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  • br O superoxide anion radical br SOD superoxide

    2019-10-21


    O2%− superoxide anion radical
    SOD superoxide dismutase
    MFI median fluorescent intensity
    mPTP mitochondrial permeability transition pore
    MTP mitochondrial transmembrane potential
    7‑AAD 7‑Aminoactinomycin D
    EB ethidium bromide
    CT calf thymus
    S-V Stern-Volmer (equation)
    Acknowledgements
    The Ministry of Education, Science and Technological Development of the Republic of Serbia under Grant 172055 supported this work. Appendix A. Supplementary data
    References
    S. Bjelogrlić et al.
    D. Radanovic, S. Radulovic, G. Pelizzi, K. Andelkovic, Synthesis, structure and characterization of novel Cd(II) and Zn(II) complexes with the condensation product of 2‑formylpyridine and selenosemicarbazide. Antiproliferative activity of the synthesized complexes and related selenosemicarbazone complexes, J. Inorg. Biochem. 104 (2010) 673–682, https://doi.org/10.1016/j.jinorgbio.2010.02.009.
    S. Bjelogrlić et al.
    M. Milczarek, An efficient process to directly convert  Journal of Inorganic Biochemistry 190 (2019) 45–66
    K. Anđelković, Synthesis, characterization and biological activities of
    S. Bjelogrlić et al.
    N.R. Filipović, K.K. Anđelković, Synthesis and characterization of novel Cd(II), Zn
    [128] C.M. Sorenson, A. Eastman, Influence of cis‑diamminedichloroplatinum(II) on DNA synthesis and Ruxolitinib (INCB018424) progression in excision repair proficient and deficient Chinese hamster ovary cells, Cancer Res. 48 (1988) 6703–6707. [129] C. Demarcq, R.T. Bunch, D. Creswell, A. Eastman, The role of cell cycle progres-sion in cisplatin-induced apoptosis in Chinese hamster ovary cells, Cell Growth Differ. 5 (1994) 983–993. [130] L.D. Attardi, A. de Vries, T. Jacks, Activation of the p53-dependent G1 checkpoint
    S. Bjelogrlić et al.
    66 Original Article
    A Novel Chimeric Poxvirus Encoding hNIS Is Tumor-Tropic, Imageable, and Synergistic with Radioiodine to Sustain Colon Cancer Regression
    Susanne G. Warner,1,2 Sang-In Kim,1 Shyambabu Chaurasiya,1 Michael P. O’Leary,1 Jianming Lu,1 Venkatesh Sivanandam,1 Yanghee Woo,1 Nanhai G. Chen,1,2 and Yuman Fong1,2
    1Department of Surgery, Division of Surgical Oncology, City of Hope National Medical Center, Duarte, CA 91010, USA; 2Center for Gene Therapy, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA 91010, USA
    Colon cancer has a high rate of recurrence even with good response to modern therapies. Novel curative adjuncts are needed. Oncolytic viral therapy has shown preclinical promise against colon cancer but lacks robust efficacy in clinical trials and raises regulatory concerns without real-time tracking of viral replication. Novel potent vectors are needed with adjunc-tive features to enhance clinical efficacy. We have Ruxolitinib (INCB018424) thus used homologous recombination and high-throughput screening to create a novel chimeric poxvirus encoding a human sodium iodide symporter (hNIS) at a redundant tk locus. The resulting virus (CF33-hNIS) consistently expresses hNIS and demon-strates replication efficiency and immunogenic cell death in colon cancer cells in vitro. Tumor-specific CF33-hNIS efficacy against colon cancer results in tumor regression in vivo in colon cancer xenograft models. Early expression of hNIS by infected cells makes viral replication reliably imageable via positron emission tomography (PET) of I-124 uptake. The intensity of I-124 uptake mirrors viral replication and tumor regression. Finally, systemic delivery of radiotherapeutic I-131 isotope following CF33-hNIS infection of colon cancer xenografts en-hances and sustains tumor regression compared with virus treatment alone in HCT116 xenografts, demonstrating synergy of oncolytic viral therapy with radioablation in vivo.
    INTRODUCTION
    Colorectal cancer is the third leading cause of cancer death in the United States.1 Improvements in treatment and screening have contributed to an increase in overall survival, but patients presenting with distant metastases still have a dismal survival, even with modern chemotherapies.2,3 Therefore, novel therapies are needed. Oncolytic viruses are naturally occurring or genetically modified viruses that infect, replicate in, and kill cancer cells, leaving healthy cells un-harmed. Viruses can also be engineered to engage the immune system and enhance local and systemic anti-tumor immune reactions.4 Despite preclinical promise, challenges related to potency, track-abil-ity of viral replication, and durable clinical responses have slowed the progression of oncolytic viruses to standard cancer therapy.5,6 The first obstacle is the relative lack of potency of existing viral vectors. In particular, the hurdle of lower potency means more viral particles