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1. Řezáčová M, Vávrová J, Vokurková D: Ionizing Radiation Sensitizes Leukemic MOLT-4 Cells to TRAIL-induced Apoptosis. Acta Medica (Hradec Kralove); 2008;51(2):101-105

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, leukemia cells studied to date have shown variable susceptibility to TRAIL.
  • Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.
  • When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

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  • (PMID = 28550838.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL
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2. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • EXPERIMENTAL DESIGN: To address this question, we analyzed 29 patients with pro-B ALL, 11 patients with CD10- pre-B ALL, 23 pre-B, and 26 cALL patients with CD10 on 20% to 80%, as well as 136 pre-B and 143 cALL patients with CD10 > or = 80% of blasts.
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • However, no 11q23/MLL translocation was identified among the CD10+ pre-B and cALL patients.
  • MLL-rearranged pro-B and CD10- pre-B ALL cases had similar clinical and immunophenotypic (coexpression of CDw65 and CD15) features at initial diagnosis.
  • CONCLUSIONS: The striking similarities between the two CD10- ALL subsets imply that CD10- pre-B ALL variants may represent pro-B ALL cases that maintained the propensity to rearrange and express their immunoglobulin heavy chain rather than actual pre-B ALL forms transformed at this later stage of B-cell differentiation.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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3. Schult C, Dahlhaus M, Ruck S, Sawitzky M, Amoroso F, Lange S, Etro D, Glass A, Fuellen G, Boldt S, Wolkenhauer O, Neri LM, Freund M, Junghanss C: The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells. BMC Cancer; 2010;10:560
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  • [Title] The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells.
  • The multikinase inhibitor Sorafenib has antitumor activity in solid tumors and its effects on acute lymphoblastic leukemia (ALL) cells are still unclear.
  • METHODS: ALL cell lines (SEM, RS4;11 and Jurkat) were treated with Sorafenib alone or in combination with cytarabine, doxorubicin or RAD001.
  • Cell count, apoptosis and necrosis rates, cell cycle distribution, protein phosphorylation and metabolic activity were determined.
  • RESULTS: Sorafenib inhibited the proliferation of ALL cells by cell cycle arrest accompanied by down-regulation of CyclinD3 and CDK4.
  • CONCLUSION: Sorafenib displays significant antileukemic activity in vitro by inducing cell cycle arrest and apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. B-Lymphocytes / pathology. Benzenesulfonates / pharmacology. Caspase 3 / metabolism. Caspase 7 / metabolism. Poly(ADP-ribose) Polymerases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Pyridines / pharmacology. T-Lymphocytes / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Jurkat Cells. Niacinamide / analogs & derivatives. Phenylurea Compounds. Phosphorylation

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  • (PMID = 20950443.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
  • [Other-IDs] NLM/ PMC2972283
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4. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
  • We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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5. Nakagawa Y, Hasegawa M, Kurata M, Yamamoto K, Abe S, Inoue M, Takemura T, Hirokawa K, Suzuki K, Kitagawa M: Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL). Am J Hematol; 2005 Mar;78(3):173-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).
  • To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.
  • These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15726601.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger
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6. De Braekeleer E, Basinko A, Douet-Guilbert N, Morel F, Le Bris MJ, Berthou C, Morice P, Férec C, De Braekeleer M: Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008. Cancer Genet Cytogenet; 2010 Jul 1;200(1):8-15
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  • [Title] Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008.
  • The detection of chromosome abnormalities by conventional cytogenetics, now combined with analyses using fluorescence in situ hybridization (FISH), is an important component in assessing the risk stratification of acute lymphoblastic leukemia (ALL).
  • Identification of specific chromosome abnormalities led to the recognition of genetic subgroups based on modal chromosomal number, reciprocal translocations in B-cell ALL, or both.
  • We report here the cytogenetic analysis of 208 patients with pre-B and B-cell ALL referred to a single laboratory between 1981 and 2008.
  • Chromosome abnormalities were observed in 82.9% of L1/L2 ALL patients and in 83.3% of L3 patients with successful analysis at diagnosis.
  • As previously reported, t(9;22)(q34;q11) and t(12;21)(p13;q21) were the most frequent structural rearrangements among adults (26.9%) and children (19.7%), respectively.
  • Almost 17% of the patients studied at diagnosis had further cytogenetic analyses at relapse, the majority showing clonal evolution toward a more complex karyotype.
  • [MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Histone-Lysine N-Methyltransferase. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Recurrence. Time Factors. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20513528.001).
  • [ISSN] 1873-4456
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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7. Magro CM, Dyrsen ME: Cutaneous lymphocyte antigen expression in benign and neoplastic cutaneous B- and T-cell lymphoid infiltrates. J Cutan Pathol; 2008 Nov;35(11):1040-9
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  • [Title] Cutaneous lymphocyte antigen expression in benign and neoplastic cutaneous B- and T-cell lymphoid infiltrates.
  • DESIGN: We investigated the expression of CLA using the HECA-452 antibody on paraffin-embedded, formalin-fixed tissue in a variety of reactive, neoplastic and preneoplastic cutaneous lymphoid infiltrates of T- and B-cell derivation.
  • High levels of CLA expression were seen in epidermotropic T-cell dyscrasias and epidermotropic T-cell lymphomas including mycosis fungoides (MF) and adult T-cell leukemia/lymphoma (ATCLL).
  • A loss of CLA in tumors normally positive for CLA was a feature of disease progression best exemplified by tumor-stage MF and acute ATCLL.
  • There was a lack of CLA expression in those lymphocytic infiltrates manifesting subcutaneous localization including lupus profundus, panniculitis-like T-cell lymphoma and atypical lymphocytic lobular panniculitis.
  • CLA expression was not only observed in primary cutaneous anaplastic large cell lymphoma but also seen in cases of nodal anaplastic large cell lymphoma secondarily involving the skin and was negative in cases of nodal anaplastic large cell lymphoma without any established skin involvement.
  • CLA was negative in the majority of B-cell lymphomas.
  • CONCLUSIONS: CLA plays a role in the pattern of T-cell lymphocyte migration in the skin and subcutis in both reactive and neoplastic states.
  • An alteration in the expression of this marker, whether it is in the context of the acquisition of expression in a cell that is normally CLA negative or its loss of expression, may define a key event in determining cutaneous and extracutaneous hematopoietic cell distribution.
  • [MeSH-major] Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Dermatitis / immunology. Lymphoma, B-Cell / immunology. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell, Cutaneous / immunology. Skin Neoplasms / immunology

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  • (PMID = 18681860.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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8. Fulci V, Colombo T, Chiaretti S, Messina M, Citarella F, Tavolaro S, Guarini A, Foà R, Macino G: Characterization of B- and T-lineage acute lymphoblastic leukemia by integrated analysis of MicroRNA and mRNA expression profiles. Genes Chromosomes Cancer; 2009 Dec;48(12):1069-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of B- and T-lineage acute lymphoblastic leukemia by integrated analysis of MicroRNA and mRNA expression profiles.
  • Acute lymphoblastic leukemia (ALL) is an heterogeneous disease comprising several subentities that differ for both immunophenotypic and molecular characteristics.
  • Furthermore, we identified miR-148, miR-151, and miR-424 as discriminative of T-lineage versus B-lineage ALL; ANOVA highlighted a set of six miRNAs-namely miR-425-5p, miR-191, miR-146b, miR-128, miR-629, and miR-126-that can discriminate B-lineage ALL subgroups harboring specific molecular lesions.
  • Signal-to-noise ratio highlighted several miRNA/gene pairs with a possible role in the disease.
  • In fact, gene set enrichment analysis of genes composing the selected miRNA/gene pairs displays over-representation of functional categories related to cancer and cell-cycle regulation.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Profiling. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line, Tumor. Cell Lineage. Cluster Analysis. Gene Expression Regulation, Leukemic. Humans. Middle Aged. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19760605.001).
  • [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 / Biomarkers, Tumor; 0 / MicroRNAs; 0 / RNA, Messenger
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9. Belov L, Huang P, Chrisp JS, Mulligan SP, Christopherson RI: Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells. J Immunol Methods; 2005 Oct 20;305(1):10-9
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  • [Title] Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells.
  • We have developed a microarray (DotScan) that enables rapid immunophenotyping and classification of leukaemias and lymphomas by measuring the capture of cells by immobilized dots of 82 CD antibodies [Belov, L., de la Vega, O., dos Remedios, C.G., Mulligan, S.P., 2001.
  • Immunophenotyping of leukemia using a cluster of differentiation antibody microarray. Cancer Res.
  • Identification of repertoires of surface antigens on leukemias using an antibody microarray.
  • After blocking the remaining nitrocellulose surface, individual arrays were incubated with each of 7 cell types from a human leukaemia cell panel consisting of three cell lines, CCRF-CEM (a T-cell acute lymphocytic leukaemia), MEC-1 (derived from B-cell chronic lymphocytic leukaemia) and HL-60 (a promyelocytic leukaemia), and four leukaemias from patients: a T-cell prolymphocytic leukaemia, a B-cell chronic lymphocytic leukaemia, and two acute myeloid leukaemias.
  • Leukaemia cells were captured by those immobilized antibodies for which they expressed the corresponding surface molecule.
  • The data obtained show the unique expression profiles of the 7 cell types in the leukaemia cell panel obtained with the DotScan microarray, and the differential capture patterns for these 7 cell types screened against the 498 antibodies in the HLDA8 microarray constructed for this study.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, CD / analysis. Leukemia / classification. Protein Array Analysis / methods
  • [MeSH-minor] Cell Line, Tumor. Collodion / chemistry. Flow Cytometry. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / immunology. Leukemia, Myeloid / classification. Leukemia, Myeloid / immunology. Leukemia, T-Cell / classification. Leukemia, T-Cell / immunology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Nitrocellulose .
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  • (PMID = 16125720.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 9004-70-0 / Collodion
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10. Davidsson J, Lilljebjörn H, Panagopoulos I, Fioretos T, Johansson B: BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias. Leukemia; 2008 Aug;22(8):1619-21
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] BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias.
  • [MeSH-major] B-Lymphocytes / immunology. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins B-raf / genetics. T-Lymphocytes / immunology

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • [CommentOn] Leukemia. 2005 Feb;19(2):310-2 [15538400.001]
  • (PMID = 18273045.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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11. Martelli MP, Manes N, Pettirossi V, Liso A, Pacini R, Mannucci R, Zei T, Bolli N, di Raimondo F, Specchia G, Nicoletti I, Martelli MF, Falini B: Absence of nucleophosmin leukaemic mutants in B and T cells from AML with NPM1 mutations: implications for the cell of origin of NPMc+ AML. Leukemia; 2008 Jan;22(1):195-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of nucleophosmin leukaemic mutants in B and T cells from AML with NPM1 mutations: implications for the cell of origin of NPMc+ AML.
  • [MeSH-major] B-Lymphocytes / metabolism. Leukemia, Myeloid / genetics. Mutation. Nuclear Proteins / genetics. T-Lymphocytes / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Acute Disease. Biopsy. Bone Marrow / metabolism. Cell Lineage. Cytoplasm / metabolism. Fluorescent Antibody Technique. Humans. Immunoenzyme Techniques. Myeloid Cells. Phosphoproteins / genetics. Subcellular Fractions

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  • (PMID = 17637812.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Phosphoproteins; 117896-08-9 / nucleophosmin
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12. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.

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  • (PMID = 27963169.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

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

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

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

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Tsujimura H, Mimura N, Ise M, Sakai C, Shimada H, Nagata M, Kumagai K: Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15663

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer.
  • METHODS: From July 2000 to March 2008, 348 patients with esophageal squamous cell carcinoma underwent CRT.
  • RESULTS: Four patients, who achieved CR after CRT, developed leukemia.
  • Case1, 60-yo-male, developed overt acute myeloid leukemia (AML) from myelodysplastic syndrome 48 months after CRT.
  • Case3, 72-yo-male, developed Burkitt leukemia with t(8;14)(q24;q32) 19 months after CRT.
  • Case4, 65-yo-male, developed myeloid crisis of chronic myelogenous leukemia with complicated abnormalities including t(9;22)(q34;q11) 48 months after CRT.
  • Case 1 and 3 had localized disease and received single course of neoadjuvant CRT.
  • Case 2 and 4 had advance disease and received 2 courses of CRT.
  • All patients eventually died of leukemia.
  • To this end, atypical cytogenetic abnormalities seen in the present cases give a new insight into the biology of therapy-related leukemia.
  • Notably, this is the first report presenting the incidence of secondary leukemia by nedaplatin.

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  • (PMID = 27962759.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Vey N, Bourhis J, Dombret H, Bordessoule D, Prebet T, Charbonnier A, Squiban P, Damholt B, Blaise D, Olive D: A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML).
  • As expected for an IgG4, NK cell numbers were unaffected by the treatment.

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  • (PMID = 27962059.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Tsai DE, Wang W, Reshef R, Vogl D, Stadtmauer E, Andreadis C, Carlson A, Luger S: Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e20533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia.
  • : e20533 Background: Bexarotene (Bex) is an oral retinoid X receptor agonist with activity against cutaneous T cell lymphoma and currently under investigation for other malignancies.
  • In patients receiving this agent for acute myeloid leukemia (AML), we noted increases in platelet counts.
  • METHODS: We analyzed platelet count data from 3 Bex clinical trials encompassing non-small cell lung cancer (NSCLC) and AML.

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  • (PMID = 27960979.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

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

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  • (PMID = 27960689.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Beltran BE, Morales D, Quiñones P, Salas R, Castillo J: Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.
  • : 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.
  • Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.
  • Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).
  • Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).
  • The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.
  • CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.
  • The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.

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  • (PMID = 27962272.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Cheng PC, Crane J, Hunter T: Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro. J Clin Oncol; 2009 May 20;27(15_suppl):e14551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14551 Background: FLT3 receptor tyrosine kinase activating mutations contribute to leukemogenesis and poor prognosis in approximately 30% of acute myeloid leukemia (AML).
  • METHODS: In the course of conducting a synthetic lethality screen with a FLT3 inhibitor on the Ba/F3 murine cell line stably expressing human FLT3 or FLT3-ITD, we identified bortezomib, a proteasome inhibitor, as having potent activity against FLT3-ITD cells.
  • The effects of drugs on proliferation, apoptosis, and phosphosignaling were quantified in Ba/F3 cells and in the HL60 (WT FLT3) and MV4-11 (FLT3-ITD) human cell lines, using an MTS- based colorimetric assay, caspase 3 and 7 activity assays, and immunoblotting, respectively.
  • When the FLT3 inhibitor and bortezomib were used at IC25 concentrations, a more pronounced inhibition of cell proliferation was observed when they were used in combination than with either alone.
  • CONCLUSIONS: Bortezomib preferentially kills FLT3- ITD cells, showing a four-fold more potent inhibition of cell proliferation, induces apoptosis, and abrogates activation of FLT3 and its downstream effector pathways.

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  • (PMID = 27963616.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).
  • For the neuroblastoma panel, the best response was progressive disease (PD) with growth delay compared to controls (PD2 response), which was observed in 5 of 6 xenografts.

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  • (PMID = 27962529.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Barret J, Dumontet C, Annereau J, Brel V, Breillout F, Guminski Y, Imbert T, Guilbaud N, Bailly C: A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512. J Clin Oncol; 2009 May 20;27(15_suppl):11087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512.
  • METHODS: The uptake of this probe was first measured by flow cytometry in a panel of human leukemia cell lines.
  • RESULTS: Data showed that high level of fluorescence was detected in F14512 -sensitive cancer cell lines whereas leukemia cells responding poorly to F14512 generally exhibited very low levels of PTS.
  • A panel of 50 fresh human acute myeloid leukemia samples showed a larger inter-individual variation and, interestingly, incorporation of the fluorescent probe was generally higher in leukemia blasts than in lymphocytes.

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  • (PMID = 27963178.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Borthakur G, Faderl S, Ravandi F, Padmanabhan S, Stock W, Wu K, Li J, Curt G, Tallman M, Minden M: Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3580

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML).
  • Eg5 inhibition is thus specific for dividing cells, resulting in monoastral mitotic spindles (monoasters) and apoptotic cell death.
  • Preclinically, hematologic tumor cell lines were generally more sensitive to AZD4877 than those derived from solid tumors.

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  • (PMID = 27961757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Yip SF, Wan TS, Chan LC, Chan GC: Trisomy 4 as sole karyotypic abnormality in acute lymphoblastic leukemia: different clinical features and treatment response between B and T phenotypes? Cancer Genet Cytogenet; 2006 Jan 1;164(1):94-5
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] Trisomy 4 as sole karyotypic abnormality in acute lymphoblastic leukemia: different clinical features and treatment response between B and T phenotypes?
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 4. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Trisomy

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  • (PMID = 16364773.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
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27. Li XL, Li R, Chen Y: [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):636-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].
  • The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of mixed-lineage acute leukemia (MAL).
  • 48 MAL patients diagnosed according to European Group of International Leukemia (EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.
  • The results showed that the incidence of MAL in acute leukemia was 9.6%.
  • The median of white blood cell count in MAL was significantly higher than that of non-mixed-lineage cases (AML and ALL) observed during the same period (P < 0.05).
  • Coexpression of myeloid and B lymphoid antigens in MAL patients was predominant, its rate was 70.9%.
  • The coexpression rate of T lymphoid and myeloid antigens was 20.8%, coexpression of B, T lymphoid and myeloid antigens was 8.3%.
  • In MAL Ph chromosome abnormality incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).
  • It is concluded that MAL is supposed to be originated from stem cells, coexpression of lymphoid/myeloid antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.

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  • (PMID = 17605883.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34
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28. Liu HX, Cao XY, Tong CR, Wu T, Wang T, Fan QZ, Wu P, Zhang X, Cai P, Zhu P: [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript]. Zhonghua Yi Xue Za Zhi; 2009 Feb 3;89(4):220-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].
  • OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with acute mixed lineage leukemia (AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.
  • Morphological analysis of the bone marrow showed the myeloid blast cells accounted for 66%, and immunophenotyping analysis showed 2 groups of aberrant blast cells: myeloid and B lineage.
  • Chemical therapy and bone marrow transplantation failed to control the disease, and a novel BCR/ABL transcript (GenBank: EF423615) was found by using several detection protocols.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Biphenotypic, Acute / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19552835.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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29. Georgy M, Yonescu R, Griffin CA, Batista DA: Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults. Cancer Genet Cytogenet; 2008 Aug;185(1):28-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.
  • Acute mixed lineage leukemia (AMLL) is a rare form of leukemia in which both myeloid and lymphoid markers are present.
  • Few chromosome abnormalities have been identified associated with this form of leukemia.
  • A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with acute leukemia and in three of these cases the diagnosis was mixed lineage.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 18656690.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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30. Teitell MA, Pandolfi PP: Molecular genetics of acute lymphoblastic leukemia. Annu Rev Pathol; 2009;4:175-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetics of acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is mainly a disease of childhood that arises from recurrent genetic insults that block precursor B and T cell differentiation and drive aberrant cell proliferation and survival.
  • Recurrent defects including chromosomal translocations, aneuploidies, and gene-specific alterations generate molecular subgroups of B- and T-ALL with differing clinical courses and distinct responses to therapy.
  • Recent discoveries arising from genome-wide surveys and adoptive transfer of leukemia-initiating cells have uncovered multiple gene copy number aberrations and have yielded new insight into at least one type of ALL-originating cell.
  • Our understanding of the pathogenesis of ALL has benefited from genetically modified mouse models that recapitulate cellular transformation at specific developmental stages of lymphoid lineage cells.
  • Here, we review the spectrum of genetic aberrations that promote acute B and T cell leukemias and the mechanisms of cell transformation and malignant progression that are reinforced by mouse models of human ALL.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Animals. Cell Differentiation / genetics. Cell Lineage / genetics. Cell Proliferation. Disease Models, Animal. Genotype. Humans. Mice. Phenotype. Signal Transduction / genetics

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  • (PMID = 18783329.001).
  • [ISSN] 1553-4014
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 153
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31. Wang Y, Chang N, Zhang T, Liu H, Ma W, Chu Q, Lai Q, Liu L, Wang W: Overexpression of human CAP10-like protein 46 KD in T-acute lymphoblastic leukemia and acute myelogenous leukemia. Genet Test Mol Biomarkers; 2010 Feb;14(1):127-33
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  • [Title] Overexpression of human CAP10-like protein 46 KD in T-acute lymphoblastic leukemia and acute myelogenous leukemia.
  • AIMS: We earlier identified a novel gene human CAP10-like protein 46 KD (hCLP46) from human acute myelogenous leukemia (AML) transformed from myelodysplastic syndrome CD34(+) cells, but the function of this gene remains unclear.
  • In this study, a real-time polymerase chain reaction-based assay was developed to quantify expression of hCLP46 in the peripheral blood of AML and T-acute lymphoblastic leukemia (T-ALL) primary samples and in six leukemic cell lines.
  • Also, we investigated expression of CDKN2A/B and the apoptosis in U937 cells when hCLP46 is downregulated in vitro.
  • RESULTS: Our findings showed that hCLP46 was overexpressed in AML, T-ALL, and the leukemic cell lines.
  • Suppressing hCLP46 overexpression had no effect on expression of CDKN2A/B and apoptosis of U937 cells.
  • CONCLUSION: Considering that hCLP46 has the capability of modifying the Notch pathway, our finding adds weight to the importance of Notch signaling in hematopoiesis and suggests that overexpression of hCLP46 might be an early event in the pathogenesis of AML and T-ALL.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteins / genetics
  • [MeSH-minor] Apoptosis / genetics. Base Sequence. Cell Line, Tumor. DNA Primers / genetics. Gene Expression. Genes, p16. Glucosyltransferases. Hematopoiesis / genetics. Hematopoiesis / physiology. Humans. RNA, Small Interfering / genetics. Receptors, Notch / physiology. Signal Transduction. Transfection. U937 Cells

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  • (PMID = 20143914.001).
  • [ISSN] 1945-0257
  • [Journal-full-title] Genetic testing and molecular biomarkers
  • [ISO-abbreviation] Genet Test Mol Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Notch; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.- / POGLUT1 protein, human
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32. Valmary S, Danjoux M, Delsol G, Brousset P: [Diagnostic value of anti-terminal deoxynucleotidyl transferase antibody (TdT) in hematologic pathology]. Ann Pathol; 2005 Feb;25(1):25-32

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Intérêt diagnostique de l'anticorps anti-terminal désoxynucleotidyl transférase (TdT) en pathologie hématologique.
  • AIMS: The diagnosis of primitive hematologic malignancies depends on a panel of monoclonal antibodies which is growing over time.
  • The distinction between immature (lymphoblastic lymphoma/acute lymphoblastic leukaemia) and mature lymphoma is sometimes difficult.
  • In this study, we evaluated anti-TdT antibody in the diagnosis and classification of these proliferations.
  • MATERIALS AND METHODS: 13 lesions were examined by immunohistochemistry: 4 B and T lymphoblastic lymphomas, 2 Burkitt's lymphomas, 5 B and T acute lymphoblastic leukemias and 2 acute monoblastic leukemias.
  • RESULTS: TdT expression is specific of immature lymphoid proliferations (T or B lymphoblasts).
  • TdT is not expressed by mature B or T cell lymphomas such as Burkitt's lymphomas.
  • Significant numbers of cases of acute myeloblastic leukemias are TdT positive but could be easily distinguished from lymphoblastic proliferations.
  • CONCLUSION: Anti-TdT antibody represents a useful marker for differentiating lymphoma/acute lymphoblastic leukemia from other lymphomas.
  • This marker, available in routine diagnosis should be systematically included in the panel of antibodies used for immunophenotyping hematologic malignancies.
  • [MeSH-major] Antibodies. DNA Nucleotidylexotransferase / analysis. DNA Nucleotidylexotransferase / immunology. Hematologic Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Burkitt Lymphoma / diagnosis. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Immunophenotyping. Leukemia, Monocytic, Acute / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, T-Cell / diagnosis. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 15981929.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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33. Ho AD, Hensel M: Pentostatin and purine analogs for indolent lymphoid malignancies. Future Oncol; 2006 Apr;2(2):169-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pentostatin and purine analogs for indolent lymphoid malignancies.
  • Pentostatin has been shown to be active in a variety of B- and T-cell malignancies.
  • The drug is a tight inhibitor of adenosine deaminase, a key degradative enzyme of purine metabolism present in all human tissues, with the highest levels found in the lymphoid system.
  • 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.
  • [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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34. Abdelhaleem M: Frequent but nonrandom expression of myeloid markers on de novo childhood acute lymphoblastic leukemia. Exp Mol Pathol; 2007 Aug;83(1):138-41
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  • [Title] Frequent but nonrandom expression of myeloid markers on de novo childhood acute lymphoblastic leukemia.
  • The expression of the myeloid markers CD13, CD33, and CD15 in two hundred and eighty-three cases of de novo childhood acute lymphoblastic leukemia (ALL) is examined.
  • The expression of at least one marker is a frequent event which is noted in 64% and 74% of B- and T-lineage ALL cases, respectively.
  • Certain patterns of myeloid antigen expression can be recognized including: no expression of CD13, CD33, and CD15 in mature B-ALL, significantly higher levels of CD13 and CD33 and significantly lower levels of CD15 in TEL-AML1-positive B cell precursor ALL, no expression of CD13 and CD33 in E2A-PBX1-positive B cell precursor ALL cases and common T-ALL (double positive for CD4 and CD8), and no expression of CD13 in MLL-AF4-positive B cell precursor ALL cases.
  • Although the numbers in some ALL subtypes are small, these patterns are consistent with nonrandom expression of myeloid markers in de novo childhood ALL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Myeloid Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD15 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Differentiation. Child. Core Binding Factor Alpha 2 Subunit / metabolism. Homeodomain Proteins / metabolism. Humans. Oncogene Proteins, Fusion / metabolism. Sialic Acid Binding Ig-like Lectin 3


35. Fett NM, Siddiqui J, Creswell CH, Zhang D, Lloyd R, Wood GS: Adult T-cell leukemia/lymphoma in a patient from Romania: a case report and review of the literature. J Cutan Pathol; 2008 Oct;35 Suppl 1:32-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma in a patient from Romania: a case report and review of the literature.
  • Adult T-cell leukemia/lymphoma (ATLL) is a rare malignancy caused by human T-cell leukemia virus-1.
  • Narrow-band ultraviolet-B (UV-B) therapy and mid-potency topical steroids resulted in skin clearing for approximately 5 months after diagnosis; however, she subsequently relapsed with disease refractory to both narrow band UV-B and psoralen plus ultraviolet A (PUV-A), progressed to acute ATLL and expired secondary to complications.
  • [MeSH-major] HTLV-I Infections / complications. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Ultraviolet Therapy

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  • [Copyright] Copyright Blackwell Munksgaard 2008.
  • (PMID = 18544058.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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36. Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX: [Study on the clinical characteristics of adult biphenotypic acute leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):18-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study on the clinical characteristics of adult biphenotypic acute leukaemia].
  • OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult biphenotypic acute leukaemia (BAL).
  • The chemotherapy regimens were accordingly for acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML) or for both ALL and AML.
  • (1) The incidence of BAL in acute leukaemias was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of myeloid and B lymphoid antigens were 81.5%, of myeloid and T lymphoid antigens 10.8%, of myeloid, B- and T lymphoid antigens 4.6%, and of B and T lymphoid antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
  • (1) High white blood cell count and coexpression of myeloid/B lymphoid antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19563029.001).
  • [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
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37. Yao L, Chen ZX, Cen JN, Liang JY, He J, Qi XF, Shen HJ: [Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in newly diagnosed adult patients with acute lymphoblastic leukemia by using multiplex PCR protocols]. Zhonghua Xue Ye Xue Za Zhi; 2008 Oct;29(10):676-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in newly diagnosed adult patients with acute lymphoblastic leukemia by using multiplex PCR protocols].
  • OBJECTIVE: To provide the evidence of RQ-PCR-based assessment of minimal residual disease (MRD), the clonal immunoglobulin and T-cell receptor (Ig/TCR) gene rearrangements were identified in newly diagnosed adult patients with acute lymphoblastic leukemia (ALL) by multiplex PCR protocols.
  • METHODS: Forty newly diagnosed adult patients with B-lineage (B-) and T cell (T-) ALL were involved in this study.
  • CONCLUSIONS: The detection rate of clonal rearrangements using the BIOMED-2 14 multiplex PCR tubes is high, which can detect virtually all clonal B and T-cell proliferations.
  • It can be used for diagnostic clonality studies as well as for the identification of PCR targets suitable for the detection of minimal residual disease.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte. Immunoglobulins / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Humans. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics

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  • (PMID = 19176062.001).
  • [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 / Immunoglobulins
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38. Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ: Acute bilineal leukemia: a rare disease with poor outcome. Leukemia; 2007 Nov;21(11):2264-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute bilineal leukemia: a rare disease with poor outcome.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • In a few cases, definitive assignment cannot be achieved because blasts express antigens of more than one lineage.
  • A subset of these, referred to as acute bilineal leukemias (aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single lineage.
  • We identified 19 cases of aBLL, including 10 mixed T and myeloid (T-My) and nine mixed B and myeloid (B-My); no mixed B and T cases were identified.
  • Of 16 patients with outcome data, only six achieved complete remission and only two remain free of disease 2.5 and 4.5 years after chemotherapy or stem cell transplantation. aBLL is a rare disease that combines B or T and myeloid blasts.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 17611554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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39. Kiyomizu K, Yagi T, Yoshida H, Minami R, Tanimura A, Karasuno T, Hiraoka A: Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia. J Infect Chemother; 2008 Oct;14(5):361-7
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  • [Title] Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia.
  • A 33-year-old man was suffering from febrile neutropenia (FN) on day 15 after the start of remission-induction therapy for biphenotypic acute leukemia under gut decontamination with polymyxin B and nystatin.
  • If B. cereus resistant to carbapem increases, our method of gut decontamination with polymyxin B and nystatin may have to be changed to one containing a new quinolone for the prevention of septicemia.
  • [MeSH-major] Bacillus cereus / drug effects. Bacteremia / microbiology. Carbapenems / therapeutic use. Leukemia, Biphenotypic, Acute / complications
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem / microbiology. Brain Stem / pathology. Fever / drug therapy. Gram-Positive Bacterial Infections / complications. Gram-Positive Bacterial Infections / diagnosis. Gram-Positive Bacterial Infections / drug therapy. Gram-Positive Bacterial Infections / pathology. Humans. Liver / microbiology. Liver / ultrastructure. Lung / microbiology. Lung / ultrastructure. Male. Microbial Sensitivity Tests. Neutropenia / drug therapy. Remission Induction. beta-Lactam Resistance

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  • (PMID = 18936889.001).
  • [ISSN] 1341-321X
  • [Journal-full-title] Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy
  • [ISO-abbreviation] J. Infect. Chemother.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Carbapenems
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40. Xu B, Li L, Tang JH, Zhou SY: Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia. Di Yi Jun Yi Da Xue Xue Bao; 2005 Oct;25(10):1207-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.
  • OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in acute lymphoblastic leukemia (ALL) patients of different immunological subtypes.
  • The positivity rate of FLT3 gene in pre-pre B-lineage ALL, pre-B-ALL, B-lineage ALL and T-lineage ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.
  • Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for myeloid antigen expression and diagnosed as acute mixed-lineage leukemia, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.
  • CONCLUSIONS: FLT3 gene can be detected in both B-and T-lineage ALL patients, but more frequently in the former.
  • In B-lineage ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.
  • FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of acute leukemia.
  • [MeSH-major] Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16234090.001).
  • [ISSN] 1000-2588
  • [Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
  • [ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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41. Guillaume N, Alleaume C, Munfus D, Capiod JC, Touati G, Pautard B, Desablens B, Lefrère JJ, Gouilleux F, Lassoued K, Gouilleux-Gruart V: ZAP-70 tyrosine kinase is constitutively expressed and phosphorylated in B-lineage acute lymphoblastic leukemia cells. Haematologica; 2005 Jul;90(7):899-905
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 tyrosine kinase is constitutively expressed and phosphorylated in B-lineage acute lymphoblastic leukemia cells.
  • BACKGROUND AND OBJECTIVES: Zeta-associated protein 70 (ZAP-70), a member of the Syk family of protein tyrosine kinases, is normally expressed in T and NK cells.
  • While little is known about ZAP-70 expression in normal human B cells, it has been reported that ZAP-70 is expressed in a subset of patients with chronic lymphocytic leukemia (CLL) with a poor prognosis.
  • In this study, we examined the expression and phosphorylation status of ZAP-70 in B-lineage acute lymphoblastic leukemia (Blin-ALL).
  • DESIGN AND METHODS: First, ZAP-70 protein expression was assessed by Western blotting and flow cytometry and ZAP-70 mRNA transcripts were analyzed by reverse transcription polymerase chain reaction (RT-PCR) on human precursor B cell lines.
  • RESULTS: ZAP-70 was constitutively expressed and phosphorylated on tyr319 in human precursor Blin-ALL cell lines as well as in primary B leukemic cells from all examined Blin-ALL patients with pro-B, pre-B and B phenotypes, but not in malignant myeloid cells.
  • Importantly, analysis of normal human bone marrow revealed expression of ZAP-70 transcripts only in the CD34+ cell fraction (either CD19-CD10- or CD19+CD10+) but not in the CD34- cell fraction (CD19+sIgM- pre-B cells or CD19+sIgM+ immature B cells).
  • INTERPRETATION AND CONCLUSIONS: ZAP-70 was found to be expressed in the CD34+ normal bone marrow compartment including earlier B-cell progenitors, but not in CD34- pre-B and immature B cells.

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  • [CommentIn] Haematologica. 2005 Jul;90(7):867 [15996917.001]
  • (PMID = 15996927.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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42. Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J: Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia. Nat Med; 2007 Jun;13(6):736-41
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  • [Title] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.
  • In the T-cell lineage, calcineurin activation is important for pre-T-cell receptor (TCR) signaling, TCR-mediated positive selection of thymocytes into mature T cells, and many aspects of the immune response.
  • We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.
  • In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.
  • In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.
  • Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.
  • Thus, calcineurin activation is critical for the maintenance of the leukemic phenotype in vivo, identifying this pathway as a relevant therapeutic target in lymphoid malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Calcineurin / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / enzymology
  • [MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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  • [CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]
  • (PMID = 17515895.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus
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43. Crazzolara R, Bendall L: Emerging treatments in acute lymphoblastic leukemia. Curr Cancer Drug Targets; 2009 Feb;9(1):19-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emerging treatments in acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a clonal proliferation of early B- and T-lymphocyte progenitors and results in the accumulation of leukemic blasts in the bone marrow and various extramedullary sites.
  • Despite current treatment protocols achieving rapid cytoreduction in the vast majority of patients, serious acute and late complications are frequent and resistance to chemotherapy often develops.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19200049.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 136
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44. Onciu M: Acute lymphoblastic leukemia. Hematol Oncol Clin North Am; 2009 Aug;23(4):655-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia and lymphoblastic lymphoma constitute a family of genetically heterogeneous lymphoid neoplasms derived from B- and T-lymphoid progenitors.
  • Diagnosis is based on morphologic, immunophenotypic, and genetic features that allow differentiation from normal progenitors and other hematopoietic and nonhematopoietic neoplasms.
  • Current intensive chemotherapy regimens have accomplished overall cure rates of 85% to 90% in children and 40% to 50% in adults, with outcomes depending on the genetic subtype of disease and clinical features at presentation.
  • Therapy is optimized using minimal residual disease studies that employ flow cytometric and molecular methodologies, and are important determinants of prognosis.
  • Genetic analyses currently underway are likely to provide insight into biology, mechanisms of relapse, pharmacogenetics, and new potential therapeutic targets, which should aid in further improvement of outcome in this disease.
  • [MeSH-major] Immunophenotyping / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Gene Rearrangement. Humans. Immunoglobulins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 19577163.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins; 0 / Receptors, Antigen, T-Cell
  • [Number-of-references] 105
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45. Akagi T, Shih LY, Ogawa S, Gerss J, Moore SR, Schreck R, Kawamata N, Liang DC, Sanada M, Nannya Y, Deneberg S, Zachariadis V, Nordgren A, Song JH, Dugas M, Lehmann S, Koeffler HP: Single nucleotide polymorphism genomic arrays analysis of t(8;21) acute myeloid leukemia cells. Haematologica; 2009 Sep;94(9):1301-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single nucleotide polymorphism genomic arrays analysis of t(8;21) acute myeloid leukemia cells.
  • Translocation of chromosomes 8 and 21, t(8;21), resulting in the AML1-ETO fusion gene, is associated with acute myeloid leukemia.
  • We searched for additional genomic abnormalities in this acute myeloid leukemia subtype by performing single nucleotide polymorphism genomic arrays (SNP-chip) analysis on 48 newly diagnosed cases.
  • Interestingly, 38% of Group B and only 13% of Group A samples had a KIT-D816 mutation, suggesting that genomic alterations are often associated with a KIT-D816 mutation.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Genome, Human. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide. Translocation, Genetic
  • [MeSH-minor] Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Humans. Loss of Heterozygosity / genetics. Mutation, Missense. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-pim-1 / genetics. Survival Rate. Tumor Cells, Cultured

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  • (PMID = 19734423.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
  • [Other-IDs] NLM/ PMC2738725
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46. Kastner P, Chan S: PU.1: a crucial and versatile player in hematopoiesis and leukemia. Int J Biochem Cell Biol; 2008;40(1):22-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PU.1: a crucial and versatile player in hematopoiesis and leukemia.
  • Purine Rich Box-1 (PU.1)/ SFFV Proviral Integration Site-1 (Spi-1) is an Ets-family transcription factor, which was first characterized as an oncogene in Friend's murine erythroleukemia, and subsequently, as a transcriptional regulator of myeloid promoters.
  • PU.1 has since emerged as a central regulator of all hematopoietic cell lineages.
  • PU.1 is essential for terminal myeloid cell differentiation, B and T cell development, erythropoiesis and hematopoietic stem cell maintenance.
  • Interestingly, recent work has provided strong evidence that suppression of PU.1 function is critical for the leukemic transformation of myeloid cells, both in mouse and man.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Hematopoiesis / physiology. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins. Trans-Activators
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Humans. Mice. Mice, Knockout. Proto-Oncogene Proteins c-ets / chemistry. Proto-Oncogene Proteins c-ets / genetics. Proto-Oncogene Proteins c-ets / metabolism. Spleen Focus-Forming Viruses. Transcriptional Activation. Tumor Suppressor Proteins / genetics

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  • (PMID = 17374502.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Trans-Activators; 0 / Tumor Suppressor Proteins; 0 / proto-oncogene protein Spi-1
  • [Number-of-references] 28
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47. Yasukawa M: [Immunotherapy and cell therapy for myeloid leukemia]. Nihon Rinsho; 2009 Oct;67(10):1938-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunotherapy and cell therapy for myeloid leukemia].
  • Recently, various leukaemia-associated antigens that are recognized by CTL in the context of HLA class I molecules have been identified.
  • On the basis of these findings, various clinical trials of immunotherapy for hematological malignancies, including peptide vaccination, dendritic cell therapy, adoptive transfer of CTL, T-cell receptor gene therapy have been ongoing.
  • Here, the current status and future feasibility of cellular immunotherapy for leukemia are discussed.
  • [MeSH-major] Cell- and Tissue-Based Therapy / methods. Immunotherapy / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adoptive Transfer. Cancer Vaccines. Core Binding Factor Alpha 2 Subunit / immunology. Dendritic Cells. Fusion Proteins, bcr-abl / immunology. Genetic Therapy. Humans. Myeloblastin / immunology. Oncogene Proteins, Fusion / immunology. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes, Cytotoxic / immunology. Vaccines, Subunit. WT1 Proteins / immunology

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  • (PMID = 19860194.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / TEL-AML1 fusion protein; 0 / Vaccines, Subunit; 0 / WT1 Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.21.76 / Myeloblastin
  • [Number-of-references] 20
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48. Armstrong SA, Look AT: Molecular genetics of acute lymphoblastic leukemia. J Clin Oncol; 2005 Sep 10;23(26):6306-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetics of acute lymphoblastic leukemia.
  • From its beginnings two decades ago with the analysis of chromosomal translocation breakpoints, research into the molecular pathogenesis of acute lymphoblastic leukemia (ALL) has now progressed to the large-scale resequencing of candidate oncogenes and tumor suppressor genes in the genomes of ALL cases blocked at various developmental stages within the B- and T-cell lineages.
  • [MeSH-major] Chromosome Aberrations. Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16155013.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
  • [Number-of-references] 126
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49. Schneider P, Costa O, Legrand E, Bigot D, Lecleire S, Grassi V, Vannier JP, Vasse M: In vitro secretion of matrix metalloprotease 9 is a prognostic marker in childhood acute lymphoblastic leukemia. Leuk Res; 2010 Jan;34(1):24-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro secretion of matrix metalloprotease 9 is a prognostic marker in childhood acute lymphoblastic leukemia.
  • Matrix metalloproteases (MMPs) are endopeptidases involved in tumor cell invasion.
  • Childhood acute lymphoblastic leukemia (ALL) is characterized by its capacity to infiltrate different organs.
  • We analyzed the expression of MMP-2, -9, -14 and TIMP-1 and -2 in a prospective study on 86 children with newly diagnosed ALL (73 B- and 13 T-lineage) and 9 children at relapse with B-ALL.
  • In patients at relapse, MMP-14 was present in a greater proportion of the B-ALL cell population than at diagnosis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Matrix Metalloproteinase 9 / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748669.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.35 / Matrix Metalloproteinase 9
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50. Zunino SJ, Storms DH: Resveratrol-induced apoptosis is enhanced in acute lymphoblastic leukemia cells by modulation of the mitochondrial permeability transition pore. Cancer Lett; 2006 Aug 18;240(1):123-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resveratrol-induced apoptosis is enhanced in acute lymphoblastic leukemia cells by modulation of the mitochondrial permeability transition pore.
  • We have previously shown that resveratrol can induce apoptotic cell death in cell lines established from patients with acute lymphoblastic leukemia (ALL).
  • These data suggest targeting the MPTP sensitizes B- and T-cell ALL to the anti-cancer activity of resveratrol, and may be particularly useful for the treatment of high-risk t(4;11) ALL.
  • [MeSH-minor] Cells, Cultured. Cyclosporine. Dose-Response Relationship, Drug. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Synergism. Humans. Isoquinolines. Jurkat Cells. Membrane Potentials. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16226372.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Isoquinolines; 0 / Mitochondrial Membrane Transport Proteins; 0 / Stilbenes; 0 / mitochondrial permeability transition pore; 83HN0GTJ6D / Cyclosporine; 85340-56-3 / PK 11195; Q369O8926L / resveratrol
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51. Jiménez-Morales S, Miranda-Peralta E, Saldaña-Alvarez Y, Perez-Vera P, Paredes-Aguilera R, Rivera-Luna R, Velázquez-Cruz R, Ramírez-Bello J, Carnevale A, Orozco L: BCR-ABL, ETV6-RUNX1 and E2A-PBX1: prevalence of the most common acute lymphoblastic leukemia fusion genes in Mexican patients. Leuk Res; 2008 Oct;32(10):1518-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCR-ABL, ETV6-RUNX1 and E2A-PBX1: prevalence of the most common acute lymphoblastic leukemia fusion genes in Mexican patients.
  • This study was conducted to determine the frequency of the most common fusion genes in Mexican pediatric patients with acute lymphoblastic leukemia (ALL).
  • Molecular analysis using RT-PCR was carried out in 53-blood samples: 52 patients with de novo ALL and one with relapsed ALL.
  • With regards to the immunophenotype, ETV6-RUNX1 was expressed in both pre-B and T-cell cases, while the presence of E2A-PBX1 and BCR-ABL was associated with the pre-B ALL phenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Homeodomain Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18455790.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 146150-85-8 / E2A-Pbx1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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52. Hodgetts A, Levin M, Kroll JS, Langford PR: Biomarker discovery in infectious diseases using SELDI. Future Microbiol; 2007 Feb;2(1):35-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been used to discover serum or tissue protein signatures and biomarkers for infectious diseases in the fields of virology (hepatitis B and C viruses, severe acute respiratory syndrome, HIV-1, human T-cell leukemia virus-1 and BK virus), parasitology (trypanosomiasis) and bacteriology (intra-amniotic inflammation, tuberculosis and bacterial endocarditis).
  • The protein signatures, or biomarkers, can be used to diagnose infection, predict disease states and to inform on disease processes.

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  • (PMID = 17661674.001).
  • [ISSN] 1746-0921
  • [Journal-full-title] Future microbiology
  • [ISO-abbreviation] Future Microbiol
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Proteome
  • [Number-of-references] 34
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53. Marculescu R, Vanura K, Montpellier B, Roulland S, Le T, Navarro JM, Jäger U, McBlane F, Nadel B: Recombinase, chromosomal translocations and lymphoid neoplasia: targeting mistakes and repair failures. DNA Repair (Amst); 2006 Sep 8;5(9-10):1246-58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recombinase, chromosomal translocations and lymphoid neoplasia: targeting mistakes and repair failures.
  • A large number of lymphoid malignancies is characterized by specific chromosomal translocations, which are closely linked to the initial steps of pathogenesis.
  • Due to the unique feature of lymphoid cells to somatically rearrange and mutate receptor genes, and to the corresponding strong activity of the immune enhancers/promoters at that stage of cell development, B- and T-cell differentiation pathways represent propitious targets for chromosomal translocations and oncogene activation.
  • Surprisingly, V(D)J-mediated translocations turn out to be restricted to two specific sub-types of lymphoid malignancies, T-cell acute lymphoblastic leukemias, and a restricted set of mature B-cell Non-Hodgkin's lymphomas.
  • [MeSH-major] DNA Repair. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, B-Cell / genetics. Recombinases / genetics. Recombination, Genetic. Translocation, Genetic

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  • (PMID = 16798110.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Recombinases
  • [Number-of-references] 88
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54. Roman-Gomez J, Jimenez-Velasco A, Barrios M, Prosper F, Heiniger A, Torres A, Agirre X: Poor prognosis in acute lymphoblastic leukemia may relate to promoter hypermethylation of cancer-related genes. Leuk Lymphoma; 2007 Jul;48(7):1269-82
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  • [Title] Poor prognosis in acute lymphoblastic leukemia may relate to promoter hypermethylation of cancer-related genes.
  • The hallmark of acute lymphoblastic leukemia (ALL) is a progressive appearance of malignant cell behavior that is triggered by the evolution of altered gene function.
  • ALL has traditionally been viewed as a genetic disease; however, epigenetic defects also play an important role.
  • Hypermethylation may contribute to the pathogenesis of leukemias providing an alternative route to gene mutation.
  • We have reported that gene methylation in ALL cells is the most important way to inactivate cancer-related genes in this disease.
  • In fact, this epigenetic event can help to inactivate tumor-suppressive apoptotic or growth-arresting responses and has prognostic impact in B- and T-ALL.
  • The presence in individual tumors of multiple genes simultaneously methylated is an independent factor of poor prognosis in both childhood and adult ALL in terms of disease-free survival and overall survival.
  • [MeSH-major] DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17613754.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 100
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55. Pike-Overzet K, van der Burg M, Wagemaker G, van Dongen JJ, Staal FJ: New insights and unresolved issues regarding insertional mutagenesis in X-linked SCID gene therapy. Mol Ther; 2007 Nov;15(11):1910-6
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  • The oncogenic potential of retrovirus-mediated gene therapy has been re-emphasized because four patients developed T-cell acute lymphoblastic leukemia (T-ALL)-like disease from an otherwise successful gene therapy trial for X-linked severe combined immunodeficiency (X-linked SCID).
  • X-linked SCID, a disease caused by inactivating mutations in the IL2Rgamma gene, is part of a heterogeneous group of SCIDs characterized by the lack of T cells in conjunction with the absence of B and/or natural killer (NK) cells.
  • In this review we discuss the various forms of SCID in relation to normal T-cell development.
  • [MeSH-minor] Animals. Cell Differentiation / immunology. Humans. Models, Immunological. Mutation / genetics. T-Lymphocytes / cytology. T-Lymphocytes / immunology

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  • (PMID = 17726455.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 56
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56. Tenney K, Shilatifard A: A COMPASS in the voyage of defining the role of trithorax/MLL-containing complexes: linking leukemogensis to covalent modifications of chromatin. J Cell Biochem; 2005 Jun 1;95(3):429-36
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  • The trithorax-related mixed lineage leukemia (Mll) gene located on chromosome 11 is rearranged in a variety of aggressive human B and T lymphoid tumors as well as acute myeloid leukemia (AML) in both children and adults.
  • [MeSH-major] Chromatin / metabolism. DNA-Binding Proteins / metabolism. Leukemia / metabolism. Multiprotein Complexes / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adult. Animals. Child. Histone-Lysine N-Methyltransferase. Humans. Methylation. Myeloid-Lymphoid Leukemia Protein. Proto-Oncogenes / genetics. Transcription, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15786493.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 1R01GM069905; United States / NCI NIH HHS / CA / 2R01CA089455
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 49
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57. Sato T, Kaneda M, Ichikawa M, Suzuki D, Nakagawa A, Kobayashi R: Current approaches to management of cerebral fungal infection in pediatric patients with hematologic disorders. J Pediatr Hematol Oncol; 2008 Mar;30(3):249-53
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  • A patient with severe aplastic anemia developed an Aspergillus species brain abscess and pulmonary aspergillosis after peripheral blood stem cell transplantation.
  • Another patient with acute myelogenous leukemia developed a huge brain abscess with histopathologic findings suspicious of mucormycosis.
  • [MeSH-major] Aspergillosis / diagnosis. Central Nervous System Fungal Infections / diagnosis. Hematologic Diseases / complications. Leukemia, Myeloid, Acute / complications. Mucormycosis / diagnosis
  • [MeSH-minor] Adolescent. Amphotericin B / administration & dosage. Anti-Bacterial Agents / administration & dosage. Antifungal Agents / administration & dosage. Child. Drug Combinations. Echinocandins / administration & dosage. Fatal Outcome. Female. Flucytosine / administration & dosage. Follow-Up Studies. Graft Rejection. Humans. Lipopeptides. Lipoproteins / administration & dosage. Magnetic Resonance Imaging. Male. Peripheral Blood Stem Cell Transplantation / adverse effects. Remission Induction. Treatment Outcome

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  • (PMID = 18376292.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents; 0 / Drug Combinations; 0 / Echinocandins; 0 / Lipopeptides; 0 / Lipoproteins; 7XU7A7DROE / Amphotericin B; D83282DT06 / Flucytosine; R10H71BSWG / micafungin
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58. Svojgr K, Burjanivova T, Vaskova M, Kalina T, Stary J, Trka J, Zuna J: Adaptor molecules expression in normal lymphopoiesis and in childhood leukemia. Immunol Lett; 2009 Feb 21;122(2):185-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adaptor molecules expression in normal lymphopoiesis and in childhood leukemia.
  • By influencing proliferation and differentiation, these molecules might play a role in ethiopathogenesis of acute lymphoblastic leukemia (ALL).
  • The aim of this study was to characterize expression of PAG, LAT, NTAL and LIME adaptors at the mRNA and protein levels in normal B- and T-precursors.
  • During normal lymphocyte development, some adaptors show significant dynamics (gradual decrease of NTAL and increase of LAT and LIME during the T-cell maturation, decrease of PAG in B-precursors, high levels of LIME in peripheral B-lymphocytes).
  • Analysis of childhood ALL samples revealed that in B-cell precursor ALL, the TEL/AML1 subgroup have unique adaptor profile compared to other leukemias.
  • Moreover, NTAL expression separates T lineage leukemias into two subgroups with good and poor response to initial prednisone therapy showing prognostic impact of this molecule in T-ALL.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. B-Lymphocytes / metabolism. Lymphopoiesis / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. T-Lymphocytes / metabolism
  • [MeSH-minor] Adaptor Proteins, Vesicular Transport / immunology. Biomarkers, Tumor. Cell Differentiation / immunology. Cell Lineage. Cell Proliferation. Child. Humans. Membrane Proteins / genetics. Membrane Proteins / immunology. Membrane Proteins / metabolism. Signal Transduction / immunology

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  • (PMID = 19183565.001).
  • [ISSN] 1879-0542
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adaptor Proteins, Vesicular Transport; 0 / Biomarkers, Tumor; 0 / LAT protein, human; 0 / LAT2 protein, human; 0 / Lck-interacting protein, human; 0 / Membrane Proteins; 0 / PAG1 protein, human
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59. de Graaf AO, van Krieken JH, Tönnissen E, Wissink W, van de Locht L, Overes I, Dolstra H, de Witte T, van der Reijden BA, Jansen JH: Expression of C-IAP1, C-IAP2 and SURVIVIN discriminates different types of lymphoid malignancies. Br J Haematol; 2005 Sep;130(6):852-9
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  • [Title] Expression of C-IAP1, C-IAP2 and SURVIVIN discriminates different types of lymphoid malignancies.
  • (De-)regulation of apoptosis plays an important role in normal and malignant lymphopoiesis.
  • To investigate whether expression of specific apoptosis-regulating genes correlated with different types of lymphoid malignancies, we measured the expression of five BCL-2 family genes, four IAP family genes and SMAC by real-time quantitative polymerase chain reaction in patient samples.
  • In total, 137 samples from B- and T-cell acute lymphoblastic leukaemia (ALL), B-cell chronic lymphocytic leukaemia (CLL), six different NHL types and three control tissue types were analysed.
  • Discriminant analysis identified three members of the IAP family, C-IAP1, C-IAP2 and SURVIVIN, as the most informative genes to discriminate between these lymphoid malignancies.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Lymphoid / diagnosis. Lymphoma, Non-Hodgkin / diagnosis. Neoplasm Proteins / metabolism
  • [MeSH-minor] Apoptosis. Diagnosis, Differential. Discriminant Analysis. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism. Polymerase Chain Reaction / methods. Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Ubiquitin-Protein Ligases

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  • (PMID = 16156855.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC2 protein, human; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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60. Berglund S, Okas M, Gertow J, Uhlin M, Mattsson J: Stable mixed donor-donor chimerism after double cord blood transplantation. Int J Hematol; 2009 Nov;90(4):526-31
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  • [Title] Stable mixed donor-donor chimerism after double cord blood transplantation.
  • In the present study, we evaluated the chimeric pattern in T-, B- and myeloid cells using PCR-based chimerism analysis in seven patients after DCBT: five patients had acute leukemia and two had lymphoma.
  • Three of the six evaluable patients showed donor-donor mixed chimerism in all cell lineages at 90 days after DCBT.
  • Interestingly, two patients in long-term follow-up showed mixed donor chimerism in all cell lineages at 25 and 35 months after DCBT, respectively.
  • In conclusion, in this study donor-donor mixed chimerism was common after high dose ATG and DCBT.
  • Further studies are warranted concerning the immunological consequences of the phenomenon of donor-donor mixed chimerism after DCBT.
  • [MeSH-major] Chimerism. Cord Blood Stem Cell Transplantation

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  • (PMID = 19697099.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum
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61. Turturro F: Denileukin diftitox: a biotherapeutic paradigm shift in the treatment of lymphoid-derived disorders. Expert Rev Anticancer Ther; 2007 Jan;7(1):11-7
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  • [Title] Denileukin diftitox: a biotherapeutic paradigm shift in the treatment of lymphoid-derived disorders.
  • Diphtheria toxin fragment A is released into the cytosol inhibiting the protein synthesis through the ADP-ribosylation of the elongation factor-2, and leading to cell death.
  • This review focuses on the clinical trials that led to the FDA approval of the drug for cutaneous T cell lymphoma in the US, and investigational studies demonstrating drug-activity against B and T-cell non-Hodgkin's lymphoma, chronic lymphocytic lymphoma and acute graft versus disease within allogeneic hematopoietic stem cell transplant.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Hodgkin Disease / drug therapy. Interleukin-2 / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Hematopoietic Stem Cell Transplantation. Humans. Recombinant Fusion Proteins / pharmacokinetics. Recombinant Fusion Proteins / therapeutic use. Safety. United States. United States Food and Drug Administration

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  • (PMID = 17187516.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 30
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62. Yang HZ, Xu S, Liao XY, Zhang SD, Liang ZL, Liu BH, Bai JY, Jiang C, Ding J, Cheng GF, Liu G: A novel immunostimulator, N-[alpha-O-benzyl-N-(acetylmuramyl)-L-alanyl-D-isoglutaminyl]-N6-trans-(m-nitrocinnamoyl)-L-lysine, and its adjuvancy on the hepatitis B surface antigen. J Med Chem; 2005 Aug 11;48(16):5112-22
The Lens. Cited by Patents in .

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  • The present study shows that MDP-C induces strong cytolytic activity by macrophages on P388 leukemia cells and cytotoxic activity by cytotoxic T lymphocytes (CTLs) on P815 mastocytoma cells.
  • Moreover, MDP-C remarkably enhances the immune system's responsiveness to hepatitis B surface antigen (HBsAg) in hepatitis B virus transgenic mice for both antibody production and specific HBsAg T-cell responses ex vivo.
  • Our results indicate that MDP-C is an apyrogenic, nonallergenic, and low-toxicity immunostimulator with great potential for diagnostic, immunotherapeutic, and prophylactic applications in diseases such as hepatitis B and cancers.
  • [MeSH-minor] Animals. Antibody Formation. Antigens, CD11c / biosynthesis. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Cell Line, Tumor. Cytotoxicity, Immunologic. Dendritic Cells / drug effects. Dendritic Cells / metabolism. Hepatitis B / immunology. Hepatitis B Vaccines / immunology. Histocompatibility Antigens Class I / biosynthesis. In Vitro Techniques. Intercellular Adhesion Molecule-1 / biosynthesis. Interleukin-12 / biosynthesis. Interleukin-2 / biosynthesis. Macrophages / drug effects. Macrophages / immunology. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Rabbits. Rats. Rats, Wistar. T-Lymphocytes, Cytotoxic / drug effects. T-Lymphocytes, Cytotoxic / immunology. Toxicity Tests, Acute

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  • (PMID = 16078831.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / U01 AI 61092-01
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, CD11c; 0 / Hepatitis B Surface Antigens; 0 / Hepatitis B Vaccines; 0 / Histocompatibility Antigens Class I; 0 / Interleukin-2; 0 / N(2)-(O-benzyl-N-(acetylmuramyl)-alanyl-isoglutaminyl)-N(6)-(3-nitrocinnamoyl)-lysine; 126547-89-5 / Intercellular Adhesion Molecule-1; 187348-17-0 / Interleukin-12; 53678-77-6 / Acetylmuramyl-Alanyl-Isoglutamine
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63. Spellman S, Bray R, Rosen-Bronson S, Haagenson M, Klein J, Flesch S, Vierra-Green C, Anasetti C: The detection of donor-directed, HLA-specific alloantibodies in recipients of unrelated hematopoietic cell transplantation is predictive of graft failure. Blood; 2010 Apr 1;115(13):2704-8
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  • [Title] The detection of donor-directed, HLA-specific alloantibodies in recipients of unrelated hematopoietic cell transplantation is predictive of graft failure.
  • Donor-directed human leukocyte antigen (HLA)-specific allo-antibodies (DSAs) cause graft failure in animal models of hematopoietic stem cell transplantation (HCT).
  • Controls were matched for disease, disease status, graft type, patient age, and transplantation year.
  • Patients had acute myeloid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome; 98% received myeloablative conditioning regimens 100% received T-replete grafts, 97% received marrow, 95% HLA-mismatched, and 97% received calcineurin-based graft-versus-host disease prophylaxis.

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  • (PMID = 20089963.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / U01 HL069294; United States / NCI NIH HHS / CA / U24 CA076518; United States / NHLBI NIH HHS / HL / 5U01HL069294; United States / NCI NIH HHS / CA / U24-CA76518
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / Immunosuppressive Agents; 0 / Isoantibodies
  • [Other-IDs] NLM/ PMC2852369
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64. Anderson MW, Zhao S, Ai WZ, Tibshirani R, Levy R, Lossos IS, Natkunam Y: C-C chemokine receptor 1 expression in human hematolymphoid neoplasia. Am J Clin Pathol; 2010 Mar;133(3):473-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recently, CCL3 (MIP-1alpha), a high-affinity CCR1 ligand, was identified as part of a model that independently predicts survival in patients with diffuse large B-cell lymphoma (DLBCL).
  • Immunohistochemical analysis of 944 cases of hematolymphoid neoplasia identified CCR1 expression in a subset of B- and T-cell lymphomas, plasma cell myeloma, acute myeloid leukemia, and classical Hodgkin lymphoma.

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  • (PMID = 20154287.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / P30 CA124435; United States / NCI NIH HHS / CA / CA34233
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR1 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, CCR1
  • [Other-IDs] NLM/ NIHMS637012; NLM/ PMC4305436
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65. Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC: The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice. Leukemia; 2006 Oct;20(10):1829-39
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  • [Title] The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
  • Rearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia.
  • Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property.
  • We also generated Mll(Een/+) chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
  • Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations.
  • We observed differential regulation of Hox genes between myeloid cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease.
  • We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myeloid Cells / pathology. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Division / physiology. Chimera. Disease Models, Animal. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Genes, Homeobox / physiology. Humans. Infant. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Translocation, Genetic

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  • (PMID = 16888613.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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66. Bardelli M, Leucci E, Schürfeld K, Bellan C, Passiatore G, Rocchigiani M, Bartolommei S, Orlandini M, Zagursky J, Lazzi S, De Falco G, Tosi P, Oliviero S, Leoncini L: VEGF-D is expressed in activated lymphoid cells and in tumors of hematopoietic and lymphoid tissues. Leuk Lymphoma; 2007 Oct;48(10):2014-21
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  • [Title] VEGF-D is expressed in activated lymphoid cells and in tumors of hematopoietic and lymphoid tissues.
  • This analysis revealed that VEGF-D is expressed in B cells of the germinal centers, scattered B and T blasts, myeloid progenitors, acute leukemia, several types of non Hodgkin lymphoma, and classical Hodgkin's lymphoma.
  • These data suggest that VEGF-D could contribute to leukemia and lymphoma growth via the induction of angiogenesis in bone marrow and lymphoid tissues.
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Biopsy. Bone Marrow Cells / metabolism. Cell Line, Tumor. HL-60 Cells. Humans. K562 Cells. Lymph Nodes / pathology. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Vascular Endothelial Growth Factor Receptor-3 / biosynthesis. Vascular Endothelial Growth Factor Receptor-3 / metabolism

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  • (PMID = 17917969.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Vascular Endothelial Growth Factor D; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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67. Kaufmann Y, Amariglio N, Rosenthal E, Hirsch YJ, Many A, Rechavi G: Proliferation response of leukemic cells to CD70 ligation oscillates with recurrent remission and relapse in a low-grade lymphoma. J Immunol; 2005 Nov 15;175(10):6940-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Interactions of the TNF-related cell surface ligand CD70 with its receptor CD27 provide a costimulatory signal in B and T cell activation.
  • Functional CD70-CD27 interactions could contribute to lymphoma and leukemia progression.
  • This possibility was studied using DNA microarrays on a unique case of low-grade lymphoma/leukemia characterized by recurrent cycles of acute leukemic phase alternating with spontaneous remission.
  • Upon induction of the acute phase expression of CD70 and CD27 in the leukemic cells increased 38- and 25-fold, respectively.
  • However, the anti-CD70 Ab specifically enhanced proliferation of the remission phase leukemic cells, whereas proliferation of the acute-phase counterparts that express higher level of membrane CD70 was unaffected.
  • Hence, in this lymphoma/leukemia, membrane CD70 is presented on the leukemic cells in a responsive state during the remission and a nonresponsive state during the attack.
  • Presumably, CD70 in its responsive state provides a costimulatory receptor for initiating the next acute phase while its nonresponsive state enables the remission.
  • [MeSH-major] Antigens, CD / metabolism. Leukemia / immunology. Leukemia / pathology. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Membrane Proteins / metabolism. Tumor Necrosis Factors / metabolism
  • [MeSH-minor] Antigens, CD27 / blood. Antigens, CD27 / genetics. Antigens, CD70. Apoptosis. Base Sequence. Cell Membrane / immunology. Cell Proliferation. DNA, Neoplasm / genetics. Gene Expression Profiling. Humans. Ligands. Recurrence

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  • (PMID = 16272354.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD27; 0 / Antigens, CD70; 0 / CD70 protein, human; 0 / DNA, Neoplasm; 0 / Ligands; 0 / Membrane Proteins; 0 / Tumor Necrosis Factors
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68. Al-Masoudi NA, Abdullah BH, Essa AH, Loddo R, LaColla P: Platinum and palladium-triazole complexes as highly potential antitumor agents. Arch Pharm (Weinheim); 2010 Apr;343(4):222-7
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  • The antiproliferative activity of the newly synthesized complexes as well as their previously prepared analogues 3-14 and 20-26 were screened against a large panel of human cancer cell lines derived from haematological CD4(+) human T-cells containing an integrated HTLV-1 genome (MT-4).
  • The complex 12a, b exhibited remarkable antiproliferative activity against MT-4, CD4(+) human acute T-lymphoblastic leukemia (CCRF-CEM), human splenic B-lymphoblastoid cells (WIL-2NS), human acute B-lymphoblastic leukemia (CCRF-SB), skin melanoma (SK-MEL-28), and prostate carcinoma (DU145) cell lines (CC(50 )= 0.5 microM, 0.4 +/- 0.05 microM, 0.6 +/- 0.05 microM, 0.4 +/- 0.1 microM, and 0.8 +/- 0.2 microM, respectively), meanwhile, 9a, b, 14a, b, and 23 showed significant activity against the CCRF-SB cell lines (CC(50) = 0.6 +/- 0.06 microM, 0.7 +/- 0.05 microM, 0.6 +/- 0.05 microM, and 0.8 +/- 0.15 microM, respectively).
  • Further, 19 exhibited activity against the CCRF-CEM cell line (CC(50 )= 0.4 +/- 0.05 microM).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Organometallic Compounds / pharmacology. Organoplatinum Compounds / pharmacology. Palladium / pharmacology. Triazoles / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Inhibitory Concentration 50. Molecular Structure. Quantitative Structure-Activity Relationship

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  • (PMID = 20222061.001).
  • [ISSN] 1521-4184
  • [Journal-full-title] Archiv der Pharmazie
  • [ISO-abbreviation] Arch. Pharm. (Weinheim)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organometallic Compounds; 0 / Organoplatinum Compounds; 0 / Triazoles; 5TWQ1V240M / Palladium
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69. Tschan MP, Reddy VA, Ress A, Arvidsson G, Fey MF, Torbett BE: PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity. Oncogene; 2008 May 29;27(24):3489-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance.
  • PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias.
  • Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression.
  • It has been hypothesized that p53-mediated expression of the p21(Cip1) cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function.
  • We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis.
  • Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21(Cip1).
  • [MeSH-minor] Apoptosis. Blotting, Western. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Humans. Immunoprecipitation. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Isoforms. RNA, Small Interfering / pharmacology. Transcriptional Activation. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 18193090.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI49165; United States / NIDDK NIH HHS / DK / DK49886
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / proto-oncogene protein Spi-1; 0 / tumor suppressor protein p73
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70. Falini B, Bolli N, Shan J, Martelli MP, Liso A, Pucciarini A, Bigerna B, Pasqualucci L, Mannucci R, Rosati R, Gorello P, Diverio D, Roti G, Tiacci E, Cazzaniga G, Biondi A, Schnittger S, Haferlach T, Hiddemann W, Martelli MF, Gu W, Mecucci C, Nicoletti I: Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AML. Blood; 2006 Jun 1;107(11):4514-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We recently identified aberrant cytoplasmic expression of nucleophosmin (NPM) as the immunohistochemical marker of a large subgroup of acute myeloid leukemia (AML) (about one-third of adult AML) that is characterized by normal karyotype and mutations occurring at the exon-12 of the NPM gene.
  • In fact, the cytoplasmic accumulation of NPM is blocked by leptomycin-B and ratjadones, specific exportin-1/Crm1-inhibitors, and by reinsertion of tryptophan residues 288 and 290, which respectively relocate NPM mutants in the nucleoplasm and nucleoli.
  • [MeSH-major] Active Transport, Cell Nucleus / genetics. Leukemia / genetics. Mutation. Nuclear Export Signals / genetics. Nuclear Proteins / genetics. Tryptophan / genetics
  • [MeSH-minor] Amino Acid Motifs. Animals. Base Sequence. Cell Line. Cell Nucleolus / metabolism. Cytoplasm / metabolism. Humans. Transfection

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  • (PMID = 16455950.001).
  • [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 / Nuclear Export Signals; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 8DUH1N11BX / Tryptophan
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71. Kraan J, Gratama JW, Haioun C, Orfao A, Plonquet A, Porwit A, Quijano S, Stetler-Stevenson M, Subira D, Wilson W: Flow cytometric immunophenotyping of cerebrospinal fluid. Curr Protoc Cytom; 2008 Jul;Chapter 6:Unit 6.25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Leptomeningeal disease is an important adverse complication occurring in patients with B and T cell lymphomas and acute leukemias of lymphoid and myeloid origin.
  • However, spinal fluid samples are frequently paucicellular with a rapidly decreasing cell viability.
  • Finally, in the Alternate Protocol, we describe a method to calculate absolute numbers of both normal and pathological cell subpopulations by adding counting beads to the assay.

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  • (PMID = 18770650.001).
  • [ISSN] 1934-9300
  • [Journal-full-title] Current protocols in cytometry
  • [ISO-abbreviation] Curr Protoc Cytom
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface
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72. Vasilatou D, Papageorgiou S, Pappa V, Papageorgiou E, Dervenoulas J: The role of microRNAs in normal and malignant hematopoiesis. Eur J Haematol; 2010 Jan 1;84(1):1-16

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because of their discovery, microRNAs have been associated with almost every normal cell function, including proliferation, differentiation and apoptosis.
  • Several lines of evidence suggest that they have an important role in normal hematopoiesis as exemplified by the role of mir-155 and mir-150 in the differentiation of B and T lymphocytes, the suppressive role of mir-221 and mir-222 in erythroid differentiation, the inhibitory effect of mir-181 on hematopoietic differentiation and the induction of myeloid differentiation by mir-223.
  • Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in chronic lymphocytic leukemia, the increased levels of mir-155 in diffuse large B-cell lymphomas and the increased levels of mir-181 in acute myeloid leukemia M1 and M2.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Down-Regulation. Erythroid Precursor Cells / cytology. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor. Humans. Invertebrates / genetics. Lymphocytes / cytology. Mice. Myeloid Cells / cytology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oncogenes. RNA, Neoplasm / antagonists & inhibitors. RNA, Neoplasm / genetics

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  • (PMID = 19744129.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm
  • [Number-of-references] 110
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73. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • The new WHO classification of hematologic tumors has adopted the EGIL criteria for BAL and introduced a new group of AL termed 'AL of ambiguous lineage'.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Chromosome abnormalities are frequent in both entities with a relatively high incidence of Philadelphia chromosome and rearrangements involving 11q23, especially in cases with B- and myeloid involvement.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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74. Correa-González LC, Mandeville PB, Manrique-Dueñas J, Alejo-González F, Salazar-Martínez A, de Pérez-Ramírez OJ, Hernández-Sierra JF: [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients]. Gac Med Mex; 2005 Nov-Dec;141(6):477-82
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  • [Title] [Prognostic value of pre-B immunophenotype in early treatment response among acute pediatric lymphoblast leukemia patients].
  • [Transliterated title] Valor pronóstico del inmunofenotipo en la respuesta temprana de la leucemia aguda linfoblástica pre-B en niños.
  • OBJECTIVE: To determine the prognostic value of preB immunophenotype and its variants on early treatment response among of acute pediatric lymphoblast leukemia.
  • PATIENTS AND METHODS: A case-control study nested in a cohort was carried out with male and female patients 15 years and younger with recently diagnosed pre-B lymphoblast leukemia.
  • A panel of B, T, monoclonal antibodies of the myelo-monocytic and megakaryocytic cell type was used.
  • We identified 29 cases with late pre-B immune phenotype, 19 cases with common pre B and 6 cases with early preB immunophenotype.
  • Eleven, patients also displayed myeloid antigens.
  • A significant association (p=0.034) was found between early treatment response and the presence of myeloid antigens.
  • CONCLUSIONS: We need to pay special emphasis on early treatment response in children with lymphoblast leukemia as our study did not corroborate the common finding that clinical factors and immune phenotype can be predictive factors.
  • [MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 16381501.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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75. Qiuping Z, Jie X, Youxin J, Qun W, Wei J, Chun L, Jin W, Yan L, Chunsong H, Mingzhen Y, Qingping G, Qun L, Kejian Z, Zhimin S, Junyan L, Jinquan T: Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia. Oncogene; 2005 Jan 20;24(4):573-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia.
  • We investigated CD4(+)CD34(+), CD8(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells from cord blood and from typical patients with T-cell-lineage acute lymphocytic leukemia and T-cell-lineage chronic lymphocytic leukemia in terms of expression and functions of CXCR5/CXCL13.
  • We found that CXCR5 was selectively frequently expressed on T-cell-lineage acute (chronic) lymphocytic leukemia (T-ALL) CD8(+)CD34(+) T cells, but not on T-ALL CD4(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells.
  • A proliferation-inducing ligand expression in T-ALL CD8(+)CD34(+) T cells was upregulated by CXCL13/BCA-1 (B-cell attracting chemokine 1).
  • In this process, cell-cell contact in culture was necessary.
  • Normal lymphocytes, especially naive B and T cells, utilized CXCR5/CXCL13 for migration, homing, maturation, and cell homeostasis, as well as secondary lymphoid tissue organogenesis.
  • [MeSH-major] Antigens, CD34 / metabolism. Apoptosis. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Cytokine / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Cell Adhesion / drug effects. Cell Line. Cell Lineage / drug effects. Chemokine CXCL13. Chemokines, CXC / metabolism. Chemokines, CXC / pharmacology. Chemotaxis / drug effects. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Nuclear Proteins / pharmacology. Receptors, CXCR5. Receptors, Chemokine / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / genetics

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  • [RetractionIn] Oncogene. 2011 Jun 16;30(24):2798 [21677655.001]
  • (PMID = 15580304.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ANP32B protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD34; 0 / BIRC7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CXCL13; 0 / Chemokines, CXC; 0 / Inhibitor of Apoptosis Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Tumor Necrosis Factor-alpha
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76. Chunsong H, Yuling H, Li W, Jie X, Gang Z, Qiuping Z, Qingping G, Kejian Z, Li Q, Chang AE, Youxin J, Jinquan T: CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells. J Immunol; 2006 Nov 15;177(10):6713-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells.
  • We have investigated expression and functions of CXCL13/CXCR5 and CCL19/CCR7 in CD23+CD5+ and CD23+CD5- B cells from cord blood (CB) and patients with B cell lineage acute or chronic lymphocytic leukemia (B-ALL or B-CLL).
  • Although no significant chemotactic responsiveness was observed, CXCL13 and CCL19 cooperatively induce significant resistance to TNF-alpha-mediated apoptosis in B-ALL and B-CLL CD23+CD5+ B cells, but not in the cells from CB.
  • B-ALL and B-CLL CD23+CD5+ B cells express elevated levels of paternally expressed gene 10 (PEG10).
  • We have found that CXCL13 and CCL19 together by means of activation of CXCR5 and CCR7 up-regulate PEG10 expression and function, subsequently stabilize caspase-3 and caspase-8 in B-ALL and B-CLL CD23+CD5+ B cells, and further rescue the cells from TNF-alpha-mediated apoptosis.
  • Therefore, we suggest that normal lymphocytes, especially naive B and T cells, use CXCL13/CXCR5 and CCL19/CCR7 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis.
  • [MeSH-major] Apoptosis / immunology. B-Lymphocyte Subsets / immunology. B-Lymphocyte Subsets / metabolism. Burkitt Lymphoma / immunology. Chemokines, CC / physiology. Chemokines, CXC / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Antigens, CD5 / biosynthesis. Cell Lineage / immunology. Chemokine CCL19. Chemokine CXCL13. Fetal Blood / cytology. Fetal Blood / immunology. Fetal Blood / metabolism. Humans. Lymphocyte Count. Proteins / metabolism. Proteins / physiology. Receptors, CCR7. Receptors, CXCR5. Receptors, Chemokine / biosynthesis. Receptors, IgE / biosynthesis

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  • (PMID = 17082584.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CCL19 protein, human; 0 / CCR7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / PEG10 protein, human; 0 / Proteins; 0 / Receptors, CCR7; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, IgE
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77. Harvey RC, Mullighan CG, Wang X, Dobbin KK, Davidson GS, Bedrick EJ, Chen IM, Atlas SR, Kang H, Ar K, Wilson CS, Wharton W, Murphy M, Devidas M, Carroll AJ, Borowitz MJ, Bowman WP, Downing JR, Relling M, Yang J, Bhojwani D, Carroll WL, Camitta B, Reaman GH, Smith M, Hunger SP, Willman CL: Identification of novel cluster groups in pediatric high-risk B-precursor acute lymphoblastic leukemia with gene expression profiling: correlation with genome-wide DNA copy number alterations, clinical characteristics, and outcome. Blood; 2010 Dec 2;116(23):4874-84
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  • [Title] Identification of novel cluster groups in pediatric high-risk B-precursor acute lymphoblastic leukemia with gene expression profiling: correlation with genome-wide DNA copy number alterations, clinical characteristics, and outcome.
  • To resolve the genetic heterogeneity within pediatric high-risk B-precursor acute lymphoblastic leukemia (ALL), a clinically defined poor-risk group with few known recurring cytogenetic abnormalities, we performed gene expression profiling in a cohort of 207 uniformly treated children with high-risk ALL.
  • These studies reveal striking clinical and genetic heterogeneity in high-risk ALL and point to novel genes that may serve as new targets for diagnosis, risk classification, and therapy.


78. Nasr MR, Rosenthal N, Syrbu S: Expression profiling of transcription factors in B- or T-acute lymphoblastic leukemia/lymphoma and burkitt lymphoma: usefulness of PAX5 immunostaining as pan-Pre-B-cell marker. Am J Clin Pathol; 2010 Jan;133(1):41-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiling of transcription factors in B- or T-acute lymphoblastic leukemia/lymphoma and burkitt lymphoma: usefulness of PAX5 immunostaining as pan-Pre-B-cell marker.
  • The optimal use of transcription factors to determine B-lineage specificity in B-acute lymphoblastic leukemia/lymphoma (B-ALL) has not been fully investigated.
  • We undertook an extensive immunohistochemical study of a panel of B-cell transcription factors in B- and T-ALL and Burkitt lymphoma to evaluate those with the best specificity and sensitivity.
  • PAX5 demonstrated better specificity for B-lineage determination than BOB.1 and PU.1 and better sensitivity than CD79a, CD22, and CD20.
  • These findings suggest that PAX5 has the greatest diagnostic usefulness and lineage determination in B-ALL, especially in cases with an inadequate specimen for flow cytometric analysis.
  • [MeSH-major] B-Cell-Specific Activator Protein / metabolism. Biomarkers, Tumor / metabolism. Burkitt Lymphoma / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Bone Marrow Cells. Cell Lineage. Flow Cytometry. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Immunophenotyping. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Tissue Array Analysis

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  • (PMID = 20023257.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
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79. Bellavia D, Mecarozzi M, Campese AF, Grazioli P, Gulino A, Screpanti I: Notch and Ikaros: not only converging players in T cell leukemia. Cell Cycle; 2007 Nov 15;6(22):2730-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch and Ikaros: not only converging players in T cell leukemia.
  • Notch3 overexpression has been observed in virtually 100% of T cell acute lymphoblastic leukemia (T-ALL).
  • A high percentage of infant B- and T-ALLs also display an increased expression of non DNA-binding Ikaros isoforms.
  • We recently suggested that pre-TCR is the missing link between Notch and Ikaros in T cell leukemogenesis.
  • Our findings may help in clarifying the regulatory mechanism of Ikaros alternative splicing and suggest a crosstalk among Notch3, pre-TCR signalling and spliced Ikaros variants in T cell leukemogenesis, mediated by HuD.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Leukemia, T-Cell / metabolism. Receptors, Notch / physiology

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  • (PMID = 18032925.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch; 148971-36-2 / Ikaros Transcription Factor
  • [Number-of-references] 66
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80. Thiede C, Koch S, Creutzig E, Steudel C, Illmer T, Schaich M, Ehninger G: Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML). Blood; 2006 May 15;107(10):4011-20
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  • [Title] Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML).
  • Mutations of the nucleophosmin (NPM1) gene have recently been described in patients with acute myeloid leukemia (AML).
  • NPM1 mutations were most prevalent in patients with normal karyotype (NK) (324 of 709; 45.7%) compared with 58 of 686 with karyotype abnormalities (8.5%; P < .001) and were significantly associated with several clinical parameters (high bone marrow [BM] blasts, high white blood cell [WBC] and platelet counts, female sex).
  • The analysis of the clinical impact in 4 groups (NPM1 and FLT3-ITD single mutants, double mutants, and wild-type [wt] for both) revealed that patients having only an NPM1 mutation had a significantly better overall and disease-free survival and a lower cumulative incidence of relapse.
  • In conclusion, NPM1 mutations represent a common genetic abnormality in adult AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics


81. Schmidt S, Irving JA, Minto L, Matheson E, Nicholson L, Ploner A, Parson W, Kofler A, Amort M, Erdel M, Hall A, Kofler R: Glucocorticoid resistance in two key models of acute lymphoblastic leukemia occurs at the level of the glucocorticoid receptor. FASEB J; 2006 Dec;20(14):2600-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucocorticoid resistance in two key models of acute lymphoblastic leukemia occurs at the level of the glucocorticoid receptor.
  • Glucocorticoids (GCs) specifically induce apoptosis in malignant lymphoblasts and are thus pivotal in the treatment of acute lymphoblastic leukemia (ALL).
  • We generated approximately 70 GC-resistant sublines from a GC-sensitive B- and a T-ALL cell line and investigated their mechanisms of resistance.
  • [MeSH-major] Drug Resistance, Neoplasm. Glucocorticoids / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Receptors, Glucocorticoid / metabolism
  • [MeSH-minor] Cell Line, Tumor. DNA Mismatch Repair. Humans. Mutation. Transcription Factors / metabolism

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  • (PMID = 17077285.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / FWF/ P 18571
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Receptors, Glucocorticoid; 0 / TSC22D3 protein, human; 0 / Transcription Factors
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82. Patel HS, Kantarjian HM, Bueso-Ramos CE, Medeiros LJ, Haidar MA: Frequent deletions at 12q14.3 chromosomal locus in adult acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2005 Jan;42(1):87-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent deletions at 12q14.3 chromosomal locus in adult acute lymphoblastic leukemia.
  • Cytogenetic abnormalities at the 12q12-q14 chromosomal locus are rarely detected in acute lymphoblastic leukemia (ALL).
  • To examine submicroscopic deletions at this locus, we analyzed 78 adult precursor B- and T-cell ALL cases [27 with Philadelphia chromosome (Ph)-negative B-cell ALL, 20 with Ph-negative B-cell ALL with expression of one or two myeloid markers, 18 with Ph-positive B-cell ALL, and 13 with T-cell ALL] using a panel of 13 microsatellite (MST) markers that span the 12q12-q14.3 region.
  • The frequency of deletions was highest in Ph-negative B-cell ALL (13 of 27, 48%) compared with that in Ph-negative B-cell ALL with expression of myeloid markers (4 of 20, 20%), Ph-positive B-cell ALL (2 of 18, 11%), and T-cell ALL (1 of 13, 8%).
  • These submicroscopic deletions at the 12q14.3 locus may play a role in the pathogenesis of ALL, particularly in Ph-negative precursor B-cell ALL.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 13 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 15495192.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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83. Williams RT, Sherr CJ: The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Adv Exp Med Biol; 2007;604:107-14
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  • [Title] The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • The prototypical Bcr-Abl chimeric oncoprotein is central to the pathogenesis of chronic myelogenous leukemias (CMLs) and a subset of acute lymphoblastic leukemias (Ph+ ALLs).
  • The constitutive tyrosine kinase transforms either hematopoietic stem cells (in CML) or committed pre-B lymphoid progenitors (in Ph+ ALL) to generate these distinct diseases.
  • The INK4A/ARF tumor suppressor locus is frequently deleted in both B- and T-lineage ALLs, including Ph+ ALL, whereas the locus remains intact in CML.
  • In murine bone marrow transplant models and after transfer of syngeneic Bcr-Abl-transformed pre-B cells into immunocompetent recipient animals, Arf gene inactivation dramatically decreases the latency and enhances the aggressiveness of Bcr-Abl-induced lymphoblastic leukemia.
  • Despite exquisite in vitro sensitivity of Arf-null, BCR-ABL+ pre-B cells to imatinib, these cells efficiently establish lethal leukemias when introduced into immunocompetent mice that receive continuous, maximal imatinib therapy.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tumor Suppressor Protein p14ARF / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Benzamides. Disease Models, Animal. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Interleukin-7 / metabolism. Mice. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 17695724.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA70089
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 20
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84. Mukherjee K, Chava AK, Bandyopadhyay S, Mallick A, Chandra S, Mandal C: Co-expression of 9-O-acetylated sialoglycoproteins and their binding proteins on lymphoblasts of childhood acute lymphoblastic leukemia: an anti-apoptotic role. Biol Chem; 2009 Apr;390(4):325-35
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  • [Title] Co-expression of 9-O-acetylated sialoglycoproteins and their binding proteins on lymphoblasts of childhood acute lymphoblastic leukemia: an anti-apoptotic role.
  • Enhanced levels of 9-O-acetylated sialoglycoproteins (Neu5,9Ac(2)GPs) as disease-associated molecules was reported to act as signaling molecules for promoting survival of lymphoblasts in childhood acute lymphoblastic leukemia (ALL).
  • Accordingly, we examined the presence of binding proteins for Neu5,9Ac(2)GPs on cell lines and primary cells of patients with B- and T-ALL, at presentation of the disease.
  • Peripheral blood mononuclear cells from normal healthy donors and cells from myeloid leukemia patients were used for comparison.
  • Neu5,9Ac(2)GPs-binding proteins (BPs) were specifically detected on the surface of both T- and B-ALL-lymphoblasts and ALL-cell lines along with the consistent presence of Neu5,9Ac(2)GPs.
  • The Neu5,9Ac(2)GPs and BPs also co-localized on the cell surface and interacted specifically in vitro.
  • This is the first report of the presence of potential physiological ligands for disease-associated molecules like Neu5,9Ac(2)GPs, the interaction of which is able to trigger an anti-apoptotic signal conferring a survival advantage to leukemic cells in childhood ALL.
  • [MeSH-major] Apoptosis. Lymphocytes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Sialoglycoproteins / metabolism
  • [MeSH-minor] Acetylation. Adolescent. Adult. Blotting, Western. Cell Cycle / drug effects. Cell Line. Child. Child, Preschool. Female. Flow Cytometry. Humans. Infant. Male. Microscopy, Confocal. Middle Aged. Protein Binding. Young Adult

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  • (PMID = 19166321.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Sialoglycoproteins
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85. Mokrzycka M, Pawlik A, Kałdońska M, Millo B: Assessment of liver function in children with acute lymphoblastic leukemia in remission. Ann Acad Med Stetin; 2006;52(3):61-5; discussion 65
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  • [Title] Assessment of liver function in children with acute lymphoblastic leukemia in remission.
  • PURPOSE: Acute lymphoblastic leukemia (ALL) is the most common malignant neoplasm in children.
  • Eleven patients were also infected with chronic viral hepatitis type B and/or type C.
  • [MeSH-major] Liver Function Tests. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
  • [MeSH-minor] Adolescent. Adult. Area Under Curve. Child. Diagnosis, Differential. Female. Half-Life. Hepatitis, Chronic / complications. Hepatitis, Chronic / diagnosis. Humans. Lidocaine / analogs & derivatives. Lidocaine / pharmacokinetics. Liver / metabolism. Male. Reference Values. Remission Induction

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  • (PMID = 17385349.001).
  • [ISSN] 1427-440X
  • [Journal-full-title] Annales Academiae Medicae Stetinensis
  • [ISO-abbreviation] Ann Acad Med Stetin
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 7728-40-7 / monoethylglycinexylidide; 98PI200987 / Lidocaine
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86. Hertoghs KM, Moerland PD, van Stijn A, Remmerswaal EB, Yong SL, van de Berg PJ, van Ham SM, Baas F, ten Berge IJ, van Lier RA: Molecular profiling of cytomegalovirus-induced human CD8+ T cell differentiation. J Clin Invest; 2010 Nov;120(11):4077-90
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  • [Title] Molecular profiling of cytomegalovirus-induced human CD8+ T cell differentiation.
  • We show here that HCMV infection induced acute and lasting changes in the transcriptomes of virus-reactive T cells collected from HCMV-seropositive patients at distinct stages of infection.
  • Enhanced cell cycle and metabolic activity was restricted to the acute phase of the response, but at all stages, HCMV-specific CD8+ T cells expressed the Th1-associated transcription factors T-bet (TBX21) and eomesodermin (EOMES), in parallel with continuous expression of IFNG mRNA and IFN-γ-regulated genes.
  • The cytolytic proteins granzyme B and perforin as well as the fractalkine-binding chemokine receptor CX3CR1 were found in virus-reactive cells throughout the response.
  • Persistent effector cell traits together with the permanent changes in chemokine receptor usage of virus-specific, nonexhausted, long-lived CD8+ T cells may be crucial to maintain lifelong protection from HCMV reactivation.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / physiology. Cell Differentiation / immunology. Cytomegalovirus / immunology. Cytomegalovirus Infections / immunology
  • [MeSH-minor] Biomarkers / metabolism. Cell Separation. Flow Cytometry. Gene Expression Profiling. Humans. Lymphocyte Activation / immunology. Microarray Analysis. Virus Latency

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  • (PMID = 20921622.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Other-IDs] NLM/ PMC2964975
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87. Alousi AM, Uberti J, Ratanatharathorn V: The role of B cell depleting therapy in graft versus host disease after allogeneic hematopoietic cell transplant. Leuk Lymphoma; 2010 Mar;51(3):376-89
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  • [Title] The role of B cell depleting therapy in graft versus host disease after allogeneic hematopoietic cell transplant.
  • Graft versus host disease (GVHD) remains a common complication following allogeneic hematopoietic cell transplant (HCT).
  • The role of B lymphocytes in the pathogenesis of this disease was brought to prominence following a case report of a patient with chronic GVHD who responded to B cell depletion therapy with rituximab.
  • Since this original observation, several clinical trials and case series have been published on the use of B cell depletion using rituximab in the treatment of chronic GVHD.
  • Corresponding to this clinical experience, considerable laboratory evidence has revealed the complex interactions between B and T cells which culminate in acute and chronic GVHD.
  • More recently, researchers have examined the link between B cell immune reconstitution following HCT and the development of chronic GVHD.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / pharmacology. Antibodies, Monoclonal, Murine-Derived / therapeutic use. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. Graft vs Host Disease / drug therapy. Hematopoietic Stem Cell Transplantation. Lymphocyte Depletion

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  • (PMID = 20141428.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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88. Tsapis M, Lieb M, Manzo F, Shankaranarayanan P, Herbrecht R, Lutz P, Gronemeyer H: HDAC inhibitors induce apoptosis in glucocorticoid-resistant acute lymphatic leukemia cells despite a switch from the extrinsic to the intrinsic death pathway. Int J Biochem Cell Biol; 2007;39(7-8):1500-9
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  • [Title] HDAC inhibitors induce apoptosis in glucocorticoid-resistant acute lymphatic leukemia cells despite a switch from the extrinsic to the intrinsic death pathway.
  • We have compared the growth inhibitory and apoptogenic potential of the pan-HDACi SAHA and the sub-class I selective HDAC inhibitor MS275, as well as valproic acid (VPA) on glucocorticoid sensitive and resistant B (B-ALL) and T (T-ALL) cell acute lymphoblastic leukemia cells and patients blasts.
  • In contrast, to our previous results with U937 acute myeloid leukemia (AML) cells which showed a similar activity of MS275 and SAHA in growth inhibition and apoptosis induction, both B and T-ALL cells were much more efficiently killed by SAHA and VPA than by MS275.
  • However, SAHA induces, in addition to p21(WAF1/CIP1) also re-expression of DR5.
  • [MeSH-major] Apoptosis. Benzamides / pharmacology. Burkitt Lymphoma / pathology. Drug Resistance, Neoplasm. Glucocorticoids / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Pyridines / pharmacology

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  • (PMID = 17499001.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glucocorticoids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Pyridines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 1ZNY4FKK9H / entinostat; 58IFB293JI / vorinostat; 614OI1Z5WI / Valproic Acid; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.98 / Histone Deacetylases
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89. Sanyal M, Tung JW, Karsunky H, Zeng H, Selleri L, Weissman IL, Herzenberg LA, Cleary ML: B-cell development fails in the absence of the Pbx1 proto-oncogene. Blood; 2007 May 15;109(10):4191-9
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  • [Title] B-cell development fails in the absence of the Pbx1 proto-oncogene.
  • Pbx1, a homeodomain transcription factor that was originally identified as the product of a proto-oncogene in acute pre-B-cell leukemia, is a global regulator of embryonic development.
  • However, embryonic lethality in its absence has prevented an assessment of its role in B-cell development.
  • Here, using Rag1-deficient blastocyst complementation assays, we demonstrate that Pbx1 null embryonic stem (ES) cells fail to generate common lymphoid progenitors (CLPs) resulting in a complete lack of B and NK cells, and a partial impairment of T-cell development in chimeric mice.
  • A critical role for Pbx1 was confirmed by rescue of B-cell development from CLPs following restoration of its expression in Pbx1-deficient ES cells.
  • In adoptive transfer experiments, B-cell development from Pbx1-deficient fetal liver cells was also severely compromised, but not erased, since transient B lymphopoiesis was detected in Rag-deficient recipients.
  • Conditional inactivation of Pbx1 in pro-B (CD19(+)) cells and thereafter revealed that Pbx1 is not necessary for B-cell development to proceed from the pro-B-cell stage.
  • Thus, Pbx1 critically functions at a stage between hematopoietic stem cell development and B-cell commitment and, therefore, is one of the earliest-acting transcription factors that regulate de novo B-lineage lymphopoiesis.

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  • (PMID = 17244677.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI047458; United States / NICHD NIH HHS / HD / R01 HD043997; United States / NCI NIH HHS / CA / R37 CA042971; United States / NIAID NIH HHS / AI / R01 AI047458; United States / NCI NIH HHS / CA / CA90735; United States / NCI NIH HHS / CA / R01 CA090735; United States / NIAID NIH HHS / AI / R21 AI047458; United States / NCI NIH HHS / CA / CA42971; United States / NICHD NIH HHS / HD / HD43997
  • [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 / Homeodomain Proteins; 0 / Pbx1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1885499
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90. Lozzi GP, Massone C, Citarella L, Kerl H, Cerroni L: Rimming of adipocytes by neoplastic lymphocytes: a histopathologic feature not restricted to subcutaneous T-cell lymphoma. Am J Dermatopathol; 2006 Feb;28(1):9-12
MedlinePlus Health Information. consumer health - Skin Cancer.

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  • [Title] Rimming of adipocytes by neoplastic lymphocytes: a histopathologic feature not restricted to subcutaneous T-cell lymphoma.
  • Subcutaneous panniculitis-like T-cell lymphoma (SPTCL) is a rare cytotoxic T-cell lymphoma of the skin presenting with histopathologic features simulating those of a lobular panniculitis.
  • The presence of neoplastic T-lymphocytes forming a rim around the individual fat cells in the subcutaneous lobules, so-called "rimming" of adipocytes, is considered a characteristic morphologic feature of this type of cutaneous lymphoma.
  • In this study we reviewed a series of 45 biopsy specimens of primary and secondary cutaneous B- and T-cell lymphomas and one of myeloid leukemia involving the subcutaneous tissues and showing rimming of adipocytes (subcutaneous panniculitis-like T-cell lymphoma: n = 16; mycosis fungoides, tumor stage: n = 3; aggressive epidermotropic CD8(+) T-cell lymphoma: n = 2; cutaneous gamma/delta T-cell lymphoma: n = 4; extranodal NK/T-cell lymphoma, nasal type: n = 4; cutaneous medium-large pleomorphic T-cell lymphoma, NOS: n = 5; CD4(+)/CD56(+) hematodermic neoplasm (blastic NK-cell lymphoma): n = 7; secondary cutaneous large B-cell lymphoma: n = 3; secondary cutaneous lymphoplasmacytic lymphoma: n = 1; specific cutaneous manifestations of acute myelogenous leukemia: n = 1).
  • We could demonstrate that rimming of adipocytes by neoplastic cells can be recognized not only in subcutaneous panniculitis-like T-cell lymphoma, but also in several different entities of malignant lymphoma with skin involvement.
  • Rimming of adipocytes should not be considered specific of subcutaneous panniculitis-like T-cell lymphoma.
  • [MeSH-major] Adipocytes / pathology. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology. Skin Neoplasms / pathology. T-Lymphocytes / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Gene Rearrangement. Genes, T-Cell Receptor gamma / genetics. Humans. Immunoglobulin Heavy Chains / genetics. Male. Middle Aged. Panniculitis / metabolism. Panniculitis / pathology. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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  • (PMID = 16456318.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta
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91. Peter A, Heiden T, Taube T, Körner G, Seeger K: Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes. Eur J Haematol; 2009 Nov;83(5):420-32
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  • [Title] Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes.
  • OBJECTIVES: TEL/AML1 (ETV6/RUNX1) fusion resulting from the translocation t(12;21)(p13;q22) constitutes the most common chimeric fusion gene in initial childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) (19-27%) and has been associated with good prognosis.
  • Many studies have explored such aberrations in initial disease, while only few reports have investigated them in relapses.
  • RESULTS: In children with TEL/AML1 positive ALL relapse, additional (a) TEL loss, (b) combined AML1 and der(21) gain, (c) combined TEL loss and AML1 gain as well as (d) the occurrence of a subpopulation with the signal pattern 1T/3A/1TA appear to be related to higher peripheral blast counts (PBCs) at relapse diagnosis (a and d) or a tendency towards the occurrence of a subsequent relapse (b and c) (P-values <0.05).
  • CONCLUSIONS: Our data together with published results on TEL/AML1 positive ALL suggest that frequencies of additional TEL and AML1 mutations are, with the exception of loss of untranslocated TEL, higher in first relapses than in initial disease.
  • They also show that it is important to consider combined mutations in the analysis of this leukemia entity.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Dosage. In Situ Hybridization, Fluorescence. Interphase. Mutation. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19594616.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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92. Adams H, Schmid P, Dirnhofer S, Tzankov A: Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases. Pathol Res Pract; 2008;204(8):569-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases.
  • Using tissue microarray technology, we tested 1059 lymphoma and acute leukemia cases, covering the most common disease entities, for aberrant CK expression, using CK22.
  • In total, 866 of the arrayed cases were evaluable (80%), and 13 positive cases (1.5%) were found: 1 out of 230 Hodgkin lymphomas (0.4%), 1 plasma cell myeloma, 2 out of 326 diffuse large B-cell lymphomas (0.6%), 5 out of 18 mantle cell lymphomas (26%), 3 out of 70 small cell lymphomas/chronic lymphocytic leukemias (4%) and 1 out of 27 peripheral T-cell lymphomas, not otherwise specified (4%).
  • All CK22-positive cases, except for one mantle cell lymphoma, expressed the specific simple epithelial CK8 but not the basal/stratified epithelial CK5/6.
  • Aberrant CK expression can be encountered in a small subset of otherwise characteristic B- and T-cell lymphomas, but not in acute leukemias, which should be considered in difficult differential diagnostic settings.
  • [MeSH-major] Keratins / analysis. Leukemia / metabolism. Lymphoma / chemistry. Tissue Array Analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Europe. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 18436389.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 68238-35-7 / Keratins
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93. Gros F, Sebti Y, de Guibert S, Branger B, Bernard M, Fauchet R, Amiot L: Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages. Neoplasia; 2006 Mar;8(3):223-30
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] Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages.
  • Assay of these molecules by enzyme-linked immunosorbent assay in patients suffering from another hematologic disorder (acute leukemia) highlights increased sHLA-G secretion.
  • This increased secretion seems more marked in acute leukemia subtypes affecting monocytic and lymphoid lineages such as FABM4 and FABM5, as well as both B and T acute lymphoblastic leukemia (ALL).
  • All these findings suggest that sHLA-G molecules could be a factor in tumoral escape from immune survey during acute leukemia.
  • [MeSH-major] Antigens, Neoplasm / blood. HLA Antigens / blood. Histocompatibility Antigens Class I / blood. Leukemia / blood
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / blood. Burkitt Lymphoma / blood. Burkitt Lymphoma / genetics. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Line, Tumor / chemistry. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cytokines / blood. Cytokines / pharmacology. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Leukemic / drug effects. HLA-G Antigens. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Retrospective Studies. Solubility. Tumor Escape

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  • (PMID = 16611416.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
  • [Other-IDs] NLM/ PMC1578523
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94. Matulić M, Paradzik M, Puskarić BJ, Stipić J, Antica M: Analysis of Ikaros family splicing variants in human hematopoietic lineages. Coll Antropol; 2010 Mar;34(1):59-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been suggested that disregulation of transcription factors from the Ikaros family is associated with the development of different human leukemias.
  • In this work we analyzed the state of Ikaros family members in different leukemic cells with the aim to explore the transcriptional control of human hematopoietic lineages and shed some new light on our understanding of transcription factor significance in human leukemias.
  • By means of RT-PCR and specific primers we investigated the expression of Ikaros, Aiolos and Helios transcription factors and their splicing variants in seven leukemia cell lines derived from different types of leukemia (ALL, CML, AML) and lymphoma (histiocytic lymphoma, Burkitt lymphoma and anaplastic large cell lymphoma).
  • In all of the cell lines examined Ikaros was present in dominant Ik1 to Ik4 isoforms and small Ik6 isoform was absent.
  • Aiolos was expressed in the majority of the cell lines, of both, B and T origin, in the form of the full length Aio1.
  • Similar distribution of positive and negative expression of Aiolos and Helios found in various types of leukemias could implicate common pathways of their regulation.
  • [MeSH-minor] Burkitt Lymphoma / genetics. Burkitt Lymphoma / pathology. Cell Differentiation / genetics. Cell Lineage / genetics. Gene Expression Regulation, Leukemic. Gene Expression Regulation, Neoplastic. HL-60 Cells. Humans. Jurkat Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / pathology. Multigene Family / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells

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  • (PMID = 20432734.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / IKZF2 protein, human; 0 / IKZF3 protein, human; 148971-36-2 / Ikaros Transcription Factor
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95. Si J, Collins SJ: Activated Ca2+/calmodulin-dependent protein kinase IIgamma is a critical regulator of myeloid leukemia cell proliferation. Cancer Res; 2008 May 15;68(10):3733-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activated Ca2+/calmodulin-dependent protein kinase IIgamma is a critical regulator of myeloid leukemia cell proliferation.
  • Ca(2+) signaling is an important component of signal transduction pathways regulating B and T lymphocyte proliferation, but the functional role of Ca(2+) signaling in regulating myeloid leukemia cell proliferation has been largely unexplored.
  • We observe that the activated (autophosphorylated) Ca(2+)/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma) is invariably present in myeloid leukemia cell lines as well as in the majority of primary acute myelogenous leukemia patient samples.
  • In contrast, myeloid leukemia cells induced to terminally differentiate or undergo growth arrest display a marked reduction in this CaMKIIgamma autophosphorylation.
  • Moreover, inhibition of CaMKIIgamma activity with pharmacologic agents, dominant-negative constructs, or short hairpin RNAs inhibits the proliferation of myeloid leukemia cells, and this is associated with the inactivation/down-regulation of multiple critical signal transduction networks involving the mitogen-activated protein kinase, Janus-activated kinase/signal transducers and activators of transcription (Jak/Stat), and glycogen synthase kinase (GSK3beta)/beta-catenin pathways.
  • In myeloid leukemia cells, CaMKIIgamma directly phosphorylates Stat3 and enhances its transcriptional activity.
  • Thus, CaMKIIgamma is a critical regulator of multiple signaling networks regulating the proliferation of myeloid leukemia cells.
  • Inhibiting CaMKIIgamma may represent a novel approach in the targeted therapy of myeloid leukemia.

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  • (PMID = 18483256.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA118971-02; United States / NCI NIH HHS / CA / R01 CA118971; United States / NCI NIH HHS / CA / R01 CA118971-01A1; United States / NCI NIH HHS / CA / CA118971-01A1; United States / NCI NIH HHS / CA / R01 CA118971-02
  • [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; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.17 / CAMK2G protein, human; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ NIHMS46214; NLM/ PMC2443690
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96. Giralt S: The role of alemtuzumab in nonmyeloablative hematopoietic transplantation. Semin Oncol; 2006 Apr;33(2 Suppl 5):S36-43
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.
  • Nonmyeloablative stem cell transplants provide a viable therapeutic option for older patients or patients with comorbid conditions, who were previously deemed to be ineligible for transplantation.
  • Despite improvements in clinical outcomes, graft-versus-host disease (GVHD) remains a significant and potentially lethal complication.
  • Alemtuzumab is a humanized monoclonal antibody that targets the CD52 antigen, which is highly expressed on both B and T lymphocytes.
  • By depleting T cells in both the donor and the recipient, alemtuzumab has been shown to prevent development of both acute and chronic GVHD, without inhibiting the benefits associated with the graft-versus-leukemia effect.
  • Clinical trials have shown that alemtuzumab is able to decrease the incidence of acute and chronic GVHD without impairing engraftment.
  • Furthermore, in chronic lymphocytic leukemia therapy, alemtuzumab has been shown to purge malignant cells from the host to allow for harvesting for the purpose of autologous transplantation.
  • Greater insight into alemtuzumab's pharmacokinetic activity would assist in developing a schedule that can optimize alemtuzumab-mediated T-cell depletion to prevent GVHD, while retaining sufficient host T-cell activity to encourage the graft-versus-leukemia effect and prevent relapse.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Graft vs Host Disease / prevention & control. Graft vs Leukemia Effect. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphocyte Depletion. T-Lymphocytes / drug effects. Transplantation Conditioning / methods

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  • (PMID = 16720202.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 33
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97. Parmar S, Del Lima M, Zou Y, Patah PA, Liu P, Cano P, Rondon G, Pesoa S, de Padua Silva L, Qazilbash MH, Hosing C, Popat U, Kebriaei P, Shpall EJ, Giralt S, Champlin RE, Stastny P, Fernandez-Vina M: Donor-recipient mismatches in MHC class I chain-related gene A in unrelated donor transplantation lead to increased incidence of acute graft-versus-host disease. Blood; 2009 Oct 01;114(14):2884-7
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Donor-recipient mismatches in MHC class I chain-related gene A in unrelated donor transplantation lead to increased incidence of acute graft-versus-host disease.
  • MICA expression is limited to gut epithelium and may play a role in triggering acute graft-versus-host disease (aGVHD).
  • Because of physical vicinity of the loci, MICA mismatch was significantly associated with mismatch at HLA-B and HLA-C.
  • [MeSH-major] Blood Donors. Genes, MHC Class I / genetics. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Hematopoietic Stem Cell Transplantation. Histocompatibility. Leukemia, Myeloid, Acute / therapy


98. Nakamura S, Yamashita M, Yokota D, Hirano I, Ono T, Fujie M, Shibata K, Niimi T, Suyama T, Maddali K, Asai K, Yamashita J, Iguchi Y, Ohnishi K: Development and pharmacologic characterization of deoxybromophospha sugar derivatives with antileukemic activity. Invest New Drugs; 2010 Aug;28(4):381-91
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we synthesized two phospha sugar derivatives, 2,3,4-tribromo-3-methyl-1-phenylphospholane 1-oxide (TMPP) and 2,3-dibromo-3-methyl-1-phenylphospholane 1-oxide (DMPP) by reacting 3-methyl-1-phenyl-2-phospholene 1-oxide with bromine, and investigated their potential as antileukemic agents in cell lines.
  • Both agents showed inhibitory effects on leukemia cell proliferation, with mean IC(50) values of 6.25 micromol/L for TMPP and 23.7 micromol/L for DMPP, indicating that inhibition appeared to be dependent on the number of bromine atoms in the structure.
  • Further, TMPP at 10 micromol/L and DMPP at 20 micromol/L induced G2/M cell cycle block in leukemia cells, and TMPP at 20 micromol/L induced apoptosis in these cells.
  • TMPP treatment effected a reduction in both cell cycle progression signals (FoxM1, KIS, Cdc25B, Cyclin D1, Cyclin A, and Aurora-B) and tumor cell survival (p27(Kip1) and p21(Cip1)), as well as induced the activation of caspase-3 and -9.
  • Here, we report on the synthesis of TMPP and DMPP and demonstrate that these agents hinder proliferation of leukemia cells by FoxM1 suppression, which leads to G2/M cell cycle block and subsequent caspase-3-dependent apoptosis in acute leukemia cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cyclic P-Oxides / pharmacology. Drug Screening Assays, Antitumor / methods. Leukemia / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Organophosphorus Compounds / pharmacology
  • [MeSH-minor] Adult. Aged. Apoptosis / drug effects. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Forkhead Transcription Factors / metabolism. Humans. Middle Aged

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  • (PMID = 19436953.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2,3,4-tribromo-3-methyl-1-phenylphospholane 1-oxide; 0 / 2,3-dibromo-3-methyl-1-phenylphospholane 1-oxide; 0 / Antineoplastic Agents; 0 / Cyclic P-Oxides; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Organophosphorus Compounds; 0 / phospholenes; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
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99. Lawce H, Olson S: FISH testing for deletions of chromosome 6q21 and 6q23 in hematologic neoplastic disorders. J Assoc Genet Technol; 2009;35(4):167-9

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  • Chromosome 6q deletions are also commonly found in lymphoid malignancies such as acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), multiple myeloma (MM), mantle zone lymphoma (MZL), and Waldenström's macroglobulinemia (WM).
  • In childhood B- and T-cell ALL a deletion of 6q is the hallmark of a neutral prognosis; however, it may be cytogenetically obscure or cryptic, requiring interphase FISH analysis.
  • In adult ALL it indicates a favorable prognosis, but in CLL, B-cell small lymphocytic lymphoma (SLL), WM, and MM it has a poor prognosis.
  • Since the deletion of 6q has prognostic implications and may be used to monitor residual disease, FISH analysis remains a valuable tool in treatment of these disorders.
  • We report the results of the first three patients in our laboratory with deletions of 6q in lymphoid malignancies using this cocktail.

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  • (PMID = 19952391.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. di Carlo E, de Totero D, Piazza T, Fabbi M, Ferrini S: Role of IL-21 in immune-regulation and tumor immunotherapy. Cancer Immunol Immunother; 2007 Sep;56(9):1323-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These include regulation of T, B and NK cell proliferation, survival, differentiation, and effector functions.
  • Besides its activities on normal lymphoid cells, IL-21 is an in vitro growth factor for myeloma and acute-T cell leukemia cells, whereas it induces the apoptosis of B-CLL (chronic lymphocytic leukemia) cells.
  • These findings indicate that the IL-21/IL-21R system exerts opposite functions in different lymphoid neoplasias, and suggest its employment in B-CLL therapy.
  • Since IL-2, but not IL-21, is specifically required for the development of regulatory T (Treg) cell immune-suppressive functions, IL-21 may be a new tool for cancer immunotherapy.

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  • (PMID = 17447063.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukins; 0 / interleukin-21
  • [Number-of-references] 92
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