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  1. Article ; Online: Mitochondrial DNA mutations in ageing and cancer.

    Smith, Anna L M / Whitehall, Julia C / Greaves, Laura C

    Molecular oncology

    2022  Volume 16, Issue 18, Page(s) 3276–3294

    Abstract: Advancing age is a major risk factor for malignant transformation and the development of cancer. As such, over 50% of neoplasms occur in individuals over the age of 70. The pathologies of both ageing and cancer have been characterized by respective ... ...

    Abstract Advancing age is a major risk factor for malignant transformation and the development of cancer. As such, over 50% of neoplasms occur in individuals over the age of 70. The pathologies of both ageing and cancer have been characterized by respective groups of molecular hallmarks, and while some features are divergent between the two pathologies, several are shared. Perturbed mitochondrial function is one such common hallmark, and this observation therefore suggests that mitochondrial alterations may be of significance in age-related cancer development. There is now considerable evidence documenting the accumulation of somatic mitochondrial DNA (mtDNA) mutations in ageing human postmitotic and replicative tissues. Similarly, mutations of the mitochondrial genome have been reported in human cancers for decades. The plethora of functions in which mitochondria partake, such as oxidative phosphorylation, redox balance, apoptosis and numerous biosynthetic pathways, manifests a variety of ways in which alterations in mtDNA may contribute to tumour growth. However, the specific mechanisms by which mtDNA mutations contribute to tumour progression remain elusive and often contradictory. This review aims to consolidate current knowledge and describe future direction within the field.
    MeSH term(s) Aging/genetics ; Aging/metabolism ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Humans ; Mitochondria/metabolism ; Mutation/genetics ; Neoplasms/pathology
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2022-07-28
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.13291
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6637: Show issues Location:
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  2. Article ; Online: Aberrant mitochondrial function in ageing and cancer.

    Whitehall, Julia C / Greaves, Laura C

    Biogerontology

    2019  Volume 21, Issue 4, Page(s) 445–459

    Abstract: Alterations in mitochondrial metabolism have been described as one of the major hallmarks of both ageing cells and cancer. Age is the biggest risk factor for the development of a significant number of cancer types and this therefore raises the question ... ...

    Abstract Alterations in mitochondrial metabolism have been described as one of the major hallmarks of both ageing cells and cancer. Age is the biggest risk factor for the development of a significant number of cancer types and this therefore raises the question of whether there is a link between age-related mitochondrial dysfunction and the advantageous changes in mitochondrial metabolism prevalent in cancer cells. A common underlying feature of both ageing and cancer cells is the presence of somatic mutations of the mitochondrial genome (mtDNA) which we postulate may drive compensatory alterations in mitochondrial metabolism that are advantageous for tumour growth. In this review, we discuss basic mitochondrial functions, mechanisms of mtDNA mutagenesis and their metabolic consequences, and review the evidence for and against a role for mtDNA mutations in cancer development.
    MeSH term(s) Aging/pathology ; Cellular Senescence ; DNA, Mitochondrial/genetics ; Humans ; Mitochondria/genetics ; Mitochondria/pathology ; Mutation ; Neoplasms/pathology
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2019-12-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2047160-9
    ISSN 1573-6768 ; 1389-5729
    ISSN (online) 1573-6768
    ISSN 1389-5729
    DOI 10.1007/s10522-019-09853-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5706: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Mitochondrial complex I subunit deficiency promotes pancreatic α-cell proliferation.

    Yu, Xuefei / Arden, Catherine / Berlinguer-Palmini, Rolando / Chen, Chun / Bradshaw, Carla / Smith, Anna Lm / Whitehall, Julia / White, Michael / Anderson, Scott / Kattner, Nicole / Shaw, James / Turnbull, Doug / Greaves, Laura C / Walker, Mark

    Molecular metabolism

    2022  Volume 60, Page(s) 101489

    Abstract: Objective: There is strong evidence that mitochondrial DNA mutations and mitochondrial dysfunction play a role in diabetes pathogenesis. The homozygous knock-in mtDNA mutator mouse is a model of premature aging due to the accumulation of mitochondrial ... ...

    Abstract Objective: There is strong evidence that mitochondrial DNA mutations and mitochondrial dysfunction play a role in diabetes pathogenesis. The homozygous knock-in mtDNA mutator mouse is a model of premature aging due to the accumulation of mitochondrial DNA mutations. We used this mouse model to investigate the relationship between mitochondrial subunit expression and pancreatic islet cell composition.
    Methods: Quadruple immunofluorescence was used to quantify mitochondrial subunit expression (complex I and IV) and cell composition in pancreatic islets from mitochondrial DNA mutator mice (PolgA
    Results: Mitochondrial complex I subunit expression was decreased in islets from 12 week PolgA
    Conclusion: Complex I deficiency promotes α-cell proliferation and alters islet cell composition.
    MeSH term(s) Animals ; Cell Proliferation ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Electron Transport Complex I/deficiency ; Mice ; Mice, Inbred C57BL ; Mitochondrial Diseases
    Chemical Substances DNA, Mitochondrial ; Electron Transport Complex I (EC 7.1.1.2)
    Language English
    Publishing date 2022-04-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2022.101489
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Age-associated mitochondrial complex I deficiency is linked to increased stem cell proliferation rates in the mouse colon.

    Stamp, Craig / Whitehall, Julia C / Smith, Anna L M / Houghton, David / Bradshaw, Carla / Stoll, Elizabeth A / Blain, Alasdair P / Turnbull, Doug M / Greaves, Laura C

    Aging cell

    2021  Volume 20, Issue 3, Page(s) e13321

    Abstract: One of the hallmarks of aging is an accumulation of cells with defects in oxidative phosphorylation (OXPHOS) due to mutations of mitochondrial DNA (mtDNA). Rapidly dividing tissues maintained by stem cells, such as the colonic epithelium, are ... ...

    Abstract One of the hallmarks of aging is an accumulation of cells with defects in oxidative phosphorylation (OXPHOS) due to mutations of mitochondrial DNA (mtDNA). Rapidly dividing tissues maintained by stem cells, such as the colonic epithelium, are particularly susceptible to accumulation of OXPHOS defects over time; however, the effects on the stem cells are unknown. We have crossed a mouse model in which intestinal stem cells are labelled with EGFP (Lgr5-EGFP-IRES-creERT2) with a model of accelerated mtDNA mutagenesis (PolgA
    MeSH term(s) Aging/pathology ; Animals ; Cell Proliferation ; Colon/pathology ; Electron Transport Complex I/deficiency ; Female ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Mitochondrial Diseases/pathology ; Oxidative Phosphorylation ; Stem Cells/pathology ; Thymidine/metabolism ; Mice
    Chemical Substances Electron Transport Complex I (EC 7.1.1.2) ; Thymidine (VC2W18DGKR)
    Language English
    Publishing date 2021-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13321
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6581: Show issues Location:
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  5. Article ; Online: Author Correction: Age-associated mitochondrial DNA mutations cause metabolic remodeling that contributes to accelerated intestinal tumorigenesis.

    Smith, Anna L M / Whitehall, Julia C / Bradshaw, Carla / Gay, David / Robertson, Fiona / Blain, Alasdair P / Hudson, Gavin / Pyle, Angela / Houghton, David / Hunt, Matthew / Sampson, James N / Stamp, Craig / Mallett, Grace / Amarnath, Shoba / Leslie, Jack / Oakley, Fiona / Wilson, Laura / Baker, Angela / Russell, Oliver M /
    Johnson, Riem / Richardson, Claire A / Gupta, Bhavana / McCallum, Iain / McDonald, Stuart A C / Kelly, Seamus / Mathers, John C / Heer, Rakesh / Taylor, Robert W / Perkins, Neil D / Turnbull, Doug M / Sansom, Owen J / Greaves, Laura C

    Nature cancer

    2022  Volume 2, Issue 1, Page(s) 129

    Language English
    Publishing date 2022-02-04
    Publishing country England
    Document type Published Erratum
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-020-00156-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: A Bioreactor Technology for Modeling Fibrosis in Human and Rodent Precision-Cut Liver Slices.

    Paish, Hannah L / Reed, Lee H / Brown, Helen / Bryan, Mark C / Govaere, Olivier / Leslie, Jack / Barksby, Ben S / Garcia Macia, Marina / Watson, Abigail / Xu, Xin / Zaki, Marco Y W / Greaves, Laura / Whitehall, Julia / French, Jeremy / White, Steven A / Manas, Derek M / Robinson, Stuart M / Spoletini, Gabriele / Griffiths, Clive /
    Mann, Derek A / Borthwick, Lee A / Drinnan, Michael J / Mann, Jelena / Oakley, Fiona

    Hepatology (Baltimore, Md.)

    2019  Volume 70, Issue 4, Page(s) 1377–1391

    Abstract: Precision cut liver slices (PCLSs) retain the structure and cellular composition of the native liver and represent an improved system to study liver fibrosis compared to two-dimensional mono- or co-cultures. The aim of this study was to develop a ... ...

    Abstract Precision cut liver slices (PCLSs) retain the structure and cellular composition of the native liver and represent an improved system to study liver fibrosis compared to two-dimensional mono- or co-cultures. The aim of this study was to develop a bioreactor system to increase the healthy life span of PCLSs and model fibrogenesis. PCLSs were generated from normal rat or human liver, or fibrotic rat liver, and cultured in our bioreactor. PCLS function was quantified by albumin enzyme-linked immunosorbent assay (ELISA). Fibrosis was induced in PCLSs by transforming growth factor beta 1 (TGFβ1) and platelet-derived growth factor (PDGFββ) stimulation ± therapy. Fibrosis was assessed by gene expression, picrosirius red, and α-smooth muscle actin staining, hydroxyproline assay, and soluble ELISAs. Bioreactor-cultured PCLSs are viable, maintaining tissue structure, metabolic activity, and stable albumin secretion for up to 6 days under normoxic culture conditions. Conversely, standard static transwell-cultured PCLSs rapidly deteriorate, and albumin secretion is significantly impaired by 48 hours. TGFβ1/PDGFββ stimulation of rat or human PCLSs induced fibrogenic gene expression, release of extracellular matrix proteins, activation of hepatic myofibroblasts, and histological fibrosis. Fibrogenesis slowly progresses over 6 days in cultured fibrotic rat PCLSs without exogenous challenge. Activin receptor-like kinase 5 (Alk5) inhibitor (Alk5i), nintedanib, and obeticholic acid therapy limited fibrogenesis in TGFβ1/PDGFββ-stimulated PCLSs, and Alk5i blunted progression of fibrosis in fibrotic PCLS. Conclusion: We describe a bioreactor technology that maintains functional PCLS cultures for 6 days. Bioreactor-cultured PCLSs can be successfully used to model fibrogenesis and demonstrate efficacy of antifibrotic therapies.
    MeSH term(s) Animals ; Biopsy, Needle ; Bioreactors ; Coculture Techniques/methods ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sensitivity and Specificity ; Time Factors ; Tissue Culture Techniques/methods
    Language English
    Publishing date 2019-05-28
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30651
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: 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)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Age-associated mitochondrial DNA mutations cause metabolic remodelling that contributes to accelerated intestinal tumorigenesis.

    Smith, Anna Lm / Whitehall, Julia C / Bradshaw, Carla / Gay, David / Robertson, Fiona / Blain, Alasdair P / Hudson, Gavin / Pyle, Angela / Houghton, David / Hunt, Matthew / Sampson, James N / Stamp, Craig / Mallett, Grace / Amarnath, Shoba / Leslie, Jack / Oakley, Fiona / Wilson, Laura / Baker, Angela / Russell, Oliver M /
    Johnson, Riem / Richardson, Claire A / Gupta, Bhavana / McCallum, Iain / McDonald, Stuart Ac / Kelly, Seamus / Mathers, John C / Heer, Rakesh / Taylor, Robert W / Perkins, Neil D / Turnbull, Doug M / Sansom, Owen J / Greaves, Laura C

    Nature cancer

    2020  Volume 1, Issue 10, Page(s) 976–989

    Abstract: Oxidative phosphorylation (OXPHOS) defects caused by somatic mitochondrial DNA (mtDNA) mutations increase with age in human colorectal epithelium and are prevalent in colorectal tumours, but whether they actively contribute to tumorigenesis remains ... ...

    Abstract Oxidative phosphorylation (OXPHOS) defects caused by somatic mitochondrial DNA (mtDNA) mutations increase with age in human colorectal epithelium and are prevalent in colorectal tumours, but whether they actively contribute to tumorigenesis remains unknown. Here we demonstrate that mtDNA mutations causing OXPHOS defects are enriched during the human adenoma/carcinoma sequence, suggesting they may confer a metabolic advantage. To test this we deleted the tumour suppressor Apc in OXPHOS deficient intestinal stem cells in mice. The resulting tumours were larger than in control mice due to accelerated cell proliferation and reduced apoptosis. We show that both normal crypts and tumours undergo metabolic remodelling in response to OXPHOS deficiency by upregulating the
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; DNA, Mitochondrial/genetics ; Intestinal Neoplasms/genetics ; Mice ; Mitochondria/genetics ; Mitochondrial Diseases ; Mutation
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2020-09-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-020-00112-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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