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  1. AU="Trivedi, Pritesh S"
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  1. Article: Bcl-6 and c-Myc are rarely co-expressed in adult diffuse large B-cell lymphoma.

    Wagner, Simon D / Amen, Furrat / Trivedi, Pritesh S / Horncastle, Donna / Elderfield, Kay / Naresh, Kikkeri N

    Leukemia & lymphoma

    2007  Volume 48, Issue 8, Page(s) 1510–1513

    Abstract: Bcl-6 is expressed in germinal centre derived B-cell non-Hodgkin lymphomas including diffuse large B-cell lymphoma (DLBCL) and is likely to play a major role in driving proliferation of a subset of DLBCLs, especially those of germinal centre B-cell ... ...

    Abstract Bcl-6 is expressed in germinal centre derived B-cell non-Hodgkin lymphomas including diffuse large B-cell lymphoma (DLBCL) and is likely to play a major role in driving proliferation of a subset of DLBCLs, especially those of germinal centre B-cell subtype, but the role of c-Myc, which is important for proliferation in various lineages is not known. We used the highly standardised staining conditions of a tissue microarray to characterise co-expression of c-Myc and Bcl-6 in DLBCL. We carried out immunohistochemistry of 73 arrayed cases. The majority (62/73) did not express c-Myc, but 11 cases (15%) showed nuclear staining. 5/53 (9%) of Bcl-6 expressing cases co-expressed c-Myc, whereas a much higher proportion, 6/20 (30%), of Bcl-6 negative cases were positive for c-Myc. Overall survival of c-Myc expressing cases was the same as those that had absent expression. There was no significant correlation between c-Myc expression and DLBCL subtype (germinal centre or non-germinal centre subtypes).
    MeSH term(s) Adult ; Germinal Center/metabolism ; Germinal Center/pathology ; Humans ; Immunoenzyme Techniques ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Lymphoma, Large B-Cell, Diffuse/metabolism ; Lymphoma, Large B-Cell, Diffuse/pathology ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Tissue Array Analysis
    Chemical Substances Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogene Proteins c-myc
    Language English
    Publishing date 2007-08-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1042374-6
    ISSN 1029-2403 ; 1042-8194
    ISSN (online) 1029-2403
    ISSN 1042-8194
    DOI 10.1080/10428190701458491
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2997: Show issues Location:
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  2. Article ; Online: Nicastrin regulates breast cancer stem cell properties and tumor growth in vitro and in vivo.

    Lombardo, Ylenia / Filipović, Aleksandra / Molyneux, Gemma / Periyasamy, Manikandan / Giamas, Georgios / Hu, Yunhui / Trivedi, Pritesh S / Wang, Jayson / Yagüe, Ernesto / Michel, Loren / Coombes, R Charles

    Proceedings of the National Academy of Sciences of the United States of America

    2012  Volume 109, Issue 41, Page(s) 16558–16563

    Abstract: Nicastrin (NCT) is a crucial component of the γ-secretase (GS) enzyme, which prompted investigations into its biological role in cancer. We have previously shown that nicastrin is overexpressed in breast cancer (BC), conferring worse overall survival in ... ...

    Abstract Nicastrin (NCT) is a crucial component of the γ-secretase (GS) enzyme, which prompted investigations into its biological role in cancer. We have previously shown that nicastrin is overexpressed in breast cancer (BC), conferring worse overall survival in invasive, ERα negative patients. Here, we used 2D and 3D Matrigel, anchorage-independent growth conditions and a breast cancer xenograft mouse model to assess the impact of nicastrin on breast cancer stem cell (BCSC) propagation and invasion in vitro and tumor growth in vivo. Stable knockdown of nicastrin in HCC1806 breast cancer cells reduced cell invasion by 51.4 ± 1.7%, accompanied by a morphological change to a rounded cell phenotype and down-regulation of vimentin, Snail, Twist, MMP2, and MMP9. We observed a reduction of the pool of CD44(+)/CD24(-) and ALDH1 high breast cancer stem cells by threefold and twofold, respectively, and a reduction by 2.6-fold of the mammospheres formation. Nicastrin overexpression in nontransformed MCF10A cells caused an induction of epithelial to mesenchymal regulators, as well as a fivefold increased ALDH1 activity, a threefold enrichment for CD44(+)/CD24(-) stem cells, and a 3.2-fold enhanced mammosphere-forming capacity. Using the γ-sescretase inhibiton, Notch1/4 siRNA, and Akt inhibition, we show that nicastrin regulates breast cancer stem cells partly through Notch1 and the Akt pathway. Exploiting serial dilution transplantation of the HCC1806 cells expressing nicastrin and HCC1806 stably depleted of nicastrin, in vivo, we demonstrate that nicastrin inhibition may be relevant for the reduced tumorigenicity of breast cancer cells. These data could serve as a benchmark for development of nicastrin-targeted therapies in breast cancer.
    MeSH term(s) Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Animals ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Culture Techniques ; Cell Line ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/genetics ; Transplantation, Heterologous ; Tumor Burden/genetics
    Chemical Substances Membrane Glycoproteins ; Receptors, Notch ; nicastrin protein ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
    Language English
    Publishing date 2012-09-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1206268109
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article: Nicastrin regulates breast cancer stem cell properties and tumor growth in vitro and in vivo

    Lombardo, Ylenia / Filipović, Aleksandra / Molyneux, Gemma / Periyasamy, Manikandan / Giamas, Georgios / Hu, Yunhui / Trivedi, Pritesh S. / Wang, Jayson / Yagüe, Ernesto / Michel, Loren / Coombes, R. Charles

    Proceedings of the National Academy of Sciences of the United States of America

    Volume v. 109,, Issue no. 4

    Abstract: Nicastrin (NCT) is a crucial component of the γ-secretase (GS) enzyme, which prompted investigations into its biological role in cancer. We have previously shown that nicastrin is overexpressed in breast cancer (BC), conferring worse overall survival in ... ...

    Abstract Nicastrin (NCT) is a crucial component of the γ-secretase (GS) enzyme, which prompted investigations into its biological role in cancer. We have previously shown that nicastrin is overexpressed in breast cancer (BC), conferring worse overall survival in invasive, ERα negative patients. Here, we used 2D and 3D Matrigel, anchorage-independent growth conditions and a breast cancer xenograft mouse model to assess the impact of nicastrin on breast cancer stem cell (BCSC) propagation and invasion in vitro and tumor growth in vivo. Stable knockdown of nicastrin in HCC1806 breast cancer cells reduced cell invasion by 51.4 ± 1.7%, accompanied by a morphological change to a rounded cell phenotype and down-regulation of vimentin, Snail, Twist, MMP2, and MMP9. We observed a reduction of the pool of CD44 ⁺/CD24 ⁻ and ALDH1 high breast cancer stem cells by threefold and twofold, respectively, and a reduction by 2.6-fold of the mammospheres formation. Nicastrin overexpression in nontransformed MCF10A cells caused an induction of epithelial to mesenchymal regulators, as well as a fivefold increased ALDH1 activity, a threefold enrichment for CD44 ⁺/CD24 ⁻ stem cells, and a 3.2-fold enhanced mammosphere-forming capacity. Using the γ-sescretase inhibiton, Notch1/4 siRNA, and Akt inhibition, we show that nicastrin regulates breast cancer stem cells partly through Notch1 and the Akt pathway. Exploiting serial dilution transplantation of the HCC1806 cells expressing nicastrin and HCC1806 stably depleted of nicastrin, in vivo, we demonstrate that nicastrin inhibition may be relevant for the reduced tumorigenicity of breast cancer cells. These data could serve as a benchmark for development of nicastrin-targeted therapies in breast cancer.
    Keywords patients ; stem cells ; cell invasion ; vimentin ; animal models ; phenotype ; small interfering RNA ; neoplasm cells ; gene expression regulation ; breast neoplasms
    Language English
    Document type Article
    ISSN 0027-8424
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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