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  1. AU="Stößer, Sandra"
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  1. Artikel ; Online: Role of Epigenetics for the Efficacy of Cisplatin.

    Lumpp, Tatjana / Stößer, Sandra / Fischer, Franziska / Hartwig, Andrea / Köberle, Beate

    International journal of molecular sciences

    2024  Band 25, Heft 2

    Abstract: The clinical utility of the chemotherapeutic agent cisplatin is restricted by cancer drug resistance, which is either intrinsic to the tumor or acquired during therapy. Epigenetics is increasingly recognized as a factor contributing to cisplatin ... ...

    Abstract The clinical utility of the chemotherapeutic agent cisplatin is restricted by cancer drug resistance, which is either intrinsic to the tumor or acquired during therapy. Epigenetics is increasingly recognized as a factor contributing to cisplatin resistance and hence influences drug efficacy and clinical outcomes. In particular, epigenetics regulates gene expression without changing the DNA sequence. Common types of epigenetic modifications linked to chemoresistance are DNA methylation, histone modification, and non-coding RNAs. This review provides an overview of the current findings of various epigenetic modifications related to cisplatin efficacy in cell lines in vitro and in clinical tumor samples. Furthermore, it discusses whether epigenetic alterations might be used as predictors of the platinum agent response in order to prevent avoidable side effects in patients with resistant malignancies. In addition, epigenetic targeting therapies are described as a possible strategy to render cancer cells more susceptible to platinum drugs.
    Mesh-Begriff(e) Humans ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Platinum ; Epigenesis, Genetic ; DNA Methylation ; Neoplasms/drug therapy ; Neoplasms/genetics
    Chemische Substanzen Cisplatin (Q20Q21Q62J) ; Platinum (49DFR088MY)
    Sprache Englisch
    Erscheinungsdatum 2024-01-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25021130
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Effect of Long-Term Low-Dose Arsenic Exposure on DNA Methylation and Gene Expression in Human Liver Cells.

    Stößer, Sandra / Lumpp, Tatjana / Fischer, Franziska / Gunesch, Sarah / Schumacher, Paul / Hartwig, Andrea

    International journal of molecular sciences

    2023  Band 24, Heft 20

    Abstract: Millions of people around the world are exposed to elevated levels of arsenic through food or drinking water. Epidemiological studies have linked chronic arsenic exposure to an increased risk of several cancers, cardiovascular disease, central nervous ... ...

    Abstract Millions of people around the world are exposed to elevated levels of arsenic through food or drinking water. Epidemiological studies have linked chronic arsenic exposure to an increased risk of several cancers, cardiovascular disease, central nervous system neuropathies, and genotoxic as well as immunotoxic effects. In addition to the induction of oxidative stress and inhibition of DNA repair processes, epigenetic effects, including altered DNA methylation patterns resulting in aberrant gene expression, may contribute to carcinogenicity. However, the underlying mechanisms by which chronic micromolar concentrations of arsenite affect the methylation status of DNA are not fully understood. In this study, human HepG2 hepatocarcinoma cells were treated with 0.5-10 μM sodium arsenite for 24 h, 10, or 20 days. During these periods, the effects on global DNA methylation, cell cycle phase distribution, and gene expression were investigated. While no impact on DNA methylation was seen after short-term exposure, global hypomethylation was observed at both long-term exposure periods, with concomitant induction of the DNA methyltransferase genes
    Mesh-Begriff(e) Humans ; DNA Methylation ; Arsenites/toxicity ; Arsenic/toxicity ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; Liver Neoplasms/genetics ; DNA/metabolism ; Gene Expression
    Chemische Substanzen arsenite (N5509X556J) ; Arsenites ; Arsenic (N712M78A8G) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2023-10-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242015238
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Arsenite Impairs BRCA1-Dependent DNA Double-Strand Break Repair, a Mechanism Potentially Contributing to Genomic Instability.

    Matthäus, Tizia / Stößer, Sandra / Seren, Hatice Yasemin / Haberland, Vivien M M / Hartwig, Andrea

    International journal of molecular sciences

    2023  Band 24, Heft 18

    Abstract: BRCA1 is a key player in maintaining genomic integrity with multiple functions in DNA damage response (DDR) mechanisms. Due to its thiol-rich zinc-complexing domain, the protein may also be a potential target for redox-active and/or thiol-reactive (semi) ... ...

    Abstract BRCA1 is a key player in maintaining genomic integrity with multiple functions in DNA damage response (DDR) mechanisms. Due to its thiol-rich zinc-complexing domain, the protein may also be a potential target for redox-active and/or thiol-reactive (semi)metal compounds. The latter includes trivalent inorganic arsenic, which is indirectly genotoxic via induction of oxidative stress and inhibition of DNA repair pathways. In the present study, we investigated the effect of NaAsO
    Mesh-Begriff(e) Humans ; DNA Breaks, Double-Stranded ; Arsenites/toxicity ; Arsenic ; DNA ; DNA Repair ; Genomic Instability ; BRCA1 Protein/genetics
    Chemische Substanzen arsenite (N5509X556J) ; Arsenites ; Arsenic (N712M78A8G) ; DNA (9007-49-2) ; BRCA1 protein, human ; BRCA1 Protein
    Sprache Englisch
    Erscheinungsdatum 2023-09-21
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241814395
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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