The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform

Fumiaki Nakayama - One of the best experts on this subject based on the ideXlab platform.

  • Strong radioprotective FGF1 signaling down-regulates proliferative and metastatic capabilities of the angiosarcoma cell line, ISOS-1, through the dual inhibition of EGFR and VEGFR pathways.
    Clinical and translational radiation oncology, 2017
    Co-Authors: Taichi Miura, Toru Imamura, Takeshi Yasuda, Mayumi Fujita, Takashi Imai, Mitsuko Kawano, Kaori Imadome, Shoko Nishihara, Mikio Masuzawa, Fumiaki Nakayama
    Abstract:

    Abstract Background and purpose Angiosarcoma is associated with a poor prognosis and is treated with radiotherapy. Although FGF1 is a potential Radioprotector, the influence of FGF1 on the malignancy of angiosarcoma remains unknown. Materials and methods Highly stable FGF1 mutants, which exhibit stronger mitogenic activity than wild-type FGF1, were examined as strong Radioprotectors and signaling agonists to clarify the effects of FGF1 on the murine angiosarcoma cell line ISOS-1. Results FGF1 mutants reduced colony formation by and the in vitro invasion and migration of ISOS-1 cells, in addition to an increase in radiosensitivity to X-rays. In contrast, an FGFR inhibitor blocked the inhibitory effects of FGF1 mutants on colony formation, invasion, and migration. siRNA targeting the Fgfr1 gene showed that strong FGFR1 signaling reduced colony formation by ISOS-1 cells. However, the FGF1 mutant reduced the activation of VEGFRs and EGFRs in ISOS-1 cells more strongly than wild-type FGF1. Moreover, the inhibition of VEGFRs and EGFRs synergistically reduced colony formation by and invasion and migration of ISOS-1 cells. Conclusion These results suggest that strong FGF1 signaling exerts not only radioprotective effects, but also inhibitory effects on proliferative and metastatic capacities of angiosarcoma through the dual inhibition of EGFR and VEGFR pathways.

  • Strong radioprotective FGF1 signaling down-regulates proliferative and metastatic capabilities of the angiosarcoma cell line, ISOS-1, through the dual inhibition of EGFR and VEGFR pathways
    Elsevier, 2017
    Co-Authors: Taichi Miura, Toru Imamura, Takeshi Yasuda, Mayumi Fujita, Takashi Imai, Mitsuko Kawano, Kaori Imadome, Shoko Nishihara, Mikio Masuzawa, Fumiaki Nakayama
    Abstract:

    Background and purpose: Angiosarcoma is associated with a poor prognosis and is treated with radiotherapy. Although FGF1 is a potential Radioprotector, the influence of FGF1 on the malignancy of angiosarcoma remains unknown. Materials and methods: Highly stable FGF1 mutants, which exhibit stronger mitogenic activity than wild-type FGF1, were examined as strong Radioprotectors and signaling agonists to clarify the effects of FGF1 on the murine angiosarcoma cell line ISOS-1. Results: FGF1 mutants reduced colony formation by and the in vitro invasion and migration of ISOS-1 cells, in addition to an increase in radiosensitivity to X-rays. In contrast, an FGFR inhibitor blocked the inhibitory effects of FGF1 mutants on colony formation, invasion, and migration. siRNA targeting the Fgfr1 gene showed that strong FGFR1 signaling reduced colony formation by ISOS-1 cells. However, the FGF1 mutant reduced the activation of VEGFRs and EGFRs in ISOS-1 cells more strongly than wild-type FGF1. Moreover, the inhibition of VEGFRs and EGFRs synergistically reduced colony formation by and invasion and migration of ISOS-1 cells. Conclusion: These results suggest that strong FGF1 signaling exerts not only radioprotective effects, but also inhibitory effects on proliferative and metastatic capacities of angiosarcoma through the dual inhibition of EGFR and VEGFR pathways. Keywords: Angiosarcoma, EGFR, FGF1, Metastasis, Radioprotector, VEGF

Vijay K. Singh - One of the best experts on this subject based on the ideXlab platform.

  • BIO 300: a promising radiation countermeasure under advanced development for acute radiation syndrome and the delayed effects of acute radiation exposure.
    Expert opinion on investigational drugs, 2020
    Co-Authors: Vijay K. Singh, Thomas M. Seed
    Abstract:

    There are no Radioprotectors currently approved by the United States Food and Drug Administration (US FDA) for either the hematopoietic acute radiation syndrome (H-ARS) or for the acute radiation g...

  • cblb613 a tlr 2 6 agonist natural lipopeptide of mycoplasma arginini as a novel radiation countermeasure
    Radiation Research, 2012
    Co-Authors: Vijay K. Singh, Elizabeth J Ducey, Oluseyi O Fatanmi, Pankaj Kumar Singh, Darren S Brown, Andrei A Purmal, Vera V Shakhova, Andrei V Gudkov, Elena Feinstein, Alexander N Shakhov
    Abstract:

    To date, there are no safe and effective drugs available for protection against ionizing radiation damage. Therefore, a great need exists to identify and develop non-toxic agents that will be useful as Radioprotectors or postirradiation therapies under a variety of operational scenarios. We have developed a new pharmacological agent, CBLB613 (a naturally occurring Mycoplasma-derived lipopeptide ligand for Toll-like receptor 2/6), as a novel radiation countermeasure. Using CD2F1 mice, we investigated CBLB613 for toxicity, immunogenicity, radioprotection, radiomitigation and pharmacokinetics. We also evaluated CBLB613 for its effects on cytokine induction and radiation-induced cytopenia in unirradiated and irradiated mice. The no-observable-adverse-effect level of CBLB613 was 1.79 mg/kg and 1 mg/kg for single and repeated doses, respectively. CBLB613 significantly protected mice against a lethal dose of 60Co γ radiation. The dose reduction factor of CBLB613 as a Radioprotector was 1.25. CBLB613 also mitigat...

James B. Mitchell - One of the best experts on this subject based on the ideXlab platform.

  • An efficient synthesis of 3-(N-piperidinemethyl)-2, 2, 5, 5-tetramethyl-1-oxy-3-pyrroline, a promising Radioprotector for cancer radiotherapy
    Tetrahedron Letters, 2014
    Co-Authors: Vincent Coble, Murali C. Krishna, Olga Vasalatiy, Rolf E. Swenson, James B. Mitchell
    Abstract:

    Nitroxides can ameliorate the toxic effects of radiation during cancer therapy. Nitroxides are paramagnetic and can be used in magnetic resonance imaging (MRI) and electron paramagnetic resonance imaging (EPRI) to monitor in vivo oxidative stress status. Compound 5 (3-(N-piperidinemethyl)-2,2,5,5-tetramethyl-1-oxy-3-pyrroline) was found to be the most effective nitroxide Radioprotector. An efficient synthesis for this promising Radioprotector was developed.

  • A Novel Nitroxide is an Effective Brain Redox Imaging Contrast Agent and in vivo Radioprotector
    Free radical biology & medicine, 2011
    Co-Authors: Ryan M. Davis, Anastasia L. Sowers, William Degraff, Marcelino Bernardo, Angela Thetford, Murali C. Krishna, James B. Mitchell
    Abstract:

    ABSTRACT Individuals are exposed to ionizing radiation during medical procedures and nuclear disasters, and this exposure can be carcinogenic, toxic, and sometimes fatal. Drugs that protect individuals from the adverse effects of radiation may therefore be valuable countermeasures against the health risks of exposure. In the current study, the LD50/30 (the dose resulting in 50% of exposed mice surviving 30 days after exposure) was determined in control C3H mice and mice treated with the nitroxide Radioprotectors Tempol, 3-CP, 16c, 22c, and 23c. The pharmacokinetics of 22c and 23c were measured with magnetic resonance imaging (MRI) in the brain, blood, submandibular salivary gland, liver, muscle, tongue, and myocardium. It was found that 23c was the most effective Radioprotector of the five studied: 23c increased the LD50/30 in mice from 7.9 ± 0.15 Gy (treated with saline) to 11.47 ± 0.13 Gy (an increase of 45%). Additionally, MRI-based pharmacokinetic studies revealed that 23c is an effective redox imaging agent in the mouse brain, and that 23c may allow functional imaging of the myocardium. The data in this report suggest that 23c is currently the most potent known nitroxide Radioprotector, and that it may also be useful as a contrast agent for functional imaging.

  • Radioprotectors and Mitigators of Radiation-Induced Normal Tissue Injury
    The oncologist, 2010
    Co-Authors: Deborah Citrin, Murali C. Krishna, Ana P. Cotrim, Fuminori Hyodo, Bruce J. Baum, James B. Mitchell
    Abstract:

    Radiation is used in the treatment of a broad range of malignancies. Exposure of normal tissue to radiation may result in both acute and chronic toxicities that can result in an inability to deliver the intended therapy, a range of symptoms, and a decrease in quality of life. Radioprotectors are compounds that are designed to reduce the damage in normal tissues caused by radiation. These compounds are often antioxidants and must be present before or at the time of radiation for effectiveness. Other agents, termed mitigators, may be used to minimize toxicity even after radiation has been delivered. Herein, we review agents in clinical use or in development as Radioprotectors and mitigators of radiation-induced normal tissue injury. Few agents are approved for clinical use, but many new compounds show promising results in preclinical testing.

Taichi Miura - One of the best experts on this subject based on the ideXlab platform.

  • Strong radioprotective FGF1 signaling down-regulates proliferative and metastatic capabilities of the angiosarcoma cell line, ISOS-1, through the dual inhibition of EGFR and VEGFR pathways.
    Clinical and translational radiation oncology, 2017
    Co-Authors: Taichi Miura, Toru Imamura, Takeshi Yasuda, Mayumi Fujita, Takashi Imai, Mitsuko Kawano, Kaori Imadome, Shoko Nishihara, Mikio Masuzawa, Fumiaki Nakayama
    Abstract:

    Abstract Background and purpose Angiosarcoma is associated with a poor prognosis and is treated with radiotherapy. Although FGF1 is a potential Radioprotector, the influence of FGF1 on the malignancy of angiosarcoma remains unknown. Materials and methods Highly stable FGF1 mutants, which exhibit stronger mitogenic activity than wild-type FGF1, were examined as strong Radioprotectors and signaling agonists to clarify the effects of FGF1 on the murine angiosarcoma cell line ISOS-1. Results FGF1 mutants reduced colony formation by and the in vitro invasion and migration of ISOS-1 cells, in addition to an increase in radiosensitivity to X-rays. In contrast, an FGFR inhibitor blocked the inhibitory effects of FGF1 mutants on colony formation, invasion, and migration. siRNA targeting the Fgfr1 gene showed that strong FGFR1 signaling reduced colony formation by ISOS-1 cells. However, the FGF1 mutant reduced the activation of VEGFRs and EGFRs in ISOS-1 cells more strongly than wild-type FGF1. Moreover, the inhibition of VEGFRs and EGFRs synergistically reduced colony formation by and invasion and migration of ISOS-1 cells. Conclusion These results suggest that strong FGF1 signaling exerts not only radioprotective effects, but also inhibitory effects on proliferative and metastatic capacities of angiosarcoma through the dual inhibition of EGFR and VEGFR pathways.

  • Strong radioprotective FGF1 signaling down-regulates proliferative and metastatic capabilities of the angiosarcoma cell line, ISOS-1, through the dual inhibition of EGFR and VEGFR pathways
    Elsevier, 2017
    Co-Authors: Taichi Miura, Toru Imamura, Takeshi Yasuda, Mayumi Fujita, Takashi Imai, Mitsuko Kawano, Kaori Imadome, Shoko Nishihara, Mikio Masuzawa, Fumiaki Nakayama
    Abstract:

    Background and purpose: Angiosarcoma is associated with a poor prognosis and is treated with radiotherapy. Although FGF1 is a potential Radioprotector, the influence of FGF1 on the malignancy of angiosarcoma remains unknown. Materials and methods: Highly stable FGF1 mutants, which exhibit stronger mitogenic activity than wild-type FGF1, were examined as strong Radioprotectors and signaling agonists to clarify the effects of FGF1 on the murine angiosarcoma cell line ISOS-1. Results: FGF1 mutants reduced colony formation by and the in vitro invasion and migration of ISOS-1 cells, in addition to an increase in radiosensitivity to X-rays. In contrast, an FGFR inhibitor blocked the inhibitory effects of FGF1 mutants on colony formation, invasion, and migration. siRNA targeting the Fgfr1 gene showed that strong FGFR1 signaling reduced colony formation by ISOS-1 cells. However, the FGF1 mutant reduced the activation of VEGFRs and EGFRs in ISOS-1 cells more strongly than wild-type FGF1. Moreover, the inhibition of VEGFRs and EGFRs synergistically reduced colony formation by and invasion and migration of ISOS-1 cells. Conclusion: These results suggest that strong FGF1 signaling exerts not only radioprotective effects, but also inhibitory effects on proliferative and metastatic capacities of angiosarcoma through the dual inhibition of EGFR and VEGFR pathways. Keywords: Angiosarcoma, EGFR, FGF1, Metastasis, Radioprotector, VEGF

Thomas M. Seed - One of the best experts on this subject based on the ideXlab platform.