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41. Gutiérrez NC, Ocio EM, de Las Rivas J, Maiso P, Delgado M, Fermiñán E, Arcos MJ, Sánchez ML, Hernández JM, San Miguel JF: Gene expression profiling of B lymphocytes and plasma cells from Waldenström's macroglobulinemia: comparison with expression patterns of the same cell counterparts from chronic lymphocytic leukemia, multiple myeloma and normal individuals. Leukemia; 2007 Mar;21(3):541-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling of B lymphocytes and plasma cells from Waldenström's macroglobulinemia: comparison with expression patterns of the same cell counterparts from chronic lymphocytic leukemia, multiple myeloma and normal individuals.
  • The tumoral clone of Waldenström's macroglobulinemia (WM) shows a wide morphological heterogeneity, which ranges from B lymphocytes (BL) to plasma cells (PC).
  • By means of genome-wide expression profiling we have been able to identify genes exclusively deregulated in BL and PC from WM, but with a similar expression pattern in their corresponding cell counterparts from chronic lymphocytic leukemia (CLL) and multiple myeloma (MM), as well as normal individuals.
  • The differentially expressed genes have important functions in B-cell differentiation and oncogenesis.
  • Thus, two of the genes downregulated in WM-BL were IL4R, which plays a relevant role in CLL B-cell survival, and BACH2, which participates in the development of class-switched PC.
  • A set of four genes was able to discriminate clonal BL from WM and CLL: LEF1 (WNT/beta-catenin pathway), MARCKS, ATXN1 and FMOD.
  • We also found deregulation of genes involved in plasma cell differentiation such as PAX5, which was overexpressed in WM-PC, and IRF4 and BLIMP1, which were underexpressed.
  • In summary, these results indicate that both PC and BL from WM are genetically different from the MM and CLL cell counterpart.
  • [MeSH-major] B-Lymphocytes / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Multiple Myeloma / pathology. Plasma Cells / metabolism. Waldenstrom Macroglobulinemia / pathology


42. Buhl AM, Jurlander J, Geisler CH, Pedersen LB, Andersen MK, Josefsson P, Petersen JH, Leffers H: CLLU1 expression levels predict time to initiation of therapy and overall survival in chronic lymphocytic leukemia. Eur J Haematol; 2006 Jun;76(6):455-64
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  • [Title] CLLU1 expression levels predict time to initiation of therapy and overall survival in chronic lymphocytic leukemia.
  • OBJECTIVES: Chronic lymphocytic leukemia (CLL) is an incurable disease with a highly variable clinical course.
  • IgV(H) mutational status, chromosomal aberrations, CD38 expression and ZAP-70 expression are prognostic markers in CLL, however, they are not exclusively confined to this disease.
  • We recently identified a novel CLL-specific gene (CLL upregulated gene1, CLLU1) that is exclusively upregulated in CLL cells.
  • Here we describe our evaluation of the prognostic significance of CLLU1 in CLL.
  • METHODS: A cohort of 59 previously untreated CLL patients was studied.
  • RESULTS: Analyzed as a continuous, quantitative parameter CLLU1 levels significantly predicted time from diagnosis to initiation of therapy (P < or = 0.0003) Analyzed as a categorical parameter, by segregation of the patients into groups with cDNA1 or CDS expression above or below the median, the CLLU1 levels significantly predicted time from diagnosis to initiation of therapy (P = 0.001) and predicted overall survival with borderline significance (P < or = 0.05).
  • Patient stratification according to clinical stage, cytogenetics, IgV(H) mutational status, ZAP-70 and CD38, demonstrated significantly increased CLLU1 expression in all investigated CLL poor risk groups.
  • CONCLUSIONS: CLLU1 is the first identified CLL specific gene.
  • The CLLU1 mRNA expression level can predict time to initiation of treatment and survival in CLL patients.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm Proteins / biosynthesis

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  • [CommentIn] Eur J Haematol. 2006 Aug;77(2):177; author reply 178 [16856913.001]
  • (PMID = 16529606.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLLU1 protein, human; 0 / DNA, Complementary; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38
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43. Chae HW, Kim IW, Jin HE, Kim DD, Chung SJ, Shim CK: Effect of ion-pair formation with bile salts on the in vitro cellular transport of berberine. Arch Pharm Res; 2008 Jan;31(1):103-10
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  • The objective of this study was to examine the effect of ion-pair complexation with endogenous bile salts on the transport of a quarternary ammonium organic cationic (OC) drug, berberine, across the Caco-2 and LLC-PK1 cell monolayers.
  • Similar results were observed for the transport of berberine across the LLC-PK1 cells.
  • These results suggest that an efflux transporter, probably P-gp, is involved in the Caco-2 cell transport.
  • The apparent partition coefficient (APC) of berberine between n-octanol and a phosphate buffer (pH 7.4) was increased by the presence of an organic anion (OA), taurodeoxycholate (TDC, a bile salt), suggesting the formation of a lipophilic ion-pair complex between an OC (berberine) and an OA (TDC).
  • Despite the ion-pair complexation, however, the BL-AP transport of berberine across the Caco-2 and LLC-PK1 cells was not altered by the cis-presence of bile salts or the rat bile juice.
  • This is consistent with the reportedly unaltered secretory transport of a quarternary ammonium compound, tributylmethylammonium (TBuMA), across the Caco-2 cell monolayers in the cis-presence of bile salts or the rat bile juice, but not with our previous report in which the secretory transport of TBuMA across the LLC-PK1 cell was increased in the cis-presence of TDC.
  • Therefore, the effect of ion-pair formation with the bile components or bile salts on the secretory transport of OCs appears to depend on the molecular properties of OCs (e.g., molecular weight, lipophilicity and affinity to relevant transporters) and the characteristics of cell strains (e.g., expression and contribution of responsible transporters to the transport).
  • [MeSH-minor] Animals. Biological Transport, Active. Caco-2 Cells. Cell Membrane / metabolism. Chemistry, Physical. Chromatography, High Pressure Liquid. Data Interpretation, Statistical. Humans. LLC-PK1 Cells. P-Glycoprotein / antagonists & inhibitors. P-Glycoprotein / metabolism. Physicochemical Phenomena. Solubility. Swine. Taurodeoxycholic Acid / chemistry

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  • (PMID = 18277615.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / P-Glycoprotein; 0I8Y3P32UF / Berberine; 516-50-7 / Taurodeoxycholic Acid
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4
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4. Moore DA, Fuller B, Hazzan M, Jones JW: Development of a security vulnerability assessment process for the RAMCAP chemical sector. J Hazard Mater; 2007 Apr 11;142(3):689-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a security vulnerability assessment process for the RAMCAP chemical sector.
  • The Department of Homeland Security (DHS), Directorate of Information Analysis & Infrastructure Protection (IAIP), Protective Services Division (PSD), contracted the American Society of Mechanical Engineers Innovative Technologies Institute, LLC (ASME ITI, LLC) to develop guidance on Risk Analysis and Management for Critical Asset Protection (RAMCAP).
  • AcuTech Consulting Group (AcuTech) has been contracted by ASME ITI, LLC, to provide assistance by facilitating the development of sector-specific guidance on vulnerability analysis and management for critical asset protection for the chemical manufacturing, petroleum refining, and liquefied natural gas (LNG) sectors.
  • This activity involves two key tasks for these three sectors: Development of a screening to supplement DHS understanding of the assets that are important to protect against terrorist attack and to prioritize the activities.
  • Development of a standard security vulnerability analysis (SVA) framework for the analysis of consequences, vulnerabilities, and threats.
  • This project involves the cooperative effort of numerous leading industrial companies, industry trade associations, professional societies, and security and safety consultants representative of those sectors.
  • Jones is the chief technology officer for ASME-ITI, LLC for RAMCAP.

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  • (PMID = 16920260.001).
  • [ISSN] 0304-3894
  • [Journal-full-title] Journal of hazardous materials
  • [ISO-abbreviation] J. Hazard. Mater.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hazardous Substances
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45. Fernàndez V, Jares P, Salaverria I, Giné E, Beà S, Aymerich M, Colomer D, Villamor N, Bosch F, Montserrat E, Campo E: Gene expression profile and genomic changes in disease progression of early-stage chronic lymphocytic leukemia. Haematologica; 2008 Jan;93(1):132-6
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  • [Title] Gene expression profile and genomic changes in disease progression of early-stage chronic lymphocytic leukemia.
  • The biologic mechanisms involved in the clinical progression from early stages of patients with chronic lymphocytic leukemia (CLL) are not well known.
  • We investigated sequential samples from 16 untreated CLL patients obtained at diagnosis in early stage and after progression before treatment.
  • One patient had a p16 (INK4a) homozygous deletion at diagnosis and progression, and 3 patients acquired a p53 mutation, gains of 5q21-q23 and 11pter-p14, and a gain of chromosome 12 respectively, during the progression of the disease.
  • Gene expression profile analysis showed a significant modulation of 58 genes with a particular downregulation of genes that are inhibitors of cell adhesion and motility.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genome. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Disease Progression. Female. Genes, p53 / genetics. Humans. Male. Middle Aged. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis

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  • (PMID = 18166798.001).
  • [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 / Cyclin-Dependent Kinase Inhibitor p16
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61. Wei J, Zhou S, Bachem MG, Debatin KM, Beltinger C: Infiltration of blood outgrowth endothelial cells into tumor spheroids: role of matrix metalloproteinases and irradiation. Anticancer Res; 2007 May-Jun;27(3B):1415-21
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  • MATERIALS AND METHODS: Infiltration of BOECs into spheroids made of tumor cells and fibroblasts was determined in the presence of low-dose EDTA, a potent inhibitor of MMPs.
  • RESULTS: Infiltration of BOECs into spheroids was blocked by low-dose EDTA.
  • Irradiation enhanced secretion of MMP-2 and, less so, of MMP-9 by tumor-stromal cells and tumor cells, and increased the amount of MMP-2 and -9 in subcutaneous LLC tumors.
  • [MeSH-major] Blood Cells / physiology. Cell Movement. Endothelial Cells / physiology. Matrix Metalloproteinase 2 / physiology. Matrix Metalloproteinase 9 / physiology. Spheroids, Cellular / physiology

  • Hazardous Substances Data Bank. Disodium EDTA .
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  • (PMID = 17595756.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Matrix Metalloproteinase Inhibitors; 9G34HU7RV0 / Edetic Acid; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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62. Manolov I, Machulla HJ, Momekov G: Synthesis, physicochemical characterization and preliminary pharmacological in vitro evaluation of two novel cytotoxic benzophenone-linked 3,3-dimethyltriazenes. Pharmazie; 2006 Jun;61(6):511-6
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  • The cytotoxicity of the novel benzophenone-linked triazenes and of ten other 1-phenyl-3,3-dimethyl triazene derivatives as well as of the referent alkylating drug melphalan was assessed using the MTT-dye reduction assay.
  • A panel of human tumor cell lines was used: the chronic lymphoid leukemia SKW-3, the acute promyelocyte leukemia HL-60 and its multi-drug-resistant subline HL-60/Dox.
  • DNA-fragmentation analysis indicated that after 24 h treatment the novel benzophenone-linked triazenes induced programmed cell death in HL-60 cells.
  • [MeSH-minor] Cell Line. Chemistry, Physical. DNA Fragmentation / drug effects. DNA, Neoplasm / biosynthesis. HL-60 Cells. Humans. Models, Molecular. Physicochemical Phenomena. Structure-Activity Relationship. Tetrazolium Salts. Thiazoles

  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
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  • (PMID = 16826969.001).
  • [ISSN] 0031-7144
  • [Journal-full-title] Die Pharmazie
  • [ISO-abbreviation] Pharmazie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzophenones; 0 / DNA, Neoplasm; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Triazenes; 298-93-1 / thiazolyl blue
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63. Rankin JS, Orozco RE, Rodgers TL, Alfery DD, Glower DD: "Adjustable" artificial chordal replacement for repair of mitral valve prolapse. Ann Thorac Surg; 2006 Apr;81(4):1526-8
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  • Gore & Associates Inc, Flagstaff, AZ) artificial chordal replacement and Carpentier ring annuloplasty (Edwards Lifesciences LLC, Irvine, CA), without leaflet resection.
  • Only 1 of 52 patients (1.9%) experienced late failure, and this patient was re-repaired with artificial chords.
  • Thus, "adjustable" artificial chordal replacement facilitates uniform repair of mitral valve prolapse with a low late failure rate.

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  • (PMID = 16564319.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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64. Suresh K, Rodriguez-Lecompte JC, Gauldie J, Foley R: Recent advances in immunotherapy of B-CLL using ex vivo modified dendritic cells. Hematology; 2005 Jun;10(3):189-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent advances in immunotherapy of B-CLL using ex vivo modified dendritic cells.
  • Chronic lymphocytic leukemia (CLL) results from the relentless accumulation of small mature, slowly dividing, monoclonal B-lymphocytes.
  • The clinical course is heterogeneous, some patients with aggressive form of the disease progressing rapidly with early death while others exhibit a more stable, possibly, non-progressing indolent type of the disease lasting many years.
  • Despite progress in modern treatment modalities, relapse invariably occurs and disease still remains incurable.
  • The clinical management of CLL is therefore challenging and considerable effort has been directed towards novel therapeutic strategies aimed at reducing minimal residual disease which can increase remission duration.
  • Ex-vivo modified and monocyte-derived DCs represents a promising approach within the context of CLL.
  • After a brief survey of general properties of DCs, this review focuses on the different approaches exploiting monocyte-derived DCs in CLL, which may help to design novel strategies for phase-I clinical trials.
  • [MeSH-major] Dendritic Cells / transplantation. Immunotherapy, Adoptive. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Monocytes / transplantation

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  • (PMID = 16019468.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 109
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65. Hwang HS, Min YS, Lee SC, Sun MK, Lim HS: Change of lip-line cant after 1-jaw orthognathic surgery in patients with mandibular asymmetry. Am J Orthod Dentofacial Orthop; 2009 Oct;136(4):564-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: The purpose of this study was to investigate the change of lip-line cant (LLC) after 1-jaw orthognathic surgery in mandibular asymmetry patients.
  • LLC was measured in the preoperative and postoperative frontal photographs, and its change was correlated with various craniofacial measurements obtained from preoperative and postoperative frontal cephalograms and maxillofacial 3-dimensional computed tomography images.
  • RESULTS: Although these subjects had 2.4 degrees of LLC on average before surgery, LLC improved to 0.5 degrees after surgery, and the change (1.9 degrees ) was statistically significant.
  • In the correlation analysis, preoperative LLC showed positive correlations with menton deviation and mandibular anterior occlusal plane cant.
  • In the correlation analysis of LLC change, it had positive correlations with preoperative LLC and mandibular anterior occlusal plane cant and preoperative and postoperative change of menton deviation.
  • CONCLUSIONS: These results suggest that LLC is present with chin deviation, even without significant maxillary canting, and can be improved considerably by 1-jaw surgery alone.

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  • (PMID = 19815160.001).
  • [ISSN] 1097-6752
  • [Journal-full-title] American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics
  • [ISO-abbreviation] Am J Orthod Dentofacial Orthop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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66. Collins SA, Buhles A, Scallan MF, Harrison PT, O'Hanlon DM, O'Sullivan GC, Tangney M: AAV2-mediated in vivo immune gene therapy of solid tumours. Genet Vaccines Ther; 2010;8:8
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  • METHODS: Immune-competent Balb/C or C57 mice bearing subcutaneous JBS fibrosarcoma or Lewis Lung Carcinoma (LLC) tumour xenografts respectively were treated by intra-tumoural administration of AAV2 vector encoding the immune up-regulating cytokine granulocyte macrophage-colony stimulating factor (GM-CSF) and the co-stimulatory molecule B7-1 to subcutaneous tumours, either alone or in combination with intra-muscular (IM) delivery of AAV2 vector encoding Nk4 14 days prior to tumour induction.
  • Cured animals were re-challenged with tumourigenic doses of the original tumour type.
  • In vivo cytotoxicity assays were used to investigate establishment of cell-mediated responses in treated animals.
  • RESULTS: AAV2-mediated GM-CSF, B7-1 treatment resulted in a significant reduction in tumour growth and an increase in survival in both tumour models.
  • Cured animals were resistant to re-challenge, and induction of T cell mediated anti-tumour responses were demonstrated.
  • CONCLUSIONS: Overall, this study demonstrates the potential for in vivo AAV2 mediated immune gene therapy, and provides data on the inter-relationship between tumour vasculature and immune cell recruitment.

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  • [Cites] Tissue Antigens. 2003 Mar;61(3):211-9 [12694570.001]
  • [Cites] Crit Rev Oncol Hematol. 1999 Feb;29(3):209-48 [10226727.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2442-50 [16489051.001]
  • [Cites] Clin Cancer Res. 2008 Feb 1;14(3):939-49 [18245558.001]
  • [Cites] Gene Ther. 2008 Jun;15(11):808-16 [18385765.001]
  • [Cites] Curr Gene Ther. 2008 Apr;8(2):66-78 [18393828.001]
  • [Cites] Genet Vaccines Ther. 2009;7:5 [19272140.001]
  • [Cites] Neuromolecular Med. 2009;11(1):43-52 [19306089.001]
  • [Cites] J Cell Biol. 1996 May;133(3):709-18 [8636243.001]
  • [Cites] J Biol Chem. 1996 May 31;271(22):13110-5 [8662798.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Oct 29;239(3):639-44 [9367820.001]
  • [Cites] Cancer. 2000 Sep 15;89(6):1181-94 [11002212.001]
  • [Cites] Clin Experiment Ophthalmol. 2000 Oct;28(5):382-6 [11097287.001]
  • [Cites] Cell. 1992 Dec 24;71(7):1093-102 [1335364.001]
  • [Cites] Cancer Gene Ther. 2006 Dec;13(12):1061-71 [16874363.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5031-5 [2164219.001]
  • [Cites] Nat Immun Cell Growth Regul. 1990;9(3):165-72 [2370876.001]
  • [Cites] Cancer Res. 1985 Jun;45(6):2560-6 [2580624.001]
  • [Cites] CA Cancer J Clin. 1972 Jul-Aug;22(4):226-9 [4625047.001]
  • [Cites] J Exp Med. 1983 Mar 1;157(3):1040-52 [6187879.001]
  • [Cites] Nature. 1984 Oct 25-31;311(5988):750-2 [6333639.001]
  • [Cites] J Immunol. 1993 Apr 15;150(8 Pt 1):3161-9 [7682233.001]
  • [Cites] FEBS Lett. 1997 Dec 22;420(1):1-6 [9450538.001]
  • [Cites] Cell Growth Differ. 1998 May;9(5):355-65 [9607557.001]
  • [Cites] Nat Med. 1999 Jan;5(1):56-63 [9883840.001]
  • [Cites] J Immunol. 2001 Aug 1;167(3):1204-11 [11466335.001]
  • [Cites] Int J Cancer. 2002 Feb 20;97(6):719-25 [11857345.001]
  • [Cites] Cancer Sci. 2003 Apr;94(4):321-7 [12824898.001]
  • [Cites] Ernst Schering Res Found Workshop. 2003;(43):107-14 [12894454.001]
  • [Cites] Int J Cardiol. 2003 Aug;90(2-3):229-38 [12957756.001]
  • [Cites] J Immunol. 1961 Feb;86:228-39 [13785862.001]
  • [Cites] Dis Esophagus. 2003;16(3):218-23 [14641313.001]
  • [Cites] Gene Ther. 2004 Mar;11(6):534-43 [14999225.001]
  • [Cites] Eur J Immunol. 2004 Oct;34(10):2635-41 [15368278.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 29;333(2):316-27 [15950947.001]
  • [Cites] Cancer Gene Ther. 2005 Dec;12(12):913-25 [15962012.001]
  • [Cites] Gene Ther. 2005 Oct;12 Suppl 1:S159-69 [16231050.001]
  • [Cites] Cancer Immunol Immunother. 2006 Nov;55(11):1443-50 [16612593.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):523-32 [7507508.001]
  • [Cites] J Exp Med. 1994 Apr 1;179(4):1205-14 [7511683.001]
  • [Cites] Cancer Res. 1994 Dec 15;54(24):6477-83 [7527298.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1995 Nov;15(11):1857-65 [7583565.001]
  • [Cites] Cancer Gene Ther. 1996 May-Jun;3(3):202-14 [8725885.001]
  • [Cites] Gene Ther. 1997 Mar;4(3):181-8 [9135731.001]
  • [Cites] Ciba Found Symp. 1997;212:119-30; discussion 130-2, 148-54 [9524767.001]
  • [Cites] Nat Med. 1998 May;4(5 Suppl):525-31 [9585204.001]
  • [Cites] Hum Gene Ther. 1999 Jan 20;10(2):201-13 [10022545.001]
  • [Cites] Nat Biotechnol. 1999 Feb;17(2):181-6 [10052356.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3906-10 [10097136.001]
  • [Cites] Nat Genet. 2000 Mar;24(3):257-61 [10700178.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1317-26 [10942373.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Dec 29;279(3):846-52 [11162438.001]
  • [Cites] Mod Pathol. 2001 Jun;14(6):604-8 [11406663.001]
  • [Cites] Hum Gene Ther. 2001 Oct 10;12(15):1907-16 [11589832.001]
  • [Cites] Cytokine Growth Factor Rev. 2002 Apr;13(2):185-93 [11900993.001]
  • [Cites] J Virol. 2002 Dec;76(24):12900-7 [12438615.001]
  • [Cites] Nat Med. 2008 Jan;14(1):28-36 [18157142.001]
  • [Cites] Nature. 2008 May 15;453(7193):410-4 [18418378.001]
  • [Cites] Ultrasound Med Biol. 2010 Mar;36(3):430-40 [20133039.001]
  • [Cites] Cancer Gene Ther. 2010 Jul;17(7):501-11 [20186173.001]
  • [Cites] Postgrad Med. 2010 May;122(3):166-80 [20463426.001]
  • [Cites] Gene Ther. 2010 Aug;17(8):1042-51 [20596059.001]
  • [Cites] Trends Cell Biol. 1998 Oct;8(10):404-10 [9789329.001]
  • [Cites] Kidney Int. 2004 Aug;66(2):586-90 [15253710.001]
  • (PMID = 21172020.001).
  • [ISSN] 1479-0556
  • [Journal-full-title] Genetic vaccines and therapy
  • [ISO-abbreviation] Genet Vaccines Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3016353
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67. Küçköztaş MF, Ozgünes N, Yazici S: [Investigation of the relationship between hepatitis c virus (HCV) genotypes with HCV-RNA and alanine aminotransferase levels in chronic hepatitis c patients]. Mikrobiyol Bul; 2010 Jan;44(1):111-5
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  • [Title] [Investigation of the relationship between hepatitis c virus (HCV) genotypes with HCV-RNA and alanine aminotransferase levels in chronic hepatitis c patients].
  • The objective of this retrospective study was to determine the distribution of HCV genotypes in patients with chronic hepatitis C infection at our region and to investigate the relation between genotypes and serum alanine aminotransferase (ALT) and HCV-RNA levels.
  • Serum samples from 52 patients (26 females, 26 males; mean age: 51.07 +/- 13.13 years) with chronic HCV infection were analyzed in this study.
  • Viral genotypes were determined by using the Versant HCV genotype assay (LiPA) 2.0 system (Bayer HealthCare LLC, USA) according to the manufacturer's instructions.
  • The mean age of the patients infected with genotype 1 (51.4 +/- 12.6 years) we e statistically significantly higher than the mean age of the patients infected with type 2 and 3 (37.8 +/- 12.3 years), (p = 0.023).
  • [MeSH-major] Alanine Transaminase / blood. Hepacivirus / genetics. Hepatitis C, Chronic / enzymology. Hepatitis C, Chronic / virology. RNA, Viral / blood

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  • (PMID = 20455406.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / RNA, Viral; EC 2.6.1.2 / Alanine Transaminase
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68. Kano R, Sato E, Okamura T, Watanabe S, Hasegawa A: Expression of Bcl-2 in feline lymphoma cell lines. Vet Clin Pathol; 2008 Mar;37(1):57-60
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  • [Title] Expression of Bcl-2 in feline lymphoma cell lines.
  • Bcl-2 has been shown to repress cell death triggered by a diverse array of stimuli, including chemotherapy and gamma irradiation.
  • OBJECTIVE: The purpose of this study was to determine feline Bcl-2 expression level in feline lymphoma cells using an immunoblot assay with anti-human and anti-canine Bcl-2 monoclonal antibodies.
  • An immunoblot assay using the monoclonal antibodies was carried out to determine the level of feline Bcl-2 expression in lymphoma and lymphocytic leukemia cell lines.
  • RESULTS: The recombinant feline Bcl-2 protein produced in E. coli had a molecular weight of about 26 kDa and was detected by immunoblot assay by using anti-human Bcl-2 mouse monoclonal antibody.
  • Feline Bcl-2 expression was high in lymphoma cell lines (FL-74-UDC-1 and FT-1) and low in the cell line from peripheral blood mononuclear cells from a healthy cat (FeTJ-1) but not low in freshly isolated peripheral blood mononuclear cells from a healthy cat.
  • CONCLUSIONS: These results confirm the expression of Bcl-2 in T-cell lymphoma cell lines and indicate that it is suitable to detect feline Bcl-2 using an immunoblot assay.
  • Pending further evaluation, Bcl-2 expression might be useful in the differential diagnosis of feline tumors.


69. Edwards TB, Gartsman GM, O'Connor DP, Sarin VK: Safety and utility of computer-aided shoulder arthroplasty. J Shoulder Elbow Surg; 2008 May-Jun;17(3):503-8
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  • This study evaluated the safety and utility of a novel, image-free, shoulder navigation system in a cadaver and in an initial cohort of shoulder arthroplasty patients.
  • Shoulder arthroplasty was performed on a cadaver and 27 patients using an image-free navigation system (NaviProtrade mark; Kinamed Navigation Systems LLC, Camarillo, CA).

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  • (PMID = 18262802.001).
  • [ISSN] 1532-6500
  • [Journal-full-title] Journal of shoulder and elbow surgery
  • [ISO-abbreviation] J Shoulder Elbow Surg
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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70. Yang C, Kaushal V, Shah SV, Kaushal GP: Mcl-1 is downregulated in cisplatin-induced apoptosis, and proteasome inhibitors restore Mcl-1 and promote survival in renal tubular epithelial cells. Am J Physiol Renal Physiol; 2007 Jun;292(6):F1710-7
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  • Mcl-1 is an antiapoptotic member of the Bcl-2 family that plays an important role in cell survival.
  • We demonstrate that proteasome-dependent regulation of Mcl-1 plays a critical role in renal tubular epithelial cell injury from cisplatin.
  • Protein levels of Mcl-1 rapidly declined in a time-dependent manner following cisplatin treatment of LLC-PK(1) cells.
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Survival / drug effects. Fluorescent Antibody Technique. LLC-PK1 Cells. Myeloid Cell Leukemia Sequence 1 Protein. Reverse Transcriptase Polymerase Chain Reaction. Swine

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  • (PMID = 17311906.001).
  • [ISSN] 1931-857X
  • [Journal-full-title] American journal of physiology. Renal physiology
  • [ISO-abbreviation] Am. J. Physiol. Renal Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.- / Caspase 3; Q20Q21Q62J / Cisplatin
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71. Saygili EI, Aksoy N, Pehlivan M, Sever T, Yilmaz M, Cimenci IG, Pehlivan S: Enzyme levels and G-463A polymorphism of myeloperoxidase in chronic lymphocytic leukemia and multiple myeloma. Leuk Lymphoma; 2009 Dec;50(12):2030-7
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  • [Title] Enzyme levels and G-463A polymorphism of myeloperoxidase in chronic lymphocytic leukemia and multiple myeloma.
  • The aim of this study was to investigate how myeloperoxidase (MPO) G-463A gene polymorphism and enzyme levels varied among patients with chronic lymphocytic leukemia (CLL) and multiple myeloma (MM) and to find the relationship between the MPO gene, enzyme levels, and clinical parameters.
  • We studied the sera from 40 healthy volunteers, patients with CLL (n = 34) and MM (n = 28).
  • In subjects with homozygote GG genotype, MPO levels were higher in the patients with both CLL and MM than in the control group.
  • This difference was statistically significant in patients with CLL.
  • In accordance with the results of the study, we assess that the increase in the MPO enzyme level in the patient groups with CLL and MM generated bactericidal effects as well as the increased formation of ROP, thus setting off a pro-cell death pathway and playing a role on the pathogenesis of lymphoproliferative malignancies through this mechanism.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Multiple Myeloma / genetics. Peroxidase / genetics


72. Kojima M, Sato E, Oshimi K, Murase T, Koike T, Tsunoda S, Matsumoto T, Marutsuka K, Ogiya D, Moriuchi M, Tokunaka M, Yara Kikuti Y, Kikuchi T, Nakamura N, Ando K: Characteristics of CD5-positive splenic marginal zone lymphoma with leukemic manifestation ; clinical, flow cytometry, and histopathological findings of 11 cases. J Clin Exp Hematop; 2010;50(2):107-12
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  • [Title] Characteristics of CD5-positive splenic marginal zone lymphoma with leukemic manifestation ; clinical, flow cytometry, and histopathological findings of 11 cases.
  • Splenic marginal zone lymphoma (SP-MZL) is a rare low-grade B-cell neoplasm that often shows leukemic manifestation.
  • The clinical characteristics of these cases did not differ from those of CD5-negative SP-MZL.
  • Flow cytometry revealed positive results as follows : CD3, 0/9 ; CD5, 11/11 ; CD10, 0/11 ; CD11c, 4/10, CD13, 5/11 ; CD19, 11/11 ; CD20, 10/11 ; CD21, 4/4 ; CD22, 7/7 ; CD23, 5/10 ; CD25, 8/11 ; FMC7, 5/7 ; κ type 6/9, and λ type 2/9.
  • Immunohistochemistry showed that the lymphoma cells were positive for CD5, CD20, and BCL-2 and negative for CD3, CD10, cyclin D1, BCL-6, and MUM-1 in all 11 cases.
  • These results suggest that CD5-positive SP-MZL differs from B-cell chronic lymphocytic leukemia, that CD13 expression is found in about half of CD5-positive SP-MZL cases, and that CD5-positive SP-MZL may be related to memory B-cell neoplasm or plasma cell differentiation.
  • [MeSH-major] Antigens, CD5 / metabolism. Lymphoma, B-Cell, Marginal Zone / metabolism. Lymphoma, B-Cell, Marginal Zone / pathology. Splenic Neoplasms / metabolism. Splenic Neoplasms / pathology

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  • (PMID = 21123968.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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73. Kreitman RJ, Pastan I: Immunotoxins in the treatment of hematologic malignancies. Curr Drug Targets; 2006 Oct;7(10):1301-11
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  • Immunotoxins, composed of protein toxins connected to cell binding ligands including monoclonal antibodies and growth factors, have been developed for several decades to target hematologic malignancies.
  • Plant toxins, particularly ricin, are useful for chemically conjugating to monoclonal antibodies, and have shown clinical activity in several types of lymphoma and leukemia.
  • Their dose is generally limited by vascular leak syndrome.
  • Denileukin diftitox has shown efficacy in cutaneous T-cell lymphoma, chronic lymphocytic leukemia, and non-Hodgkin's lymphoma.
  • Recombinant immunotoxin BL22 is an anti-CD22 Fv fragment fused to truncated Pseudomonas exotoxin; it induces complete remissions in a high percentage of patients with chemoresistant hairy cell leukemia.

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  • (PMID = 17073592.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunotoxins
  • [Number-of-references] 235
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74. Marina O, Hainz U, Biernacki MA, Zhang W, Cai A, Duke-Cohan JS, Liu F, Brusic V, Neuberg D, Kutok JL, Alyea EP, Canning CM, Soiffer RJ, Ritz J, Wu CJ: Serologic markers of effective tumor immunity against chronic lymphocytic leukemia include nonmutated B-cell antigens. Cancer Res; 2010 Feb 15;70(4):1344-55
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  • [Title] Serologic markers of effective tumor immunity against chronic lymphocytic leukemia include nonmutated B-cell antigens.
  • Patients with chronic lymphocytic leukemia (CLL) who relapse after allogeneic transplant may achieve durable remission following donor lymphocyte infusion (DLI), showing the potency of donor-derived immunity in eradicating tumors.
  • We sought to elucidate the antigenic basis of the effective graft-versus-leukemia (GvL) responses associated with DLI for the treatment of CLL by analyzing the specificity of plasma antibody responses developing in two DLI-treated patients who achieved long-term remission without graft-versus-host disease.
  • Along with additional candidate antigens DAPK3, SERBP1, and OGFOD1, these proteins showed higher transcript and protein expression in B cells and CLL cells compared with normal peripheral blood mononuclear cells.
  • Although ZFYVE19, DAPK3, and OGFOD1 elicited minimal antibody reactivity in 12 normal subjects and 12 chemotherapy-treated CLL patients, 5 of 12 CLL patients with clinical GvL responses were serologically reactive to these antigens.
  • Moreover, antibody reactivity against these antigens was temporally correlated with clinical disease regression.
  • These B-cell antigens represent promising biomarkers of effective anti-CLL immunity.

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  • [Cites] Bone Marrow Transplant. 2005 Nov;36(9):825-30 [16151430.001]
  • [Cites] Genome Biol. 2001;2(11):SOFTWARE0002 [16173164.001]
  • [Cites] Exp Hematol. 2006 Jan;34(1):44-53 [16413390.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1724-30 [16239425.001]
  • [Cites] Methods Enzymol. 2005;403:1-10 [16473572.001]
  • [Cites] Cancer Biol Ther. 2006 Feb;5(2):145-9 [16357522.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):210-9 [16616068.001]
  • [Cites] Adv Immunol. 2006;90:133-73 [16730263.001]
  • [Cites] Leuk Lymphoma. 2006 Oct;47(10):2028-36 [17071473.001]
  • [Cites] Leukemia. 2007 Jan;21(1):12-7 [17109028.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D680-4 [17132831.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1355-62 [17008540.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8947-52 [17517626.001]
  • [Cites] Proteomics. 2007 Mar;7(6):976-91 [17370257.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Sep;20(3):557-68 [17707840.001]
  • [Cites] Gynecol Oncol. 2007 Nov;107(2):266-73 [17698176.001]
  • [Cites] Science. 2008 Jan 11;319(5860):215-20 [18187659.001]
  • [Cites] J Proteome Res. 2008 May;7(5):2059-68 [18393456.001]
  • [Cites] Clin Cancer Res. 2009 Jul 15;15(14):4759-68 [19567591.001]
  • [Cites] Nat Med. 2000 Jun;6(6):667-72 [10835683.001]
  • [Cites] J Clin Invest. 2000 Sep;106(5):705-14 [10974024.001]
  • [Cites] Leukemia. 2001 Mar;15(3):445-51 [11237069.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2101-5 [11474067.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1625-38 [11733577.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2123-31 [12200376.001]
  • [Cites] Oncogene. 2003 Mar 6;22(9):1400-10 [12618766.001]
  • [Cites] Clin Cancer Res. 2003 May;9(5):1656-65 [12738718.001]
  • [Cites] EMBO J. 2003 Jul 15;22(14):3664-74 [12853481.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2747-53 [12860954.001]
  • [Cites] Bioinformatics. 2004 Aug 12;20(12):1962-3 [14988114.001]
  • [Cites] J Clin Oncol. 2004 Oct 1;22(19):3937-49 [15459216.001]
  • [Cites] Genome Res. 2004 Oct;14(10B):2128-35 [15489335.001]
  • [Cites] Genomics. 1996 Apr 1;33(1):151-2 [8617505.001]
  • [Cites] Bone Marrow Transplant. 1996 Sep;18(3):669-72 [8879640.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] J Exp Med. 1998 Jan 19;187(2):265-70 [9432985.001]
  • [Cites] Immunol Res. 1997;16(4):313-39 [9439758.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1642-51 [9488481.001]
  • [Cites] Blood. 1998 May 15;91(10):3671-80 [9573003.001]
  • [Cites] J Exp Med. 1999 Jan 18;189(2):371-80 [9892619.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2973-8 [15613541.001]
  • [Cites] Blood. 2005 May 15;105(10):3945-50 [15692072.001]
  • [Cites] Int J Androl. 2005 Jun;28(3):163-70 [15910542.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5788-94 [16043827.001]
  • [Cites] J Biol Chem. 2005 Aug 26;280(34):30564-73 [15985431.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4389-96 [16131571.001]
  • (PMID = 20124481.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5R21CA115043-2; United States / NCI NIH HHS / CA / R21 CA132232-02; United States / NCI NIH HHS / CA / P01 CA078378; United States / NCI NIH HHS / CA / P01 CA155258; United States / NCI NIH HHS / CA / CA132232-02; United States / NCI NIH HHS / CA / R21 CA132232; United States / NCI NIH HHS / CA / R21 CA115043; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / P50 CA100707
  • [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.; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / Immunodominant Epitopes
  • [Other-IDs] NLM/ NIHMS167268; NLM/ PMC2852266
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75. Kokhaei P, Palma M, Mellstedt H, Choudhury A: Biology and treatment of chronic lymphocytic leukemia. Ann Oncol; 2005;16 Suppl 2:ii113-23
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  • [Title] Biology and treatment of chronic lymphocytic leukemia.

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  • (PMID = 15958440.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Genetic Markers
  • [Number-of-references] 90
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76. Majumder D, Banerjee D, Chandra S, Banerjee S, Chakrabarti A: Red cell morphology in leukemia, hypoplastic anemia and myelodysplastic syndrome. Pathophysiology; 2006 Dec;13(4):217-25
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  • [Title] Red cell morphology in leukemia, hypoplastic anemia and myelodysplastic syndrome.
  • In the present work, we have studied the overall morphology of intact red cells in different leukemic patients along with patients of hypoplastic anemia (HPA) by scanning electron microscopy.
  • We have also studied the ultrastructure of the red cell surface membranes by transmission electron microscopy.
  • We have shown direct evidence of the altered red cell (RBC) membrane morphology irrespective of the hemoglobin status of the patients which includes (1) presence of large central holes in RBCs of acute myeloid leukemia (AML), (2) presence of thorn- and horn-like structure in RBCs of acute lymphoblastic leukemia (ALL) and chronic myeloid leukemia (CML) and (3) flaccid appearance of RBCs in chronic lymphocytic leukemia (CLL) patients.
  • TEM studies revealed presence of pores with diameters ranging from 100 to 200nm on the RBC membrane surface of myeloid leukemia with AML being the most prominent among others.
  • Such pathophysiological alterations of the RBC morphology in leukemic patients could be identified as characteristic signature of the onset of anemia associated with the disease.

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  • (PMID = 16876391.001).
  • [ISSN] 0928-4680
  • [Journal-full-title] Pathophysiology : the official journal of the International Society for Pathophysiology
  • [ISO-abbreviation] Pathophysiology
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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77. Trachootham D, Zhang H, Zhang W, Feng L, Du M, Zhou Y, Chen Z, Pelicano H, Plunkett W, Wierda WG, Keating MJ, Huang P: Effective elimination of fludarabine-resistant CLL cells by PEITC through a redox-mediated mechanism. Blood; 2008 Sep 1;112(5):1912-22
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  • [Title] Effective elimination of fludarabine-resistant CLL cells by PEITC through a redox-mediated mechanism.
  • Chronic lymphocytic leukemia (CLL) is the most common adult leukemia, and resistance to fludarabine-based therapies is a major challenge in CLL treatment.
  • Because CLL cells are known to have elevated levels of reactive oxygen species (ROS), we aimed to test a novel ROS-mediated strategy to eliminate fludarabine-resistant CLL cells based on this redox alteration.
  • Using primary CLL cells and normal lymphocytes from patients (n = 58) and healthy subjects (n = 12), we showed that both fludarabine-resistant and -sensitive CLL cells were highly sensitive to beta-phenylethyl isothiocyanate (PEITC) with mean IC(50) values of 5.4 microM and 5.1 microM, respectively.
  • Normal lymphocytes were significantly less sensitive to PEITC (IC(50) = 27 microM, P < .001).
  • CLL cells exhibited intrinsically higher ROS level and lower cellular glutathione, which were shown to be the critical determinants of CLL sensitivity to PEITC.
  • Exposure of CLL cells to PEITC induced severe glutathione depletion, ROS accumulation, and oxidation of mitochondrial cardiolipin leading to massive cell death.
  • Such ROS stress also caused deglutathionylation of MCL1, followed by a rapid degradation of this cell survival molecule.
  • Our study demonstrated that the natural compound PEITC is effective in eliminating fludarabine-resistant CLL cells through a redox-mediated mechanism with low toxicity to normal lymphocytes, and warrants further clinical evaluation.

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  • [Cites] Oncogene. 2004 Jun 17;23(28):4818-27 [15122313.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:153-75 [14633781.001]
  • [Cites] Am J Hematol. 2004 Jan;75(1):22-33 [14695629.001]
  • [Cites] Drug Resist Updat. 2003 Dec;6(6):323-8 [14744496.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Mar;53(3):209-19 [14610616.001]
  • [Cites] Arch Biochem Biophys. 2004 Mar 1;423(1):37-46 [14989263.001]
  • [Cites] Drug Resist Updat. 2004 Apr;7(2):97-110 [15158766.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Sep;20(3):499-512 [17707836.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8653-61 [17875705.001]
  • [Cites] J Biol Chem. 2007 Nov 2;282(44):32233-42 [17823113.001]
  • [Cites] Am J Hematol. 1988 Nov;29(3):152-63 [3189311.001]
  • [Cites] Br J Haematol. 1989 May;72(1):32-5 [2786733.001]
  • [Cites] Cancer Res. 1991 Feb 1;51(3):794-8 [1846317.001]
  • [Cites] Blood. 1993 Jan 1;81(1):143-50 [8093345.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Jan 17;206(2):748-55 [7826396.001]
  • [Cites] Jpn J Pharmacol. 1996 Aug;71(4):299-305 [8886927.001]
  • [Cites] Blood. 1998 May 1;91(9):3379-89 [9558396.001]
  • [Cites] Semin Liver Dis. 1998;18(4):389-401 [9875556.001]
  • [Cites] Free Radic Biol Med. 2004 Dec 1;37(11):1821-33 [15528041.001]
  • [Cites] Leukemia. 2004 Dec;18(12):1934-40 [15483672.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):640-5 [15577914.001]
  • [Cites] J Biol Chem. 2005 Feb 11;280(6):4738-44 [15550399.001]
  • [Cites] Biochemistry. 2005 Apr 19;44(15):5899-906 [15823049.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4820-7 [15728130.001]
  • [Cites] Nature. 2005 Jul 7;436(7047):123-7 [16001073.001]
  • [Cites] Free Radic Res. 2005 Jun;39(6):573-80 [16036334.001]
  • [Cites] EMBO J. 2005 Oct 5;24(19):3482-92 [16163384.001]
  • [Cites] Braz J Med Biol Res. 2006 Mar;39(3):327-33 [16501812.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):437-45 [16272172.001]
  • [Cites] Crit Rev Clin Lab Sci. 2006;43(2):143-81 [16517421.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):210-9 [16616068.001]
  • [Cites] Science. 2006 Jun 16;312(5780):1650-3 [16728594.001]
  • [Cites] Expert Opin Pharmacother. 2006 Aug;7(12):1641-51 [16872267.001]
  • [Cites] Cancer Cell. 2006 Sep;10(3):241-52 [16959615.001]
  • [Cites] Leuk Lymphoma. 2007 Feb;48(2):311-20 [17325891.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):799-804 [17283363.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2144-50 [17404098.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6217-22 [17389404.001]
  • [Cites] Biochemistry. 2007 Jul 3;46(26):7765-80 [17555331.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6409-16 [17616701.001]
  • [Cites] Clin Chim Acta. 2000 Mar;293(1-2):53-62 [10699422.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1405-13 [10942236.001]
  • [Cites] Biochem J. 2000 Oct 1;351(Pt 1):183-93 [10998361.001]
  • [Cites] Free Radic Biol Med. 2001 Jun 1;30(11):1286-92 [11368926.001]
  • [Cites] Anal Biochem. 2001 Apr 15;291(2):279-89 [11401302.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1795-801 [12176902.001]
  • [Cites] J Biol Chem. 2002 Nov 15;277(46):43730-4 [12223490.001]
  • [Cites] Blood. 2003 May 15;101(10):4098-104 [12531810.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37832-9 [12853461.001]
  • [Cites] Cell Death Differ. 2004 Jul;11 Suppl 1:S73-85 [15105835.001]
  • (PMID = 18574029.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100428; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA085563; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA109041; United States / NCI NIH HHS / CA / R01 CA109041; United States / NCI NIH HHS / CA / CA100428; United States / NCI NIH HHS / CA / CA085563
  • [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 / Antineoplastic Agents; 0 / Isothiocyanates; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Reactive Oxygen Species; 6U7TFK75KV / phenethyl isothiocyanate; 9007-43-6 / Cytochromes c; EC 1.11.1.9 / Glutathione Peroxidase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; FA2DM6879K / Vidarabine; GAN16C9B8O / Glutathione; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2518893
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78. Reuters I, Weber M, Schulze-Lohoff E: Rho/Rho kinase pathway regulates maintenance of the differentiated tubular epithelial cell phenotype on laminin-1. Nephron Physiol; 2006;104(2):p95-p106
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  • [Title] Rho/Rho kinase pathway regulates maintenance of the differentiated tubular epithelial cell phenotype on laminin-1.
  • BACKGROUND: Maintenance of a polarized tubular epithelium by appropriate intracellular signaling and extracellular matrix is critical both in normal renal function as well as in acute and chronic tubular injury.
  • We examined the hypothesis that maintenance of a differentiated epithelial phenotype on the basement membrane glycoprotein laminin-1 is controlled by the Rho/Rho kinase pathway.
  • METHODS: Using the tubular epithelial cell lines LLC-PK1 and MDCK which were cultured on laminin-1 vs. collagen IV, we analyzed cell morphology and motility (cohort migration assay) as well as expression of differentiation and dedifferentiation markers (immunofluorescence microscopy).
  • RESULTS: Cohort migration of LLC-PK1 cells was significantly slowed down on laminin-1 (10.7 +/- 2.2 m.u. (migratory units)) compared with collagen IV (16.6 +/- 2.3 m.u.
  • In parallel to the increased migratory activity, inhibition of the Rho/Rho kinase pathway resulted in a more mesenchymal phenotype of LLC-PK1 cells on laminin-1 with increased formation of lamellopodia and filopodia, distinct loss of focal contacts and stress fibers, upregulation of the dedifferentiation marker vimentin, and loss of cell-cell contacts with translocation of beta-catenin from the adherens junctions to the cytosol and nucleus.
  • Similarly, cohort migration of MDCK cells was retarded on laminin-1 when compared with collagen IV, and addition of the Rho kinase inhibitor Y27632 resulted in enhanced motility and a change in cell morphology.
  • CONCLUSION: The study demonstrates that the Rho/Rho kinase pathway is required to maintain a non-migratory epithelial phenotype of cultured renal tubular LLC-PK1 and MDCK cells on the basement membrane glycoprotein laminin-1.
  • [MeSH-minor] Animals. Cell Differentiation. Cell Line. Cell Movement. Dogs. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Phenotype. Signal Transduction / drug effects. Signal Transduction / physiology. Swine. rho-Associated Kinases

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16847378.001).
  • [ISSN] 1660-2137
  • [Journal-full-title] Nephron. Physiology
  • [ISO-abbreviation] Nephron Physiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Laminin; 0 / laminin 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / rho-Associated Kinases; EC 3.6.5.2 / rho GTP-Binding Proteins
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79. Virgin F, Zhang S, Schuster D, Azbell C, Fortenberry J, Sorscher EJ, Woodworth BA: The bioflavonoid compound, sinupret, stimulates transepithelial chloride transport in vitro and in vivo. Laryngoscope; 2010 May;120(5):1051-6
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  • OBJECTIVES/HYPOTHESIS: Dehydration of airway surface liquid (ASL) disrupts normal mucociliary clearance in sinonasal epithelium leading to chronic rhinosinusitis.
  • Abnormal chloride (Cl(-)) transport is one mechanism that contributes to this disorder, as demonstrated by the disease cystic fibrosis.
  • Sinupret (Bionorica, LLC, San Clemente, CA), a combination of naturally occurring bioflavonoids, is a widely used treatment for respiratory ailments in Europe.
  • METHODS: Well characterized murine nasal septal epithelial (MNSE) cultures, and murine nasal potential difference (NPD) techniques were used to evaluate the effects of Sinupret on Cl(-) secretion.

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  • (PMID = 20422703.001).
  • [ISSN] 1531-4995
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chloride Channels; 0 / Chlorides; 0 / Flavonoids; 0 / Plant Extracts; 1F7A44V6OU / Colforsin; 77321-52-9 / Sinupret
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80. Biebinger R, Zimmermann MB, Al-Hooti SN, Al-Hamed N, Al-Salem E, Zafar T, Kabir Y, Al-Obaid I, Petry N, Hurrell RF: Efficacy of wheat-based biscuits fortified with microcapsules containing ferrous sulfate and potassium iodate or a new hydrogen-reduced elemental iron: a randomised, double-blind, controlled trial in Kuwaiti women. Br J Nutr; 2009 Nov;102(9):1362-9
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  • The first objective of the study was to measure the efficacy in wheat flour of two newly developed Fe compounds, an H-reduced Fe powder (NutraFine RS; North America Höganäs High Alloys LLC, Johnstown, PA, USA) and small particle-sized (40 microm) encapsulated FeSO4.
  • A randomised, double-blind controlled intervention trial was conducted in Kuwaiti women (n 279; aged 18-35 years) with low body Fe stores (serum ferritin (SF) < 25 microg/l) randomly assigned to one of three groups (20 mg Fe as NutraFine RS, 10 mg Fe as encapsulated FeSO4 and 150 microg iodine, or no fortification Fe) who consumed wheat-based biscuits 5 d per week.
  • Relative to control, mean SF in the encapsulated FeSO4 group increased by 88 % (P < 0.001) and body Fe stores increased from - 0.96 to 2.24 mg/kg body weight (P < 0.001), while NutraFine RS did not significantly increase SF or body Fe stores.
  • The median urinary iodine concentration increased from 140 to 213 microg/l (P < 0.01).

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  • (PMID = 19653920.001).
  • [ISSN] 1475-2662
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Capsules; 0 / Ferrous Compounds; 0 / Hemoglobins; 0 / Iodates; 0 / Iron, Dietary; 0 / Potassium Compounds; 0 / Transferrin; 39R4TAN1VT / ferrous sulfate; E1UOL152H7 / Iron; I139E44NHL / potassium iodate
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81. Chen Z, Wang Y, Ratia K, Mesecar AD, Wilkinson KD, Baker SC: Proteolytic processing and deubiquitinating activity of papain-like proteases of human coronavirus NL63. J Virol; 2007 Jun;81(11):6007-18
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  • Human coronavirus NL63 (HCoV-NL63), a common human respiratory pathogen, is associated with both upper and lower respiratory tract disease in children and adults.
  • We generated polyclonal antisera directed against two of the predicted replicase nonstructural proteins (nsp3 and nsp4) and detected replicase proteins from HCoV-NL63-infected LLC-MK2 cells by immunofluorescence, immunoprecipitation, and Western blot assays.

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  • [Cites] J Virol. 2004 Jun;78(11):5957-65 [15140993.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10012-7 [15226499.001]
  • [Cites] Nucleic Acids Res. 2004;32(14):e115 [15304544.001]
  • [Cites] J Virol. 2004 Sep;78(18):9977-86 [15331731.001]
  • [Cites] Proc Natl Acad Sci U S A. 1967 Apr;57(4):933-40 [5231356.001]
  • [Cites] J Virol. 1999 Apr;73(4):2658-66 [10074111.001]
  • [Cites] J Virol. 1999 Jul;73(7):5957-69 [10364348.001]
  • [Cites] J Virol. 2004 Dec;78(24):13600-12 [15564471.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1374-8 [15531891.001]
  • [Cites] Curr Top Microbiol Immunol. 2005;287:57-94 [15609509.001]
  • [Cites] J Virol. 2005 Jan;79(2):884-95 [15613317.001]
  • [Cites] J Infect Dis. 2005 Feb 15;191(4):503-6 [15655772.001]
  • [Cites] J Med Virol. 2005 Mar;75(3):463-5 [15648061.001]
  • [Cites] J Med Virol. 2005 Mar;75(3):455-62 [15648064.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 15;102(7):2430-5 [15695582.001]
  • [Cites] J Virol. 2005 Apr;79(7):4550-1 [15767458.001]
  • [Cites] Clin Infect Dis. 2005 Jun 15;40(12):1721-9 [15909257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 31;102(22):7988-93 [15897467.001]
  • [Cites] Pediatr Infect Dis J. 2005 Jul;24(7):645-6 [15999010.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):599-609 [16064136.001]
  • [Cites] Emerg Infect Dis. 2005 Aug;11(8):1225-9 [16102311.001]
  • [Cites] Mol Cell. 2005 Aug 19;19(4):547-57 [16109378.001]
  • [Cites] PLoS Med. 2005 Aug;2(8):e240 [16104827.001]
  • [Cites] J Clin Microbiol. 2005 Sep;43(9):4567-73 [16145108.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14040-5 [16169905.001]
  • [Cites] PLoS Biol. 2005 Oct;3(10):e324 [16128623.001]
  • [Cites] Essays Biochem. 2005;41:139-56 [16250903.001]
  • [Cites] J Med Chem. 2005 Nov 3;48(22):6767-71 [16250632.001]
  • [Cites] Science. 2005 Oct 28;310(5748):676-9 [16195424.001]
  • [Cites] Structure. 2005 Nov;13(11):1665-75 [16271890.001]
  • [Cites] J Gen Virol. 1967 Apr;1(2):175-8 [4293939.001]
  • [Cites] Virology. 1992 Jul;189(1):274-84 [1318604.001]
  • [Cites] Virology. 1995 Jun 1;209(2):420-7 [7778277.001]
  • [Cites] Virology. 1995 Jun 1;209(2):489-97 [7539970.001]
  • [Cites] J Virol. 1997 Feb;71(2):900-9 [8995606.001]
  • [Cites] J Virol. 2000 Feb;74(4):1674-85 [10644337.001]
  • [Cites] J Virol. 2000 Sep;74(17):7911-21 [10933699.001]
  • [Cites] J Biol Chem. 2001 Aug 31;276(35):33220-32 [11431476.001]
  • [Cites] Virology. 1995 Apr 1;208(1):1-8 [11831690.001]
  • [Cites] J Virol. 2002 Apr;76(8):3697-708 [11907209.001]
  • [Cites] J Virol. 2002 Jun;76(12):6323-31 [12021365.001]
  • [Cites] Chem Biol. 2002 Oct;9(10):1149-59 [12401499.001]
  • [Cites] Lancet. 2003 Apr 19;361(9366):1319-25 [12711465.001]
  • [Cites] N Engl J Med. 2003 May 15;348(20):1967-76 [12690091.001]
  • [Cites] N Engl J Med. 2003 May 15;348(20):1953-66 [12690092.001]
  • [Cites] J Virol. 2003 Jul;77(13):7376-82 [12805436.001]
  • [Cites] J Gen Virol. 2003 Sep;84(Pt 9):2305-15 [12917450.001]
  • [Cites] J Virol. 2003 Oct;77(19):10515-27 [12970436.001]
  • [Cites] Annu Rev Cell Dev Biol. 2003;19:141-72 [14570567.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):10136-41 [14699140.001]
  • [Cites] Emerg Infect Dis. 2004 Feb;10(2):320-6 [15030705.001]
  • [Cites] Nat Med. 2004 Apr;10(4):368-73 [15034574.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6212-6 [15073334.001]
  • [Cites] Pediatr Infect Dis J. 2005 Nov;24(11):1015-7 [16282944.001]
  • [Cites] J Virol. 2005 Dec;79(24):15189-98 [16306590.001]
  • [Cites] J Virol. 2005 Dec;79(24):15199-208 [16306591.001]
  • [Cites] J Virol. 2005 Dec;79(24):15582-5 [16306630.001]
  • [Cites] Virol J. 2004;1:7 [15548333.001]
  • [Cites] Cell. 2005 Dec 2;123(5):773-86 [16325574.001]
  • [Cites] Proteins. 2006 Mar 15;62(3):760-75 [16358325.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5717-22 [16581910.001]
  • [Cites] J Virol. 2006 May;80(9):4211-9 [16611880.001]
  • [Cites] Antimicrob Agents Chemother. 2006 Jun;50(6):2000-8 [16723558.001]
  • [Cites] J Virol. 2006 Jun;80(12):5927-40 [16731931.001]
  • [Cites] J Virol. 2006 Jun;80(12):6003-12 [16731939.001]
  • [Cites] PLoS Pathog. 2005 Dec;1(4):e39 [16341254.001]
  • [Cites] Clin Infect Dis. 2006 Sep 1;43(5):585-92 [16886150.001]
  • [Cites] J Virol. 2006 Sep;80(17):8639-52 [16912312.001]
  • [Cites] J Virol. 2006 Dec;80(23):11610-20 [16971428.001]
  • (PMID = 17392370.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P01 AI060915; United States / NIAID NIH HHS / AI / P01-AI060915; United States / PHS HHS / / R01-A1045798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ubiquitin; 0 / Viral Envelope Proteins; EC 3.4.22.- / 3C-like proteinase, Coronavirus; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.2 / Papain
  • [Other-IDs] NLM/ PMC1900296
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82. Mowery YM, Weinberg JB, Kennedy MN, Bond KM, Moore JO, Lanasa MC, Gockerman JP, Diehl LF, Pizzo SV, Cianciolo GJ, Friedman DR: LMP-420: a novel purine nucleoside analog with potent cytotoxic effects for CLL cells and minimal toxicity for normal hematopoietic cells. Leukemia; 2010 Sep;24(9):1580-7
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  • [Title] LMP-420: a novel purine nucleoside analog with potent cytotoxic effects for CLL cells and minimal toxicity for normal hematopoietic cells.
  • B-cell chronic lymphocytic leukemia (CLL) is characterized by slow accumulation of malignant cells, which are supported in the microenvironment by cell-cell interactions and soluble cytokines such as tumor necrosis factor (TNF).
  • We evaluated the effect of the small molecule TNF inhibitor LMP-420 on primary CLL cells.
  • CLL cells from patients with poor prognostic indicators showed LMP-420 sensitivity equal to that for cells from patients with favorable characteristics.
  • In addition, LMP-420 potentiated the cytotoxic effect of fludarabine and inhibited in vitro proliferation of stimulated CLL cells.
  • Gene expression profiling indicated that the mechanism of action of LMP-420 may involve suppression of nuclear factor-kappaB and immune response pathways in CLL cells.
  • LMP-420 had minimal effects on normal peripheral blood mononuclear cell, B- and T-cell function, and hematopoietic colony formation.
  • Our data suggest that LMP-420 may be a useful treatment for CLL with negligible hematologic toxicities.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boron Compounds / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Purines / pharmacology. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Synergism. Female. Flow Cytometry. Gene Expression Profiling. Humans. Male. Prognosis. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 20613784.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-6-chloro-9-((5-dihydroxyboryl)pentyl)purine; 0 / Antineoplastic Agents; 0 / Boron Compounds; 0 / Purines; 0 / Tumor Necrosis Factor-alpha; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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83. Rezvany MR, Kazemi A, Hajifathali A, Kaviani S, Mellstedt H: Analysis of HLA-G gene expression in B-lymphocytes from chronic lymphocytic leukemia patients. Iran Biomed J; 2007 Apr;11(2):125-9
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  • [Title] Analysis of HLA-G gene expression in B-lymphocytes from chronic lymphocytic leukemia patients.
  • BACKGROUND: The human leukocyte antigen G (HLA-G) molecule exhibits limited tissue distribution, low polymorphism and alternative splicings that generate seven HLA-G isoforms.
  • This study it is an effort to clarify the presence of HLA-G in B-cell chronic lymphocytic leukemia (B-CLL) patients.
  • METHODS: HLA-G mRNA expression was studied in a pilot study in circulating B-CLL and also healthy controls by reverse transcription (RT)-PCR using a set of pan-HLA-G primers.
  • RESULTS: RT-PCR was performed on B-cells from 74 B-CLL patients and 12 healthy controls.
  • The data showed HLA-G gene expression in 20% of the B-CLL patients.
  • CONCLUSION: These data suggest that HLA-G is expressed at the gene level in B cells from B-CLL patients but not in B cells from healthy controls.
  • Further study is required to clarify the role of HLA-G as a regulatory factor that could affect immune response in B-CLL patients.
  • [MeSH-major] B-Lymphocytes / immunology. Gene Expression Regulation / immunology. HLA Antigens / genetics. Histocompatibility Antigens Class I / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • (PMID = 18051955.001).
  • [ISSN] 1028-852X
  • [Journal-full-title] Iranian biomedical journal
  • [ISO-abbreviation] Iran. Biomed. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / DNA Primers; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
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84. Lu CM, Murata-Collins JL, Wang E, Siddiqi I, Lawrence H: Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: molecular evidence of two separate diseases. Am J Hematol; 2006 Dec;81(12):963-8
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  • [Title] Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: molecular evidence of two separate diseases.
  • Acute myeloid leukemia (AML) occurring concurrently with or after untreated chronic lymphocytic leukemia (CLL) is rare.
  • We report a case of a 59-year-old man who was evaluated for anemia, thrombocytopenia, and leukocytosis with circulating blasts.
  • On the basis of the morphology and immunophenotyping results, a preliminary diagnosis of chronic myelomonocytic leukemia with concurrent CLL was considered.
  • Subsequently, cytogenetic analysis of the leukemic blood specimen revealed inv(16)(p13.1q22) with secondary trisomy 22 in a sideline clone.
  • Fluorescence in situ hybridization confirmed the CBFbeta rearrangement associated with inv(16) in myeloblasts and myelomonocytic cells, but not in CLL cells.
  • Therefore, a final diagnosis of AML with inv(16) with concurrent CLL was made.
  • After standard chemotherapy for AML, the patient achieved complete remission for both his AML and CLL.
  • The unique aspects of this case include concomitant AML and CLL, which do not share clonality, complex cytogenetic abnormalities with trisomy 22 as a secondary abnormality associated with inv(16), and achievement of remission for both AML and CLL by AML chemotherapy regimen.
  • This case also represents one of the rare instances where a diagnosis of AML can be established even when the blast percentage in the marrow and blood is less than 20%.
  • [MeSH-major] Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Trisomy / genetics
  • [MeSH-minor] Blast Crisis / diagnosis. Blast Crisis / drug therapy. Blast Crisis / genetics. Blast Crisis / pathology. Bone Marrow / pathology. Humans. In Situ Hybridization, Fluorescence / methods. Male. Middle Aged. Remission Induction


85. Caraway NP, Thomas E, Khanna A, Payne L, Zhang HZ, Lin E, Keating MJ, Katz RL: Chromosomal abnormalities detected by multicolor fluorescence in situ hybridization in fine-needle aspirates from patients with small lymphocytic lymphoma are useful for predicting survival. Cancer; 2008 Oct 25;114(5):315-22
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  • [Title] Chromosomal abnormalities detected by multicolor fluorescence in situ hybridization in fine-needle aspirates from patients with small lymphocytic lymphoma are useful for predicting survival.
  • BACKGROUND: Fine-needle aspiration (FNA) of lymph nodes is commonly used to assess disease progression in patients with small lymphocytic lymphoma (SLL).
  • Although cytologic features are helpful for diagnosing typical SLL and transformed large-cell lymphoma (tLCL), SLL in accelerated phase (SLLacc) is more difficult to diagnose.
  • Additional tests are needed to identify those patients who are transforming to a higher-grade lymphoma.
  • This study evaluated the use of a multicolor fluorescence in situ hybridization (FISH) probe panel specifically designed for chronic lymphocytic leukemia (CLL)/SLL and assessed the association between FISH findings and cytologic diagnosis, proliferation index, and risk of death.
  • METHODS: FNA specimens from 50 patients (32 men and 18 women; mean age, 57 years [range, 36-77 years]) with histologically confirmed CLL and/or SLL were evaluated in this study for chromosomal abnormalities of 11q22 (ATM), 12, 13q14.3, 13q34.3 (LAMP1), and 17p13.1 (p53) by using a multiprobe FISH kit.
  • CONCLUSIONS: FISH can be performed on FNA specimens from patients with a history of SLL/CLL.
  • [MeSH-major] Biopsy, Fine-Needle. Chromosome Aberrations. In Situ Hybridization, Fluorescence. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / mortality

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18683215.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
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86. Storey R, Gatt M, Bradford I: Mucosa associated lymphoid tissue lymphoma presenting within a solitary anti-mesenteric dilated segment of ileum: a case report. J Med Case Rep; 2009;3:6
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  • [Title] Mucosa associated lymphoid tissue lymphoma presenting within a solitary anti-mesenteric dilated segment of ileum: a case report.
  • INTRODUCTION: Mucosa associated lymphoid tissue (MALT) lymphoma is the third most common non-Hodgkin's lymphoma subtype.
  • Clinical presentation is often insidious as a low-grade lesion and disease tends to remain localised for a long period of time.
  • Histology of this segment demonstrated MALT lymphoma of the small bowel.

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  • [Cites] Scand J Gastroenterol. 2008;43(4):497-505 [18365916.001]
  • [Cites] Ann Surg. 2005 Mar;241(3):529-33 [15729078.001]
  • [Cites] Leuk Lymphoma. 1997 Aug;26(5-6):527-37 [9389360.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2486-92 [10561313.001]
  • [Cites] Arch Surg. 1994 Jun;129(6):659-61 [8204043.001]
  • [Cites] Cancer. 1983 Jan 1;51(1):80-91 [6336974.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • (PMID = 19126231.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2627909
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87. Stilgenbauer S, Zenz T, Winkler D, Bühler A, Schlenk RF, Groner S, Busch R, Hensel M, Dührsen U, Finke J, Dreger P, Jäger U, Lengfelder E, Hohloch K, Söling U, Schlag R, Kneba M, Hallek M, Döhner H, German Chronic Lymphocytic Leukemia Study Group: Subcutaneous alemtuzumab in fludarabine-refractory chronic lymphocytic leukemia: clinical results and prognostic marker analyses from the CLL2H study of the German Chronic Lymphocytic Leukemia Study Group. J Clin Oncol; 2009 Aug 20;27(24):3994-4001
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  • [Title] Subcutaneous alemtuzumab in fludarabine-refractory chronic lymphocytic leukemia: clinical results and prognostic marker analyses from the CLL2H study of the German Chronic Lymphocytic Leukemia Study Group.
  • PURPOSE: The phase II CLL2H trial evaluated safety and efficacy of subcutaneous alemtuzumab in patients with fludarabine-refractory chronic lymphocytic leukemia (CLL).
  • The median progression-free survival was 7.7 months, and the median overall survival (OS) was 19.1 months.
  • In multivariate analysis of clinical and biologic variables, age, performance status, beta2-MG, and TK were independent prognostic factors for OS.
  • CONCLUSION: Subcutaneous alemtuzumab appears as effective and safe as intravenous alemtuzumab in fludarabine-refractory CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Vidarabine / analogs & derivatives

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  • (PMID = 19597025.001).
  • [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] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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88. Giannopoulos K, Schmitt M, Własiuk P, Chen J, Bojarska-Junak A, Kowal M, Roliñski J, Dmoszyñska A: The high frequency of T regulatory cells in patients with B-cell chronic lymphocytic leukemia is diminished through treatment with thalidomide. Leukemia; 2008 Jan;22(1):222-4
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  • [Title] The high frequency of T regulatory cells in patients with B-cell chronic lymphocytic leukemia is diminished through treatment with thalidomide.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. T-Lymphocytes, Regulatory / immunology. Thalidomide / therapeutic use
  • [MeSH-minor] Adult. Aged. CD4-Positive T-Lymphocytes / metabolism. Female. Forkhead Transcription Factors / metabolism. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Male. Middle Aged

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  • (PMID = 17657216.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Immunosuppressive Agents; 0 / Interleukin-2 Receptor alpha Subunit; 4Z8R6ORS6L / Thalidomide
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89. Morrison VA: Infectious complications of chronic lymphocytic leukaemia: pathogenesis, spectrum of infection, preventive approaches. Best Pract Res Clin Haematol; 2010 Mar;23(1):145-53
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  • [Title] Infectious complications of chronic lymphocytic leukaemia: pathogenesis, spectrum of infection, preventive approaches.
  • Infectious complications continue to be a major cause of morbidity and mortality in patients with chronic lymphocytic leukaemia (CLL).
  • This review focuses on the pathogenesis and risk factors for infections in patients with CLL, the spectrum of infectious complications and preventive approaches to infection in these patients, using antimicrobial and immunoglobulin prophylaxis and vaccination strategies.
  • [MeSH-major] Infection / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • [Copyright] Published by Elsevier Ltd.
  • (PMID = 20620978.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 70
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90. Goldin LR, Lanasa MC, Slager SL, Cerhan JR, Vachon CM, Strom SS, Camp NJ, Spector LG, Leis JF, Morrison VA, Glenn M, Rabe KG, Achenbach SJ, Algood SD, Abbasi F, Fontaine L, Yau M, Rassenti LZ, Kay NE, Call TG, Hanson CA, Weinberg JB, Marti GE, Caporaso NE: Common occurrence of monoclonal B-cell lymphocytosis among members of high-risk CLL families. Br J Haematol; 2010 Oct;151(2):152-8
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  • [Title] Common occurrence of monoclonal B-cell lymphocytosis among members of high-risk CLL families.
  • Monoclonal B-cell lymphocytosis (MBL) is an asymptomatic haematological condition characterized by low absolute levels of B-cell clones with a surface immunophenotype similar to that of chronic lymphocytic leukaemia (CLL).
  • It has been reported to be higher among first-degree relatives from CLL families.
  • We report results of multi-parameter flow cytometry among 505 first-degree relatives with no personal history of lymphoproliferative disease from 140 families having at least two cases of CLL.
  • MBL clustered in certain families but clustering was independent of the number of known CLL cases in a family.
  • As is the case with CLL, males had a significantly higher risk for MBL than did females (P = 0·04).
  • MBL patients had significantly higher mean absolute lymphocyte counts (2·4 × 10(9) /l) and B-cell counts (0·53 × 10(9) /l) than those with a normal B-cell immuno-phenotype.
  • Our findings show that MBL occurs at a very high rate in high risk CLL families.
  • Both the age and gender distribution of MBL are parallel to CLL, implying a shared inherited risk.

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  • [Copyright] Published 2010. This article is a US Government work and is in the public domain in the USA.
  • [Cites] Br J Haematol. 2009 Nov;147(3):339-46 [19709083.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):3959-63 [19620484.001]
  • [Cites] Leukemia. 2010 Mar;24(3):512-20 [20090778.001]
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2289-90 [12239136.001]
  • [Cites] Cytometry B Clin Cytom. 2003 Mar;52(1):1-12 [12599176.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2337-42 [14630808.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):325-32 [16042682.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1087-91 [17577771.001]
  • [Cites] Cytometry B Clin Cytom. 2007 Sep;72(5):344-53 [17266153.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] Mayo Clin Proc. 2008 Jul;83(7):776-85 [18613994.001]
  • [Cites] N Engl J Med. 2008 Aug 7;359(6):575-83 [18687638.001]
  • [Cites] N Engl J Med. 2009 Feb 12;360(7):659-67 [19213679.001]
  • [Cites] Leuk Lymphoma. 2009 Mar;50(3):493-7 [19347733.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4188-96 [19015397.001]
  • [Cites] Haematologica. 2009 May;94(5):647-53 [19286886.001]
  • [Cites] Blood. 2009 Jul 2;114(1):26-32 [19029437.001]
  • [Cites] Blood. 2009 Jul 2;114(1):33-7 [19420353.001]
  • [Cites] Leukemia. 2010 Jan;24(1):133-40 [19946263.001]
  • (PMID = 20738309.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA118444; United States / NCI NIH HHS / PC / N01-PC-35141; United States / NCI NIH HHS / CA / N01PC35141; United States / NIAID NIH HHS / AI / P30 AI051445; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R43 CA137941; United States / NCI NIH HHS / CA / CA137941; United States / NIAID NIH HHS / AI / AI-51445; United States / NCI NIH HHS / CA / CA116237; United States / NCI NIH HHS / CA / U01 CA118444; United States / NCI NIH HHS / CA / R01 CA116237
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS230867; NLM/ PMC2966536
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91. Dreger P, Corradini P, Kimby E, Michallet M, Milligan D, Schetelig J, Wiktor-Jedrzejczak W, Niederwieser D, Hallek M, Montserrat E, Chronic Leukemia Working Party of the EBMT: Indications for allogeneic stem cell transplantation in chronic lymphocytic leukemia: the EBMT transplant consensus. Leukemia; 2007 Jan;21(1):12-7
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  • [Title] Indications for allogeneic stem cell transplantation in chronic lymphocytic leukemia: the EBMT transplant consensus.
  • The aim of this project was to identify situations where allogeneic stem cell transplantation (allo-SCT) might be considered as a preferred treatment option for patients with B-cell chronic lymphocytic leukemia (CLL).
  • Key elements of the consensus are (1) allo-SCT is a procedure with evidence-based efficacy in poor-risk CLL;.
  • (2) although definition of 'poor-risk CLL' requires further investigation, allo-SCT is a reasonable treatment option for younger patients with (i) non-response or early relapse (within 12 months) after purine analogues, (ii) relapse within 24 months after having achieved a response with purine-analogue-based combination therapy or autologous transplantation, and (iii) patients with p53 abnormalities requiring treatment; and (3) optimum transplant strategies may vary according to distinct clinical situations and should be defined in prospective trials.
  • This is the first attempt to define standard indications for allo-SCT in CLL.
  • Nevertheless, whenever possible, allo-SCT should be performed within disease-specific prospective clinical protocols in order to continuously refine transplant indications according to new developments in risk assessment and treatment of CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Stem Cell Transplantation

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  • (PMID = 17109028.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Consensus Development Conference; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Number-of-references] 43
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92. Hamblin TJ: Chronic lymphocytic leukaemia: clinical translations of biological features. Curr Top Microbiol Immunol; 2005;294:165-85
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  • [Title] Chronic lymphocytic leukaemia: clinical translations of biological features.
  • The chronic lymphatic leukaemia (CLL) world was surprised to find that the disease split so neatly down the middle into those patients with unmutated immunoglobulin genes who were mainly men, had aggressive disease and were destined to die from their disease, on average at about 8 years from diagnosis, and those with mutated immunoglobulin genes who were equally distributed between the sexes, had indolent disease and usually died of something else a quarter of a century later.
  • This discovery gave fresh impetus to the investigation into the biology of CLL.
  • We now know more about, though we are still not certain of, the cell of origin of the disease and how it functions and fails to function.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] B-Lymphocytes / immunology. Biomarkers, Tumor. Female. Genes, Immunoglobulin. Germinal Center / immunology. Humans. Immunologic Memory. Male. Mutation. Prognosis

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  • (PMID = 16323432.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 77
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93. Masago M, Takaai M, Sakata J, Horie A, Ito T, Ishida K, Taguchi M, Hashimoto Y: Membrane transport mechanisms of quinidine and procainamide in renal LLC-PK1 and intestinal LS180 cells. Biol Pharm Bull; 2010;33(8):1407-12
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  • [Title] Membrane transport mechanisms of quinidine and procainamide in renal LLC-PK1 and intestinal LS180 cells.
  • The aim of the present study was to compare the membrane transport mechanisms of procainamide with those of quinidine using renal epithelial LLC-PK(1) and intestinal epithelial LS180 cells.
  • In LLC-PK(1) cells, the transcellular transport of 10 microM quinidine in the basolateral-to-apical direction was similar to that in the opposite direction, and 1 mM tetraethylammonium (TEA) did not affect the transcellular transport of the drug.
  • On the other hand, the transcellular transport of 10 microM TEA and procainamide in LLC-PK(1) cells was directional from the basolateral side to the apical side.
  • [MeSH-major] Anti-Arrhythmia Agents / pharmacokinetics. Cell Membrane / metabolism. Intestines / metabolism. Kidney / metabolism. Procainamide / pharmacokinetics. Quinidine / pharmacokinetics
  • [MeSH-minor] Animals. Biological Transport, Active. Caco-2 Cells. Cation Transport Proteins / metabolism. Drug Interactions. Epithelial Cells / metabolism. Humans. Hydrogen-Ion Concentration. LLC-PK1 Cells. Swine. Temperature. Tetraethylammonium / pharmacology

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  • (PMID = 20686239.001).
  • [ISSN] 1347-5215
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Arrhythmia Agents; 0 / Cation Transport Proteins; 66-40-0 / Tetraethylammonium; ITX08688JL / Quinidine; L39WTC366D / Procainamide
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94. Cerezo M, Bandelt HJ, Martín-Guerrero I, Ardanaz M, Vega A, Carracedo A, García-Orad A, Salas A: High mitochondrial DNA stability in B-cell chronic lymphocytic leukemia. PLoS One; 2009;4(11):e7902
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  • [Title] High mitochondrial DNA stability in B-cell chronic lymphocytic leukemia.
  • BACKGROUND: Chronic Lymphocytic Leukemia (CLL) leads to progressive accumulation of lymphocytes in the blood, bone marrow, and lymphatic tissues.
  • Previous findings have suggested that the mtDNA could play an important role in CLL.
  • METHODOLOGY/PRINCIPAL FINDINGS: The mitochondrial DNA (mtDNA) control-region was analyzed in lymphocyte cell DNA extracts and compared with their granulocyte counterpart extract of 146 patients suffering from B-Cell CLL; B-CLL (all recruited from the Basque country).
  • Only twenty instabilities were finally confirmed, most of them affecting the homopolymeric stretch located in the second hypervariable segment (HVS-II) around position 310, which is well known to constitute an extreme mutational hotspot of length polymorphism, as these mutations are frequently observed in the general human population.
  • A critical revision of the findings in previous studies indicates a lack of proper methodological standards, which eventually led to an overinterpretation of the role of the mtDNA in CLL tumorigenesis.
  • CONCLUSIONS/SIGNIFICANCE: Our results suggest that mtDNA instability is not the primary causal factor in B-CLL.
  • [MeSH-major] DNA, Mitochondrial / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism
  • [MeSH-minor] Base Sequence. DNA Primers / genetics. Databases, Genetic. Granulocytes / cytology. Haplotypes. Humans. Lymphocytes / cytology. Models, Statistical. Molecular Sequence Data. Mutation. Phylogeny. Sequence Analysis, DNA

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  • [Cites] BMC Cancer. 2009;9:113 [19371404.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 22;333(1):122-30 [15958208.001]
  • [Cites] Forensic Sci Int. 2000 May 8;110(1):47-59 [10802200.001]
  • [Cites] Am J Hum Genet. 2000 Nov;67(5):1251-76 [11032788.001]
  • [Cites] Leukemia. 2001 Mar;15(3):445-51 [11237069.001]
  • [Cites] Int J Legal Med. 2001;114(3):186-90 [11296893.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1317-25 [11516091.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 30;335(3):891-9 [16102729.001]
  • [Cites] Electrophoresis. 2005 Sep;26(18):3414-29 [16167362.001]
  • [Cites] J Med Genet. 2005 Dec;42(12):957-60 [15923271.001]
  • [Cites] Leukemia. 2006 Feb;20(2):362-3 [16357835.001]
  • [Cites] Genetics. 2006 Jan;172(1):373-87 [16172508.001]
  • [Cites] PLoS Med. 2005 Nov;2(11):e296 [16187796.001]
  • [Cites] Hum Genet. 2006 Jun;119(5):505-15 [16528519.001]
  • [Cites] Blood. 2007 Jan 15;109(2):756-62 [16946307.001]
  • [Cites] Mol Biol Evol. 2007 Feb;24(2):436-48 [17099056.001]
  • [Cites] Mol Biol Evol. 2007 Mar;24(3):868-74 [17218641.001]
  • [Cites] Forensic Sci Int. 2007 May 3;168(1):1-13 [16814504.001]
  • [Cites] PLoS One. 2008;3(4):e2062 [18446216.001]
  • [Cites] J Med Genet. 2008 Dec;45(12):769-72 [18611982.001]
  • [Cites] PLoS One. 2009;4(4):e5112 [19340307.001]
  • [Cites] Am J Hum Genet. 2002 May;70(5):1152-71 [11938495.001]
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Am J Hum Genet. 2002 Nov;71(5):1150-60 [12384858.001]
  • [Cites] Am J Phys Anthropol. 2003 Apr;120(4):391-404 [12627534.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3118-25 [12446454.001]
  • [Cites] Electrophoresis. 2003 Apr;24(7-8):1159-65 [12707907.001]
  • [Cites] Int J Legal Med. 2003 Jun;117(3):180-4 [12799738.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1437-47 [12886229.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2487-91 [14523470.001]
  • [Cites] Leukemia. 2004 Jan;18(1):18-22 [14614516.001]
  • [Cites] Oncogene. 2004 Feb 12;23(6):1314-20 [14647457.001]
  • [Cites] Forensic Sci Int. 2004 Feb 10;140(1):1-11 [15013160.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1966-71 [15026331.001]
  • [Cites] Forensic Sci Int. 2004 Mar 10;140(2-3):251-7 [15036446.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1313-6 [15129223.001]
  • [Cites] Science. 2004 Sep 3;305(5689):1402-4 [15353782.001]
  • [Cites] Am J Hum Genet. 2004 Nov;75(5):910-8 [15382008.001]
  • [Cites] Ann Hum Genet. 1991 Jan;55(Pt 1):51-67 [2042936.001]
  • [Cites] Int J Legal Med. 1993;105(5):251-6 [8471542.001]
  • [Cites] N Engl J Med. 1995 Oct 19;333(16):1052-7 [7675049.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Int J Cancer. 1998 May 18;76(4):495-8 [9590124.001]
  • [Cites] Ann Intern Med. 1998 Oct 1;129(7):559-66 [9758577.001]
  • [Cites] Leukemia. 1998 Oct;12(10):1612-7 [9766507.001]
  • [Cites] Eur J Hum Genet. 1998 Jul-Aug;6(4):365-75 [9781045.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):147 [10508508.001]
  • [Cites] Forensic Sci Int. 2005 Mar 10;148(2-3):191-8 [15639614.001]
  • [Cites] Int J Legal Med. 2004 Oct;118(5):267-73 [15257464.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Am J Hum Genet. 2005 May;76(5):883-6 [15791543.001]
  • [Cites] Electrophoresis. 2000 Feb;21(3):548-53 [10726758.001]
  • (PMID = 19924307.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Mitochondrial
  • [Other-IDs] NLM/ PMC2775629
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95. Wang J, Zhang B, Guo Y, Li G, Xie Q, Zhu B, Gao J, Chen Z: Artemisinin inhibits tumor lymphangiogenesis by suppression of vascular endothelial growth factor C. Pharmacology; 2008;82(2):148-55
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  • We have previously reported that dihydroartemisinin is found to have a potent ability in influencing lymphatic endothelial cell migration and tube formation.
  • In this study, we investigated the effect of artemisinin on tumor growth, lymphangiogenesis, metastasis and survival in mouse Lewis lung carcinoma (LLC) models.
  • Furthermore, IL-1beta-induced p38 mitogen-activated protein kinase (MAPK) activation and upregulation of VEGF-C mRNA and protein in LLC cells was also suppressed by artemisinin or by the p38 MAPK inhibitor SB-203580, suggesting that p38 MAPK could serve as a mediator of proinflammatory cytokine-induced VEGF-C expression.
  • [MeSH-minor] Administration, Oral. Animals. Female. Gene Expression Regulation, Neoplastic / drug effects. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Lymphangiogenesis / drug effects. Lymphatic Metastasis / prevention & control. Mice. Mice, Inbred C57BL. Neoplasm Metastasis / prevention & control. Survival Rate. p38 Mitogen-Activated Protein Kinases / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18667841.001).
  • [ISSN] 1423-0313
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Artemisinins; 0 / Vascular Endothelial Growth Factor C; 9RMU91N5K2 / artemisinine; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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96. Sleep 2009. Abstracts of the 23rd Annual Meeting of the Associated Professional Sleep Societies, LLC. June 6-11, 2009. Seattle, Washington, USA. Sleep; 2009;32 Suppl:A1-427
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  • [Title] Sleep 2009. Abstracts of the 23rd Annual Meeting of the Associated Professional Sleep Societies, LLC. June 6-11, 2009. Seattle, Washington, USA.

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  • (PMID = 19760817.001).
  • [ISSN] 0161-8105
  • [Journal-full-title] Sleep
  • [ISO-abbreviation] Sleep
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] United States
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97. Szmigielska-Kapłon A, Jesionek-Kupnicka D, Góra-Tybor J, Błonski JZ, Lech-Marańda E, Kordek R, Kasznicki M, Robak T: Influence of cladribine alone and in combination with cyclophosphamide or cyclophosphamide and mitoxantrone on bone marrow angiogenesis in chronic lymphocytic leukemia. Leuk Lymphoma; 2007 May;48(5):1042-4
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  • [Title] Influence of cladribine alone and in combination with cyclophosphamide or cyclophosphamide and mitoxantrone on bone marrow angiogenesis in chronic lymphocytic leukemia.
  • [MeSH-major] Bone Marrow Cells / drug effects. Cladribine / administration & dosage. Cladribine / therapeutic use. Cyclophosphamide / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Mitoxantrone / administration & dosage. Neovascularization, Pathologic

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  • Hazardous Substances Data Bank. CLADRIBINE .
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  • (PMID = 17487753.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone
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98. Payne PR, Borlawsky TB, Stephens W, Barrett MC, Nguyen-Pham T, Greaves AW: The TRITON Project: Design and Implementation of an Integrative Translational Research Information Management Platform. AMIA Annu Symp Proc; 2010 Nov 13;2010:617-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Chronic Lymphocytic Leukemia (CLL) Research Consortium (CRC), a s a prototypical instance of such a consortia, uses numerous loosely coupled web applications to address its informatics needs.

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  • [Cites] J Am Med Inform Assoc. 2008 Mar-Apr;15(2):138-49 [18096909.001]
  • [Cites] AMIA Annu Symp Proc. 2007;:433-7 [18693873.001]
  • [Cites] AMIA Annu Symp Proc. 2008;:1087 [18998940.001]
  • [Cites] AMIA Annu Symp Proc. 2008;:566-70 [18998958.001]
  • [Cites] Mol Cell Biochem. 2009 May;325(1-2):41-51 [19139973.001]
  • [Cites] J Am Med Inform Assoc. 2009 May-Jun;16(3):305-15 [19261933.001]
  • [Cites] Bioinformatics. 2006 Aug 1;22(15):1910-6 [16766552.001]
  • (PMID = 21347052.001).
  • [ISSN] 1942-597X
  • [Journal-full-title] AMIA ... Annual Symposium proceedings. AMIA Symposium
  • [ISO-abbreviation] AMIA Annu Symp Proc
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / R01 CA134232
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 30IQX730WE / Polyethylene Glycols
  • [Other-IDs] NLM/ PMC3041280
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99. Carulli G, Cannizzo E, Zucca A, Buda G, Orciuolo E, Marini A, Petrini M: CD45 expression in low-grade B-cell non-Hodgkin's lymphomas. Leuk Res; 2008 Feb;32(2):263-7
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  • [Title] CD45 expression in low-grade B-cell non-Hodgkin's lymphomas.
  • Few data are available about CD45 expression in the various types of low-grade B-cell non-Hodgkin's lymphomas (NHL).
  • Low levels of CD45 have been reported in pathologic lymphocytes from typical chronic lymphocytic leukemia (CLL) and higher levels of this antigen have been observed in some cases of atypical CLL and in some cases of other types of NHL.
  • One hundred and seven bone marrow samples of NHL with bone marrow infiltration were investigated: 45 typical CLL, 15 atypical CLL, 9 mantle cell lymphomas (MCL), 1 MCL with CD23 expression, 18 marginal zone lymphomas (MZL), 6 lymphoplasmacytic lymphomas (LPL), 6 follicular lymphomas (FL), and 7 hairy cell leukemias (HCL).
  • CD45 expression was evaluated by flow cytometry: pathologic lymphocytes were identified on the basis of specific immunophenotypic profile, CD19/K or CD19/lambda co-expression.
  • CD45 expression was measured also on autologous T-lymphocytes and a "CD45 index" was calculated as the ratio MFI of pathologic B-lymphocytes/MFI of T-lymphocytes, to normalize the results obtained.
  • We found four CD45 expression patterns: very low in typical CLL; relatively low in MCL; intermediate intensity in MZL, LPL, and FL; very high expression in HCL.
  • Among the atypical cases, very high CD45 expression was found in one case of CD23-negative CLL, in CD23-positive MCL, and CLL with atypical morphology.
  • The results indicate different levels of maturation in low-grade NHL and may help to characterize such neoplasias.
  • [MeSH-major] Antigens, CD45 / biosynthesis. Lymphoma, Non-Hodgkin / metabolism
  • [MeSH-minor] Flow Cytometry. Humans. Immunophenotyping. Leukemia, Hairy Cell / metabolism. Leukemia, Hairy Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, Follicular / metabolism. Lymphoma, Follicular / pathology. Lymphoma, Mantle-Cell / metabolism. Lymphoma, Mantle-Cell / pathology. Polymerase Chain Reaction

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  • (PMID = 17692374.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
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100. Giannopoulos K, Schmitt M: Targets and strategies for T-cell based vaccines in patients with B-cell chronic lymphocytic leukemia. Leuk Lymphoma; 2006 Oct;47(10):2028-36
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  • [Title] Targets and strategies for T-cell based vaccines in patients with B-cell chronic lymphocytic leukemia.
  • T-cell based immunotherapies might be a novel option for the treatment of B-cell chronic lymphocytic leukemia (B-CLL), a disease characterized by a prolonged natural course.
  • Different strategies of active immunotherapy have been tested in vitro to enhance a specific T-cell response against tumor cells and an anti-leukemic effect has been observed in B-CLL patients after allogenic stem cell transplantation.
  • Several antigens have been characterized as tumor/leukemia associated antigens (T/LAAs) in B-CLL with the potential to elicit specific anti-tumor response encompassing idiotype immunoglobulin, oncofetal antigen-immature laminin receptor protein (OFAiLRP), survivin, as well as fibromodulin, the receptor for hyaluronic acid mediated motility (RHAMM/CD168) and the murine double-minute 2 oncoprotein (MDM2).
  • This study presents an overview of possible targets and genetherapeutical maneuvers for future immunotherapies of B-CLL patients and summarizes recent clinical vaccination trials with dendritic cells (DCs) for B-CLL.
  • [MeSH-major] Cancer Vaccines. Leukemia, Lymphocytic, Chronic, B-Cell / prevention & control. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. T-Lymphocytes / metabolism






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