig scFv fragment in patients with chronic B cell leukemia.
  • The expression vector of SmIg scFv fragment was constructed in patient with B cell chronic lymphocyte leukemia (B-CLL) and expressed in E. coli to obtain scFv fragment, and the effect of the protein on the proliferation of stimulated peripheral blood mononuclear cells (PBMC) was investigated in vitro.
  • [MeSH-major] Genetic Vectors / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Cell Proliferation. Cells, Cultured. Cloning, Molecular. Electrophoresis, Polyacrylamide Gel. Escherichia coli / genetics. Genes, Immunoglobulin Heavy Chain / genetics. Genes, Immunoglobulin Light Chain / genetics. Humans. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / metabolism. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Single-Chain Antibodies

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  • [Cites] FASEB J. 1995 Jan;9(1):73-80 [7821762.001]
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  • (PMID = 16850734.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Recombinant Fusion Proteins; 0 / Single-Chain Antibodies; 0 / scFv fragment SW1
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26. Sprangers M, Feldhahn N, Liedtke S, Jumaa H, Siebert R, Müschen M: SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells. Oncogene; 2006 Aug 24;25(37):5180-6
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  • [Title] SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells.
  • Perpetual V(D)J recombinase activity involving multiple DNA double-strand break events in B-cell lineage leukemia and lymphoma cells may introduce secondary genetic aberrations leading towards malignant progression.
  • Here, we investigated defective negative feedback signaling through the (pre-) B-cell receptor as a possible reason for deregulated V(D)J recombinase activity in B-cell malignancy.
  • On studying 28 cases of pre-B-lymphoblastic leukemia and 27 B-cell lymphomas, expression of the (pre-) B-cell receptor-related linker molecule SLP65 (SH2 domain-containing lymphocyte protein of 65 kDa) was found to be defective in seven and five cases, respectively.
  • Reconstitution of SLP65 expression in SLP65-deficient leukemia and lymphoma cells results in downregulation of RAG1/2 expression and prevents both de novo V(H)-DJ(H) rearrangements and secondary V(H) replacement.
  • [MeSH-major] Burkitt Lymphoma / genetics. Carrier Proteins / genetics. Lymphoma, B-Cell / genetics. Phosphoproteins / deficiency. Phosphoproteins / genetics. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Base Sequence. Cell Line, Tumor. DNA Damage. Gene Rearrangement. Genes, Immunoglobulin. Humans. Molecular Sequence Data. Sequence Deletion

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  • (PMID = 16636677.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Carrier Proteins; 0 / Phosphoproteins; EC 2.7.7.- / VDJ Recombinases
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27. Merimi M, Ozkan Y, Cleuter Y, Griebel P, Burny A, Martiat P, Van den Broeke A: Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model. Front Biosci (Schol Ed); 2009;1:154-63
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  • [Title] Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model.
  • Bovine Leukemia Virus (BLV)-induced B-cell leukemia in sheep is a valuable large animal model for investigating oncogenic mechanisms, particularly those associated with human T-cell leukemia virus 1 (HTLV-1).
  • Multiple factors including viral genes, genetic and epigenetic alterations, and the host immune system are likely to contribute and cooperate in the leukemogenesis of adult T-cell leukemia (ATL) in human and B-cell leukemia in sheep.
  • Future studies in sheep will increase the number of genes identified that are aberrantly regulated by epigenetic processes and identify potential biomarkers which may be used as therapeutic targets in leukemia.
  • [MeSH-major] Epigenesis, Genetic. Leukemia / virology. Leukemia Virus, Bovine / pathogenicity. Oncogenes

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  • (PMID = 19482691.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 93
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28. Petricevic B, Wessner B, Sachet M, Vrbanec D, Spittler A, Bergmann M: CL097, a TLR7/8 ligand, inhibits TLR-4--dependent activation of IRAK-M and BCL-3 expression. Shock; 2009 Nov;32(5):484-90
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  • Two negative regulators of TLR-4 signaling are IL-1 receptor-associated kinase M and B-cell leukemia 3.
  • Reduction of IL-1 receptor-associated kinase M and B-cell leukemia 3 was paralleled by a significant increased cytokine induction of TNF-alpha, IL-10, and IL-12 observed after intracellular and extracellular TLR stimulation.

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  • (PMID = 19333135.001).
  • [ISSN] 1540-0514
  • [Journal-full-title] Shock (Augusta, Ga.)
  • [ISO-abbreviation] Shock
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CL097 compound; 0 / Imidazoles; 0 / Ligands; 0 / Lipopolysaccharides; 0 / Proto-Oncogene Proteins; 0 / Quinolines; 0 / TLR4 protein, human; 0 / TLR7 protein, human; 0 / TLR8 protein, human; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 0 / Toll-Like Receptors; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / proto-oncogene protein bcl-3; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 9004-61-9 / Hyaluronic Acid; EC 2.7.11.1 / IRAK3 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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29. Attarbaschi A, Dworzak M, Steiner M, Urban C, Fink FM, Reiter A, Gadner H, Mann G: Outcome of children with primary resistant or relapsed non-Hodgkin lymphoma and mature B-cell leukemia after intensive first-line treatment: a population-based analysis of the Austrian Cooperative Study Group. Pediatr Blood Cancer; 2005 Jan;44(1):70-6
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  • [Title] Outcome of children with primary resistant or relapsed non-Hodgkin lymphoma and mature B-cell leukemia after intensive first-line treatment: a population-based analysis of the Austrian Cooperative Study Group.
  • BACKGROUND: Children and adolescents with Non-Hodgkin lymphoma (NHL) and mature B-cell leukemia (B-ALL) have an excellent prognosis with contemporary chemotherapy stratified according to the histologic subtype and clinical stage of disease.
  • RESULTS: Nine of 140 (6.5%) patients with B-cell NHL/B-ALL (relapse, n = 6; progress, n = 3) failed initial treatment.
  • Four of them underwent a hematopoietic stem cell transplantation (HSCT) as second-line therapy, two patients received intensive chemotherapy alone and in three patients treatment was palliative.
  • Eight of the nine patients died of their disease.
  • Three of the four patients died of resistant disease.
  • Nine of 29 (31%) patients with anaplastic large cell lymphoma (ALCL) (relapse, n = 7; progress, n = 2) failed first-line therapy.
  • CONCLUSIONS: Conclusively, patients with early relapsed and progressive B-cell neoplasia or LBL have a very poor prognosis with current treatment approaches, while those with ALCL have a respectable chance to achieve a sustained complete second remission with high-dose chemotherapy and HSCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Infant. Male. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368550.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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30. Fang MH, Liu WL, Meng FK, Sun HY: [Aberrant methylation at promoter region of HOX A gene cluster in leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jul;30(7):468-72
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  • [Title] [Aberrant methylation at promoter region of HOX A gene cluster in leukemia cells].
  • OBJECTIVE: To explore the characteristics of CpG islands methylation at promoter region of HOX A gene cluster in leukemia cells before and after all-trans retinoic acid (ATRA) treatment.
  • METHODS: Eleven human leukemia cell lines, bone marrow cells from leukemia patients before and after therapy and white blood cells from normal subjects were collected.
  • In HOX A4, A6, A7, A9, A10 and A11, many CpG sites were methylated (>20%) or hypermethylated (>50%) in leukemia cell lines.
  • Percentages of methylated CpGs were higher in T-cell leukemia (71.4%) and B-cell leukemia (85.7%) than in others.
  • For individual CpGs methylations there were HOX A4 in all leukemia cells, HOX A6 and HOX A7 in most of the leukemia samples and HOX A10 and HOX A11 in K562 and HL-60 cells (38%-86%).
  • HOX A9 CpGs showed hypomethylation in most of myeloid leukemia cells, whereas HOX A11 CpGs were hypermethylated in B-cell leukemia (>50%).
  • CONCLUSIONS: In all leukemia cell lines, aberrant methylation of CpGs was observed at promoter regions of 6 HOX A cluster genes, and some of these genes showed leukemia-type-specific hypermethylation.
  • CpGs methylation of some HOX A genes in leukemia cell lines, especially in HL-60 cells, were down-regulated by ATRA.
  • [MeSH-major] DNA Methylation. Homeodomain Proteins / genetics. Leukemia / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Cell Line, Tumor. CpG Islands / genetics. Humans. Multigene Family

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  • (PMID = 19954601.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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31. Ikewaki N, Nakaichi M, Mizuno T, Takamura N, Tokunaga J, Ogata K, Inoko H, Otsu R: Anti-human very late antigen-alpha4 (CD49d) monoclonal antibody (BU49) cross-reacts with the canine B-cell leukemia cell line GL-1, resulting in the induction of homotypic cell aggregation. Cell Immunol; 2010;263(1):55-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-human very late antigen-alpha4 (CD49d) monoclonal antibody (BU49) cross-reacts with the canine B-cell leukemia cell line GL-1, resulting in the induction of homotypic cell aggregation.
  • We have found that the anti-human very late antigen-alpha4 (VLA-alpha4) (CD49d) monoclonal antibody (mAb) BU49 cross-reacts with the canine B-cell leukemia cell line GL-1.
  • Interestingly, the BU49 mAb specifically induced the homotypic cell aggregation of GL-1 cells accompanied by morphological changes.
  • Homotypic cell aggregates induced by BU49 mAb were blocked by the presence of a protein kinase C inhibitor, a protein kinase A inhibitor, an actin filament formation inhibitor, and an EDTA.
  • On the other hand, a protein tyrosine kinase inhibitor, a DNA-synthesis inhibitor, and an anti-canine CD45 mAb did not affect the GL-1 homotypic cell aggregation induced by BU49 mAb.
  • The BU49 mAb immunoprecipitated at a molecular weight of about 150kDa in the GL-1 cells, similar to the results in the human monocyte-like cell line U937.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Cell Aggregation / immunology. Integrin alpha4beta1 / immunology. Leukemia, B-Cell / immunology. Leukocytes, Mononuclear / drug effects
  • [MeSH-minor] Actin Cytoskeleton / immunology. Animals. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / immunology. Cyclic AMP-Dependent Protein Kinases / metabolism. Dogs. Edetic Acid / pharmacology. Humans. Male. Protein Kinase C / immunology. Protein Kinase C / metabolism. U937 Cells

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20304388.001).
  • [ISSN] 1090-2163
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Integrin alpha4beta1; 9G34HU7RV0 / Edetic Acid; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.13 / Protein Kinase C
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32. Quiney C, Billard C, Mirshahi P, Fourneron JD, Kolb JP: Hyperforin inhibits MMP-9 secretion by B-CLL cells and microtubule formation by endothelial cells. Leukemia; 2006 Apr;20(4):583-9
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  • We previously reported that hyperforin (HF), a natural phloroglucinol purified from Saint John's wort, can induce the apoptosis of leukemic cells from patients with B-cell lymphocytic leukemia (B-CLL) ex vivo.
  • [MeSH-major] Apoptosis / drug effects. Endothelial Cells / drug effects. Leukemia, B-Cell / metabolism. Matrix Metalloproteinase Inhibitors. Microtubules / metabolism. Phloroglucinol / analogs & derivatives. Terpenes / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bicyclo Compounds / pharmacology. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Cell Line. Cells, Cultured. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Female. Gelatinases / drug effects. Gelatinases / metabolism. Humans. In Vitro Techniques. Male. Matrix Metalloproteinase 9 / metabolism. Matrix Metalloproteinase 9 / secretion. Middle Aged. Vascular Endothelial Growth Factors / antagonists & inhibitors

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  • (PMID = 16467866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bicyclo Compounds; 0 / Matrix Metalloproteinase Inhibitors; 0 / Terpenes; 0 / Vascular Endothelial Growth Factors; DHD7FFG6YS / Phloroglucinol; EC 3.4.24.- / Gelatinases; EC 3.4.24.35 / Matrix Metalloproteinase 9; RM741E34FP / hyperforin
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33. Atmar J: Review of the safety and feasibility of rapid infusion of rituximab. J Oncol Pract; 2010 Mar;6(2):91-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Added to standard chemotherapy, rituximab improved survival in patients with non-Hodgkin's lymphoma; added to fludarabine-based regimens, it improved response and survival in patients with chronic B-cell lymphocytic leukemia.

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  • (PMID = 20592783.001).
  • [ISSN] 1935-469X
  • [Journal-full-title] Journal of oncology practice
  • [ISO-abbreviation] J Oncol Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2835489
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34. Yang I, Weiss L, Abdul-Hai A, Kasir J, Reich S, Slavin S: Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease. Cancer Res; 2005 Nov 1;65(21):9735-40
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  • [Title] Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease.
  • Graft-versus-leukemia (GVL) effects can be induced in tolerant mixed chimeras prepared with nonmyeloablative conditioning.
  • Unfortunately, DLI is frequently associated with graft-versus-host disease (GVHD).
  • We investigated the feasibility of induction of potent GVL effects by DLI using intentionally mismatched lymphocytes followed by elimination of alloreactive donor T cells by cyclophosphamide for prevention of lethal GVHD following induction of very short yet most potent GVL effects.
  • Mice inoculated with B-cell leukemia (BCL1) and mismatched donor lymphocytes were treated 2 weeks later with low-dose or high-dose cyclophosphamide.
  • All mice receiving cyclophosphamide 2 weeks after DLI survived GVHD, and no residual disease was detected by PCR; all control mice receiving DLI alone died of GVHD.
  • Our working hypothesis suggests that short-term yet effective and safe adoptive immunotherapy of leukemia may be accomplished early post-transplantation using alloreactive donor lymphocytes, with prevention of GVHD by elimination of GVL effector cells.
  • [MeSH-major] Graft vs Host Disease / prevention & control. Isoantigens / immunology. Leukemia, B-Cell / immunology. Leukemia, B-Cell / therapy. Lymphocytes / immunology
  • [MeSH-minor] Animals. Bone Marrow Transplantation / immunology. Cyclophosphamide / pharmacology. Graft vs Leukemia Effect. Immunosuppressive Agents / pharmacology. Lymphocyte Transfusion. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm, Residual. Transplantation Chimera

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  • [ErratumIn] Cancer Res. 2006 Jul 1;66(13):6894. Yung, Iris [corrected to Yang, Iris]
  • (PMID = 16266994.001).
  • [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 / Immunosuppressive Agents; 0 / Isoantigens; 8N3DW7272P / Cyclophosphamide
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35. Büchau AS, MacLeod DT, Morizane S, Kotol PF, Hata T, Gallo RL: Bcl-3 acts as an innate immune modulator by controlling antimicrobial responses in keratinocytes. J Invest Dermatol; 2009 Sep;129(9):2148-55
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  • We report here the identification of B-cell leukemia (Bcl)-3 as a modulator of innate immune signaling in keratinocytes.

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  • (PMID = 19282837.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI052453-08; United States / NIAMS NIH HHS / AR / AR45676; United States / NIAID NIH HHS / AI / AI052453-08; United States / NIAMS NIH HHS / AR / R01 AR045676; United States / NIAID NIH HHS / AI / R01 AI052453; United States / NIAID NIH HHS / AI / AI052453
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,25-dihydroxy-16,23-diene vitamin D3; 0 / Antimicrobial Cationic Peptides; 0 / Interleukin-13; 0 / Interleukin-6; 0 / Interleukin-8; 0 / NF-kappa B p50 Subunit; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3; 143108-26-3 / CAP18 lipopolysaccharide-binding protein; 1C6V77QF41 / Cholecalciferol; 207137-56-2 / Interleukin-4
  • [Other-IDs] NLM/ NIHMS148559; NLM/ PMC2758924
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36. Gertz MA, Geyer SM, Badros A, Kahl BS, Erlichman C: Early results of a phase I trial of oblimersen sodium for relapsed or refractory Waldenstrom's macroglobulinemia. Clin Lymphoma; 2005 Mar;5(4):282-4
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  • Oblimersen sodium is an antisense oligonucleotide to the first 6 codons of the B-cell leukemia gene 2 (bcl-2) open reading frame.
  • It prevents the expression of the bcl-2 gene product and leads to apoptosis in cells that express Bcl-2. bcl-2 is one of the major apoptosis regulatory gene families and is found in a variety of low-grade B-cell non-Hodgkin's lymphomas.
  • The in vitro use of oblimersen in Waldenstrom's macroglobulinemia (WM) cell line results in enhanced toxicity when exposed to fludarabine, dexamethasone, or rituximab.

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  • (PMID = 15794866.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01 CM 17104
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
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37. Joshi AD, Dickinson JD, Hegde GV, Sanger WG, Armitage JO, Bierman PJ, Bociek RG, Devetten MP, Vose JM, Joshi SS: Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion. Cancer Genet Cytogenet; 2007 Jan 15;172(2):120-6
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  • [Title] Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common B-cell leukemia among older populations in Western countries.
  • The clinical course of B-CLL is heterogeneous: in some patients the disease course is indolent, in others it is aggressive.
  • The B-CLL subgroups with chromosome 11q23 deletion have been associated with aggressive disease course involving ATM deletion, extensive bulky lymphadenopathy (BLA), and inferior clinical outcome.
  • Moreover, gene expression analysis in B-CLL patients with and without BLA revealed differences in expression for genes involved in apoptosis, cell cycle, and cell adhesion.
  • These results indicate an association between BLA and reduced expression of ATM, suggesting a role for ATM in disease progression in B-CLL.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Down-Regulation / genetics. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphatic Diseases / genetics. Protein-Serine-Threonine Kinases / biosynthesis. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Cell Adhesion / genetics. Cell Cycle / genetics. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 17213020.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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38. Abdul-Hai A, Weiss L, Ergas D, Resnick IB, Slavin S, Shapira MY: The effect of high-dose thiotepa, alone or in combination with other chemotherapeutic agents, on a murine B-cell leukemia model simulating autologous stem cell transplantation. Bone Marrow Transplant; 2007 Nov;40(9):891-6
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  • [Title] The effect of high-dose thiotepa, alone or in combination with other chemotherapeutic agents, on a murine B-cell leukemia model simulating autologous stem cell transplantation.
  • The use of thiotepa (TH) is increasing, especially in stem cell transplantation, mainly due to its safety and blood-brain barrier penetration.
  • We evaluated the use of TH in a murine model simulating autologous stem cell transplantation, with or without additional agents.
  • Between 1 and 11 days following inoculation of BALB/c mice with 10(5)-10(8) B-cell leukemia (BCL1) cells (simulating pre-transplant leukemia loads), each group received an 'induction-like' irradiation and/or cytotoxic regimen.
  • Administered alone without AT, high-dose TH did not change the time to appearance of leukemia.
  • Moreover, a synergistic effect was seen in the TH-CY combination (none of the animals developed leukemia, whereas 4/10 animals in the CY-TBI group developed leukemia (P=0.029)).
  • In conclusion, although TH produced only a moderate effect against BCL1 leukemia when used alone, its combination with CY is promising and should be tested further in allogeneic murine models and clinical studies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, B-Cell / drug therapy. Thiotepa / therapeutic use
  • [MeSH-minor] Animals. Busulfan / therapeutic use. Cyclophosphamide / therapeutic use. Disease Models, Animal. Drug Synergism. Mice. Mice, Inbred BALB C. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 17768389.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; G1LN9045DK / Busulfan
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39. Zhu L, Wang HX, Lui J, Yan HM, Xue M: [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):400-2
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  • [Title] [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation].
  • To investigate the leukemia relapse of AL patients after HLA haploidentical bone marrow transplantation (HLA HBMT), 2 relapsed leukemia patients received HLA HBMT were studied, peripheral blood simples and bone marrow smear were examined, morphologic change of bone marrow cells was observed, while the HLA genotype and chromosome karyotye were analyzed by PCR and routine G-banding methods, respectively.
  • The results indicated that the two cases were diagnosed primarily as acute lymphocytic leukemia (common cell subtype) and acute megakaryocytic leukemia, in which chromosome abnormalities or activation of protooncogene in leukemic cells were observed.
  • The complete hematopuietie reconstitution of donor origin was obtained in these 2 cases after HLA HBMT, but the leukemic cells in these 2 leukemia patients were confirmed to be donor origin after relapse, their blood groups and HLA genotype were found to be originated from donor.
  • These 2 relapsed leukemia patients were diagnosed as acute lymphocytic leukemia (B cell subtype) and acute megakaryocytic leukemia.
  • It is suggested that high-dose of immunosuppressive agents used in transplantation may contribute to leukemia relapse of donor origin in these patients.
  • Abnormalities in hematopoietic microenvironment may be also involved in the leukemia development.
  • Donor-cell leukemia after allogeneic hematopoietic stem cell transplantation can be an ideal model to investigate the related events in human leukemogenesis.

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  • (PMID = 16638225.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HLA Antigens
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40. Weiser KC, Liu B, Hansen GM, Skapura D, Hentges KE, Yarlagadda S, Morse Iii HC, Justice MJ: Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma. Mamm Genome; 2007 Oct;18(10):709-22
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  • [Title] Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma.
  • AKXD recombinant inbred (RI) strains develop a variety of leukemias and lymphomas due to somatically acquired insertions of retroviral DNA into the genome of hematopoetic cells that can mutate cellular proto-oncogenes and tumor suppressor genes.
  • We generated a new set of tumors from nine AKXD RI strains selected for their propensity to develop B-cell tumors, the most common type of human hematopoietic cancers.
  • Furthermore, numerous previously uncharacterized genes lie near CISs, providing a pool of candidate disease genes for future research.
  • This tumor collection represents the most comprehensive study of the genetics of B-cell leukemia and lymphoma development in mice.

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  • (PMID = 17926094.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA063229; United States / NCI NIH HHS / CA / R29 CA063229; United States / NCI NIH HHS / CA / R01 CA63229; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
  • [Other-IDs] NLM/ PMC2042025
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41. Damron TA, Horton JA, Naqvi A, Loomis RM, Margulies BS, Strauss JA, Farnum CE, Spadaro JA: Combination radioprotectors maintain proliferation better than single agents by decreasing early parathyroid hormone-related protein changes after growth plate irradiation. Radiat Res; 2006 Mar;165(3):350-8
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  • While all treatments had a positive effect in reversing the decrease in B-cell leukemia 2 protein and coincident increase in Bax previously observed 2 weeks postirradiation, the two combination groups had a more robust effect.
  • [MeSH-minor] Animals. Caspase 3. Caspases / metabolism. Cell Proliferation / drug effects. Cell Proliferation / radiation effects. Extremities / anatomy & histology. Extremities / radiation effects. Immunohistochemistry. Male. Rats. Rats, Sprague-Dawley. Receptors, Parathyroid Hormone / metabolism. Time Factors

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  • (PMID = 16494524.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA83892
  • [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 / Parathyroid Hormone-Related Protein; 0 / Radiation-Protective Agents; 0 / Receptors, Parathyroid Hormone; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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42. Giné E, Martinez A, Villamor N, López-Guillermo A, Camos M, Martinez D, Esteve J, Calvo X, Muntañola A, Abrisqueta P, Rozman M, Rozman C, Bosch F, Campo E, Montserrat E: Expanded and highly active proliferation centers identify a histological subtype of chronic lymphocytic leukemia ("accelerated" chronic lymphocytic leukemia) with aggressive clinical behavior. Haematologica; 2010 Sep;95(9):1526-33
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  • [Title] Expanded and highly active proliferation centers identify a histological subtype of chronic lymphocytic leukemia ("accelerated" chronic lymphocytic leukemia) with aggressive clinical behavior.
  • BACKGROUND: The concept of "accelerated" chronic lymphocytic leukemia is frequently used by both pathologists and clinicians.
  • However, neither histological criteria to define this form of chronic lymphocytic leukemia nor its clinical correlates and prognostic impact have been formally defined in large series of patients.
  • DESIGN AND METHODS: Tissue biopsies from 100 patients with chronic lymphocytic leukemia were analyzed for the size of proliferation centers and their proliferation rate as assessed by mitosis count and Ki-67 immunostaining.
  • RESULTS: A suspicion of disease transformation was the main reason for carrying out tissue biopsy, which was performed at a median time of 14 months (range, 0 to 204 months) after the diagnosis of chronic lymphocytic leukemia.
  • The biopsy showed histological transformation to diffuse large B-cell lymphoma in 22 cases.
  • Thus, 23 patients with either expanded proliferation centers or high proliferation rate were considered as having "accelerated" chronic lymphocytic leukemia.
  • The median survival from biopsy of patients with "non-accelerated" chronic lymphocytic leukemia, "accelerated" chronic lymphocytic leukemia and transformation to diffuse large B-cell leukemia was 76, 34, and 4.3 months, respectively (P<0.001).
  • CONCLUSIONS: The presence of expanded and/or highly active proliferation centers identifies a group of patients with "accelerated" chronic lymphocytic leukemia characterized by an aggressive clinical behavior.
  • [MeSH-major] Cell Proliferation. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymph Nodes / pathology

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  • (PMID = 20421272.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  • [Other-IDs] NLM/ PMC2930954
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43. Usui T, Konnai S, Ohashi K, Onuma M: Interferon-gamma expression associated with suppression of bovine leukemia virus at the early phase of infection in sheep. Vet Immunol Immunopathol; 2007 Jan 15;115(1-2):17-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interferon-gamma expression associated with suppression of bovine leukemia virus at the early phase of infection in sheep.
  • Immunological control of bovine leukemia virus (BLV)-infection has been reported as dependent on the expression balance of types 1 and 2 cytokines.
  • The virus did not propagate well in three sheep, which showed augmented mRNA expression of IFN-gamma, a strong indicator of cell-mediated immunity, immediately after BLV-infection.
  • Among the other five sheep having more than 2% of BLV-infected cells among PBMC at 12 weeks post infection, four sheep developed B-cell leukemia or lymphoma within 2 years after infection.
  • [MeSH-major] Enzootic Bovine Leukosis / immunology. Interferon-gamma / genetics. Leukemia Virus, Bovine. Sheep Diseases / immunology

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  • (PMID = 17064782.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / RNA, Messenger; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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44. Kolmannskog S, Flaegstad T, Helgestad J, Hellebostad M, Zeller B, Glomstein A: [Childhood acute lymphoblastic leukemia in Norway 1992-2000]. Tidsskr Nor Laegeforen; 2007 May 31;127(11):1493-5
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  • [Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].
  • BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.
  • Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 17551551.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
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45. Chanan-Khan A, Kipps T, Stilgenbauer S: Clinical roundtable monograph. New alternatives in CLL therapy: managing adverse events. Clin Adv Hematol Oncol; 2010 Aug;8(8):suppl 1-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic lymphocytic leukemia (CLL) is a B-cell leukemia mainly affecting older adults.
  • Historically, CLL has been regarded as an incurable disease, and treatment has been confined to cytotoxic chemotherapy regimens.
  • The introduction of rituximab, a CD20-targeted monoclonal antibody, revolutionized the treatment for this disease.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • (PMID = 21192630.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
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46. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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47. Lucas DM, Edwards RB, Lozanski G, West DA, Shin JD, Vargo MA, Davis ME, Rozewski DM, Johnson AJ, Su BN, Goettl VM, Heerema NA, Lin TS, Lehman A, Zhang X, Jarjoura D, Newman DJ, Byrd JC, Kinghorn AD, Grever MR: The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo. Blood; 2009 May 7;113(19):4656-66
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  • [Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.
  • Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.
  • Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.
  • In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.
  • We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.
  • In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.
  • These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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  • (PMID = 19190247.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956
  • [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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol
  • [Other-IDs] NLM/ PMC2680369
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48. Chen CZ, Lodish HF: MicroRNAs as regulators of mammalian hematopoiesis. Semin Immunol; 2005 Apr;17(2):155-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Many miRNAs cloned from mouse bone marrow cells are differentially regulated in various hematopoietic lineages, suggesting that they might influence hematopoietic lineage differentiation. miR-181, a miRNA specifically expressed in B cells within mouse bone marrow, promotes B-cell differentiation when expressed in hematopoietic stem/progenitor cells.
  • Some human miRNAs are linked to leukemias: the miR-15a/miR-16 locus is frequently deleted or down-regulated in patients with B-cell chronic lymphocytic leukemia and miR-142 is at a translocation site found in a case of aggressive B-cell leukemia.

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  • (PMID = 15737576.001).
  • [ISSN] 1044-5323
  • [Journal-full-title] Seminars in immunology
  • [ISO-abbreviation] Semin. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NHLBI NIH HHS / HL / R01 HL081612-01; United States / NHLBI NIH HHS / HL / R01 HL081612-02; United States / NIDDK NIH HHS / DK / R01 DK068348
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Number-of-references] 114
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49. Cook JR, Aguilera NI, Reshmi S, Huang X, Yu Z, Gollin SM, Abbondanzo SL, Swerdlow SH: Deletion 6q is not a characteristic marker of nodal lymphoplasmacytic lymphoma. Cancer Genet Cytogenet; 2005 Oct 1;162(1):85-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Lymphoplasmacytic lymphoma (LPL) is a small B-cell neoplasm with plasmacytic differentiation that does not fulfill the criteria for any other type of B-cell leukemia or lymphoma.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6. Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • [MeSH-minor] Biomarkers, Tumor. Humans. In Situ Hybridization, Fluorescence / methods. Lymphoma, B-Cell / genetics

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  • (PMID = 16157207.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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50. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
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  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • On the other hand, the inverse relationship between severity of anemia and survival found within specific subgroups suggests that very low hemoglobin levels at diagnosis are associated with more advanced disease in these subgroups.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome


51. Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB: Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids. Cancer Cell Int; 2007 Nov 28;7:18
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  • Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
  • GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.
  • Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).
  • To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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  • (PMID = 18045478.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041407
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2228275
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52. Foss F: Clinical experience with denileukin diftitox (ONTAK). Semin Oncol; 2006 Feb;33(1 Suppl 3):S11-6
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The high-affinity form of this receptor is expressed on activated T lymphocytes, activated B lymphocytes, and activated macrophages.
  • A number of leukemias and lymphomas, including cutaneous T-cell lymphoma, chronic lymphocytic leukemia, and B-cell non-Hodgkin's lymphoma, express a component of the receptor.
  • Ex vivo studies have shown that denileukin diftitox interacts with the high- and intermediate-affinity IL-2 receptor on the cell surface and undergoes internalization.
  • Subsequent cleavage in the endosome releases the diphtheria toxin into the cytosol, which then inhibits cellular protein synthesis, resulting in rapid cell death.
  • This article examines the clinical profile and potential benefits of denileukin diftitox in the treatment of cutaneous T-cell lymphoma and other hematologic disorders.
  • [MeSH-minor] Graft vs Host Disease / drug therapy. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell, Cutaneous / drug therapy. Receptors, Interleukin-2 / metabolism. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 16516670.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 15
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53. Dai ZS, Chen QF, Lu HZ, Xie Y: Defective expression and modulation of B7-2/CD86 on B cells in B cell chronic lymphocytic leukemia. Int J Hematol; 2009 Jun;89(5):656-63
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defective expression and modulation of B7-2/CD86 on B cells in B cell chronic lymphocytic leukemia.
  • Malignant monoclonal B cells of chronic B cell lymphocytic leukemia (B-CLL) usually fail to be cleared, which indicates important costimulatory molecules may be lacking.
  • In this study, B7-1 and B7-2 expression on B cells in chronic B cell lymphocytic leukemia patients were detected.
  • Data showed that B7-2 expression in chronic B cell lymphocytic leukemia patients is significantly lower than in normal people, which suggests defective B7-2 expression may be one of the pathogenic mechanisms of chronic B cell lymphocytic leukemia.
  • Further, we confirmed interferon-gamma could induce B7-2 expression slightly and promote T-cell response against chronic B cell lymphocytic leukemia cells, indicating interferon-gamma has clinical value in chronic leukemia immunotherapy based on modulating B7-2 expression.
  • [MeSH-major] Antigens, CD86 / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD80 / analysis. B-Lymphocytes / pathology. Case-Control Studies. Female. Humans. Interferon-gamma / pharmacology. Male. Middle Aged

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  • (PMID = 19430862.001).
  • [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] Japan
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD86; 82115-62-6 / Interferon-gamma
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54. Ho AD, Hensel M: Pentostatin and purine analogs for indolent lymphoid malignancies. Future Oncol; 2006 Apr;2(2):169-83
Hazardous Substances Data Bank. PENTOSTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pentostatin has been shown to be active in a variety of B- and T-cell malignancies.
  • Early clinical trials indicated that this agent was highly active in acute lymphoblastic leukemias with high intracellular adenosine deaminase levels.
  • Through the efforts of a few investigators, better tolerated, low-dose regimens have been shown to be extremely active in lymphoproliferative diseases with very low intracellular adenosine deaminase levels such as hairy cell leukemia, B- and T-cell chronic leukemias, T-cell cutaneous lymphomas and low-grade non-Hodgkin lymphomas.
  • Although all the purine analogs have shown similar activity, the advantage of pentostatin is the relatively specific cytotoxicity against lymphocytes, which permits treatment even in patients with severe cytopenias.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Leukemia, Hairy Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Pentostatin / therapeutic use. Purine Nucleosides / therapeutic use

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  • (PMID = 16563086.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin
  • [Number-of-references] 92
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55. Hatakeyama N, Tamura Y, Sahara H, Suzuki N, Suzuki K, Hori T, Mizue N, Torigoe T, Tsutsumi H, Sato N: Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells. Exp Hematol; 2006 Feb;34(2):197-207

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells.
  • OBJECTIVE: Several studies have demonstrated that dendritic cells (DCs) pulsed with tumor lysate or apoptotic tumor cells can elicit effective T-cell responses.
  • We applied this approach to induce HLA class I- and class II-restricted T-cell responses directed against autologous acute lymphocytic leukemia (B-ALL) cell line NH-1.
  • METHODS: Autologous T cells were stimulated by apoptotic tumor cell-loaded DCs generated from a patient with ALL.
  • The stimulated and expanded T cells were isolated into CD8(+) T-cell line and CD4(+) T-cell line, and each of them was examined as to their functions.
  • RESULTS: Both CD8(+) and CD4(+) T-cell lines demonstrated cytotoxicity against NH-1 in an major histocompatibility complex-dependent manner.
  • Finally, we established two independent CD4(+) T-cell clones restricted to HLA-DR.
  • The CD4(+) T-cell line responded strongly to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) but not to autologous normal cells.
  • Furthermore, the T-cell clones also responded to allogeneic EBV-LCLs and B-ALL cell lines in the context of the HLA-DRB1( *)04051 molecule.
  • Interestingly, 293T and COS-7 cells, which had been transfected with the HLA-DRB1( *)04051, were also recognized by T-cell clones.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Fusion. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Apoptosis / immunology. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. Epitopes / immunology. Epstein-Barr Virus Nuclear Antigens / immunology. Female. HLA-DR Antigens / classification. HLA-DR Antigens / immunology. Histocompatibility Antigens Class II / immunology. Histocompatibility Antigens Class II / pharmacology. Humans. Infant. Lymphocyte Activation

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  • (PMID = 16459188.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Epitopes; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / HLA-DR Antigens; 0 / Histocompatibility Antigens Class II
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56. Kraigher-Krainer E, Lackner H, Sovinz P, Schwinger W, Benesch M, Urban C: Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):426-8
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] Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia.
  • We report on an 11-year-old male who presented with NCS as initial manifestation of acute lymphoblastic leukemia of B-cell type.
  • [MeSH-major] Chin / pathology. Hypesthesia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18506757.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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57. McCarthy BA, Boyle E, Wang XP, Guzowski D, Paul S, Catera R, Trott J, Yan XJ, Croce CM, Damle R, Yancopoulos S, Messmer BT, Lesser M, Allen SL, Rai KR, Chiorazzi N: Surface expression of Bcl-2 in chronic lymphocytic leukemia and other B-cell leukemias and lymphomas without a breakpoint t(14;18). Mol Med; 2008 Sep-Oct;14(9-10):618-27
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surface expression of Bcl-2 in chronic lymphocytic leukemia and other B-cell leukemias and lymphomas without a breakpoint t(14;18).
  • Here we show that Bcl-2 also can position on the outer cell surface membrane of B cells from patients with chronic lymphocytic leukemia (B-CLL) and certain other leukemias that do not classically possess the chromosomal breakpoint t(14;18).
  • It is not clear if this surface membrane expression is a passive consequence of the apoptotic process or an active attempt by the B cell to abort cell death by stabilizing the plasma membrane.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • Genetic Alliance. consumer health - B-Cell Lymphomas.
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  • (PMID = 18633450.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA087956; United States / NCI NIH HHS / CA / R01 CA87956
  • [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 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2464573
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58. Chiorazzi N: Cell proliferation and death: forgotten features of chronic lymphocytic leukemia B cells. Best Pract Res Clin Haematol; 2007 Sep;20(3):399-413
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell proliferation and death: forgotten features of chronic lymphocytic leukemia B cells.
  • Chronic lymphocytic leukemia (CLL) results from an accumulation of abnormal B cells due to an imbalance between birth and death rates such that the former exceeds the latter.
  • CLL has long been considered a disease in which cell accumulation results from decreased death, due to a genetic defect, with minimal birth of the leukemic clone.
  • CLL cells appeared as resting lymphocytes by light microscopy and responded poorly to mitogens (primarily T-cell mitogens)--at a time when T- and B-cell discrimination was not well appreciated.
  • However, recent studies using more sophisticated measures suggest that the initial characterization of CLL biology needs re-evaluation.
  • Using a safe, non-radioactive in-vivo labeling method that permits the determination of CLL-cell birth rates, we have directly documented that a small fraction of the clone (approximately 0.1-1.75%), i.e., between approximately 1x10(9) and 1x10(12) cells are born each day in all patients studied.
  • Thus the dynamic interplay between birth and death that characterizes other leukemias and lymphomas applies to CLL.
  • Therefore, CLL is a disease of both proliferation and accumulation in which a homeostatic balance exists in patients with stable lymphocyte counts or an imbalance exists in patients with rising lymphocyte counts.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Death / physiology. Cell Proliferation. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
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  • (PMID = 17707829.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA81554; United States / NCI NIH HHS / CA / R01 CA87956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 83
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59. Kiss F, Buslig J, Szegedi I, Scholtz B, Kappelmayer J, Kiss C: Early relapse after rituximab chemoimmunotherapy. Pediatr Blood Cancer; 2008 Feb;50(2):372-5
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In relapsed/refractory childhood acute lymphoblastic leukemia (ALL) of the B-cell lineage rituximab, a monoclonal anti-CD20 antibody was used successfully in some cases.
  • We report on a 15-year-old female with relapsed CD20-positive B-cell progenitor ALL treated with rituximab because of positive minimal residual disease signals after chemotherapy, as checked by flow cytometry and real time quantitative-PCR.
  • The patient died with fulminant aspergillosis before hematopoietic stem cell transplantation could be performed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Humans. Neoplasm, Residual / pathology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973316.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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60. Kuramochi K, Yukizawa S, Ikeda S, Sunoki T, Arai S, Matsui R, Morita A, Mizushina Y, Sakaguchi K, Sugawara F, Ikekita M, Kobayashi S: Syntheses and applications of fluorescent and biotinylated epolactaene derivatives: Epolactaene and its derivative induce disulfide formation. Bioorg Med Chem; 2008 May 1;16(9):5039-49
Hazardous Substances Data Bank. N-ACETYLCYSTEINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BM 1689-P mycelium, induces neurite outgrowth and arrests the cell cycle of the human neuroblastoma cell line, SH-SY5Y, at the G1 phase.
  • We have found that epolactaene and its derivatives induce apoptosis in the human leukemia B-cell line, BALL-1.
  • [MeSH-minor] Acetylcysteine / analogs & derivatives. Acetylcysteine / chemistry. Biotinylation. Cell Death / drug effects. Drug Screening Assays, Antitumor. Epoxy Compounds / chemical synthesis. Epoxy Compounds / chemistry. Epoxy Compounds / pharmacology. Fluorescence. Humans. Molecular Structure. Polyenes / chemical synthesis. Polyenes / chemistry. Polyenes / pharmacology. Stereoisomerism. Tumor Cells, Cultured

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  • (PMID = 18375133.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Disulfides; 0 / Epoxy Compounds; 0 / Polyenes; 0 / epolactaene; 6SO6U10H04 / Biotin; WYQ7N0BPYC / Acetylcysteine
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61. Carmody RJ, Ruan Q, Palmer S, Hilliard B, Chen YH: Negative regulation of toll-like receptor signaling by NF-kappaB p50 ubiquitination blockade. Science; 2007 Aug 3;317(5838):675-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulator of TLR signaling.
  • [MeSH-minor] Animals. Cell Line. Cells, Cultured. DNA / metabolism. Female. Half-Life. Immune Tolerance. Immunity, Innate. Lipopolysaccharides / immunology. Macrophage Activation. Male. Mice. Mice, Inbred C57BL. Promoter Regions, Genetic. Transcription Factor RelA / metabolism. Transcription, Genetic. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism. Ubiquitin / metabolism

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  • (PMID = 17673665.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI069289; United States / NIAID NIH HHS / AI / AI50059; United States / NIDDK NIH HHS / DK / DK070691
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / NF-kappa B p50 Subunit; 0 / Proto-Oncogene Proteins; 0 / Rela protein, mouse; 0 / Toll-Like Receptors; 0 / Transcription Factor RelA; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Ubiquitin; 0 / proto-oncogene protein bcl-3; 9007-49-2 / DNA
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62. Kuramochi K, Matsui R, Matsubara Y, Nakai J, Sunoki T, Arai S, Nagata S, Nagahara Y, Mizushina Y, Ikekita M, Kobayashi S: Apoptosis-inducing effect of epolactaene derivatives on BALL-1 cells. Bioorg Med Chem; 2006 Apr 1;14(7):2151-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Epolactaene, a neuritogenic compound in human neuroblastoma SH-SY5Y, induces apoptosis in a human leukemia B-cell line, BALL-1.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, B-Cell / drug therapy
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Drug Screening Assays, Antitumor. Epoxy Compounds / chemical synthesis. Epoxy Compounds / chemistry. Epoxy Compounds / pharmacology. Humans. Hydrolysis. Molecular Structure. Polyenes / chemical synthesis. Polyenes / chemistry. Polyenes / pharmacology. Stereoisomerism. Structure-Activity Relationship

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  • (PMID = 16298530.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Epoxy Compounds; 0 / Polyenes; 0 / epolactaene
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63. Boström H, Leuchowius KJ, Hallböök H, Nordgren A, Thörn I, Thorselius M, Rosenquist R, Söderberg O, Sundström C: U-2973, a novel B-cell line established from a patient with a mature B-cell leukemia displaying concurrent t(14;18) and MYC translocation to a non-IG gene partner. Eur J Haematol; 2008 Sep;81(3):218-25
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  • [Title] U-2973, a novel B-cell line established from a patient with a mature B-cell leukemia displaying concurrent t(14;18) and MYC translocation to a non-IG gene partner.
  • B-cell lymphomas/leukemias with simultaneous t(14;18)(q32;q21) and MYC rearrangements have recently been shown to constitute a separate diagnostic entity, presenting with a rapid clinical course and a very poor prognosis.
  • We describe the establishment of an Epstein-Barr virus negative cell line, designated U-2973, from a male patient with a de novo aggressive B-cell lymphoma/leukemia and very high peripheral blast cell count.
  • Flow cytometry of bone marrow cells and U-2973 displayed a mature B-cell phenotype, and immunostaining showed expression of MYC and BCL2.
  • [MeSH-major] Cell Line. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. Leukemia, B-Cell / genetics. Lymphoma, B-Cell / genetics. Proto-Oncogene Proteins c-myc / genetics. Translocation, Genetic

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  • (PMID = 18510704.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc
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64. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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65. Chiron D, Bekeredjian-Ding I, Pellat-Deceunynck C, Bataille R, Jego G: Toll-like receptors: lessons to learn from normal and malignant human B cells. Blood; 2008 Sep 15;112(6):2205-13
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  • These encounters promote plasma cell differentiation and antibody production.
  • In hematologic malignancies, cells often retain B cell-specific receptors and associated functions.
  • Among these, TLRs are currently exploited to target different subclasses of B-cell leukemia, and TLR agonists are currently being evaluated in clinical trials.
  • However, accumulating evidence suggests that endogenous TLR ligands or chronic infections promote tumor growth, thus providing a need for further investigations to decipher the exact function of TLRs in the B-cell lineage and in neoplastic B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Toll-Like Receptors / immunology
  • [MeSH-minor] Antibody Formation. Humans. Leukemia, B-Cell / pathology. Ligands. Lymphoma, B-Cell / pathology

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  • (PMID = 18591383.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Toll-Like Receptors
  • [Number-of-references] 80
  • [Other-IDs] NLM/ PMC2532798
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66. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
SciCrunch. DrugBank: Data: Chemical .

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  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Nelarabine is water soluble and rapidly converted to ara-G, which is specifically cytotoxic to T-lymphocytes and T-lymphoblastoid cells.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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67. Hasselbach HC, Fickenscher H, Nölle B, Roider J: [Atypical ocular toxoplasmosis with concomitant ocular reactivation of varicella-zoster virus and cytomegalovirus in an immunocompromised host]. Klin Monbl Augenheilkd; 2008 Mar;225(3):236-9
Hazardous Substances Data Bank. PREDNISOLONE .

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  • HISTORY AND SIGNS: A case of an initially therapy-resistant, necrotizing retinopathy is presented in a 65-year-old immunocompromised male patient suffering from chronic B-cell leukemia.
  • [MeSH-major] Chorioretinitis / diagnosis. Cytomegalovirus / physiology. Cytomegalovirus Infections / diagnosis. Herpes Zoster Ophthalmicus / diagnosis. Herpesvirus 3, Human. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Opportunistic Infections / diagnosis. Toxoplasmosis, Ocular / diagnosis. Virus Activation

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  • (PMID = 18351539.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 18D0SL7309 / Chlorambucil; 9PHQ9Y1OLM / Prednisolone
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68. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
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  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.
  • CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
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69. Waldmann TA, Morris JC: Development of antibodies and chimeric molecules for cancer immunotherapy. Adv Immunol; 2006;90:83-131
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  • Monoclonal antibodies targeting non-Hodgkin's lymphoma (NHL), Her-2/neu highly expressing metastatic breast cancer, colorectal cancer, acute myelogenous leukemia, and B-cell chronic lymphocytic leukemia (CLL) have received FDA approval.

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  • (PMID = 16730262.001).
  • [ISSN] 0065-2776
  • [Journal-full-title] Advances in immunology
  • [ISO-abbreviation] Adv. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins
  • [Number-of-references] 194
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70. Kawahara T, Kawaguchi-Ihara N, Okuhashi Y, Itoh M, Nara N, Tohda S: Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells. Anticancer Res; 2009 Nov;29(11):4629-32
Hazardous Substances Data Bank. CYCLOPAMINE .

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  • [Title] Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells.
  • BACKGROUND: Hedgehog (Hh) and Wnt signaling pathways are involved in the stimulation of growth of leukemia and lymphoma cells.
  • In the present study, whether or not the Hh inhibitor, cyclopamine, and the Wnt inhibitor, quercetin, suppress cell growth was investigated.
  • MATERIALS AND METHODS: The effects of cyclopamine and quercetin on the in vitro growth and protein expression of ten acute leukemia and B-cell lymphoma cell lines were examined.
  • RESULTS: Cyclopamine and quercetin suppressed cell growth and induced apoptosis in seven and eight cell lines respectively.
  • Quercetin decreased the level of Notch1 protein and its active fragment in the DND-41 T-lymphoblastic leukemia cell line with constitutive Notch activation.
  • CONCLUSION: Cyclopamine and quercetin suppress the growth of a number of leukemia and lymphoma cells.
  • This finding suggests the potential use of these compounds in molecularly-targeted therapy for leukemia and lymphoma.
  • [MeSH-major] Leukemia / drug therapy. Lymphoma / drug therapy. Quercetin / pharmacology. Veratrum Alkaloids / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. Protein Biosynthesis / drug effects. Receptor, Notch1 / biosynthesis. Transcription Factors / biosynthesis

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  • (PMID = 20032413.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Transcription Factors; 0 / Veratrum Alkaloids; 9IKM0I5T1E / Quercetin; ZH658AJ192 / cyclopamine
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71. Hatakeyama M: [Oncogenic mechanism of Helicobacter pylori]. Nihon Rinsho Meneki Gakkai Kaishi; 2008 Jun;31(3):132-40
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  • As a result, CagA causes aberrant mitogenic signal as well as elevated cell motility in gastric epithelial cells.
  • Also, CagA specifically interacts with and inhibits PAR1b/MARK2 polarity-regulating kinase to disrupt tight junctions and cause loss of epithelial apical-basolateral cell polarity.
  • Indeed, recently generated cagA-transgenic mice expressing CagA systemically developed gastrointestinal carcinomas as well hematopoietic malignancies such as myeloid leukemia and B-cell lymphoma.

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  • (PMID = 18587223.001).
  • [ISSN] 1349-7413
  • [Journal-full-title] Nihon Rinshō Men'eki Gakkai kaishi = Japanese journal of clinical immunology
  • [ISO-abbreviation] Nihon Rinsho Meneki Gakkai Kaishi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / Oncogene Proteins; 0 / cagA protein, Helicobacter pylori
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72. Simeonova A, Abo-Madyan Y, Ströbel P, Kleine W, Schwarzbach M, Fleckenstein K, Wenz F: Bone marrow-sparing intensity-modulated radiotherapy (IMRT) for neo-adjuvant therapy of inoperable cervical cancer in a patient with severe thrombocytopenia. Onkologie; 2010;33(4):189-92
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  • CASE REPORT: We describe a 50-year-old woman with inoperable cervical carcinoma and chronic lymphatic B cell leukemia (B-CLL).


73. Chen X, Estévez MC, Zhu Z, Huang YF, Chen Y, Wang L, Tan W: Using aptamer-conjugated fluorescence resonance energy transfer nanoparticles for multiplexed cancer cell monitoring. Anal Chem; 2009 Aug 15;81(16):7009-14
The Lens. Cited by Patents in .

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  • [Title] Using aptamer-conjugated fluorescence resonance energy transfer nanoparticles for multiplexed cancer cell monitoring.
  • These FRET nanoparticles were then modified by a few aptamers specific for different cancer cell lines, in this case, T-cell leukemia and B-cell lymphoma.
  • As a result, simultaneous and sensitive detection of multiple cancer cell targets was achieved.

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  • (PMID = 19572554.001).
  • [ISSN] 1520-6882
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] eng
  • [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 / Aptamers, Nucleotide
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74. Su X, Della-Valle V, Delabesse E, Azgui Z, Berger R, Merle-Béral H, Bernard OA, Nguyen-Khac F: Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder. Haematologica; 2008 Jul;93(7):1081-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder.
  • Study of T-cell acute lymphoblastic leukemia identified the related non-clustered homeobox transcription factors, TLX1 and TLX3, as frequently ectopically expressed as a result of chromosomal translocations.
  • We report the deregulation of a non-clustered homeobox gene in a new type of t(5;14)(q35;q11) translocation in a mature peripheral B-cell leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Gene Expression Regulation. Homeodomain Proteins / genetics. Lymphoproliferative Disorders / genetics. Lymphoproliferative Disorders / pathology. Transcription Factors / genetics. Transcriptional Activation
  • [MeSH-minor] Cell Proliferation. Chronic Disease. Cytogenetics. Female. Humans. Middle Aged. Models, Biological. Mutation. Sequence Analysis, DNA. Translocation, Genetic

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  • (PMID = 18492690.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Transcription Factors
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75. Senawong T, Peterson VJ, Leid M: BCL11A-dependent recruitment of SIRT1 to a promoter template in mammalian cells results in histone deacetylation and transcriptional repression. Arch Biochem Biophys; 2005 Feb 15;434(2):316-25
Hazardous Substances Data Bank. NICOTINAMIDE .

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  • The B cell leukemia 11A protein (BCL11A/Evi9/CTIP1) has been implicated in hematopoietic cell development and malignancies.

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  • (PMID = 15639232.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES00210; United States / NIGMS NIH HHS / GM / R01 GM060852-02; United States / NIEHS NIH HHS / ES / ES000210-35; United States / NIGMS NIH HHS / GM / GM60852; United States / NIEHS NIH HHS / ES / P30 ES000210-35; United States / NIGMS NIH HHS / GM / R01 GM060852; United States / NIGMS NIH HHS / GM / GM060852-02; United States / NIEHS NIH HHS / ES / P30 ES000210
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL11A protein, human; 0 / Carrier Proteins; 0 / Histones; 0 / Hydroxamic Acids; 0 / Nuclear Proteins; 25X51I8RD4 / Niacinamide; 3X2S926L3Z / trichostatin A; EC 2.5.1.18 / Glutathione Transferase; EC 3.5.1.- / SIRT1 protein, human; EC 3.5.1.- / Sirtuin 1; EC 3.5.1.- / Sirtuins; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ NIHMS173222; NLM/ PMC2819353
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76. Loisel S, Le Ster K, Meyer M, Berthou C, Youinou P, Kolb JP, Billard C: Therapeutic activity of two xanthones in a xenograft murine model of human chronic lymphocytic leukemia. J Hematol Oncol; 2010;3:49
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  • [Title] Therapeutic activity of two xanthones in a xenograft murine model of human chronic lymphocytic leukemia.
  • BACKGROUND: We previously reported that allanxanthone C and macluraxanthone, two xanthones purified from Guttiferae trees, display in vitro antiproliferative and proapoptotic activities in leukemic cells from chronic lymphocytic leukemia (CLL) and leukemia B cell lines.
  • RESULTS: Here, we investigated the in vivo therapeutic effects of the two xanthones in a xenograft murine model of human CLL, developed by engrafting CD5-transfected chronic leukemia B cells into SCID mice.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Xanthones / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, SCID. Xenograft Model Antitumor Assays

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  • (PMID = 21138552.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Xanthones; 0 / allanxanthone C
  • [Other-IDs] NLM/ PMC3016254
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77. van Zelm MC, van der Burg M, de Ridder D, Barendregt BH, de Haas EF, Reinders MJ, Lankester AC, Révész T, Staal FJ, van Dongen JJ: Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression. J Immunol; 2005 Nov 1;175(9):5912-22
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  • [Title] Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression.
  • The role of specific transcription factors in the initiation and regulation of Ig gene rearrangements has been studied extensively in mouse models, but data on normal human precursor B cell differentiation are limited.
  • We purified five human precursor B cell subsets, and assessed and quantified their IGH, IGK, and IGL gene rearrangement patterns and gene expression profiles.
  • Transcripts of the RAG1 and RAG2 genes and earlier defined transcription factors, such as E2A, early B cell factor, E2-2, PAX5, and IRF4, were specifically up-regulated at stages undergoing Ig gene rearrangements.
  • Based on the combined Ig gene rearrangement status and gene expression profiles of consecutive precursor B cell subsets, we identified 16 candidate genes involved in initiation and/or regulation of Ig gene rearrangements.
  • These analyses provide new insights into early human precursor B cell differentiation steps and represent an excellent template for studies on oncogenic transformation in precursor B acute lymphoblastic leukemia and B cell differentiation blocks in primary Ab deficiencies.
  • [MeSH-minor] Adolescent. Cell Separation. Child. Child, Preschool. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Humans

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  • [ErratumIn] J Immunol. 2006 Jun 15;176(12):7787
  • (PMID = 16237084.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
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78. Viny AD, Lichtin A, Pohlman B, Loughran T, Maciejewski J: Chronic B-cell dyscrasias are an important clinical feature of T-LGL leukemia. Leuk Lymphoma; 2008 May;49(5):932-8
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  • [Title] Chronic B-cell dyscrasias are an important clinical feature of T-LGL leukemia.
  • T cell large granular lymphocyte leukemia (T-LGL) is characterised by semiautonomous proliferation of monoclonal cytotoxic T lymphocytes, which can result in neutropenia, splenomegaly, and is associated with various autoimmune disorders, particularly rheumatoid arthritis.
  • The coexistence of T-LGL leukemia with B cell abnormalities has previously been identified in case reports.
  • We identified coexisting B cell dyscrasias in 17 T-LGL patients (27% of total), of whom 12 had monoclonal gammopathy of unknown significance (MGUS) (19%), and 5 had chronic lymphocytic leukemia (CLL) (8%).
  • Additionally, polyclonal hypergammaglobulinemia or hypogammaglobulinemia was found in 10 additional LGL leukemia patients bringing the total frequency of B cell abnormalities in T-LGL leukemia to 43% in our cohort.
  • The co-association of B cell pathology with T-LGL suggests that either a common antigen drives clonal B and T cells, or that humoral malignancy could serve as the stimulus for lymphocyte expansion representing an overactive anti-tumour surveillance.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Large Granular Lymphocytic / etiology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Agammaglobulinemia / complications. Comorbidity. Humans. Hypergammaglobulinemia / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Lymphoma, Follicular / complications. Monoclonal Gammopathy of Undetermined Significance / complications

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  • [CommentIn] Leuk Lymphoma. 2008 May;49(5):845-6 [18464104.001]
  • (PMID = 18452068.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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79. Mühlbauer M, Chilton PM, Mitchell TC, Jobin C: Impaired Bcl3 up-regulation leads to enhanced lipopolysaccharide-induced interleukin (IL)-23P19 gene expression in IL-10(-/-) mice. J Biol Chem; 2008 May 23;283(21):14182-9
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  • Lipopolysaccharide (LPS)-induced B cell leukemia 3 (Bcl3) expression was strongly impaired (90% decrease) in IL-10(-/-) BMDC compared with WT BMDC.

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  • (PMID = 18375954.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI071047; United States / NIDDK NIH HHS / DK / R01 DK047700; United States / NIDDK NIH HHS / DK / R01 DK 47700; United States / NIDDK NIH HHS / DK / R01 DK 73338
  • [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 / Interleukin-23; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Toll-Like Receptors; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3; 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ PMC2386919
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80. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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81. Kawamata N, Ogawa S, Zimmermann M, Niebuhr B, Stocking C, Sanada M, Hemminki K, Yamatomo G, Nannya Y, Koehler R, Flohr T, Miller CW, Harbott J, Ludwig WD, Stanulla M, Schrappe M, Bartram CR, Koeffler HP: Cloning of genes involved in chromosomal translocations by high-resolution single nucleotide polymorphism genomic microarray. Proc Natl Acad Sci U S A; 2008 Aug 19;105(33):11921-6
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  • Using this technique, we found that the PAX5 gene was rearranged to a variety of partner genes including ETV6, FOXP1, AUTS2, and C20orf112 in pediatric acute lymphoblastic leukemia (ALL).
  • In human B cell leukemia cells, binding of wild-type PAX5 to a regulatory region of BLK, one of the direct downstream target genes of PAX5, was diminished by expression of the PAX5-fusion protein, leading to repression of BLK.
  • [MeSH-minor] Animals. B-Cell-Specific Activator Protein / genetics. B-Cell-Specific Activator Protein / metabolism. Base Sequence. Cell Line. Cloning, Molecular. DNA / genetics. Humans. Mice. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Transcription, Genetic / genetics

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  • (PMID = 18697940.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ EU784145/ EU784146/ EU784147/ EU784148
  • [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 / PAX5 protein, human; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2575257
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82. Meng H, Yang C, Ni W, Ding W, Yang X, Qian W: Antitumor activity of fludarabine against human multiple myeloma in vitro and in vivo. Eur J Haematol; 2007 Dec;79(6):486-93
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  • Fludarabine, a nucleoside analogue, plays a major role in the treatment of B-cell lymphocytic leukemia, hairy cell leukemia, and indolent lymphomas.
  • We demonstrated that myeloma cell line RPMI8226 was efficiently inhibited by fludarabine, concomitantly with decreased phosphorylation of Akt, down-regulation of the inhibitor of apoptosis proteins (IAP) family, including XIAP and survivin, and induction of apoptosis related to activation of caspase cascade.
  • [MeSH-minor] Animals. Apoptosis. Cell Cycle. Dexamethasone / pharmacology. Female. Humans. In Vitro Techniques. Inhibitory Concentration 50. Mice. Mice, SCID. Neoplasm Transplantation


83. Yao J, Duan L, Fan M, Wu X: Gamma-secretase inhibitors exerts antitumor activity via down-regulation of Notch and Nuclear factor kappa B in human tongue carcinoma cells. Oral Dis; 2007 Nov;13(6):555-63
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  • Cell growth was determined by the methylthiazole tetrazolium method.
  • Cell cycle and apoptosis were analyzed by flow cytometry and/or confocal microscopy.
  • RESULTS: L-685,458 dose-dependently inhibited the growth of human tongue carcinoma Tca8113 cells by inducing G0-G1 cell cycle arrest and apoptosis.
  • Furthermore, L-685,458 down-regulated cyclin D1, B-cell lymphocytic-leukemia proto-oncogene 2 and c-Myc expressions, which are regulated by the transcription factor NF-kappaB.
  • [MeSH-minor] Analysis of Variance. Apoptosis / drug effects. Cell Cycle / drug effects. Down-Regulation. Drug Screening Assays, Antitumor. Humans. Tumor Cells, Cultured

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  • (PMID = 17944672.001).
  • [ISSN] 1354-523X
  • [Journal-full-title] Oral diseases
  • [ISO-abbreviation] Oral Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Carbamates; 0 / Dipeptides; 0 / Enzyme Inhibitors; 0 / L 685458; 0 / NF-kappa B; 0 / Receptors, Notch; EC 3.4.- / Amyloid Precursor Protein Secretases
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84. Tamura K, Arai H, Ueno E, Saito C, Yagihara H, Isotani M, Ono K, Washizu T, Bonkobara M: Comparison of dendritic cell-mediated immune responses among canine malignant cells. J Vet Med Sci; 2007 Sep;69(9):925-30
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  • [Title] Comparison of dendritic cell-mediated immune responses among canine malignant cells.
  • Dendritic cell (DC) vaccination is one of the most attractive immunotherapies for malignancies in dogs.
  • To examine the differences in DC-mediated immune responses from different types of malignancies in dogs, we vaccinated dogs using autologous DCs pulsed with keyhole limpet hemocyanin (KLH) and cell lysate prepared from squamous cell carcinoma SCC2/88 (SCC-KLH-DC), histiocytic sarcoma CHS-5 (CHS-KLH-DC), or B cell leukemia GL-1 (GL-KLH-DC) in vitro.
  • By contrast, neither CD8 nor CD4 T cell infiltration was found at the DTH challenge site in the dogs vaccinated with CHS-KLH-DC or GL-KLH-DC.
  • These findings may reflect that the efficacy of immune induction by DC vaccination varies among tumor types and that immune responses could be inducible in squamous cell carcinoma.
  • Our results encouraged further investigation of therapeutic vaccination for dogs with advanced squamous cell carcinoma in clinical trials.

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  • (PMID = 17917377.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines
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85. Hebeis B, Vigorito E, Kovesdi D, Turner M: Vav proteins are required for B-lymphocyte responses to LPS. Blood; 2005 Jul 15;106(2):635-40
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  • B lymphocytes respond to bacterial lipopolysaccharide (LPS) through Toll-like receptor 4 (TLR4) and CD180 (previously called RP105).
  • We show here that the responses of B lymphocytes to LPS require the function of the Vav family of guanine nucleotide exchange factors.
  • Induction of CD86 and CD25 by anti-CD180 also required Vav function, as did the induction of the anti-apoptotic protein Bcl-xL (B-cell leukemia XL).
  • [MeSH-major] B-Lymphocytes / drug effects. B-Lymphocytes / metabolism. Cell Cycle Proteins / immunology. Lipopolysaccharides / pharmacology. Oncogene Proteins / immunology. Proto-Oncogene Proteins / immunology

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  • (PMID = 15811961.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBS/E/B/0000M050; United Kingdom / Medical Research Council / / G117/424
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Bcl2l1 protein, mouse; 0 / Cell Cycle Proteins; 0 / Immunoglobulin G; 0 / Lipopolysaccharides; 0 / Ly78 protein, mouse; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-vav; 0 / Receptors, Immunologic; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 4; 0 / Vav1 protein, mouse; 0 / Vav2 protein, mouse; 0 / bcl-X Protein
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86. De Keersmaecker K, Graux C, Odero MD, Mentens N, Somers R, Maertens J, Wlodarska I, Vandenberghe P, Hagemeijer A, Marynen P, Cools J: Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32). Blood; 2005 Jun 15;105(12):4849-52
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  • [Title] Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32).
  • The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Fusion Proteins, bcr-abl / chemistry. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, T-Cell / pathology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Base Sequence. Benzamides. Blotting, Western. Cell Line. Cell Survival. DNA, Complementary / metabolism. DNA-Binding Proteins / metabolism. Female. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Microtubules / metabolism. Milk Proteins / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Genetic. Molecular Sequence Data. Open Reading Frames. Phenotype. Phosphorylation. Piperazines / pharmacology. Polymerase Chain Reaction. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Pyrimidines / pharmacology. Recombinant Fusion Proteins / metabolism. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Signal Transduction. Time Factors. Trans-Activators / metabolism

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  • (PMID = 15713800.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / EML1-ABL1 fusion protein, human; 0 / Milk Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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87. Sand SL, Oppegård C, Ohara S, Iijima T, Naderi S, Blomhoff HK, Nissen-Meyer J, Sand O: Plantaricin A, a peptide pheromone produced by Lactobacillus plantarum, permeabilizes the cell membrane of both normal and cancerous lymphocytes and neuronal cells. Peptides; 2010 Jul;31(7):1237-44
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  • [Title] Plantaricin A, a peptide pheromone produced by Lactobacillus plantarum, permeabilizes the cell membrane of both normal and cancerous lymphocytes and neuronal cells.
  • To investigate if preferential effect on cancerous cells is a general feature of PlnA, we have studied effects of the peptide on normal and cancerous lymphocytes and neuronal cells.
  • Normal human B and T cells, Reh cells (from human B cell leukemia), and Jurkat cells (from human T cell leukemia) were studied by flow cytometry to detect morphological changes (scatter) and viability (propidium iodide uptake), and by patch clamp recordings to monitor membrane conductance.
  • All the tested cell types were affected by 10-100 microM PlnA, whereas concentrations below 10 microM had no significant effect.
  • We conclude that normal and cancerous lymphocytes and neuronal cells show similar sensitivity to PlnA.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bacteriocins / pharmacology. Cell Membrane Permeability / drug effects. Lactobacillus plantarum / metabolism
  • [MeSH-minor] Animals. Cell Membrane / drug effects. Cell Membrane / metabolism. Flow Cytometry. Humans. Jurkat Cells. Leukemia / metabolism. Leukemia / pathology. Lymphocytes / cytology. Lymphocytes / drug effects. Lymphocytes / metabolism. Mice. Neurons / drug effects. Neurons / metabolism. Pheromones / biosynthesis. Rats

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20416350.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bacteriocins; 0 / Pheromones; 131463-18-8 / plantaricin A
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88. Morecki S, Yacovlev E, Gelfand Y, Shabat Y, Slavin S: Induction of graft-versus-leukemia (GVL) effect without graft-versus-host disease (GVHD) by pretransplant donor treatment with immunomodulators. Biol Blood Marrow Transplant; 2009 Apr;15(4):406-15
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  • [Title] Induction of graft-versus-leukemia (GVL) effect without graft-versus-host disease (GVHD) by pretransplant donor treatment with immunomodulators.
  • Pretransplant donor treatment with immunomodulators such as complete Freund's adjuvant (CFA) or oligodeoxynucleotide sequences expressing CpG motifs (CpG), was applied in sublethally irradiated host mice inoculated with murine models of mammary carcinoma (4T1) or B cell leukemia (BCL1).
  • Spleen cells or IL-2 activated splenocytes (lymphokine activated killer [LAK]) derived from donor mice treated with CpG emulsified in incomplete Freund's adjuvant (IFA), (CpG + IFA) did not cause graft-versus-host disease (GVHD), but were not efficient enough to induce a significant graft-versus-tumor (GVT) response against 4T1 cells.
  • In contrast, an efficient graft-versus-leukemia (GVL) effect was evident in BCL1-bearing mice inoculated with spleen cells from donors pretreated with CFA or CpG + IFA.
  • Pretransplant donor treatment with CFA prolonged survival to a median of 62 days with 3 of 27 mice remaining GVHD- and leukemia-free for >200 days, compared to GVHD-related death of all mice inoculated with naïve cells (median 17 days), or leukemia-related death of all mice inoculated with leukemia cells (median of 27 days).
  • Pretransplant donor treatment with CpG + IFA exerted a more efficient GVL effect with reduced GVHD resulting in 12 of 26 GVHD- and leukemia-free survivors for >200 days.
  • Our results suggest that it may be possible to prevent GVHD while sparing an efficient GVL effect by using pretransplant donor treatment with immunomodulators prior to allogeneic stem cell transplantation and/or donor lymphocyte infusions in hematologic malignancies.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Freund's Adjuvant / pharmacology. Graft vs Leukemia Effect / drug effects. Leukemia, B-Cell / therapy. Lymphocyte Transfusion. Oligodeoxyribonucleotides / pharmacology. Stem Cell Transplantation

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  • (PMID = 19285627.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / CPG-oligonucleotide; 0 / Oligodeoxyribonucleotides; 9007-81-2 / Freund's Adjuvant
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89. Antosz H, Sajewicz J, Marzec-Kotarska B, Kocki J, Dmoszyńska A: Different expression of CD180, CD284 and CD14 receptors on the CD19+ subpopulation of normal and B-CLL lymphocytes. Folia Histochem Cytobiol; 2009;47(4):593-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different expression of CD180, CD284 and CD14 receptors on the CD19+ subpopulation of normal and B-CLL lymphocytes.
  • TLRs are currently used to target different subclasses of B-cell leukemia, and TLR agonists are being evaluated in clinical trials.
  • The aim of the study was to assess the CD180, CD284 and mCD14 levels in CD19+ subpopulation of B-CLL peripheral blood lymphocytes and compare them with respective levels in the normal B-cells of adult volunteers, before and after LPS stimulation.

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  • (PMID = 20430725.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD19; 0 / CD180 protein, human; 0 / Lipopolysaccharides; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4
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90. Bhatia S, Kaul D, Varma N: Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia. Mol Cell Biochem; 2010 Jul;340(1-2):97-106
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] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.
  • Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).
  • Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.
  • Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.
  • Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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  • (PMID = 20549547.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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91. Tomomatsu J, Isobe Y, Oshimi K, Tabe Y, Ishii K, Noguchi M, Hirano T, Komatsu N, Sugimoto K: Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior. Leuk Lymphoma; 2010 Dec;51(12):2230-9
Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior.
  • Chronic lymphocytic leukemia (CLL) is relatively rare in Japan.
  • Among 46 cases of mature B-cell leukemia, we identified 28 Japanese patients with CLL, including prolymphocytoid and lymphoplasmacytoid morphological variants.
  • [MeSH-major] Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Disease Progression. Female. Gene Frequency. Genes, Immunoglobulin Heavy Chain / genetics. Genes, bcl-2 / genetics. Humans. Immunoglobulin Variable Region / genetics. Male. Middle Aged. Mutation. Population. Prognosis

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  • (PMID = 21067444.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IGH-CCND1 fusion protein, human; 0 / Immunoglobulin Variable Region; 0 / Oncogene Proteins, Fusion
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92. Kanno S, Kitajima Y, Kakuta M, Osanai Y, Kurauchi K, Ujibe M, Ishikawa M: Costunolide-induced apoptosis is caused by receptor-mediated pathway and inhibition of telomerase activity in NALM-6 cells. Biol Pharm Bull; 2008 May;31(5):1024-8
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  • We investigated the induction mechanism of apoptosis by costunolide in a human B cell leukemia NALM-6 cell culture system.
  • [MeSH-minor] Apoptosis Regulatory Proteins / physiology. Blotting, Western. Caspases / physiology. Cell Differentiation / drug effects. Cell Line, Tumor. Humans. RNA / biosynthesis. RNA / genetics. Receptors, Drug / drug effects. Receptors, Drug / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18451540.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Regulatory Proteins; 0 / Enzyme Inhibitors; 0 / Receptors, Drug; 0 / Sesquiterpenes; 4IK578SA7Z / costunolide; 63231-63-0 / RNA; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
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93. Erlacher M, Michalak EM, Kelly PN, Labi V, Niederegger H, Coultas L, Adams JM, Strasser A, Villunger A: BH3-only proteins Puma and Bim are rate-limiting for gamma-radiation- and glucocorticoid-induced apoptosis of lymphoid cells in vivo. Blood; 2005 Dec 15;106(13):4131-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Numerous p53 target genes have been implicated in DNA damage-induced apoptosis signaling, but proapoptotic Bcl-2 (B-cell leukemia 2) family members of the BH3 (Bcl-2 homolog region [BH] 3)-only subgroup appear to play the critical initiating role.
  • In various types of cultured cells, 3 BH3-only proteins, namely Puma (p53 up-regulated modulator of apoptosis), Noxa, and Bim (Bcl-2 interacting mediator of cell death), have been shown to initiate p53-dependent as well as p53-independent apoptosis in response to DNA damage and treatment with anticancer drugs or glucocorticoids.
  • In particular, the absence of Puma or Bim renders thymocytes and mature lymphocytes refractory to varying degrees to death induced in vitro by growth factor withdrawal, DNA damage, or glucocorticoids.
  • Absence of Puma or Bcl-2 overexpression efficiently protected diverse types of lymphocytes from the effects of gamma-radiation in vivo, and loss of Bim provided lower but significant protection in most lymphocytes, whereas Noxa deficiency had no impact.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis / radiation effects. Apoptosis Regulatory Proteins / metabolism. Glucocorticoids / pharmacology. Lymphocytes / drug effects. Lymphocytes / radiation effects. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Dexamethasone / pharmacology. Gamma Rays. Mice. Mice, Knockout. Spleen / cytology. Spleen / drug effects. Spleen / metabolism. Spleen / radiation effects. Thymus Gland / cytology. Thymus Gland / drug effects. Thymus Gland / metabolism. Thymus Gland / radiation effects

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  • (PMID = 16118324.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Glucocorticoids; 0 / Membrane Proteins; 0 / PUMA protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC1895232
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94. Squires MS, Cooke L, Lock V, Qi W, Lewis EJ, Thompson NT, Lyons JF, Mahadevan D: AT7519, a cyclin-dependent kinase inhibitor, exerts its effects by transcriptional inhibition in leukemia cell lines and patient samples. Mol Cancer Ther; 2010 Apr;9(4):920-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AT7519, a cyclin-dependent kinase inhibitor, exerts its effects by transcriptional inhibition in leukemia cell lines and patient samples.
  • B-cell lymphoproliferative disorders, including chronic lymphocytic leukemia, rely on the expression of transcripts with a short half-life, such as Mcl-1, Bcl-2, and XIAP, for survival.
  • Here, we describe the characterization of AT7519 in leukemia cell lines, and compare and contrast the response in cell lines derived from solid tumors.
  • Finally, we use these mechanistic insights to show activity in peripheral blood mononuclear cells isolated from 16 chronic lymphocytic leukemia patients.
  • Together the data suggest AT7519 offers a promising treatment for patients with advanced B-cell leukemia.
  • [MeSH-major] Cyclin-Dependent Kinases / antagonists & inhibitors. Leukemia / enzymology. Leukemia / genetics. Piperidines / pharmacology. Pyrazoles / pharmacology. Transcription, Genetic / drug effects
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Cell Death / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. RNA Polymerase II / antagonists & inhibitors. Time Factors. Xenograft Model Antitumor Assays

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  • (PMID = 20354122.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxylic acid piperidin-4-ylamide; 0 / Apoptosis Regulatory Proteins; 0 / Piperidines; 0 / Pyrazoles; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 2.7.7.- / RNA Polymerase II
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95. Au WY, Wong KY, Leung RY, Tong AC: Isolated gingival relapse of acute lymphoblastic leukemia after transplantation. J Oral Pathol Med; 2008 Apr;37(4):249-51
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated gingival relapse of acute lymphoblastic leukemia after transplantation.
  • A patient with a history of precursor B-cell leukemia presented with an isolated ulcerating gum lesion 8 years after allogeneic stem cell transplantation with severe graft versus host disease.
  • Molecular studies confirmed clonal relationship between the gum lesion with the original marrow disease, despite the anatomical, histological and chronological separations.
  • [MeSH-major] Gingival Neoplasms / pathology. Graft vs Leukemia Effect. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / surgery. Fatal Outcome. Female. Graft vs Host Disease / etiology. Hematopoiesis, Extramedullary. Humans. Recurrence. Stem Cell Transplantation / adverse effects

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • (PMID = 18321346.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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96. Bourdeau A, Dubé N, Heinonen KM, Théberge JF, Doody KM, Tremblay ML: TC-PTP-deficient bone marrow stromal cells fail to support normal B lymphopoiesis due to abnormal secretion of interferon-{gamma}. Blood; 2007 May 15;109(10):4220-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • The T-cell protein tyrosine phosphatase (TC-PTP) is a negative regulator of the Jak/Stat cytokine signaling pathway.
  • Our study shows that the absence of TC-PTP leads to an early bone marrow B-cell deficiency characterized by hindered transition from the pre-B cell to immature B-cell stage.
  • Our results unraveled a new role for TC-PTP in normal B lymphopoiesis and suggest that modulation of bone marrow microenvironment is a potential therapeutic approach for selected B-cell leukemia.
  • [MeSH-major] B-Lymphocytes / cytology. Bone Marrow Cells / metabolism. Interferon-gamma / secretion. Lymphopoiesis / genetics. Protein Tyrosine Phosphatases / genetics. Stromal Cells / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Cells, Cultured. Homeostasis / genetics. Interleukin-7 / pharmacology. Mice. Mice, Knockout. Models, Biological. Phosphorylation. Protein Kinases / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 2. STAT1 Transcription Factor / metabolism

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  • (PMID = 17234741.001).
  • [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 / Interleukin-7; 0 / STAT1 Transcription Factor; 0 / Stat1 protein, mouse; 82115-62-6 / Interferon-gamma; EC 2.7.- / Protein Kinases; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 2; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Ptpn2 protein, mouse
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97. Ishdorj G, Johnston JB, Gibson SB: Inhibition of constitutive activation of STAT3 by curcurbitacin-I (JSI-124) sensitized human B-leukemia cells to apoptosis. Mol Cancer Ther; 2010 Dec;9(12):3302-14
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  • [Title] Inhibition of constitutive activation of STAT3 by curcurbitacin-I (JSI-124) sensitized human B-leukemia cells to apoptosis.
  • Phosphorylation of STAT3 on serine 727 regulates gene expression and is found to be elevated in many B-leukemia cells including chronic lymphocytic leukemia (CLL).
  • JSI-124 potently induces apoptosis in 3 B-leukemia cell lines (BJAB, I-83, and NALM-6) and in primary CLL cells and was associated with a reduction in serine 727 phosphorylation of STAT3.
  • Similarly, knockdown of STAT3 expression induced apoptosis in these leukemia cells.
  • Besides apoptosis, we found that JSI-124 also induced cell-cycle arrest prior to apoptosis in B-leukemia cells.
  • This corresponded with reduced expression of the cell-cycle regulatory gene, cdc-2.
  • Thus, we present here for the first time that JSI-124 induced suppression of serine 727 phosphorylation of STAT3, leading to apoptosis and cell-cycle arrest through alterations in gene transcription in B-leukemia cells.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, B-Cell / pathology. STAT3 Transcription Factor / metabolism. Triterpenes / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. Gene Knockdown Techniques. Histone Deacetylase 1 / metabolism. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Phosphoserine / metabolism. RNA, Small Interfering / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Up-Regulation / drug effects. X-Linked Inhibitor of Apoptosis Protein / metabolism

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  • [Copyright] ©2010 AACR.
  • (PMID = 21159613.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Triterpenes; 0 / X-Linked Inhibitor of Apoptosis Protein; 17885-08-4 / Phosphoserine; 2222-07-3 / cucurbitacin I; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1
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98. Domart MC, Esposti DD, Sebagh M, Olaya N, Harper F, Pierron G, Franc B, Tanabe KK, Debuire B, Azoulay D, Brenner C, Lemoine A: Concurrent induction of necrosis, apoptosis, and autophagy in ischemic preconditioned human livers formerly treated by chemotherapy. J Hepatol; 2009 Nov;51(5):881-9
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  • IP induced a twofold increase in B-cell leukemia/ lymphoma 2 (Bcl-2; p<0.05), which was localized to hepatocytes of centrolobular and peliotic areas and colocalized with the autophagy protein beclin-1 in livers with IP, suggesting their coordinated role in autophagy.
  • Bcl-2 and beclin-1 could be major targets in the regulation of cell death during I/R injury.

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  • (PMID = 19765849.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-bcl-2
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99. Cui W, Kong NR, Ma Y, Amin HM, Lai R, Chai L: Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia. Mod Pathol; 2006 Dec;19(12):1585-92
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  • [Title] Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.
  • Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia.
  • In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody.
  • Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines.
  • In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia.
  • Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/lymphomas were positive.
  • The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells.
  • We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development.
  • The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis.
  • More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Plasmacytoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Separation. Flow Cytometry. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Immunoenzyme Techniques. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16998462.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK063220
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SALL4 protein, human; 0 / Transcription Factors
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100. Klener P, Szynal M, Cleuter Y, Merimi M, Duvillier H, Lallemand F, Bagnis C, Griebel P, Sotiriou C, Burny A, Martiat P, Van den Broeke A: Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells. J Virol; 2006 Feb;80(4):1922-38
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  • [Title] Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells.
  • Large-animal models for leukemia have the potential to aid in the understanding of networks that contribute to oncogenesis.
  • Infection of cattle and sheep with bovine leukemia virus (BLV), a complex retrovirus related to human T-cell leukemia virus type 1 (HTLV-1), is associated with the development of B-cell leukemia.
  • Whereas the natural disease in cattle is characterized by a low tumor incidence, experimental infection of sheep leads to overt leukemia in the majority of infected animals, providing a model for studying the pathogenesis associated with BLV and HTLV-1.
  • Using cDNA-spotted microarrays comprising 10,336 human genes/expressed sequence tags, we identified a cohort of differentially expressed genes, including genes related to apoptosis, DNA transcription, and repair; proto-oncogenes; cell cycle regulators; transcription factors; small Rho GTPases/GTPase-binding proteins; and previously reported Tax(HTLV-1)-responsive genes.
  • Interestingly, genes known to be associated with human neoplasia, especially B-cell malignancies, were extensively represented.
  • Although cross-species approaches do not permit a comprehensive analysis of gene expression patterns, they can provide initial clues for the functional roles of genes that participate in B-cell transformation and pinpoint molecular targets not identified using other methods in animal models.
  • [MeSH-major] B-Lymphocytes / physiology. B-Lymphocytes / virology. Cell Transformation, Viral / genetics. Gene Expression Profiling. Gene Expression Regulation. Gene Products, tax / physiology. Leukemia Virus, Bovine / physiology

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  • (PMID = 16439548.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax
  • [Other-IDs] NLM/ PMC1367148
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