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  1. Article: PPAR

    Glazer, Robert I

    PPAR research

    2016  Volume 2016, Page(s) 3082340

    Abstract: ... ...

    Abstract PPAR
    Language English
    Publishing date 2016-12-18
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 2237981-2
    ISSN 1687-4765 ; 1687-4757
    ISSN (online) 1687-4765
    ISSN 1687-4757
    DOI 10.1155/2016/3082340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book: Developments in cancer chemotherapy / 2

    Glazer, Robert I.

    1989  

    Author's details ed. Robert I. Glazer
    Collection Developments in cancer chemotherapy
    Size 200 S. : Ill., graph. Darst.
    Publisher CRC Pr
    Publishing place Boca Raton, Fla
    Publishing country United States
    Document type Book
    HBZ-ID HT003203882
    ISBN 0-8493-5770-5 ; 978-0-8493-5770-1
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1986 A 3734 -2- order for loan Magazin

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  3. Article ; Online: PPARs as determinants of the estrogen receptor lineage: use of synthetic lethality for the treatment of estrogen receptor-negative breast cancer.

    Glazer, Robert I / Kopelovich, Levy

    Oncotarget

    2017  Volume 8, Issue 31, Page(s) 50337–50341

    Abstract: The dilemma: Estrogen receptora-negative (ER-) breast cancer lacks a specific critical target to control tumor progression.: The objective: To identify mechanisms that enable increased expression of the ER+ lineage in an otherwise ER- breast cancer.!# ...

    Abstract The dilemma: Estrogen receptora-negative (ER-) breast cancer lacks a specific critical target to control tumor progression.
    The objective: To identify mechanisms that enable increased expression of the ER+ lineage in an otherwise ER- breast cancer.
    Preface: The nuclear receptor superfamily members PPARγ and PPARδ regulate gene expression associated with a multitude of pathways, including intermediary metabolism, angiogenesis, proliferation and inflammation (see reviews [1-3]). Recent developments using transgenic and knockout mice, as well as pharmacologic intervention with PPARγ and PPARδ agonists, have revealed a previously unknown relationship between PPARγ suppression and PPARδ activation that leads to the appearance of ER+ tumors, enabling a synthetic lethality approach by anti-ER therapy. The ability to selectively affect the ER+ lineage by modulating PPARγ and PPARδ activity represents a new clinical paradigm and opportunity to treat ER- cancer with PPARγ and PPARδ modulating agents, ultimately rendering them more responsive to adjuvant therapy.
    Language English
    Publishing date 2017-04-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.17302
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: PPARδ as a Metabolic Initiator of Mammary Neoplasia and Immune Tolerance

    Robert I. Glazer

    PPAR Research, Vol

    2016  Volume 2016

    Abstract: PPARδ is a ligand-activated nuclear receptor that regulates the transcription of genes associated with proliferation, metabolism, inflammation, and immunity. Within this transcription factor family, PPARδ is unique in that it initiates oncogenesis in a ... ...

    Abstract PPARδ is a ligand-activated nuclear receptor that regulates the transcription of genes associated with proliferation, metabolism, inflammation, and immunity. Within this transcription factor family, PPARδ is unique in that it initiates oncogenesis in a metabolic and tissue-specific context, especially in mammary epithelium, and can regulate autoimmunity in some tissues. This review discusses its role in these processes and how it ultimately impacts breast cancer.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: A new therapeutic basis for treating Li-Fraumeni Syndrome breast tumors expressing mutated TP53.

    Glazer, Robert I

    Oncotarget

    2011  Volume 1, Issue 7, Page(s) 470–471

    MeSH term(s) Apoptosis/genetics ; Apoptosis/physiology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Carcinoma/genetics ; Carcinoma/pathology ; Carcinoma/therapy ; Cell Line, Tumor ; Cell Survival/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Li-Fraumeni Syndrome/genetics ; Li-Fraumeni Syndrome/pathology ; Li-Fraumeni Syndrome/therapy ; Models, Biological ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Therapies, Investigational/methods ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Mutant Proteins ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2011-02-13
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.101008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Multicenter Validation of a T2-Weighted MRI Calculator to Differentiate Adrenal Adenoma From Adrenal Metastases.

    Tu, Wendy / Badawy, Mohamed / Carney, Benjamin W / Caoili, Elaine M / Corwin, Michael T / Elsayes, Khaled M / Mayo-Smith, William / Glazer, Daniel I / Bagga, Barun / Petrocelli, Robert / Taffel, Myles T / Schieda, Nicola

    AJR. American journal of roentgenology

    2023  Volume 222, Issue 1, Page(s) e2329727

    MeSH term(s) Humans ; Adrenocortical Adenoma ; Adrenal Gland Neoplasms/pathology ; Adenoma/pathology ; Magnetic Resonance Imaging ; Diagnosis, Differential
    Language English
    Publishing date 2023-08-09
    Publishing country United States
    Document type Multicenter Study ; Journal Article
    ZDB-ID 82076-3
    ISSN 1546-3141 ; 0361-803X ; 0092-5381
    ISSN (online) 1546-3141
    ISSN 0361-803X ; 0092-5381
    DOI 10.2214/AJR.23.29727
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  7. Article ; Online: Resistance of MMTV-NeuT/ATTAC mice to anti-PD-1 immune checkpoint therapy is associated with macrophage infiltration and Wnt pathway expression.

    Yuan, Hongyan / Jin, Lu / Xiang, Handan / Bhattacharya, Anannya / Brandish, Philip E / Baltus, Gretchen / Tong, Alexander / Zhou, Changyan / Glazer, Robert I

    Oncotarget

    2022  Volume 13, Page(s) 1350–1358

    Abstract: One of the central challenges for cancer therapy is the identification of factors in the tumor microenvironment that increase tumor progression and immune tolerance. In breast cancer, fibrosis is a histopathologic criterion for invasive cancer and poor ... ...

    Abstract One of the central challenges for cancer therapy is the identification of factors in the tumor microenvironment that increase tumor progression and immune tolerance. In breast cancer, fibrosis is a histopathologic criterion for invasive cancer and poor survival that results from inflammatory factors and remodeling of the extracellular matrix to produce an immune tolerant microenvironment. To determine whether tolerance is associated with the immune checkpoint, Programmed Cell Death 1 (PD-1), NeuT/ATTAC mice, a conditional model of mammary fibrosis that we recently developed, were administered a murine-specific anti-PD-1 mAb related to pembrolizumab, and drug response was monitored by tumor development, imaging mass cytometry, immunohistochemistry and tumor gene expression by RNAseq. Tumor progression in NeuT/ATTAC mice was unaffected by weekly injection of anti-PD-1 over four months. Insensitivity to anti-PD-1 was associated with several processes, including increased tumor-associated macrophages (TAM), epithelial to mesenchymal transition (EMT), fibroblast proliferation, an enhanced extracellular matrix and the Wnt signaling pathway, including increased expression of Fzd5, Wnt5a, Vimentin, Mmp3, Col2a1 and Tgfβ1. These results suggest potential therapeutic avenues that may enhance PD-1 immune checkpoint sensitivity, including the use of tumor microenvironment targeted agents and Wnt pathway inhibitors.
    MeSH term(s) Mice ; Animals ; Wnt Signaling Pathway ; Epithelial-Mesenchymal Transition ; Neoplasms ; Antineoplastic Agents/pharmacology ; Macrophages ; Tumor Microenvironment ; Cell Line, Tumor
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2022-12-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.28330
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: MicroRNA analysis in maternal blood of pregnancies with preterm premature rupture of membranes reveals a distinct expression profile.

    Spiliopoulos, Michail / Haddad, Andrew / Al-Kouatly, Huda B / Haleema, Saeed / Paidas, Michael J / Iqbal, Sara N / Glazer, Robert I

    PloS one

    2022  Volume 17, Issue 11, Page(s) e0277098

    Abstract: Objective: To determine the expression profile of microRNAs in the peripheral blood of pregnant women with preterm premature rupture of membranes (PPROM) compared to that of healthy pregnant women.: Study design: This was a pilot study with case- ... ...

    Abstract Objective: To determine the expression profile of microRNAs in the peripheral blood of pregnant women with preterm premature rupture of membranes (PPROM) compared to that of healthy pregnant women.
    Study design: This was a pilot study with case-control design in pregnant patients enrolled between January 2017 and June 2019. Patients with healthy pregnancies and those affected by PPROM between 20- and 33+6 weeks of gestation were matched by gestational age and selected for inclusion to the study. Patients were excluded for multiple gestation and presence of a major obstetrical complication such as preeclampsia, diabetes, fetal growth restriction and stillbirth. A total of ten (n = 10) controls and ten (n = 10) patients with PPROM were enrolled in the study. Specimens were obtained before administration of betamethasone or intravenous antibiotics. MicroRNA expression was analyzed for 800 microRNAs in each sample using the NanoString nCounter Expression Assay. Differential expression was calculated after normalization and log2- transformation using the false discovery rate (FDR) method at an alpha level of 5%.
    Results: Demographic characteristics were similar between the two groups. Of the 800 miRNAs analyzed, 116 were differentially expressed after normalization. However, only four reached FDR-adjusted statistical significance. Pregnancies affected by PPROM were characterized by upregulation of miR-199a-5p, miR-130a-3p and miR-26a-5p and downregulation of miR-513b-5p (FDR adjusted p-values <0.05). The differentially expressed microRNAs participate in pathways associated with altered collagen and matrix metalloprotease expression in the extracellular matrix.
    Conclusion: Patients with PPROM have a distinct peripheral blood microRNA profile compared to healthy pregnancies as measured by the NanoString Expression Assay.
    MeSH term(s) Infant, Newborn ; Humans ; Pregnancy ; Female ; MicroRNAs/metabolism ; Pilot Projects ; Fetal Membranes, Premature Rupture/genetics ; Gestational Age ; Pregnancy, Multiple
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2022-11-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0277098
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  9. Article ; Online: Development and Validation of a Risk Model for Predicting Contrast-Associated Acute Kidney Injury in Patients With Cancer: Evaluation in Over 46,000 CT Examinations.

    Gupta, Shruti / Motwani, Shveta S / Seitter, Robert H / Wang, Wei / Mu, Yi / Chute, Donald F / Sise, Meghan E / Glazer, Daniel I / Rosner, Bernard A / Curhan, Gary C

    AJR. American journal of roentgenology

    2023  Volume 221, Issue 4, Page(s) 486–501

    Abstract: BACKGROUND. ...

    Abstract BACKGROUND.
    MeSH term(s) Male ; Adult ; Humans ; Female ; Middle Aged ; Aged ; Retrospective Studies ; Contrast Media/adverse effects ; Acute Kidney Injury/chemically induced ; Acute Kidney Injury/diagnostic imaging ; Acute Kidney Injury/epidemiology ; Risk Factors ; Renal Insufficiency, Chronic ; Neoplasms/complications ; Tomography, X-Ray Computed/adverse effects
    Chemical Substances Contrast Media
    Language English
    Publishing date 2023-05-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 82076-3
    ISSN 1546-3141 ; 0361-803X ; 0092-5381
    ISSN (online) 1546-3141
    ISSN 0361-803X ; 0092-5381
    DOI 10.2214/AJR.23.29139
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    In stock of ZB MED Cologne/Königswinter

    Ue I Zs.57: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  10. Book: Developments in cancer chemotherapy / [1]

    Glazer, Robert I.

    1984  

    Author's details ed. Robert I. Glazer
    Collection Developments in cancer chemotherapy
    Keywords Krebs ; Chemotherapie ; Cytostatikum ; Tumor
    Subject Carcinom ; Malignom ; Maligner Tumor ; Neoplasma ; Karzinom ; Bösartiger Tumor ; Krebserkrankung ; Blastom ; Geschwulst ; Neoplasie ; Zytostatikum ; Cancerotoxischer Stoff ; Carcinostatikum ; Krebsmittel ; Antineoplastikum ; Anticarcinogen ; Antikarzinogen ; Anticancerogen ; Antineoplastisches Mittel
    Size 290 S. : Ill., graph. Darst.
    Publisher CRC Pr
    Publishing place Boca Raton, Fla
    Publishing country United States
    Document type Book
    HBZ-ID HT003203875
    ISBN 0-8493-5778-0 ; 978-0-8493-5778-7
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1986 A 3734 -[1]- order for loan Magazin

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