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  1. Article ; Online: Pancreatic cancer patients with germline BRCA mutations can benefit from olaparib treatment.

    Mukherjee, Shibani / Asaithamby, Aroumougame

    Translational cancer research

    2022  Volume 9, Issue 4, Page(s) 2154–2156

    Language English
    Publishing date 2022-01-15
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2901601-0
    ISSN 2219-6803 ; 2218-676X
    ISSN (online) 2219-6803
    ISSN 2218-676X
    DOI 10.21037/tcr.2020.03.07
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  2. Article: Cellular senescence and lung cancer prognosis.

    Asaithamby, Aroumougame / Shay, Jerry W / Minna, John D

    Translational lung cancer research

    2022  Volume 11, Issue 10, Page(s) 1982–1987

    Language English
    Publishing date 2022-11-07
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2754335-3
    ISSN 2226-4477 ; 2218-6751
    ISSN (online) 2226-4477
    ISSN 2218-6751
    DOI 10.21037/tlcr-22-678
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  3. Article ; Online: Nuclear Foci Assays in Live Cells.

    Mori, Eiichiro / Asaithamby, Aroumougame

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 1984, Page(s) 75–85

    Abstract: DNA double strand breaks (DSBs) are a serious threat to genome stability and cell viability. Accurate detection of DSBs is critical for the basic understanding of cellular response to ionizing radiation. Recruitment and retention of DNA repair and ... ...

    Abstract DNA double strand breaks (DSBs) are a serious threat to genome stability and cell viability. Accurate detection of DSBs is critical for the basic understanding of cellular response to ionizing radiation. Recruitment and retention of DNA repair and response proteins at DSBs can be conveniently visualized by fluorescence imaging (often called ionizing radiation-induced foci) both in live and fixed cells. In this chapter, we describe a live cell imaging methodology that directly monitors induction and repair of single DSB, recruitment kinetics of DSB repair/sensor factors to DSB sites, and dynamic interaction of DSB repair/sensor proteins with DSBs at single-cell level. Additionally, the methodology described in this chapter can be readily adapted to other DSBs repair/sensor factors and cell types.
    MeSH term(s) Biological Assay/methods ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Survival ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA Repair ; Fluorescence Recovery After Photobleaching ; Humans ; Kinetics ; Tumor Suppressor p53-Binding Protein 1/metabolism
    Chemical Substances Tumor Suppressor p53-Binding Protein 1
    Language English
    Publishing date 2019-07-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9432-8_9
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  4. Article: Repurposing DNA repair factors to eradicate tumor cells upon radiotherapy.

    Bhattacharya, Souparno / Asaithamby, Aroumougame

    Translational cancer research

    2018  Volume 6, Issue Suppl 5, Page(s) S822–S839

    Abstract: Cancer is the leading cause of death worldwide. Almost 50% of all cancer patients undergo radiation therapy (RT) during treatment, with varying success. The main goal of RT is to kill tumor cells by damaging their DNA irreversibly while sparing the ... ...

    Abstract Cancer is the leading cause of death worldwide. Almost 50% of all cancer patients undergo radiation therapy (RT) during treatment, with varying success. The main goal of RT is to kill tumor cells by damaging their DNA irreversibly while sparing the surrounding normal tissue. The outcome of RT is often determined by how tumors recognize and repair their damaged DNA. A growing body of evidence suggests that tumors often show abnormal expression of DNA double-strand break (DSB) repair genes that are absent from normal cells. Defects in a specific DNA repair pathway make tumor cells overly dependent on alternative or backup pathways to repair their damaged DNA. These tumor cell-specific abnormalities in the DNA damage response (DDR) machinery can potentially be used as biomarkers for treatment outcomes or as targets for sensitization to ionizing radiation (IR). An improved understanding of genetic or epigenetic alterations in the DNA repair pathways specific to cancer cells has paved the way for new treatments that combine pharmacological exploitation of tumor-specific molecular vulnerabilities with IR. Inhibiting DNA repair pathways has the potential to greatly enhance the therapeutic ratio of RT. In this review, we will discuss DNA repair pathways in active cells and how these pathways are deregulated in tumors. We will also describe the impact of targeting cancer-specific aberrations in the DDR as a treatment strategy to improve the efficacy of RT. Finally, we will address the current roadblocks and future prospects of these approaches.
    Language English
    Publishing date 2018-12-20
    Publishing country China
    Document type Journal Article
    ZDB-ID 2901601-0
    ISSN 2219-6803 ; 2218-676X
    ISSN (online) 2219-6803
    ISSN 2218-676X
    DOI 10.21037/tcr.2017.05.22
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  5. Article ; Online: Tumor treating fields cause replication stress and interfere with DNA replication fork maintenance: Implications for cancer therapy.

    Karanam, Narasimha Kumar / Ding, Lianghao / Aroumougame, Asaithamby / Story, Michael D

    Translational research : the journal of laboratory and clinical medicine

    2019  Volume 217, Page(s) 33–46

    Abstract: Tumor treating fields (TTFields) is a noninvasive physical modality of cancer therapy that applies low-intensity, intermediate frequency, and alternating electric fields to a tumor. Interference with mitosis was the first mechanism describing the effects ...

    Abstract Tumor treating fields (TTFields) is a noninvasive physical modality of cancer therapy that applies low-intensity, intermediate frequency, and alternating electric fields to a tumor. Interference with mitosis was the first mechanism describing the effects of TTFields on cancer cells; however, TTFields was shown to not only reduce the rejoining of radiation-induced DNA double-strand breaks (DSBs), but to also induce DNA DSBs. The mechanism(s) by which TTFields generates DNA DSBs is related to the generation of replication stress including reduced expression of the DNA replication complex genes MCM6 and MCM10 and the Fanconi's Anemia pathway genes. When markers of DNA replication stress as a result of TTFields exposure were examined, newly replicated DNA length was reduced with TTFields exposure time and there was increased R-loop formation. Furthermore, as cells were exposed to TTFields a conditional vulnerability environment developed which rendered cells more susceptible to DNA damaging agents or agents that interfere with DNA repair or replication fork maintenance. The effect of TTFields exposure with concomitant exposure to cisplatin or PARP inhibition, the combination of TTFields plus concomitant PARP inhibition followed by radiation, or radiation alone at the end of a TTFields exposure were all synergistic. Finally, gene expression analysis of 47 key mitosis regulator genes suggested that TTFields-induced mitotic aberrations and DNA damage/replication stress events, although intimately linked to one another, are likely initiated independently of one another. This suggests that enhanced replication stress and reduced DNA repair capacity are also major mechanisms of TTFields effects, effects for which there are therapeutic implications.
    MeSH term(s) Cell Line, Tumor ; Cisplatin/pharmacology ; DNA Damage ; DNA Replication ; Electric Stimulation Therapy/methods ; Humans ; Neoplasms/genetics ; Neoplasms/therapy ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerases
    Chemical Substances Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2019-10-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2246684-8
    ISSN 1878-1810 ; 1532-6543 ; 1931-5244
    ISSN (online) 1878-1810 ; 1532-6543
    ISSN 1931-5244
    DOI 10.1016/j.trsl.2019.10.003
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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs 42: 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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  6. Article ; Online: Ionizing radiation and heart risks.

    Bhattacharya, Souparno / Asaithamby, Aroumougame

    Seminars in cell & developmental biology

    2016  Volume 58, Page(s) 14–25

    Abstract: Cardiovascular disease and cancer are the two leading causes of morbidity and mortality worldwide. As advancements in radiation therapy (RT) have significantly increased the number of cancer survivors, the risk of radiation-induced cardiovascular disease ...

    Abstract Cardiovascular disease and cancer are the two leading causes of morbidity and mortality worldwide. As advancements in radiation therapy (RT) have significantly increased the number of cancer survivors, the risk of radiation-induced cardiovascular disease (RICD) in this group is a growing concern. Recent epidemiological data suggest that accidental or occupational exposure to low dose radiation, in addition to therapeutic ionizing radiation, can result in cardiovascular complications. The progression of radiation-induced cardiotoxicity often takes years to manifest but is also multifaceted, as the heart may be affected by a variety of pathologies. The risk of cardiovascular disease development in RT cancer survivors has been known for 40 years and several risk factors have been identified in the last two decades. However, most of the early work focused on clinical symptoms and manifestations, rather than understanding cellular processes regulating homeostatic processes of the cardiovascular system in response to radiation. Recent studies have suggested that a different approach may be needed to refute the risk of cardiovascular disease following radiation exposure. In this review, we will focus on how different radiation types and doses may induce cardiovascular complications, highlighting clinical manifestations and the mechanisms involved in the pathophysiology of radiation-induced cardiotoxicity. We will finally discuss how current and future research on heart development and homeostasis can help reduce the incidence of RICD.
    Language English
    Publishing date 2016-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2016.01.045
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2918: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  7. Article ; Online: Immunomodulatory Effects of Radiotherapy.

    Kumari, Sharda / Mukherjee, Shibani / Sinha, Debapriya / Abdisalaam, Salim / Krishnan, Sunil / Asaithamby, Aroumougame

    International journal of molecular sciences

    2020  Volume 21, Issue 21

    Abstract: Radiation therapy (RT), an integral component of curative treatment for many malignancies, can be administered via an increasing array of techniques. In this review, we summarize the properties and application of different types of RT, specifically, ... ...

    Abstract Radiation therapy (RT), an integral component of curative treatment for many malignancies, can be administered via an increasing array of techniques. In this review, we summarize the properties and application of different types of RT, specifically, conventional therapy with x-rays, stereotactic body RT, and proton and carbon particle therapies. We highlight how low-linear energy transfer (LET) radiation induces simple DNA lesions that are efficiently repaired by cells, whereas high-LET radiation causes complex DNA lesions that are difficult to repair and that ultimately enhance cancer cell killing. Additionally, we discuss the immunogenicity of radiation-induced tumor death, elucidate the molecular mechanisms by which radiation mounts innate and adaptive immune responses and explore strategies by which we can increase the efficacy of these mechanisms. Understanding the mechanisms by which RT modulates immune signaling and the key players involved in modulating the RT-mediated immune response will help to improve therapeutic efficacy and to identify novel immunomodulatory drugs that will benefit cancer patients undergoing targeted RT.
    MeSH term(s) Animals ; DNA Breaks, Double-Stranded ; DNA Repair ; Genomic Instability ; Humans ; Immunity, Cellular/immunology ; Immunity, Cellular/radiation effects ; Immunologic Factors ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/radiotherapy
    Chemical Substances Immunologic Factors
    Language English
    Publishing date 2020-10-31
    Publishing country Switzerland
    Document type 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/ijms21218151
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  8. Article ; Online: Mitochondrial fatty acid utilization increases chromatin oxidative stress in cardiomyocytes.

    Menendez-Montes, Ivan / Abdisalaam, Salim / Xiao, Feng / Lam, Nicholas T / Mukherjee, Shibani / Szweda, Luke I / Asaithamby, Aroumougame / Sadek, Hesham A

    Proceedings of the National Academy of Sciences of the United States of America

    2021  Volume 118, Issue 34

    Abstract: The inability of adult mammalian cardiomyocytes to proliferate underpins the development of heart failure following myocardial injury. Although the newborn mammalian heart can spontaneously regenerate for a short period of time after birth, this ability ... ...

    Abstract The inability of adult mammalian cardiomyocytes to proliferate underpins the development of heart failure following myocardial injury. Although the newborn mammalian heart can spontaneously regenerate for a short period of time after birth, this ability is lost within the first week after birth in mice, partly due to increased mitochondrial reactive oxygen species (ROS) production which results in oxidative DNA damage and activation of DNA damage response. This increase in ROS levels coincides with a postnatal switch from anaerobic glycolysis to fatty acid (FA) oxidation by cardiac mitochondria. However, to date, a direct link between mitochondrial substrate utilization and oxidative DNA damage is lacking. Here, we generated ROS-sensitive fluorescent sensors targeted to different subnuclear compartments (chromatin, heterochromatin, telomeres, and nuclear lamin) in neonatal rat ventricular cardiomyocytes, which allowed us to determine the spatial localization of ROS in cardiomyocyte nuclei upon manipulation of mitochondrial respiration. Our results demonstrate that FA utilization by the mitochondria induces a significant increase in ROS detection at the chromatin level compared to other nuclear compartments. These results indicate that mitochondrial metabolic perturbations directly alter the nuclear redox status and that the chromatin appears to be particularly sensitive to the prooxidant effect of FA utilization by the mitochondria.
    MeSH term(s) Animals ; Cell Line ; Cell Proliferation ; DNA Damage ; Fatty Acids/metabolism ; Mice ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism
    Chemical Substances Fatty Acids ; Reactive Oxygen Species
    Language English
    Publishing date 2021-08-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2101674118
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
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  9. Article ; Online: Immunomodulatory Effects of Radiotherapy

    Sharda Kumari / Shibani Mukherjee / Debapriya Sinha / Salim Abdisalaam / Sunil Krishnan / Aroumougame Asaithamby

    International Journal of Molecular Sciences, Vol 21, Iss 8151, p

    2020  Volume 8151

    Abstract: Radiation therapy (RT), an integral component of curative treatment for many malignancies, can be administered via an increasing array of techniques. In this review, we summarize the properties and application of different types of RT, specifically, ... ...

    Abstract Radiation therapy (RT), an integral component of curative treatment for many malignancies, can be administered via an increasing array of techniques. In this review, we summarize the properties and application of different types of RT, specifically, conventional therapy with x-rays, stereotactic body RT, and proton and carbon particle therapies. We highlight how low-linear energy transfer (LET) radiation induces simple DNA lesions that are efficiently repaired by cells, whereas high-LET radiation causes complex DNA lesions that are difficult to repair and that ultimately enhance cancer cell killing. Additionally, we discuss the immunogenicity of radiation-induced tumor death, elucidate the molecular mechanisms by which radiation mounts innate and adaptive immune responses and explore strategies by which we can increase the efficacy of these mechanisms. Understanding the mechanisms by which RT modulates immune signaling and the key players involved in modulating the RT-mediated immune response will help to improve therapeutic efficacy and to identify novel immunomodulatory drugs that will benefit cancer patients undergoing targeted RT.
    Keywords radiation therapy ; charged particle therapy ; carbon ion therapy ; clustered DNA damage ; immune signaling ; cancer vaccines ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 616
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Mechanistic link between DNA damage sensing, repairing and signaling factors and immune signaling.

    Mukherjee, Shibani / Abdisalaam, Salim / Bhattacharya, Souparno / Srinivasan, Kalayarasan / Sinha, Debapriya / Asaithamby, Aroumougame

    Advances in protein chemistry and structural biology

    2019  Volume 115, Page(s) 297–324

    Abstract: Previously, DNA damage sensing, repairing and signaling machineries were thought to mainly suppress genomic instability in response to genotoxic stress. Emerging evidence indicates a crosstalk between DNA repair machinery and the immune system. In this ... ...

    Abstract Previously, DNA damage sensing, repairing and signaling machineries were thought to mainly suppress genomic instability in response to genotoxic stress. Emerging evidence indicates a crosstalk between DNA repair machinery and the immune system. In this chapter, we attempt to decipher the molecular choreography of how factors, including ATM, BRCA1, DNA-PK, FANCA/D2, MRE11, MUS81, NBS1, RAD51 and TREX1, of multiple DNA metabolic processes are directly or indirectly involved in suppressing cytosolic DNA sensing pathway-mediated immune signaling. We provide systematic details showing how different DDR factors' roles in modulating immune signaling are not direct, but are rather a consequence of their inherent ability to sense, repair and signal in response to DNA damage. Unexpectedly, most DDR factors negatively impact the immune system; that is, the immune system shows defective signaling if there are defects in DNA repair pathways. Thus, in addition to their known DNA repair and replication functions, DDR factors help prevent erroneous activation of immune signaling. A more precise understanding of the mechanisms by which different DDR factors function in immune signaling can be exploited to redirect the immune system for both preventing and treating autoimmunity, cellular senescence and cancer in humans.
    MeSH term(s) DNA/genetics ; DNA/immunology ; DNA Damage/immunology ; DNA Repair/immunology ; Humans ; Signal Transduction/immunology
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2019-01-03
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 1876-1631 ; 1876-1623
    ISSN (online) 1876-1631
    ISSN 1876-1623
    DOI 10.1016/bs.apcsb.2018.11.004
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