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    DNA Damage as Target for Therapeutic Intervention

    Submission Deadline: June 10, 2023

    Guest Editor

    Prof. Thomas Efferth E-Mail

    Director, Institute of Pharmaceutical and Biomedical Sciences, Johannes-Gutenberg University of Mainz, Mainz, Germany


    About the Special Issue

    DNA damage is an ever-present challenge to all forms of life on earth and DNA repair is of fundamental importance to maintain the integrity of the genetic material. From endogenous and exogenous DNA damaging agents. Thus, it comes as no surprise that all organisms from pro- to eukaryotes have developed very efficient repair mechanisms during evolution of life of life on earth (e.g., direct lesion reversal, single-strand repair, double-strand repair, translesion synthesis). Nevertheless, DNA damage occur as rare event in the body and contributes to malignancies as initial step in tumorigenesis. DNA-damaging chemotherapeutics and radiotherapy belong to the standard armamentarium of cancer therapy. In the context of a tumor cells, the DNA repair machinery does not contribute to the health maintenance of the body but, by contrast, to resistance to DNA-damaging drugs and eventually to failure of chemotherapy and the death of cancer patients. While numerous compounds have been described in the past to inhibit DNA repair in tumor cells in an attempt to re-sensitize tumor cells to chemo- and radiotherapy. In the recent years, there has been a paradigm change from cytotoxic to targeted treatment to improve the efficacy and specificity of tumor therapy. In this context, DNA recognition and repair proteins gained much attention as exquisite targets for cancer therapy.
    With the current special issue, we provide a forum to open an interdisciplinary discussion for scientists and clinicians from diverse disciplines to present innovative and thriving concepts how current cancer treatment could benefit from targeting DNA damage and repair. We welcome manuscript from diverse fields such as pharmacology (of synthetic and natural compounds), medicinal chemistry, cell and molecular biology, systems and network pharmacology, and all related disciplines in medicine dealing with DNA damage as target for therapeutic intervention.
    The aim is to provide a comprehensive overview of the current understanding and span a bow from basic to translational and clinical aspects. This special issue should enable the reader to gain the fundamental knowledge of current cutting-edge research.

    Keywords: Cell biology; DNA repair mechanisms; targeted chemo- and radiotherapy; medicinal chemistry; molecular biology; pharmacology; radiotherapy; oncology

    Call for Papers

    Published Articles

    Open Access
    Original Article
    Aflatoxin B1-DNA adducts modify the effects of post-operative adjuvant transarterial chemoembolization improving hepatocellular carcinoma prognosis
    Aim: DNA damage involves in the carcinogenesis of some cancer and may act as a target for therapeutic intervention of cancers. However, it is unclear whether aflatoxin B1 (AFB1)-DNA adducts (ADAs) [...] Read more.

    Aim:

    DNA damage involves in the carcinogenesis of some cancer and may act as a target for therapeutic intervention of cancers. However, it is unclear whether aflatoxin B1 (AFB1)-DNA adducts (ADAs), an important kind of DNA damage caused by AFB1, affect the efficiency of post-operative adjuvant transarterial chemoembolization (po-TACE) treatment improving hepatocellular carcinoma (HCC) survival.

    Methods:

    A hospital-based retrospective study, including 318 patients with Barcelona Clinic Liver Cancer (BCLC)-C stage HCC from high AFB1 exposure areas, to investigate the potential effects of ADAs in the tissues with HCC on po-TACE treatment. The amount of ADAs in the cancerous tissues was tested by competitive enzyme-linked immunosorbent assay (c-ELISA).

    Results:

    Among these patients with HCC, the average amount of ADAs was 3.00 µmol/mol ± 1.51 µmol/mol DNA in their tissues with cancer. For these patients, increasing amount of ADAs was significantly associated with poorer overall survival (OS) and tumor reoccurrence-free survival (RFS), with corresponding death risk (DR) of 3.69 (2.78–4.91) and tumor recurrence risk (TRR) of 2.95 (2.24–3.88). The po-TACE therapy can efficiently improve their prognosis [DR = 0.59 (0.46–0.76), TRR = 0.63 (0.49–0.82)]. Interestingly, this improving role was more noticeable among these patients with high ADAs [DR = 0.36 (0.24–0.53), TRR = 0.40 (0.28–0.59)], but not among those with low ADAs (P > 0.05).

    Conclusions:

    These results suggest that increasing ADAs in the cancerous tissues may be beneficial for po-TACE in ameliorating the survival of patients with HCC.

    Liyan Huang ... Xidai Long
    Published: August 31, 2023 Explor Target Antitumor Ther. 2023;4:780–792
    DOI: https://doi.org/10.37349/etat.2023.00167
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    Aim:

    DNA damage involves in the carcinogenesis of some cancer and may act as a target for therapeutic intervention of cancers. However, it is unclear whether aflatoxin B1 (AFB1)-DNA adducts (ADAs), an important kind of DNA damage caused by AFB1, affect the efficiency of post-operative adjuvant transarterial chemoembolization (po-TACE) treatment improving hepatocellular carcinoma (HCC) survival.

    Methods:

    A hospital-based retrospective study, including 318 patients with Barcelona Clinic Liver Cancer (BCLC)-C stage HCC from high AFB1 exposure areas, to investigate the potential effects of ADAs in the tissues with HCC on po-TACE treatment. The amount of ADAs in the cancerous tissues was tested by competitive enzyme-linked immunosorbent assay (c-ELISA).

    Results:

    Among these patients with HCC, the average amount of ADAs was 3.00 µmol/mol ± 1.51 µmol/mol DNA in their tissues with cancer. For these patients, increasing amount of ADAs was significantly associated with poorer overall survival (OS) and tumor reoccurrence-free survival (RFS), with corresponding death risk (DR) of 3.69 (2.78–4.91) and tumor recurrence risk (TRR) of 2.95 (2.24–3.88). The po-TACE therapy can efficiently improve their prognosis [DR = 0.59 (0.46–0.76), TRR = 0.63 (0.49–0.82)]. Interestingly, this improving role was more noticeable among these patients with high ADAs [DR = 0.36 (0.24–0.53), TRR = 0.40 (0.28–0.59)], but not among those with low ADAs (P > 0.05).

    Conclusions:

    These results suggest that increasing ADAs in the cancerous tissues may be beneficial for po-TACE in ameliorating the survival of patients with HCC.

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