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Academic literature on the topic 'Radiation induced bystander effect'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Radiation induced bystander effect"

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Rugo, Rebecca E., Michael W. Epperly, Darcy Franicola, Benjamin Greenberger, Paavani Komanduri, Hong Wang, Dominika M. Wiktor-Brown, Joel S. Greenberger, and Bevin P. Engelward. "DNA Methyltransferases Modulate the Bystander Effect in Mouse Embryonic Stem Cells." Blood 110, no. 11 (November 16, 2007): 4154. http://dx.doi.org/10.1182/blood.v110.11.4154.4154.

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Abstract Cells exposed to radiation or other genotoxic agents can induce DNA damage and other stress responses in non-irradiated cells that are either cultured with the irradiated cells or have been exposed to culture medium from irradiated cells. This is called the bystander effect. In a previous study we found that the descendents of bystander cells exposed to Mitomycin C (MMC) are themselves capable of inducing homologous recombination in un-exposed cells. This suggests that MMC induces persistent and transmissible changes in expression in bystander cells. Bystander effects are likely caused by epigenetic mechanisms rather than “classic” mutations, i.e. changes in DNA sequence. One of the epigenetic mechanisms cells employ for changing expression is DNA methylation in which DNA methyltransferases (DNMTs) add a methyl group to the 5 carbon of cytosine. In this study we asked if ionizing radiation can induce transmissible DNA damage in bystander cells by examining if bystander cells exposed to irradiated cells were themselves able to induce damage in naive cells. Furthermore, we asked if this was dependent on DNMT activity in the irradiated cells. We irradiated wild-type (WT) and DNMT triple knockout (DNMT TKO) mouse embryonic stem cells (ESCs) and after two weeks of continuous culture, we collected conditioned medium (CM). CM was then added to cultures of naive WT ESCs (primary bystanders). Three weeks later, CM was collected from the primary bystanders and added to naïve WT cells (secondary bystanders). We assessed DNA damage by evaluating strand breaks using the alkaline Comet assay and sister chromatid exchange (SCE) analysis. As expected, we found that medium from cells irradiated with 5 Gy induced modest damage in bystander cells. The median Olive tail moment was 2.8 in bystander cells exposed to conditioned medium from irradiated cells compared to 1.0 in control bystander cells (p < 0.0001). Homologous recombination was 0.15 chromatid exchanges per chromosome compared to 0.092 in control bystanders (p < 0.0001). We also observed an increase in strand breaks in secondary bystanders of a similar magnitude to that found in primary bystanders, indicating that radiation-induced bystanders are themselves able to induce damage. In contrast to WT cells, the irradiated DNMT TKO cells did not induce strand breaks in bystander cells, as measured by the Comet assay, but did induce HR. Surprisingly, we also observed that un-irradiated DNMT TKO cells induce DNA damage in bystanders, and furthermore that the magnitude of the effect is similar to that induced by irradiated WT cells. These data suggest that methyltransferases have a complex role in bystander effects. Bystander effects may be mediated by free radicals. To see if the DNMT TKO cells had changes in antioxidant levels, glutathione (GSH) and glutathione peroxidase (GPX) activity were determined. There was no significant change in GSH levels between WT and DNMT TKO cells. However, DNMT TKO cells had significantly higher levels of GPX activity (275.4 + 19.8 mU/mg protein) compared to control cells (122.0 + 16.4 mU/mg, p= 0.0001). Taken together, these results show that radiation-induced bystander cells can themselves induce damage in un-irradiated cells and suggest that cells lacking DNA methylation activity can induce bystander effects.
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Shemetun, O. V., and M. A. Pilins’ka. "Radiation-induced “bystander” effect." Cytology and Genetics 41, no. 4 (August 2007): 251–55. http://dx.doi.org/10.3103/s0095452707040111.

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Elbakrawy, Eman, Savneet Kaur Bains, Scott Bright, Raheem AL-Abedi, Ammar Mayah, Edwin Goodwin, and Munira Kadhim. "Radiation-Induced Senescence Bystander Effect: The Role of Exosomes." Biology 9, no. 8 (July 27, 2020): 191. http://dx.doi.org/10.3390/biology9080191.

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Ionizing Radiation (IR), especially at high doses, induces cellular senescence in exposed cultures. IR also induces “bystander effects” through signals released from irradiated cells, and these effects include many of the same outcomes observed following direct exposure. Here, we investigate if radiation can cause senescence through a bystander mechanism. Control cultures were exposed directly to 0, 0.1, 2, and 10 Gy. Unirradiated cells were treated with medium from irradiated cultures or with exosomes extracted from irradiated medium. The level of senescence was determined post-treatment (24 h, 15 days, 30 days, and 45 days) by β-galactosidase staining. Media from cultures exposed to all four doses, and exosomes from these cultures, induced significant senescence in recipient cultures. Senescence levels were initially low at the earliest timepoint, and peaked at 15 days, and then decreased with further passaging. These results demonstrate that senescence is inducible through a bystander mechanism. As with other bystander effects, bystander senescence was induced by a low radiation dose. However, unlike other bystander effects, cultures recovered from bystander senescence after repeated passaging. Bystander senescence may be a potentially significant effect of exposure to IR, and may have both beneficial and harmful effects in the context of radiotherapy.
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Yu, Kwan Ngok. "Radiation-Induced Rescue Effect: Insights from Microbeam Experiments." Biology 11, no. 11 (October 23, 2022): 1548. http://dx.doi.org/10.3390/biology11111548.

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The present paper reviews a non-targeted effect in radiobiology known as the Radiation-Induced Rescue Effect (RIRE) and insights gained from previous microbeam experiments on RIRE. RIRE describes the mitigation of radiobiological effects in targeted irradiated cells after they receive feedback signals from co-cultured non-irradiated bystander cells, or from the medium previously conditioning those co-cultured non-irradiated bystander cells. RIRE has established or has the potential of establishing relationships with other non-traditional new developments in the fields of radiobiology, including Radiation-Induced Bystander Effect (RIBE), Radiation-Induced Field Size Effect (RIFSE) and ultra-high dose rate (FLASH) effect, which are explained. The paper first introduces RIRE, summarizes previous findings, and surveys the mechanisms proposed for observations. Unique opportunities offered by microbeam irradiations for RIRE research and some previous microbeam studies on RIRE are then described. Some thoughts on future priorities and directions of research on RIRE exploiting unique features of microbeam radiations are presented in the last section.
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Azzam, Edouard I., and John B. Little. "The radiation-induced bystander effect: evidence and significance." Human & Experimental Toxicology 23, no. 2 (February 2004): 61–65. http://dx.doi.org/10.1191/0960327104ht418oa.

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A multitude of biological effects observed over the past two decades in various in vivo and in vitro cell culture experiments have indicated that low dose/low fluence ionizing radiation has significantly different biological responses than high dose radiation. Exposure of cell populations to very low fluences of particles or incorporated radionuclides results in significant biological effects occurring in both the irradiated and nonirradiated cells in the population. Cells recipient of growth medium from irradiated cultures can also respond to the radiation exposure. This phenomenon, termed the ‘bystander response’, has been postulated to impact both the estimation of risks of exposure to ionizing radiation and radiotherapy. Amplification of radiation-induced cyto-toxic and genotoxic effects by the bystander effect is in contrast to the observations of adaptive responses, which are generally induced following exposure to low dose, low linear energy transfer radiation and which tend to attenuate radiation-induced damage. In this article, the evidence for existence of radiation-induced bystander effects and our current knowledge of the biochemical and molecular events involved in mediating these effects are described. Potential similarities between factors that mediate the radiation-induced bystander and adaptive responses are highlighted.
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Stenerlöw, Bo. "Radiation-induced bystander effects." Acta Oncologica 45, no. 4 (January 2006): 373–74. http://dx.doi.org/10.1080/02841860600768960.

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Östreicher, Jan, Kevin M. Prise, Barry D. Michael, Jürgen Vogt, Tilman Butz, and Judith M. Tanner. "Radiation-Induced Bystander Effects." Strahlentherapie und Onkologie 179, no. 2 (February 2003): 69–77. http://dx.doi.org/10.1007/s00066-003-1000-9.

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Pilinska, M., O. Shemetun, O. Talan, O. Dibska, S. Kravchenko, and V. Sholoiko. "STUDY THE EFFECTS OF IONIZING RADIATION ON THE LEVEL OF CHROMOSOME INSTABILITY IN HUMAN SOMATIC CELLS DURING THE DEVELOPMENT OF TUMOR-INDUCED BYSTANDER EFFECT." Проблеми радіаційної медицини та радіобіології = Problems of Radiation Medicine and Radiobiology 25 (2020): 353–61. http://dx.doi.org/10.33145/2304-8336-2020-25-353-361.

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Objective. to determine the impact of the irradiated in vitro blood cells from patients with B-cell chronic lymphocytic leukemia (CLL) on the level of chromosomal instability in peripheral blood lymphocytes (PBL) from healthy persons during the development of tumor-induced bystander effect. Materials and methods. Separate and joint cultivation of PBL from healthy persons (cells-bystanders) together with blood cells from CLL patients irradiated in vitro at the G0 stage of the mitotic cycle by γ-quanta 137Cs in a dose of 0.5 Gy 137Cs (cells-inductors) was used. For joint cultivation our own model system for co-cultivation of PBL from individuals of different sex, designed by us to investigate the bystander effects at the cytogenetic level was used. Traditional cytogenetic analysis of uniformly painted chromosomes with group karyotyping was performed. The frequency of chromosome aberrations in cells-inductors and cells-bystanders as the markers of chromosome instability were determined. Results. Found that at co-cultivation of PBL from healthy individuals with irradiated blood cells from CLL patients the middle group frequency of chromosome aberrations in the bystander cells (5.18 ± 0.51 per 100 metaphases, p < 0.001) was statistically significant higher than its background level determined at a separate cultivaton (1.52 ± 0.30 per 100 metaphases), and at co-cultivation with non-irradiated blood cells from CLL patients (3.31 ± 0.50 per 100 metaphases, p < 0.01). Conclusions. Co-cultivation of in vitro irradiated blood cells from CLL patients with PBL from healthy persons leads to an increase in the level of chromosome instability in the bystander cells due to synergism between tumor-induced and radiation-induced bystander effects. Key words: human peripheral blood lymphocytes, B-cell chronic lymphocytic leukemia, ionizing radiation, chromosomal instability, tumor-induced bystander effect.
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Snyder, Andrew R. "Review of radiation-induced bystander effects." Human & Experimental Toxicology 23, no. 2 (February 2004): 87–89. http://dx.doi.org/10.1191/0960327104ht423oa.

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It is now apparent that the target for the biological effects of ionizing radiation (IR) is not solely the irradiated cell(s), but also includes the surrounding cells/tissue as well. Radiation-induced bystander effects (BSEs) are defined by the presence of the biological effects of radiation in cells that were not themselves in the field of irradiation. Decreased plating efficiency, increased sister chromatid exchanges, oncogenic transformation, among other endpoints have been used to describe the BSE. Two primary means have been established for the transmission of the bystander signal; one is mediated by gap-junction intracellular communication, and the other is initiated through the secretion of factors from irradiated cells. While the basis for these phenomena have been established in cell culture systems, there is also evidence for their presence in vivo. This in vivo effect may contribute to increased tumor cell killing, and may also play a role in the abscopal effects of radiation, where radiation responses are seen in areas separated from the irradiated tissue. Although the precise molecular components and mechanisms remain unknown, their discovery will shed new light on the role of the BSEs in radiation risk assessment, and clinical radiotherapy in the clinic.
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Faria, Fernando P., Ronald Dickman, and Carlos H. C. Moreira. "Models of the radiation-induced bystander effect." International Journal of Radiation Biology 88, no. 8 (June 11, 2012): 592–99. http://dx.doi.org/10.3109/09553002.2012.692568.

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Dissertations / Theses on the topic "Radiation induced bystander effect"

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Liu, Chang S. B. Massachusetts Institute of Technology. "Radiation-induced bystander fibroblasts both reduce and amplify micronuclei induction through the reciprocal bystander effect and the secondary bystander effect." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/106695.

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Thesis: S.B., Massachusetts Institute of Technology, Department of Nuclear Science and Engineering, 2016.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 25-27).
Aside from directly causing DNA damage, the traversal of radiation through cells also induces the bystander effect, which is the biological response of unirradiated cells that are neighboring or sharing medium with the irradiated cells. Although the mechanisms through which irradiated cells send signals to the bystander cells are not well understood, the bystander effect could potentially have clinical relevance or play a significant role in low dose radiation environments. The research in this thesis focuses on the ability of the bystander cells to influence the behavior of cells that share medium with them, which can be separated into three categories: unirradiated cells, irradiated cells, and the original irradiated cells that caused the bystander effect. These can be considered the "secondary bystanders." Human AG01522 fibroblasts were irradiated with 250 kVp X-rays and co-cultured with unirradiated fibroblasts to generate bystander cells, which were then cocultured with one of the three types of secondary bystander cells. The micronucleus assay was used to analyze the amount of chromosome aberrations present. In the unirradiated secondary bystander population, an increase in percentage of binucleated cells with micronuclei from the background level to approximately the level of the primary bystander cells was observed, indicating that bystander cells can send damaging signals. The data also showed that there was a lower frequency of micronuclei formation in the irradiated population with bystander inserts in comparison to irradiated populations without bystanders. However, there were no conclusive data on the effect of the bystander cells on other irradiated cells. Overall, the results suggest that bystander fibroblasts are capable of sending both detrimental and beneficial signals and can induce a range of behaviors in other cells.
by Chang Liu.
S.B.
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Koturbash, Igor, and University of Lethbridge Faculty of Arts and Science. "Molecular mechanisms of radiation-induced bystander effects in vivo." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/664.

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Ionizing radiation (IR), along with being an important diagnostic and treatment modality, is a potent tumor-causing agent, and the risk of secondary radiation treatment-related cancers is a growing clinical problem. Now some studies propose to link secondary radiation-induced cancers to an enigmatic phenomenon of bystander effects, whereby the exposed cells send signal damage and distress to their naïve neighbors and result in genome destabilization and carcinogenesis. Yet, no data existed on the bystander effects in an organ other than an exposed one. With this in mind, we focused on the analysis of existence and mechanisms of radiation-induced bystander effects in vivo. We have found that bystander effects occur in vivo in distant skin and spleen following half-body or cranial irradiation. These bystander effects resulted in elevated DNA damage, profound dysregulation of epigenetic machinery, and pronounced alterations in apoptosis, proliferation and gene expression. Bystander effects also exhibited persistency and sex specificity. The results obtained while using the animal model systems can potentially be extrapolated to different animals and humans.
xiii, 208 leaves : ill. ; 29 cm.
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Gonon, Géraldine. "Space radiation-induced bystander effect : kinetics of biologic responses, mechanisms, and significance of secondary radiations." Phd thesis, Université de Franche-Comté, 2011. http://tel.archives-ouvertes.fr/tel-00987717.

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Widespread evidence indicates that exposure of cell cultures to α particles results in significant biological changes in both the irradiated and non-irradiated bystander cells in the population. The induction of non-targeted biological responses in cell cultures exposed to low fluences of high charge (Z) and high energy (E) particles is relevant to estimates of the health risks of space radiation and to radiotherapy. Here, we investigated the mechanisms underlying the induction of stressful effects in confluent normal human fibroblast cultures exposed to low fluences of 1000 MeV/u iron ions (linear energy transfer (LET) ~151 keV/µm), 600 MeV/u silicon ions (LET ~50 keV/µm) or 290 MeV/u carbon ions (LET ~13 keV/µm). We compared the results with those obtained in cell cultures exposed, in parallel, to low fluences of 0.92 MeV/u α particles (LET ~109 keV/µm).Induction of DNA damage, changes in gene expression, protein carbonylation and lipid peroxidation during 24 h after exposure of confluent cultures to mean doses as low as 0.2 cGy of iron or silicon ions strongly supported the propagation of stressful effects from irradiated to bystander cells. At a mean dose of 0.2 cGy, only ~1 and 3 % of the cells would be targeted through the nucleus by an iron or silicon ion, respectively. Within 24 h post-irradiation, immunoblot analyses revealed significant increases in the levels of phospho-TP53 (serine 15), p21Waf1 (also known as CDKN1A), HDM2, phospho-ERK1/2, protein carbonylation and lipid peroxidation. The magnitude of the responses suggested participation of non-targeted cells in the response. Furthermore, when the irradiated cell populations were subcultured in fresh medium shortly after irradiation, greater than expected increases in the levels of these markers were also observed during 24 h. Together, the results imply a rapidly propagated and persistent bystander effect. In situ analyses in confluent cultures showed 53BP1 foci formation, a marker of DNA damage, in more cells than expected based on the fraction of cells traversed through the nucleus by an iron or silicon ion. The effect was expressed as early as 15 min after exposure, peaked at 1 h and decreased by 24 h. A similar tendency occurred after exposure to a mean absorbed dose of 0.2 cGy of 3.7 MeV α particles, but not after 0.2 cGy of 290 MeV/u carbon ions.Analyses in dishes that incorporate a CR-39 solid state nuclear track detector bottom identified the cells irradiated with iron or silicon ions and further supported the participation of bystander cells in the stress response. Mechanistic studies indicated that gap junction intercellular communication, DNA repair, and oxidative metabolism participate in the propagation of the induced effects.We also considered the possible contribution of secondary particles produced along the primary particle tracks to the biological responses. Simulations with the FLUKA multi-particle transport code revealed that fragmentation products, other than electrons, in cells cultures exposed to HZE particles comprise <1 % of the absorbed dose. Further, the radial spread of dose due to secondary heavy ion fragments is confined to approximately 10-20 µm Thus, the latter are unlikely to significantly contribute to the stressful effects in cells not targeted by primary HZE particles.
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Whiteside, James Roy. "Persistent genomic instability and bystander effects induced by ultraviolet radiation." Thesis, Lancaster University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444640.

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Anzenberg, Vered. "LET dependence of radiation-induced bystander effects using human prostate tumor cells." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/44795.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2008.
"June 2008."
Includes bibliographical references (leaves 133-140).
In the past fifteen years, evidence provided by many independent research groups have indicated higher numbers of cells exhibiting damage than expected based on the number of cells traversed by the radiation. This phenomenon has been coined as the "bystander effect". The purpose of this study was to characterize the ability of irradiated tumor cells to induce bystander effects in co-cultured cells. Human DU-145 prostate carcinoma cells were grown on a 1.4 [mu]m-thick mylar membrane in specially constructed cell culture dishes for irradiation with alpha particles (average energy 3.14 MeV) from a 241Am source, or in 6-well plates for irradiation with 250 kVp x-rays at 25°C. In parallel experiments, the tumor cells were incubated at 4°C for one hour prior to irradiation and irradiated on ice to test the nature of the bystander signal. Bystander cells were placed into the medium above the irradiated DU-145 and were co-incubated for a length of time. The bystander effect endpoints measured in either DU-145 tumor cells or in normal primary AGO1522 fibroblasts were micronucleus (MN) formation, [gamma]-H2AX double strand break repair foci, and survival fraction. A 1.5-2.0-fold increase in MN formation was observed in both DU-145 and AG01522 bystander cells after either alpha particle or xray irradiation of the DU-145 target cells. A 1.5-fold [gamma]-H2AX bystander increase and a survival fraction reduction to 80% were only detected in AGO1522 cells, and only after xray irradiation of target DU-145 cells. Alpha particle irradiation of the target DU-145 cells produced neither [gamma]-H2AX foci nor survival fraction bystander effect in either cell line. Lowering the temperature to 4°C during the irradiation of the DU-145 tumor cells, with either x-rays or alpha particles, eliminated both the MN formation and the decreased survival fraction bystander effects in the co-cultured AG01522 fibroblasts.
(cont.) This study demonstrates that biochemical processes in the directly-irradiated tumor cells are required for initiation of the signaling process. Low temperature during the irradiation inhibited the initiation of a bystander signal. There are also LET-dependent differences in the signal released from DU-145 human prostate carcinoma cells; and that, for some endpoints, bystander AG01522 fibroblasts and bystander DU-145 prostate carcinoma cells respond differently to the same, medium-mediated signal.
by Vered Anzenberg.
Ph.D.
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Blyth, Benjamin John, and benjamin blyth@flinders edu au. "Development and use of an adoptive transfer method for detecting radiation-induced bystander effects in vivo." Flinders University. School of Medicine, 2009. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20091008.150317.

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Ionising radiation can cause damage to DNA that can result in gene mutations contributing to carcinogenesis. Radiation-protection policy currently estimates cancer risks from exposures to radiation in terms of excess risk per unit dose. At very low radiation dose-rates, where not all cells are absorbing radiation energy, this formula carries the inherent assumption that risk is limited to those cells receiving direct energy depositions. Numerous studies have now called this assumption into question. Such low dose-rates are in the relevant range that the public receives from natural background and man-made sources, and, if this fundamental assumption proves unfounded, current estimations of radiation-induced cancer risk at low doses will be incorrect. Accurate predictions of stochastic cancer risks from low-dose radiation exposures are crucial to evaluating the safety of radiation-based technologies for industry, power generation and the increasing use of radiation for medical diagnostic and screening purposes. This thesis explores phenomena known as radiation-induced bystander effects. The term bystander effects, as used here, describes biological responses to ionising radiation (hitherto observed in vitro) in cells not directly traversed by an ionising track, due to intercellular signals received from neighbouring cells that did receive energy depositions. This study aimed to determine whether radiation effects are communicated between irradiated and unirradiated cells in vivo, and if so, whether this effect alters current estimations of cancer risk following low-dose radiation exposures. In order to answer these questions, an in vivo experimental system for studying bystander effects in mice was developed. The method was based on the adoptive transfer of irradiated splenocytes into unirradiated hosts with simultaneous identification of irradiated donor cells, and biological endpoints in unirradiated bystander cells in situ using fluorescence microscopy and image analysis. Splenocytes from donor mice were radiolabelled with 3H-thymidine or received an acute X-ray dose. The irradiated donor cells, labelled with a fluorescent probe, were then adoptively transferred into unirradiated recipient mice via the tail vein, whilst control mice received sham-irradiated donor cells. A proportion of the cells lodged in the recipient mouse spleens where they remained for a period before the tissues were cryopreserved. The locations of donor cells were identified in frozen spleen sections by the fluorescent probe, and the levels of apoptosis and proliferation were simultaneously evaluated in situ in the surrounding unirradiated bystander cells using fluorescence-based assays. Transgenic pKZ1 recipient mice were also used to quantify chromosomal inversions in bystander cells. Since three-dimensional spatial relationships were preserved, responses could be measured in the local area surrounding irradiated cells as well as further afield. Following the development of the irradiated-cell adoptive transfer protocol and validation of the sensitivity and reproducibility of the biological assays in situ, a series of experiments was performed. In the initial experiments, 500,000 radiolabelled cells (0.33 mBq.cell-1) were injected into recipient mice and the spleen tissues were isolated 22 h later. No changes in apoptosis or proliferation were detected in local bystander spleen cells or throughout the spleen, compared to mice receiving sham-radiolabelled donor cells. In subsequent experiments, the effects of a number of experimental conditions were explored including the injection of tenfold more donor cells, analysis of spleen tissues after three days lodging in vivo, radiolabelling of donor cells with 100-fold higher 3H dose-rate and irradiation of donor cells ex vivo with 0.1 or 1 Gy X-rays. In each case, no changes in apoptosis or proliferation were observed. The in vivo method described here was designed to simulate the conditions of a bystander scenario from low dose-rate exposures relevant to public radiation protection. Contrary to the many reports of bystander effects in vitro, experiments using this sensitive method for examining the in vivo responses of unirradiated cells to neighbouring low-dose irradiated cells, have so far shown no changes in bystander cells in the spleen. This adoptive transfer method is the first in vivo method for examining the effects of known irradiated cells exposed to low radiation doses at low dose-rates, on neighbouring cells in situ that are truly unirradiated. Both the irradiated and bystander cells are normal, non-transformed primary spleen cells functioning in their natural environment. This in vivo experimental system allows the examination of tens of thousands of bystander cells and has shown a remarkable sensitivity, with statistical power to rule out changes in apoptosis <10% from the control. The relevance of in vitro bystander findings is unclear. Many reported bystander effects are more analogous to the systemic communication of abscopal effects from highly irradiated tissues. Disagreement between experimental systems and difficulty in reproducing key results between laboratories further complicate the translation of bystander data in vitro to human risk-estimation. The radiation protection community has expressed its need for in vivo validation of the bystander phenomenon before it can be included into the appraisal of carcinogenic risk. This adoptive transfer method is now available to study a range of bystander endpoints and potential signalling mechanisms in vivo, and provides a way to translate the wealth of data previously collected in vitro into findings directly relevant to human risk-estimation.
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Fullerton, Natasha Eileen. "Gene therapy and targeted radiotherapy applied to bladder and prostate cancer : examination of radiation-induced bystander effects in targeted radiotherapy." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438687.

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Wordsworth, James William. "The senescent cell induced bystander effect." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2536.

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The induction of senescence in response to persistent stress induces major phenotypic changes in senescent cells, including the secretion of a host of inflammatory factors and reactive oxygen species. Recent evidence has implicated senescent cells in the diseases of ageing and cancer; however, the mechanism by which this occurs is still unknown. This thesis uses a reporter cell line with cells expressing a fluorescent conjugate that allows real time live cell imaging of a sub set of cells within a co-culture, to provide the first evidence that senescent cells can induce a DNA damage response in healthy cells, and thus implicates a potential mechanism by which senescent cells could non-autonomously contribute to the ageing process. The use of specific inhibitors, stimulation, and targeted repression indicate that gap junctions, reactive oxygen species, p38, mTOR and NF-κB all play a key role in this observed bystander effect of senescent cells, and offer potential targets for therapies designed to reduce the damaging effects of senescent cells.
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Zemp, Franz Joseph, and University of Lethbridge Faculty of Arts and Science. "The bystander effect : animal and plant models." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/685.

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Bystander effects are traditionally known as a phenomenon whereby unexposed cells exhibit the molecular symptoms of stress exposure when adjacent or nearby cells are traversed by ionizing radiation. However, the realm of bystander effects can be expanded to include any systemic changes to cellular homeostasis in response to a number of biotic or abiotic stresses, in any molecular system. This thesis encompasses three independent experiments looking at bystander and bystander-like responses in both plant and animal models. In plants, an investigation into the regulation of small RNAs has given us some insights into the regulation of the plant hormone auxin in both stress-treated and systemic (bystander) leaves. Another plant model shows that a bystander-like plant-plant signal can be induced upon ionizing radiation to increase the genome instability of neighbouring unexposed (bystander) plants. In animals, it is shown that the microRNAome is largely affected in the bystander cells in a three-dimensional human tissue model. In silico and bioinfomatic analysis of this data provide us with clues as to the nature of bystander signalling in this human ‘in vivo’ model.
xiv, 141 p. : ill. ; 29 cm.
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Lumpkins, Sarah B. "Space radiation-induced bystander signaling in 2D and 3D skin tissue models." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/70817.

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Thesis (Sc. D.)--Harvard-MIT Program in Health Sciences and Technology, 2012.
Page 157 blank. Cataloged from PDF version of thesis.
Includes bibliographical references (p. 145-156).
Space radiation poses a significant hazard to astronauts on long-duration missions, and the low fluences of charged particles characteristic of this field suggest that bystander effects, the phenomenon in which a greater number of cells exhibit damage than expected based on the number of cells traversed by radiation, could be significant contributors to overall cell damage. The purpose of this thesis was to investigate bystander effects due to signaling between different cell types cultured within 2D and 3D tissue architectures. 2D bystander signaling was investigated using a transwell insert system in which normal human fibroblasts (A) and keratinocytes (K) were irradiated with 1 GeV/n protons or iron ions at the NASA Space Radiation Laboratory using doses from either 2 Gy (protons) or 1 Gy (iron ions) down to spacerelevant low fluences. Medium-mediated bystander responses were investigated using three cell signaling combinations. Bystander signaling was also investigated in a 3D model by developing tissue constructs consisting of fibroblasts embedded in a collagen matrix with a keratinocyte epidermal layer. Bystander experiments were conducted by splitting each construct in half and exposing half to radiation then placing the other half in direct contact with the irradiated tissue on a transwell insert. Cell damage was evaluated primarily as formation of foci of the DNA repair-related protein 53BP1. In the 2D system, both protons and iron ions yielded a strong dose dependence for the induction of 53BP1 in irradiated cells, while the magnitudes and time courses of bystander responses were dependent on radiation quality. Furthermore, bystander effects were present in all three cell signaling combinations even at the low proton particle fluences used, suggesting the potential importance of including these effects in cancer risk models for low-dose space radiation exposures. Cells cultured in the 3D constructs exhibited a significant reduction in the percentages of both direct and bystander cells positive for 53BP1 foci, although the qualitative kinetics of DNA damage and repair were similar to those observed in 2D. These results provide evidence that the microenvironment significantly influences intercellular signaling and that cells may be more radioresistant in 3D compared to 2D systems.
by Sarah B. Lumpkins.
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Books on the topic "Radiation induced bystander effect"

1

Ėlango, M. A. Elementary inelastic radiation-induced processes. New York: American Institute of Physics, 1991.

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Goldstein, L. S. Radiation-induced germ cell mutations-- their detection and modification. Washington, DC: Defense Nuclear Agency, 1987.

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Goldstein, L. S. Radiation-induced germ cell mutations-- their detection and modification. Washington, DC: Defense Nuclear Agency, 1987.

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Goldstein, L. S. Radiation-induced germ cell mutations-- their detection and modification. Washington, DC: Defense Nuclear Agency, 1987.

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Laser-induced damage of optical materials. Bristol: Institute of Physics, 2003.

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Haston, Christina Kathleen. The effect of fraction spacing on radiation-induced lung damage in rats. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Robin, Russell Jones, and Southwood Richard Sir 1931-, eds. Radiation and health: The biological effectsof low-level exposure to ionizing radiation. Chichester: Wiley, 1987.

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Hardy, J. T. Human-induced global climate change: Predicted effects and implicatons for the Gulf. Leiden: Backhuys, 2002.

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International Symposium on Plasma Process-Induced Damage (4th 1999 Monterey, Calif.). 1999 4th International Symposium on Plasma Process-Induced Damage: May 9-11, 1999, Monterey, California, USA. Edited by Dao, Leanne Thuy Lien, 1958-, Koyanagi Mitsumasa, Hook Terence, IEEE Electron Devices Society, American Vacuum Society, and Ōyō Butsuri Gakkai. Sunnyvale, CA: Northern California Chapter of the American Vacuum Society, 1999.

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International, Symposium on Plasma Process-Induced Damage (1st 1996 Santa Clara Calif ). 1996 1st International Symposium on Plasma Process-Induced Damage: 13-14 May 1996, Santa Clara, California, USA. Sunnyvale, CA: Northern California Chapter of the American Vacuum Society, 1996.

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Book chapters on the topic "Radiation induced bystander effect"

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Mothersill, Carmel, and Colin Seymour. "Radiation-Induced Bystander Effects and Stress-Induced Mutagenesis." In Stress-Induced Mutagenesis, 199–222. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6280-4_10.

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Azzam, Edouard I., Sonia M. de Toledo, Andrew L. Harris, Vladimir Ivanov, Hongning Zhou, Sally A. Amundson, Howard B. Lieberman, and Tom K. Hei. "The Ionizing Radiation-Induced Bystander Effect: Evidence, Mechanism, and Significance." In Pathobiology of Cancer Regimen-Related Toxicities, 35–61. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5438-0_3.

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Lintott, Rachel, Stephen McMahon, Kevin Prise, Celine Addie-Lagorio, and Carron Shankland. "Using Process Algebra to Model Radiation Induced Bystander Effects." In Computational Methods in Systems Biology, 196–210. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12982-2_14.

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Dieriks, B., W. De Vos, and P. Van Oostveldt. "Analysis of radiation-induced bystander effects using high content screening." In EMC 2008 14th European Microscopy Congress 1–5 September 2008, Aachen, Germany, 249–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-85228-5_125.

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Ermakov, Aleksey V., Marina S. Konkova, Svetlana V. Kostyuk, Tatjana D. Smirnova, Liudmila V. Efremova, Liudmila N. Lyubchenko, and Natalya N. Veiko. "Development of the Adaptive Response and Bystander Effect Induced by Low-Dose Ionising Radiation in Human Mesenchymal Stem Cells." In Circulating Nucleic Acids in Plasma and Serum, 225–31. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9382-0_31.

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Krześlak, Michał, and Andrzej Świerniak. "Extended Spatial Evolutionary Games and Induced Bystander Effect." In Advances in Intelligent Systems and Computing, 337–48. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06593-9_30.

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Surinov, Boris P., Valentina G. Isaeva, Natalia N. Dukhova, and Andrey D. Kaprin. "The Significance of Chemosignaling Between Irradiated and Non-irradiated Organisms in Bystander Effect." In Genetics, Evolution and Radiation, 193–203. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48838-7_17.

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van der Schans, G. P. "Effect of Dose Modifiers on Radiation-Induced Cellular DNA Damage." In The Early Effects of Radiation on DNA, 347–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_36.

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Dokwal, Sumit, Suman Mahendia, Rishi Pal Chahal, Vishal Sharma, Suman B. Kuhar, and Shyam Kumar. "Irradiation-induced effect on polymer: From mechanism to biomedical applications." In Radiation Technologies and Applications in Materials Science, 149–75. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003321910-6.

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Grdina, David J., Biserka Nagy, and Paul J. Meechan. "Effect of an Aminothiol (WR-1065) on Radiation-Induced Mutagenesis and Cytotoxicity in Two Repair-Deficient Mammalian Cell Lines." In Anticarcinogenesis and Radiation Protection 2, 287–95. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3850-9_41.

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Conference papers on the topic "Radiation induced bystander effect"

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Swierniak, Andrzej, and Michal Krzeslak. "Evolutionary and Spatial Evolutionary Games and Radiation Induced Bystander Effect." In Biomedical Engineering. Calgary,AB,Canada: ACTAPRESS, 2012. http://dx.doi.org/10.2316/p.2012.764-034.

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Swierniak, Andrzej, and Michal Krzeslak. "GAME THEORETIC APPROACH TO MATHEMATICAL MODELING OF RADIATION INDUCED BYSTANDER EFFECT." In Biomedical Engineering. Calgary,AB,Canada: ACTAPRESS, 2010. http://dx.doi.org/10.2316/p.2010.723-017.

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Swierniak, Andrzej, and Michal Krzeslak. "Game Theoretic Approach to Mathematical Modeling of Radiation Induced Bystander Effect." In Biomedical Engineering. Calgary,AB,Canada: ACTAPRESS, 2011. http://dx.doi.org/10.2316/p.2011.723-017.

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Veeraraghavan, Jamunarani, Mohan Natarajan, Terence S. Herman, and Natarajan Aravindan. "Abstract 574: Mechanism of radiation-induced bystander effect: Role of NFκß pathway." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-574.

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Tubin, Slavisa, Seema Gupta, and Mansoor M. Ahmed. "Abstract LB-370: Radiation and hypoxia-induced bystander effect in human lung cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-370.

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Olivier, David, Samuel Douilard, and Thierry Patrice. "PDT-induced in vitro bystander effect." In 12th World Congress of the International Photodynamic Association, edited by David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.823471.

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Lo, Chia-Chien, Yen-Ting Chou, Su-Jun Chiu, Jeng-Jung Hwang, and Yi-Jang Lee. "Abstract 440: The sublethal dose radiation induces cellular senescence and potent bystander effects through c-Myc oncogene." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-440.

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Szilágyi, Zsófia, Bertalan Pintér, Erika Szabó, Györgyi Kubinyi, and György Thuróczy. "Pilot study of radiofrequency radiation impacted bystander effect on dermal fibroblast cells in vitro." In RAD Conference. RAD Centre, 2022. http://dx.doi.org/10.21175/rad.spr.abstr.book.2022.27.6.

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Wang, Xingmin, Yonghong Yang, and Mark M. Huycke. "Abstract 1713: Macrophage-induced bystander effect activates Wnt/β-catenin signaling and induces cellular dedifferentiation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1713.

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Prahardi, R., and Arundito Widikusumo. "Zero Dose." In Seminar Si-INTAN. Badan Pengawas Tenaga Nuklir, 2021. http://dx.doi.org/10.53862/ssi.v1.062021.008.

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Abstract:
Ionizing radiation in the medical world has long been used, both for diagnostic and therapeutic purposes. But the use of ionizing radiation, besides helping a lot in diagnosis and therapy, ionizing radiation is also hazardous for us. The effects of ionizing radiation on humans are divided into two types, namely stochastic effects, and non-stochastic (deterministic) effects. Of the two kinds of effects caused by ionizing radiation, the stochastic effect needs special attention. Because the dose-limiting parameter does not exist, how much radiation dose can cause the stochastic effect. We only have the principle that no matter how small the radiation that hits us, it will still impact us. The mechanism for this effect is either a direct effect or an indirect effect, or a newly discovered effect, namely the bystander effect, all of which lead to DNA damage. This DNA damage will cause various kinds of health problems for us. Keywords: Stochastic Effect, DNA Damage. Gene Mutation, Bystander Effect
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Reports on the topic "Radiation induced bystander effect"

1

Folkard, Melvyn, Borivoj Vojnovic, Giuseppe Schettino, Kirk Atkinson, Kevin, M. Prise, and Barry, D. Michael. A Variable-Energy Soft X-Ray Microprobe to Investigate Mechanisms of the Radiation-Induced Bystander Effect. US: Gray Cancer Institute, PO Box 100, Mount Vernon Hospital, Northwood, Middlesex, HA62JR, UK, January 2007. http://dx.doi.org/10.2172/897804.

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Kim, Hun S. Mechanisms of Radiation-Induced Bone Loss and Effect on Prostate Cancer Bone Metastases. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada581466.

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Kwon, Joong Ho, Eun Joo Lee, and Dong U. Ahn. Effect of Cooking on Radiation-induced Chemical Markers in Beef and Pork during Storage. Ames (Iowa): Iowa State University, January 2014. http://dx.doi.org/10.31274/ans_air-180814-1176.

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Little, John B. Effects of Low-Dose Alpha-Particle Irradiation in Human Cells: The Role of Induced Genes and the Bystander Effect. Final Technical Report (9/15/1998-5/31/2005). Office of Scientific and Technical Information (OSTI), September 2013. http://dx.doi.org/10.2172/1093259.

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Turkot, F., C. Hojvat, W. Anderson, C. S. Lindsey, N. Biswas, J. Piekarz, and A. Bujak. Studies of beam induced radiation for experiment 735 at the CO interaction region and its effect on detector components. Office of Scientific and Technical Information (OSTI), June 1985. http://dx.doi.org/10.2172/5934713.

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Charatsi, Dimitra, Polyxeni Vanakara, Michail Nikolaou, Aikaterini Evaggelopoulou, Dimitrios Korfias, Foteini Simopoulou, Nikolaos Charalampakis, et al. Vaginal Dilator Use to Promote Sexual Wellbeing After Radiotherapy in Gynaecological Cancer Survivors: A Prospective Observational Study. Science Repository, October 2021. http://dx.doi.org/10.31487/j.ijcst.2021.03.01.sup.

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Abstract:
Background: Since continuing advances in radiotherapy technology broaden the role of radiotherapy in the treatment of gynaecologic malignancies, the use of vaginal dilators has been introduced in order to mitigate the risk of vaginal stenosis. The main aims of this study were to investigate the vaginal dilator use efficacy in the treatment of radiation-induced vaginal stenosis and the vaginal dilator effect on sexual quality of life. Methods: We studied fifty-three patients with endometrial or cervical cancer. The participants were treated with radical or adjuvant external beam radiotherapy and/or brachytherapy. They were routinely examined at four time points post-radiotherapy when also they were asked to fill in a validated sexual function-vaginal changes questionnaire. A p-value less than 0.05 was considered statistically significant. Results: The vaginal stenosis grading score was decreased and the size of the vaginal dilator comfortably insertable was gradually increased throughout the year of vaginal dilator use while radiation-induced vaginal and sexual symptoms were improved throughout the year of VD use. All patients with initial grade 3 showed vaginal stenosis of grade 2 after 12 months of vaginal dilator use and 65.8% of the patients with grade 2 initial vaginal stenosis demonstrated final vaginal stenosis grade 1 while 77.8% of the participants with initial 1st size of vaginal dilators reached the 3rd vaginal dilator size after 12 months. Starting time of dilator therapy <= 3 months after the end of radiotherapy was associated with a significant decrease in vaginal stenosis. Additionally, there was an overall upward trend regarding patients’ satisfaction with their sexual life. Conclusion: Endometrial and cervical cancer survivors should be encouraged to use vaginal dilators for the treatment of vaginal stenosis and sexual rehabilitation after radiotherapy.
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