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  1. Article ; Online: Red blood cells function as reservoirs of tumor DNA.

    Thompson, Jeffrey C / Li, Sue / Jose, Joshua S / Predina, Jarrod / Gupta, Aasha / Eruslanov, Evgeniy / Singhal, Sunil / Albelda, Steven M / Mangalmurti, Nilam S

    American journal of physiology. Lung cellular and molecular physiology

    2024  Volume 326, Issue 5, Page(s) L646–L650

    Abstract: Novel screening techniques for early detection of lung cancer are urgently needed. Profiling circulating tumor cell-free DNA (ctDNA) has emerged as a promising tool for biopsy-free tumor genotyping. However, both the scarcity and short half-life of ctDNA ...

    Abstract Novel screening techniques for early detection of lung cancer are urgently needed. Profiling circulating tumor cell-free DNA (ctDNA) has emerged as a promising tool for biopsy-free tumor genotyping. However, both the scarcity and short half-life of ctDNA substantially limit the sensitivity and clinical utility of ctDNA detection methodologies. Our discovery that red blood cells (RBCs) sequester mitochondrial DNA opens a new avenue for detecting circulating nucleic acids, as RBCs represent an unrecognized reservoir of circulating nucleic acid. Here, we show that RBCs acquire tumor DNA following coculture with lung cancer cell lines harboring Kirsten rat sarcoma viral oncogene homolog (KRAS) and epidermal growth factor receptor (EGFR) mutations. RBC-bound tumor DNA is detectable in patients with early-stage non-small cell lung cancer (NSCLC) but not in healthy controls by qPCR. Our results collectively uncover a previously unrecognized yet easily accessible reservoir of tumor DNA, offering a promising foundation for future RBC-based tumor diagnostics.
    MeSH term(s) Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/blood ; Lung Neoplasms/pathology ; Lung Neoplasms/diagnosis ; Erythrocytes/metabolism ; Circulating Tumor DNA/genetics ; Circulating Tumor DNA/blood ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/blood ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Mutation ; Cell Line, Tumor ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/blood ; Proto-Oncogene Proteins p21(ras)/genetics ; Male ; Female ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/blood ; DNA, Neoplasm/blood ; DNA, Neoplasm/genetics
    Chemical Substances Circulating Tumor DNA ; ErbB Receptors (EC 2.7.10.1) ; DNA, Mitochondrial ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; EGFR protein, human (EC 2.7.10.1) ; KRAS protein, human ; Biomarkers, Tumor ; DNA, Neoplasm
    Language English
    Publishing date 2024-03-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00049.2024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Succinate prodrugs in combination with atropine and pralidoxime protect cerebral mitochondrial function in a rodent model of acute organophosphate poisoning.

    Piel, Sarah / Janowska, Joanna I / Ward, J Laurenson / McManus, Meagan J / Jose, Joshua S / Starr, Jonathan / Sheldon, Malkah / Clayman, Carly L / Elmér, Eskil / Hansson, Magnus J / Jang, David H / Karlsson, Michael / Ehinger, Johannes K / Kilbaugh, Todd J

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 20329

    Abstract: Pesticides account for hundreds of millions of cases of acute poisoning worldwide each year, with organophosphates (OPs) being responsible for the majority of all pesticide-related deaths. OPs inhibit the enzyme acetylcholinesterase (AChE), which leads ... ...

    Abstract Pesticides account for hundreds of millions of cases of acute poisoning worldwide each year, with organophosphates (OPs) being responsible for the majority of all pesticide-related deaths. OPs inhibit the enzyme acetylcholinesterase (AChE), which leads to impairment of the central- and peripheral nervous system. Current standard of care (SOC) alleviates acute neurologic-, cardiovascular- and respiratory symptoms and reduces short term mortality. However, survivors often demonstrate significant neurologic sequelae. This highlights the critical need for further development of adjunctive therapies with novel targets. While the inhibition of AChE is thought to be the main mechanism of injury, mitochondrial dysfunction and resulting metabolic crisis may contribute to the overall toxicity of these agents. We hypothesized that the mitochondrially targeted succinate prodrug NV354 would support mitochondrial function and reduce brain injury during acute intoxication with the OP diisopropylfluorophosphate (DFP). To this end, we developed a rat model of acute DFP intoxication and evaluated the efficacy of NV354 as adjunctive therapy to SOC treatment with atropine and pralidoxime. We demonstrate that NV354, in combination with atropine and pralidoxime therapy, significantly improved cerebral mitochondrial complex IV-linked respiration and reduced signs of brain injury in a rodent model of acute DFP exposure.
    MeSH term(s) Animals ; Rats ; Organophosphate Poisoning/drug therapy ; Atropine/pharmacology ; Atropine/therapeutic use ; Prodrugs/pharmacology ; Isoflurophate/toxicity ; Succinic Acid ; Acetylcholinesterase/metabolism ; Rodentia/metabolism ; Succinates ; Mitochondria/metabolism ; Brain Injuries/drug therapy
    Chemical Substances pralidoxime (P7MU9UTP52) ; Atropine (7C0697DR9I) ; Prodrugs ; Isoflurophate (12UHW9R67N) ; Succinic Acid (AB6MNQ6J6L) ; Acetylcholinesterase (EC 3.1.1.7) ; Succinates
    Language English
    Publishing date 2022-11-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-24472-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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