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      Radon Therapy Is Very Promising as a Primary or an Adjuvant Treatment for Different Types of Cancers: 4 Case Reports

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          Abstract

          We report on the application of radon inhalation therapy to patients with 4 types of cancer: colon, uterine, lung, and liver cell. The radon treatments were given to improve the efficacy of chemotherapy and were potent in all 4 cases. Marker values decreased and disease symptoms were alleviated. We include a lengthy discussion on the mechanism that may be responsible for the observed results. While employing the radon generator to treat the patient with hepatocellular carcinoma, we discovered that a concentration of 6 MBq/m 3 was very effective, while 1 MBq/m 3 was marginal. This implies different, and rather high, radon concentration thresholds for the treatment of different types of cancer. The evidence from these 4 cases suggests that radon inhalation may be beneficial against various cancer types as an important adjuvant therapy to conventional chemotherapy and for local high-dose radiotherapy, which would address the problem of distant metastasis. A previous case report on 2 patients with advanced breast cancer, who refused chemotherapy or radiotherapy, indicates that radon may be effective as a primary therapy for cancer. Clinical trials should be carried out to determine the best radon concentrations for treatment of other types of cancer, at different stages of progression.

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          Mortality from breast cancer after irradiation during fluoroscopic examinations in patients being treated for tuberculosis.

          The increasing use of mammography to screen asymptomatic women makes it important to know the risk of breast cancer associated with exposure to low levels of ionizing radiation. We examined the mortality from breast cancer in a cohort of 31,710 women who had been treated for tuberculosis at Canadian sanatoriums between 1930 and 1952. A substantial proportion (26.4 percent) had received radiation doses to the breast of 10 cGy or more from repeated fluoroscopic examinations during therapeutic pneumothoraxes. Women exposed to greater than or equal to 10 cGy of radiation had a relative risk of death from breast cancer of 1.36, as compared with those exposed to less than 10 cGy (95 percent confidence interval, 1.11 to 1.67; P = 0.001). The data were most consistent with a linear dose-response relation. The risk was greatest among women who had been exposed to radiation when they were between 10 and 14 years of age; they had a relative risk of 4.5 per gray, and an additive risk of 6.1 per 10(4) person-years per gray. With increasing age at first exposure, there was substantially less excess risk, and the radiation effect appeared to peak approximately 25 to 34 years after the first exposure. Our additive model for lifetime risk predicts that exposure to 1 cGy at the age of 40 increases the number of deaths from breast cancer by 42 per million women. We conclude that the risk of breast cancer associated with radiation decreases sharply with increasing age at exposure and that even a small benefit to women of screening mammography would outweigh any possible risk of radiation-induced breast cancer.
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            gamma-Irradiation induces P2X(7) receptor-dependent ATP release from B16 melanoma cells.

            Ionizing irradiation causes not only growth arrest and cell death, but also release of growth factors or signal transmitters, which promote cancer malignancy. Extracellular ATP controls cancer growth through activation of purinoceptors. However, there is no report of radiation-induced ATP release from cancer cells. Here, we examined gamma-irradiation-induced ATP release and its mechanism in B16 melanoma. Extracellular ATP was measured by luciferin-luciferase assay. To investigate mechanism of radiation-induced ATP release, we pharmacologically inhibited the ATP release and established stable P2X(7) receptor-knockdown B16 melanoma cells using two short hairpin RNAs targeting P2X(7) receptor. Cells were exposed to 0.5-8 Gy of gamma-rays. Extracellular ATP was increased, peaking at 5 min after 0.5 Gy irradiation. A selective P2X(7) receptor channel antagonist, but not anion transporter inhibitors, blocked the release of ATP. Further, radiation-induced ATP release was significantly decreased in P2X(7) receptor-knockdown cells. Our results indicate that gamma-irradiation evokes ATP release from melanoma cells, and P2X(7) receptor channel plays a significant role in mediating the ATP release. We suggest that extracellular ATP could be a novel intercellular signaling molecule released from cancer cells when cells are exposed to ionizing radiation.
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              Enhancement of antitumor immunity by low-dose total body irradiationis associated with selectively decreasing the proportion and number of T regulatory cells.

              Low-dose total body irradiation (LTBI) is used in the treatment of some cancers mainly for immune enhancement rather than cell killing. However, the mechanism underlying LTBI remains unknown. In this study, by analyzing the immune patterns of lymphocytes, we found that the percentage and absolute number of CD4(+)CD25(+)Foxp3(+) regulatory T cells are markedly decreased in naive mice following treatment with LTBI. On the contrary, the CD4(+)CD44(+)/CD8(+)CD44(+) effect or-memory T cells are greatly increased. Importantly, naive mice treated with dendritic cell-gp 100 tumor vaccines under LTBI induced an enhancement of antigen-specific proliferation and cytotoxicity as well as interferon-gamma (IFN-gamma) secretion against F10 melanoma tumor challenge, compared to treatment with either the tumor vaccine or LTBI alone. Consequently, the treatment resulted in a reduced tumor burden and prolonged mouse survival. Our data demonstrate that LTBI's enhancement of antitumor immunity was mainly associated with selectively decreasing the proportion and number of T regulatory cells,implying the potential application of the combination of LTBI and a tumor vaccine in antitumor therapy.
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                Author and article information

                Journal
                Dose Response
                Dose Response
                DOS
                spdos
                Dose-Response
                SAGE Publications (Sage CA: Los Angeles, CA )
                1559-3258
                03 June 2019
                Apr-Jun 2019
                : 17
                : 2
                : 1559325819853163
                Affiliations
                [1 ]Department of Radiation Biosciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science (TUS), Noda-city, Chiba, Japan
                [2 ]Cuttler and Associates Inc, Vaughan, Ontario, Canada
                [3 ]Drainage Co., Ltd, Minoo-city, Osaka, Japan
                [4 ]Yorozu Clinic, Totori-city, Japan
                [5 ]Horii Clinic, Nishinomiya-city, Japan
                [6 ]Faculty of Pharmaceutical Sciences, Ohu University, Koriyama, Japan
                [7 ]Lead and Company Co., Ltd., Minami-ku, Yokohama, Japan
                Author notes
                [*]Shuji Kojima, Department of Radiation Biosciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science (TUS), 2641 Yamazaki, Noda-city, Chiba 8510, Japan. Email: skjma@ 123456jcom.zaq.ne.jp
                Author information
                https://orcid.org/0000-0001-6944-9250
                Article
                10.1177_1559325819853163
                10.1177/1559325819853163
                6552369
                93b98286-f1eb-449c-9bae-2a641ea08a13
                © The Author(s) 2019

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 02 February 2019
                : 25 April 2019
                : 30 April 2019
                Categories
                Key Issues in Dose Response: Leadership Forum-Clinical Case
                Custom metadata
                April-June 2019

                radon therapy,colon uterine lung liver cancer,breast cancer,primary or adjuvant treatment,optimum radon concentration,radiation hormesis

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