Radiation Research Journal Impact Factor & Information

Publisher: Radiation Research Society (U.S.), Radiation Research Society

Current impact factor: 2.91

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.911
2013 Impact Factor 2.445
2012 Impact Factor 2.698
2011 Impact Factor 2.684
2010 Impact Factor 2.578
2009 Impact Factor 2.948
2008 Impact Factor 3.043
2007 Impact Factor 2.599
2006 Impact Factor 2.602
2005 Impact Factor 3.099
2004 Impact Factor 3.228
2003 Impact Factor 3.208
2002 Impact Factor 2.768
2001 Impact Factor 2.478
2000 Impact Factor 2.752
1999 Impact Factor 2.807
1998 Impact Factor 3.109
1997 Impact Factor 2.405
1996 Impact Factor 2.356
1995 Impact Factor 1.98
1994 Impact Factor 2.314
1993 Impact Factor 1.74
1992 Impact Factor 1.792

Impact factor over time

Impact factor

Additional details

5-year impact 2.88
Cited half-life >10.0
Immediacy index 0.57
Eigenfactor 0.01
Article influence 0.85
Other titles Radiation research (Online), Radiation research
ISSN 1938-5404
OCLC 47723402
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Radiation Research Society

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • On open access repositories or websites only
    • Publisher's version/PDF must be used
    • Publishers PDF can be obtained for a fee
    • Permission to use elsewhere must be obtained from Publisher
    • Publisher will deposit PDF in PubMed Central for NIH authors after 12 months
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The Thyrotoxicosis Therapy Follow-up Study (TTFUS) is comprised of 35,593 hyperthyroid patients treated from the mid-1940s through the mid-1960s. One objective of the TTFUS was to evaluate the long-term effects of high-dose iodine-131 ((131)I) treatment (1-4). In the TTFUS cohort, 23,020 patients were treated with (131)I, including 21,536 patients with Graves disease (GD), 1,203 patients with toxic nodular goiter (TNG) and 281 patients with unknown disease. The study population constituted the largest group of hyperthyroid patients ever examined in a single health risk study. The average number (±1 standard deviation) of (131)I treatments per patient was 1.7 ± 1.4 for the GD patients and 2.1 ± 2.1 for the TNG patients. The average total (131)I administered activity was 380 ± 360 MBq for GD patients and 640 ± 550 MBq for TNG patients. In this work, a biokinetic model for iodine was developed to derive organ residence times and to reconstruct the radiation-absorbed doses to the thyroid gland and to other organs resulting from administration of (131)I to hyperthyroid patients. Based on (131)I data for a small, kinetically well-characterized sub-cohort of patients, multivariate regression equations were developed to relate the numbers of disintegrations of (131)I in more than 50 organs and tissues to anatomical (thyroid mass) and clinical (percentage thyroid uptake and pulse rate) parameters. These equations were then applied to estimate the numbers of (131)I disintegrations in the organs and tissues of all other hyperthyroid patients in the TTFUS who were treated with (131)I. The reference voxel phantoms adopted by the International Commission on Radiological Protection (ICRP) were then used to calculate the absorbed doses in more than 20 organs and tissues of the body. As expected, the absorbed doses were found to be highest in the thyroid (arithmetic means of 120 and 140 Gy for GD and TNG patients, respectively). Absorbed doses in organs other than the thyroid were much smaller, with arithmetic means of 1.6 Gy, 1.5 Gy and 0.65 Gy for esophagus, thymus and salivary glands, respectively. The arithmetic mean doses to all other organs and tissues were more than 100 times less than those to the thyroid gland. To our knowledge, this work represents the most comprehensive study to date of the doses received by persons treated with (131)I for hyperthyroidism.
    Radiation Research 11/2015; DOI:10.1667/RR14160.1
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    ABSTRACT: Inflammatory cytokines have been implicated in the regulation of radiation-induced genomic instability in the hematopoietic system and have also been shown to induce chronic DNA damage responses in radiation-induced senescence. We have previously shown that human bronchial epithelial cells (HBEC3-KT) have increased genomic instability and IL-8 production persisting at day 7 after exposure to high-LET (600 MeV/nucleon (56)Fe ions) compared to low-LET (320 keV X rays) radiation. Thus, we investigated whether IL-8 induction is part of a broader pro-inflammatory response produced by the epithelial cells in response to damage, which influences genomic instability measured by increased micronuclei and DNA repair foci frequencies. We found that exposure to radiation induced the release of multiple inflammatory cytokines into the media, including GM-CSF, GROα, IL-1α, IL-8 and the inflammation modulator, IL-1 receptor antagonist (IL-1RA). Our results suggest that this is an IL-1α-driven response, because an identical signature was induced by the addition of recombinant IL-1α to nonirradiated cells and functional interference with recombinant IL-1RA (Anakinra) or anti-IL-1α function-blocking antibody, decreased IL-8 production induced by radiation exposure. However, genomic instability was not influenced by this pathway as addition of recombinant IL-1α to naive or irradiated cells or the presence of IL-1 RA under the same conditions as those that interfered with the induction of IL-8, did not affect micronuclei or DNA repair foci frequencies measured at day 7 after exposure. While dose-response studies revealed that genomic instability and IL-8 production are the consequences of targeted effects, experiments employing a co-culture transwell system revealed the propagation of pro-inflammatory responses but not genomic instability from irradiated to nonirradiated cells. Collectively, these results point to a cell-autonomous mechanism sustaining radiation-induced genomic instability in this model system and suggest that while molecules associated with these mechanisms could be markers for persisting damage, they reflect two different outcomes.
    Radiation Research 11/2015; DOI:10.1667/RR14045.1
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    ABSTRACT: A unique feature of the space radiation environment is the presence of high-energy charged particles, which can be significantly hazardous to space flight crews who are exposed during a mission. Health risks associated with high-LET radiation exposure include cognitive injury. The pathogenesis of this injury is unknown but may involve modifications to dendritic structure and/or alterations in dendritic spine density and morphology. In this study, 24 two-month-old C57BL6/J male mice were either whole-body irradiated with 0.5 Gy (56)Fe (600 MeV/n; n = 12) or sham irradiated (n = 12). Three months postirradiation animals were tested for locomotor activity and habituation. After behavioral testing, animals were euthanized and the brains were flash frozen. Compared to sham-irradiated mice, irradiated mice moved less when first introduced to the environment, although they did recognize the environment when re-exposed to it one day later. Exposure to (56)Fe radiation significantly compromised the dendritic architecture and reduced spine density throughout the hippocampal tri-synaptic network. To our knowledge, this data represents the first reported evidence that high-LET radiation has deleterious effects on mature neurons associated with hippocampal learning and memory.
    Radiation Research 11/2015; DOI:10.1667/RR14103.1
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    ABSTRACT: Radiation-induced heart injury is one of the major side effects of radiotherapy for thoracic malignancies. Previous studies have shown that radiotherapy induced myocardial fibrosis and intensified myocardial remodeling. In this study, we investigated whether atorvastatin could inhibit radiation-induced heart fibrosis in Sprague-Dawley rats, which were randomly divided into six groups: control; radiation only; and four treatment groups receiving atorvastatin plus radiation (E1, E2, E3 and E4). All rats, except the control group, received local heart irradiation in 7 daily fractions of 3 Gy for a total of 21 Gy. Rats in groups E1 (10 mg/kg/day) and E2 (20 mg/kg/day) received atorvastatin and radiation treatment until week 12 after exposure. Rats in groups E3 (10 mg/kg/day) and E4 (20 mg/kg/day) received atorvastatin treatment from 3 months before irradiation to week 12 after irradiation. The expressions of TGF-β1, Smad2, Smad3, fibronectin, ROCK I and p-Akt in heart tissues were evaluated using real-time PCR or Western blot analyses. Atorvastatin significantly reduced the expression of TGF-β1, Smad3/P-Smad3, ROCK I and p-Akt in rats of the E1-E4 groups and in a dose-dependent manner. Fibronectin exhibited a similar pattern of expression changes. In addition, echocardiography showed that atorvastatin treatment can inhibit the increase of left ventricular end-diastolic dimension, left ventricular end-systolic diameter and left ventricular posterior wall thickness, and prevent the decrease of ejection fraction and fraction shortening in E1-E4 groups compared with the radiation only group. This study demonstrated that radiation exposure increased the expression of fibronectin in cardiac fibroblasts and induced cardiac fibrosis through activation of the TGF-β1/Smad3, RhoA/ROCK, and PI3K/AKT signaling pathways. Statins ameliorated radiation-induced cardiac fibrosis in Sprague-Dawley rats. Our results suggest that atorvastatin is effective for the treatment of radiation-induced cardiac fibrosis, especially with longer and higher dose atorvastatin treatment, as demonstrated in experimental group E4.
    Radiation Research 11/2015; DOI:10.1667/RR14075.1

  • Radiation Research 11/2015; 184(5):559-560. DOI:10.1667/RR00WB.1
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    ABSTRACT: Low-dose ionizing radiation is known to induce radioadaptive responses in cells in vitro as well as in mice in vivo. Low-dose radiation decreases the incidence and increases latency for spontaneous and radiation-induced tumors in mice, potentially as a result of enhanced cellular DNA repair efficiency or a reduction in genomic instability. In this study, the cytokinesis-block micronucleus (CBMN) assay was used to examine dose response and potential radioadaptive response for cytogenetic damage and cell survival in C57BL/6 and BALB/c spleen cells exposed in vitro or in vivo to low-dose (60)Co gamma radiation. The effects of genetic background, radiation dose and dose rate, sampling time and cell cycle were investigated with respect to dose response and radioadaptive response. In C57BL/6 mice, a linear-quadratic dose-response relationship for the induction of micronuclei (MN) was observed for doses between 100 mGy and 2 Gy. BALB/c mice exhibited increased radiosensitivity for MN induction compared to C57BL/6 mice. A 20 mGy dose had no effect on MN frequencies in splenocytes of either mouse strain, however, increased spleen weight and a reduced number of dead cells were noted in the C57BL/6 strain only. Multiple experimental parameters were investigated in radioadaptive response studies, including dose and dose rate of the priming dose (20 mGy at 0.5 mGy/min and 100 mGy at 10 mGy/min), time interval (4 and 24 h) between priming and challenge doses, cell cycle stage (resting or proliferating) at exposure and kinetics after the challenge dose. Radioadaptive responses were not observed for MN induction for either mouse strain under any of the experimental conditions investigated. In contrast, a synergistic response for radiation-induced micronuclei in C57BL/6 spleen was detected after in vivo 20 mGy irradiation. This increase in the percentage of cells with cytogenetic damage was associated with a reduction in the number of nonviable spleen cells, suggesting that low-dose irradiation led to a reduction in the turnover of damaged cells within the spleen of C57BL/6 mice. Overall, these results indicate that long-term protective effects against tumor latency and other beneficial health outcomes observed after low-dose irradiation are not mediated by a reduction of the proportion of cells harboring radiation-induced cytogenetic damage.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14102.1
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    ABSTRACT: The non-human primate has been a useful model for studies of human acute radiation syndrome (ARS). However, to date structural changes in various parts of the intestine after total body irradiation (TBI) have not been systematically studied in this model. Here we report on our current study of TBI-induced intestinal structural injury in the non-human primate after doses typically associated with hematopoietic ARS. Twenty-four non-human primates were divided into three groups: sham-irradiated control group; and total body cobalt-60 ((60)Co) 6.7 Gy gamma-irradiated group; and total body (60)Co 7.4 Gy gamma-irradiated group. After animals were euthanized at day 4, 7 and 12 postirradiation, sections of small intestine (duodenum, proximal jejunum, distal jejunum and ileum) were collected and fixed in 10% formalin. The intestinal mucosal surface length, villus height and crypt depths were assessed by computer-assisted image analysis. Plasma citrulline levels were determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Total bone marrow cells were counted and hematopoietic stem/progenitor cells in bone marrow were analyzed by flow cytometer. Histopathologically, all segments exhibited conspicuous disappearance of plicae circulares and prominent atrophy of crypts and villi. Intestinal mucosal surface length was significantly decreased in all intestinal segments on day 4, 7 and 12 after irradiation (P < 0.02-P < 0.001). Villus height was significantly reduced in all segments on day 4 and 7 (P = 0.02-0.005), whereas it had recovered by day 12 (P > 0.05). Crypt depth was also significantly reduced in all segments on day 4, 7 and 12 after irradiation (P < 0.04-P < 0.001). Plasma citrulline levels were dramatically reduced after irradiation, consistent with intestinal mucosal injury. Both 6.7 and 7.4 Gy TBI reduced total number of bone marrow cells. And further analysis showed that the number and function of CD45(+)CD34(+) hematopoietic stem/progenitors in bone marrow decreased significantly. In summary, TBI in the hematopoietic ARS dose range induces substantial intestinal injury in all segments of the small bowel. These findings underscore the importance of maintaining the mucosal barrier that separates the gut microbiome from the body's interior after TBI.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14191.1
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    ABSTRACT: We measured and compared the circular dichroism (CD) spectra and secondary structures of histone proteins H2A, H2B and their variants extracted from X-irradiated and unirradiated human HeLa cells. Compared to unirradiated cells, a relative increase in α-helix structure and decrease in other secondary structures was observed in X-irradiated cells. These structural alterations persisted for at least 24 h, which is substantially longer than the 2 h generally known to be required for DNA double-strand break repair.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14071.1
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    ABSTRACT: We present a simple model for a component of the radiolytic production of any chemical species due to electron emission from irradiated nanoparticles (NPs) in a liquid environment, provided the expression for the G value for product formation is known and is reasonably well characterized by a linear dependence on beam energy. This model takes nanoparticle size, composition, density and a number of other readily available parameters (such as X-ray and electron attenuation data) as inputs and therefore allows for the ready determination of this contribution. Several approximations are used, thus this model provides an upper limit to the yield of chemical species due to electron emission, rather than a distinct value, and this upper limit is compared with experimental results. After the general model is developed we provide details of its application to the generation of HO(•) through irradiation of gold nanoparticles (AuNPs), a potentially important process in nanoparticle-based enhancement of radiotherapy. This model has been constructed with the intention of making it accessible to other researchers who wish to estimate chemical yields through this process, and is shown to be applicable to NPs of single elements and mixtures. The model can be applied without the need to develop additional skills (such as using a Monte Carlo toolkit), providing a fast and straightforward method of estimating chemical yields. A simple framework for determining the HO(•) yield for different NP sizes at constant NP concentration and initial photon energy is also presented.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14059.1
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    ABSTRACT: Triptolide (TPL) may mitigate radiation-induced late pulmonary side effects through its inhibition of global pro-inflammatory cytokines. In this study, we evaluated the effect of TPL in C57BL/6 mice, the animals were exposed to radiation with vehicle (15 Gy), radiation with TPL (0.25 mg/kg i.v., twice weekly for 1, 2 and 3 months), radiation and celecoxib (CLX) (30 mg/kg) and sham irradiation. Cultured supernatant of irradiated RAW 264.7 and MLE-15 cells and lung lysate in different groups were enzyme-linked immunosorbent assays at 33 h. Respiratory rate, pulmonary compliance and pulmonary density were measured at 5 months in all groups. The groups exposed to radiation with vehicle and radiation with TPL exhibited significant differences in respiratory rate and pulmonary compliance (480 ± 75/min vs. 378 ± 76/min; 0.6 ± 0.1 ml/cm H2O/p kg vs. 0.9 ± 0.2 ml/cm H2O/p kg). Seventeen cytokines were significantly reduced in the lung lysate of the radiation exposure with TPL group at 5 months compared to that of the radiation with vehicle group, including profibrotic cytokines implicated in pulmonary fibrosis, such as IL-1β, TGF- β1 and IL-13. The radiation exposure with TPL mice exhibited a 41% reduction of pulmonary density and a 25% reduction of hydroxyproline in the lung, compared to that of radiation with vehicle mice. The trichrome-stained area of fibrotic foci and pathological scaling in sections of the mice treated with radiation and TPL mice were significantly less than those of the radiation with vehicle-treated group. In addition, the radiation with TPL-treated mice exhibited a trend of improved survival rate compared to that of the radiation with vehicle-treated mice at 5 months (83% vs. 53%). Three radiation-induced profibrotic cytokines in the radiation with vehicle-treated group were significantly reduced by TPL treatment, and this partly contributed to the trend of improved survival rate and pulmonary density and function and the decreased severity of pulmonary fibrosis at 5 months. Our findings indicate that triptolide could be a potential new agent to mitigate radiation-induced pulmonary fibrosis.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR13831.1
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    ABSTRACT: Although a standardized approach to radiotherapy has been used to treat breast cancer, regardless of subtype (e.g., luminal, basal), recent clinical data suggest that radiation response may vary significantly among subtypes. We hypothesized that this clinical variability may be due, in part, to differences in cellular radiation response. In this study, we utilized RNA samples for microarray analysis from two sources: 1. Paired pre- and postirradiation breast tumor tissue from 32 early-stage breast cancer patients treated in our unique preoperative radiation Phase I trial; and 2. Sixteen biologically diverse breast tumor cell lines exposed to 0 and 5 Gy irradiation. The transcriptome response to radiation exposure was derived by comparing gene expression in samples before and after irradiation. Genes with the highest coefficient of variation were selected for further evaluation and validated at the RNA and protein level. Gene editing and agonistic antibody treatment were performed to assess the impact of gene modulation on radiation response. Gene expression in our cohort of luminal breast cancer patients was distinctly different before and after irradiation. Further, two distinct patterns of gene expression were observed in our biologically diverse group of breast cancer cell lines pre- versus postirradiation. Cell lines that showed significant change after irradiation were largely luminal subtype, while gene expression in the basal and HER2(+) cell lines was minimally impacted. The 100 genes with the most significant response to radiation in patients were identified and analyzed for differential patterns of expression in the radiation-responsive versus nonresponsive cell lines. Fourteen genes were identified as significant, including FAS, a member of the tumor necrosis factor receptor family known to play a critical role in programed cell death. Modulation of FAS in breast cancer cell lines altered radiation response phenotype and enhanced radiation sensitivity in radioresistant basal cell lines. Our findings suggest that cell-type-specific, radiation-induced FAS contributes to subtype-specific breast cancer radiation response and that activation of FAS pathways may be exploited for biologically tailored radiotherapy.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14089.1
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    ABSTRACT: We report here on a qualitative and quantitative comparison of four kinetic photon cell survival models. The commonly used linear-quadratic model extended by a dose protraction factor, the lethal potentially lethal model, the repair misrepair model and the recently reported Giant LOop Binary LEsion (GLOBLE) model are discussed with respect to the proposed underlying biological mechanisms explaining the cellular response to radiation. Furthermore, with the use of eight benchmarks, the accuracy, reliability, resolution power and robustness of the models are assessed and compared. This work demonstrates that the linear-quadratic, lethal potentially lethal and GLOBLE models often perform equivalently and that the repair misrepair model appears to have some drawbacks regarding the end points under investigation.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR13862.1
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    ABSTRACT: We examined nutrient transport in the intestines of mice exposed to chronic low-LET (137)Cs gamma rays. The mice were whole-body irradiated for 3 days at dose rates of 0, 0.13 and 0.20 Gy/h, for total dose delivery of 0, 9.6 or 14.4 Gy, respectively. The mice were fed either a control diet or a diet supplemented with high levels of vitamins A, C and E. Our results showed that nutrient transport was perturbed by the chronic irradiation conditions. However, no apparent alteration of the macroscopic intestinal structures of the small intestine were observed up to day 10 after initiating irradiation. Jejunal fructose uptake measured in vitro was strongly affected by the chronic irradiation, whereas uptake of proline, carnosine and the bile acid taurocholate in the ileum was less affected. D-glucose transport did not appear to be inhibited significantly by either 9.6 or 14.4 Gy exposure. In the 14.4 Gy irradiated groups, the diet supplemented with high levels of vitamins A, C and E increased intestinal transport of fructose compared to the control diet (day 10; t test, P = 0.032), which correlated with elevated levels of vitamins A, C and E in the plasma and jejunal enterocytes. Our earlier studies with mice exposed acutely to (137)Cs gamma rays demonstrated significant protection for transport of fructose, glucose, proline and carnosine. Taken together, these results suggest that high levels of vitamins A, C and E dietary supplements help preserve intestinal nutrient transport when intestines are irradiated chronically or acutely with low-LET gamma rays.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14043.1
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    ABSTRACT: This article provides a summary of presentations focused on critical education and training issues in radiation oncology, radiobiology and medical physics from a workshop conducted as part of the 60th Annual Meeting of the Radiation Research Society held in Las Vegas, NV (September 21-24, 2014). Also included in this synopsis are pertinent comments and concerns raised by audience members, as well as recommendations for addressing ongoing and future challenges.
    Radiation Research 10/2015; 184(5). DOI:10.1667/RR14199.1
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    ABSTRACT: Ionizing radiation induces more cell death under normoxic conditions than under hypoxic conditions. This phenomenon, which is known as the oxygen enhancement effect, occurs primarily because ionizing radiation causes more DNA lesions in the presence of oxygen than in its absence. However, the roles these lesions play in terms of cell survival and chromosome damage have not been fully characterized. We exposed a panel of chicken DT40 mutant cells to ionizing radiation to categorize the type of lesion induced and the DNA-repair pathway involved under both normoxic and hypoxic conditions. Among the mutant panel, RAD54(-/-)/KU70(-/-) cells exhibited the greatest radiosensitivity, which was found to be significantly higher under normoxic conditions. This indicates that double-strand breaks (DSBs) were the major cause of cell death and that ionizing radiation induces more DSBs under normoxic condition. Interestingly, the sensitivity of the REV3(-/-) cells increased under hypoxic conditions. Indeed, the REV3(-/-) mutant exhibited a greater number of chromosomal aberrations under hypoxic conditions than under normoxic conditions. These results suggest that the Rev3-mediated translesion-synthesis pathway is more critical for cellular tolerance to ionizing radiation in hypoxic cells than in normoxic cells, and that more chemically modified DNA might be induced under hypoxic conditions. In this study, we identify a previously unappreciated radiation-induced pattern of DNA damage under hypoxic conditions.
    Radiation Research 10/2015; 184(4). DOI:10.1667/RR14117.1
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    ABSTRACT: Protein synthesis is essential for growth, proliferation and survival of cells. Translation factors are overexpressed in many cancers and in preclinical models, their experimental inhibition has been shown to inhibit cancer growth. Differential regulation of translation also occurs upon exposure to cancer-relevant stressors such as hypoxia and ionizing radiation. The failure to regulate translation has been shown to interfere with recovery after genotoxic stress. These findings suggest that modulation of translation, alone or in conjunction with genotoxins, may be therapeutic in oncology. Yet, only two drugs that directly inhibit translation are FDA-approved for oncology therapies used today. We have previously identified the protein synthesis inhibitor, bouvardin in a screen for small molecule enhancers of ionizing radiation in Drosophila melanogaster . Bouvardin was independently identified in a screen for selective inhibitors of engineered human breast cancer stem cells. Here we report the effect of bouvardin treatment in preclinical models of head and neck cancer (HNC) and glioma, two cancer types for which radiation therapy is the most common treatment. Our data show that bouvardin treatment blocked translation elongation on human ribosomes and suggest that it did so by blocking the dissociation of elongation factor 2 from the ribosome. Bouvardin and radiation enhanced the induction of clonogenic death in HNC and glioma cells, although by different mechanisms. Bouvardin treatment enhanced the radiation-induced antitumor effects in HNC tumor xenografts in mice. These data suggest that inhibition of translation elongation, particularly in combination with radiation treatment, may be a promising treatment option for cancer.
    Radiation Research 09/2015; 184(4). DOI:10.1667/RR14068.1