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  1. Article: Omentum and bone marrow: how adipocyte‐rich organs create tumour microenvironments conducive for metastatic progression

    Chkourko Gusky, H / Diedrich, J / MacDougald, O. A / Podgorski, I

    Obesity reviews. 2016 Nov., v. 17, no. 11

    2016  

    Abstract: A number of clinical studies have linked adiposity with increased cancer incidence, progression and metastasis, and adipose tissue is now being credited with both systemic and local effects on tumour development and survival. Adipocytes, a major ... ...

    Abstract A number of clinical studies have linked adiposity with increased cancer incidence, progression and metastasis, and adipose tissue is now being credited with both systemic and local effects on tumour development and survival. Adipocytes, a major component of benign adipose tissue, represent a significant source of lipids, cytokines and adipokines, and their presence in the tumour microenvironment substantially affects cellular trafficking, signalling and metabolism. Cancers that have a high predisposition to metastasize to the adipocyte‐rich host organs are likely to be particularly affected by the presence of adipocytes. Although our understanding of how adipocytes influence tumour progression has grown significantly over the last several years, the mechanisms by which adipocytes regulate the metastatic niche are not well‐understood. In this review, we focus on the omentum, a visceral white adipose tissue depot, and the bone, a depot for marrow adipose tissue, as two distinct adipocyte‐rich organs that share common characteristic: they are both sites of significant metastatic growth. We highlight major differences in origin and function of each of these adipose depots and reveal potential common characteristics that make them environments that are attractive and conducive to secondary tumour growth. Special attention is given to how omental and marrow adipocytes modulate the tumour microenvironment by promoting angiogenesis, affecting immune cells and altering metabolism to support growth and survival of metastatic cancer cells.
    Keywords adipocytes ; adipokines ; adiposity ; angiogenesis ; bone marrow ; clinical trials ; cytokines ; lipids ; metabolism ; metastasis ; neoplasm cells ; neoplasms ; omentum ; white adipose tissue
    Language English
    Dates of publication 2016-11
    Size p. 1015-1029.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note REVIEW
    ZDB-ID 2147980-X
    ISSN 1467-789X ; 1467-7881
    ISSN (online) 1467-789X
    ISSN 1467-7881
    DOI 10.1111/obr.12450
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5908: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Omentum and bone marrow: how adipocyte-rich organs create tumour microenvironments conducive for metastatic progression.

    Chkourko Gusky, H / Diedrich, J / MacDougald, O A / Podgorski, I

    Obesity reviews : an official journal of the International Association for the Study of Obesity

    2016  Volume 17, Issue 11, Page(s) 1015–1029

    Abstract: A number of clinical studies have linked adiposity with increased cancer incidence, progression and metastasis, and adipose tissue is now being credited with both systemic and local effects on tumour development and survival. Adipocytes, a major ... ...

    Abstract A number of clinical studies have linked adiposity with increased cancer incidence, progression and metastasis, and adipose tissue is now being credited with both systemic and local effects on tumour development and survival. Adipocytes, a major component of benign adipose tissue, represent a significant source of lipids, cytokines and adipokines, and their presence in the tumour microenvironment substantially affects cellular trafficking, signalling and metabolism. Cancers that have a high predisposition to metastasize to the adipocyte-rich host organs are likely to be particularly affected by the presence of adipocytes. Although our understanding of how adipocytes influence tumour progression has grown significantly over the last several years, the mechanisms by which adipocytes regulate the metastatic niche are not well-understood. In this review, we focus on the omentum, a visceral white adipose tissue depot, and the bone, a depot for marrow adipose tissue, as two distinct adipocyte-rich organs that share common characteristic: they are both sites of significant metastatic growth. We highlight major differences in origin and function of each of these adipose depots and reveal potential common characteristics that make them environments that are attractive and conducive to secondary tumour growth. Special attention is given to how omental and marrow adipocytes modulate the tumour microenvironment by promoting angiogenesis, affecting immune cells and altering metabolism to support growth and survival of metastatic cancer cells.
    MeSH term(s) Adipocytes/metabolism ; Adipocytes/physiology ; Adipose Tissue, White/pathology ; Bone Marrow/pathology ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/pathology ; Disease Progression ; Humans ; Neoplasm Metastasis ; Neoplasms/immunology ; Neoplasms/pathology ; Obesity/complications ; Obesity/immunology ; Obesity/pathology ; Omentum/pathology ; Tumor Microenvironment/immunology ; Tumor Microenvironment/physiology
    Language English
    Publishing date 2016-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2147980-X
    ISSN 1467-789X ; 1467-7881
    ISSN (online) 1467-789X
    ISSN 1467-7881
    DOI 10.1111/obr.12450
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5908: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Missense mutations in plakophilin-2 cause sodium current deficit and associate with a Brugada syndrome phenotype.

    Cerrone, Marina / Lin, Xianming / Zhang, Mingliang / Agullo-Pascual, Esperanza / Pfenniger, Anna / Chkourko Gusky, Halina / Novelli, Valeria / Kim, Changsung / Tirasawadichai, Tiara / Judge, Daniel P / Rothenberg, Eli / Chen, Huei-Sheng Vincent / Napolitano, Carlo / Priori, Silvia G / Delmar, Mario

    Circulation

    2013  Volume 129, Issue 10, Page(s) 1092–1103

    Abstract: Background: Brugada syndrome (BrS) primarily associates with the loss of sodium channel function. Previous studies showed features consistent with sodium current (INa) deficit in patients carrying desmosomal mutations, diagnosed with arrhythmogenic ... ...

    Abstract Background: Brugada syndrome (BrS) primarily associates with the loss of sodium channel function. Previous studies showed features consistent with sodium current (INa) deficit in patients carrying desmosomal mutations, diagnosed with arrhythmogenic cardiomyopathy (or arrhythmogenic right ventricular cardiomyopathy). Experimental models showed correlation between the loss of expression of desmosomal protein plakophilin-2 (PKP2) and reduced INa. We hypothesized that PKP2 variants that reduce INa could yield a BrS phenotype, even without overt structural features characteristic of arrhythmogenic right ventricular cardiomyopathy.
    Methods and results: We searched for PKP2 variants in the genomic DNA of 200 patients with a BrS diagnosis, no signs of arrhythmogenic cardiomyopathy, and no mutations in BrS-related genes SCN5A, CACNa1c, GPD1L, and MOG1. We identified 5 cases of single amino acid substitutions. Mutations were tested in HL-1-derived cells endogenously expressing NaV1.5 but made deficient in PKP2 (PKP2-KD). Loss of PKP2 caused decreased INa and NaV1.5 at the site of cell contact. These deficits were restored by the transfection of wild-type PKP2, but not of BrS-related PKP2 mutants. Human induced pluripotent stem cell cardiomyocytes from a patient with a PKP2 deficit showed drastically reduced INa. The deficit was restored by transfection of wild type, but not BrS-related PKP2. Super-resolution microscopy in murine PKP2-deficient cardiomyocytes related INa deficiency to the reduced number of channels at the intercalated disc and increased separation of microtubules from the cell end.
    Conclusions: This is the first systematic retrospective analysis of a patient group to define the coexistence of sodium channelopathy and genetic PKP2 variations. PKP2 mutations may be a molecular substrate leading to the diagnosis of BrS.
    MeSH term(s) Adult ; Animals ; Brugada Syndrome/genetics ; Brugada Syndrome/metabolism ; Brugada Syndrome/physiopathology ; Cell Line ; Disease Models, Animal ; Female ; Genotype ; Heart Conduction System/physiopathology ; Humans ; Male ; Mice ; Mice, Mutant Strains ; Middle Aged ; Mutation, Missense ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; NAV1.5 Voltage-Gated Sodium Channel/metabolism ; Patch-Clamp Techniques ; Pedigree ; Phenotype ; Plakophilins/genetics ; Retrospective Studies ; Sodium Channels/deficiency ; Sodium Channels/metabolism
    Chemical Substances NAV1.5 Voltage-Gated Sodium Channel ; PKP2 protein, human ; Pkp2 protein, mouse ; Plakophilins ; Scn5a protein, mouse ; Sodium Channels
    Language English
    Publishing date 2013-12-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.113.003077
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.60: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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