Radiation-induced genes expressed in six murine tumors.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE15362 | GEO | 2015/03/23
SECONDARY ACCESSION(S): PRJNA117091
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression profiling was used to identify genes that display radiation-induced transcriptional change over tumor histopathology. Keywords: mouse squamous cell carcinoma, fibrosarcoma and mammary carcinoma, gamma-irradiation, carbon ion irradiation, resected sample, transplanted tissues
2009-03-20 | GSE5331 | GEO
Project description:Gene expression profiling was used to identify genes that display radiation-induced transcriptional change over tumor histopathology. Keywords: mouse squamous cell carcinoma, fibrosarcoma and mammary carcinoma, gamma-irradiation, carbon ion irradiation, resected sample, transplanted tissues C3H/HeMs male mice were irradiated by gamma-rays (30Gy, 50Gy, 70Gy) or carbon ions (30Gy) as local irradiation in single doses to hind legs where each tumor was transplanted. Animals were sacrificed either before irradiation (pre) or 1 day after irradiation (day 1) for expression analysis.
2009-03-20 | E-GEOD-5331 | biostudies-arrayexpress
Project description:This study uses microarray analysis to examine the fate of multiple C-ion-irradiated tumors in vivo to gain a comprehensive overview of the changes in gene expression induced by C-ion irradiation. Four murine tumors were irradiated in vivo with C-ions at a single dose, and gamma-rays were used as a reference beam. Keywords: mouse squamous cell carcinoma and fibrosarcoma, carbon ion-irradiation, gamma-irradiation, resected sample, transplanted tissues
2008-06-09 | GSE11629 | GEO
Project description:It is widely believed that the carcinogenic action of ionizing radiation is due to targeted DNA damage and resulting mutations, but there is also substantial evidence that non-targeted radiation effects alter epithelial phenotype and the stromal microenvironment. Activation of transforming growth factor β1 (TGFβ) is a non-targeted radiation effect that mediates cell fate decisions following DNA damage and regulates microenvironment composition; it could either suppress or promote cancer. We asked if such non-targeted radiation effects contribute to carcinogenesis by using a novel radiation chimera model. Unirradiated Trp53 null mammary epithelium was transplanted to the mammary stroma, previously divested of endogenous epithelia, of mice previously exposed to a single low (10 -100 cGy) radiation dose. By 300 days, 100% of transplants in irradiated hosts at either 10 or 100 cGy had developed Trp53 null breast carcinomas compared to 54% in unirradiated hosts. Tumor growth rate was also increased by high, but not low, dose host irradiation. In contrast, irradiation of Tgfb1 heterozygote mice prior to transplantation failed to decrease tumor latency, or increase growth rate at any dose. Host irradiation significantly reduced the latency of invasive ductal carcinoma compared to spindle cell carcinoma. However, irradiation of either host genotype significantly increased the frequency of estrogen receptor negative tumors. These data demonstrate two concepts critical to understanding radiation risks. First, non-targeted radiation effects can significantly promote the frequency and alter the features of epithelial cancer. Second, radiation-induced TGFβ activity is a key mechanism of tumor promotion. Keywords: Differential gene expression after low dose irradiation
2010-03-01 | GSE18216 | GEO
Project description:This is a genome-wide approach to identifying genes persistently induced in the mouse mammary gland by acute whole body low dose ionizing radiation (10cGy), 1 and 4 weeks after exposure. Gene expression that is modified under these parameters were compared between Tgfb1 wild type and heterozygote littermates in order to determine which genes induced or repressed by radiation were mediated via Tgfb1 status. Differential gene expression was analyzed in Tgfb1 heterozygote and wild type littermate 4th mammary glands, after whole body exposure to an acute dose of 10cGy ionizing radiation. Estrus cycle was normalized in all mice two days prior to irradiation by injection with an estrogen and progesterone mixture. It is widely believed that the carcinogenic action of ionizing radiation is due to targeted DNA damage and resulting mutations, but there is also substantial evidence that non-targeted radiation effects alter epithelial phenotype and the stromal microenvironment. Activation of transforming growth factor beta 1 (TGFbeta) is a non-targeted radiation effect that mediates cell fate decisions following DNA damage and regulates microenvironment composition; it could either suppress or promote cancer. Gene expression profiling shown herein demonstrates that low dose radiation (10 cGy) elicits persistent changes in Tgfb1 wild type and heterozygote murine mammary gland that are highly modulated by TGFbeta. We asked if such non-targeted radiation effects contribute to carcinogenesis by using a novel radiation chimera model. Unirradiated Trp53 null mammary epithelium was transplanted to the mammary stroma of mice previously exposed to a single low (10 -100 cGy) radiation dose. By 300 days, 100% of transplants in irradiated hosts at either 10 or 100 cGy had developed Trp53 null breast carcinomas compared to 54% in unirradiated hosts. Tumor growth rate was also increased by high, but not low, dose host irradiation. In contrast, irradiation of Tgfb1 heterozygote mice prior to transplantation failed to decrease tumor latency, or increase growth rate at any dose. Host irradiation significantly reduced the latency of invasive ductal carcinoma compared to spindle cell carcinoma, as well as those tumors negative for smooth muscle actin in wild type but not Tgfb1 heterozygote mice. However, irradiation of either host genotype significantly increased the frequency of estrogen receptor negative tumors. These data demonstrate two concepts critical to understanding radiation risks. First, non-targeted radiation effects can significantly promote the frequency and alter the features of epithelial cancer. Second, radiation-induced TGFbeta activity is a key mechanism of tumor promotion. Keywords: Differential gene expression after low dose irradiation Two genotypes: TGBbeta1 heterozygote and wildtype mouse mammary glands. Two time points post-10cGy-irradiation per genotype (1 week, 4 weeks); control time point was 1 week post-sham-irradiation. Two or three replicates per time point.
2010-03-07 | E-GEOD-18216 | biostudies-arrayexpress
Project description:Gene expression profiling was used to identify genes that display radiation-induced transcriptional change over mouse strain and tissue differences. Keywords: mouse strain comparison, irradiation, time course, lung, skin
2007-12-30 | GSE4312 | GEO
Project description:Breast cancer ranks top in the incidence among the main sites of female cancer in Japan. The epidemiological study on atomic bomb survivors has suggested that the excess relative risk for breast cancer is higher than any other sites. Little is known, however, about the molecular mechanisms of breast cancer induction by radiation. Therefore, we analyzed here the genome-wide copy number aberration of radiation-induced rat mammary carcinomas using microarray-based comparative genomic hybridization (array-CGH). Mammary carcinomas were induced by 2 Gy gamma irradiation of Sprague-Dawley (SD) rats at 3 or 7 weeks of age. We examined 14 mammary carcinomas induced by gamma-irradiation (2 Gy) and found 26 aberrations including trisomies of chromosomes 4 and 10 in 3 and 1 carcinomas, respectively, and deletion of chromosomes 3q35q36 and 5q32 (Cdkn2a and Cdkn2b region) in 2 and 2 carcinomas, respectively. On the other hand, only one aberration (amplification of chromosome 10q31) was observed in four spontaneous mammary carcinomas. These results suggest that the trisomy of chromosome 4 and deletion of chromosomes 3q35q36 and 5q32 were associated with radiation exposure. We performed aCGH on mammary carcinoma in Sprague-Dawley rat to identify radiation-specific DNA copy number aberration compared with spontaneous mammary carcinoma.
2010-08-08 | E-GEOD-16128 | biostudies-arrayexpress
Project description:Tardigrades can survive remarkable doses of ionizing radiation, up to about 1000 times the lethal dose for humans. How they do so is incompletely understood. We found that the tardigrade Hypsibius exemplaris suffers DNA damage upon gamma irradiation, but damage is repaired. We show that tardigrades have a specific and robust response to ionizing radiation: irradiation induces a rapid, dramatic upregulation of many DNA repair genes. By expressing tardigrade genes in bacteria, we validate that increased expression of some repair genes can suffice to increase radiation tolerance. We show that at least one such gene is necessary for tardigrade radiation tolerance. Tardigrades’ ability to sense ionizing radiation and massively upregulate specific DNA repair pathway genes may represent an evolved solution for maintaining DNA integrity.
2024-12-13 | PXD047724 | Pride
Project description:The population's increasing risk of acute large-scale radiological/nuclear exposures underlines the need for functional radiation biomarkers. As ionizing radiation triggers a complex response on the genome, proteome, and metabolome level, all were already reported as suitable indicators of radiation-induced damage in vitro or in animal models. We aim to analyze the blood of total-body irradiated (TBI) leukaemia patients using a mass spectrometry approach and to identify and quantify plasma proteins before and after irradiation. Combining two independent mass spectrometry approaches we identified 15 plasma proteins differing in the blood of TBI patients before and after irradiation. The majority of proteins were associated with the inflammatory responce of the immune system and with metabolism of lipids. These candidate radiation biomarkers might have implications for practical biological dosimetry.
2024-06-16 | PXD043516 | Pride
Project description:Radiotherapy is one of the most common therapies for cancer. Approximately half of all cancer patients will receive radiotherapy at some point during treatment. Consequences of IR treatment are dose dependent and different sensitivity to IR of various types of cells is well established. To reduce the damage of IR to most sensitive cells of normal (noncancerous) tissue radiotherapy is administered as fractionated dose treatment applying radiation in ~2 Gy fractions every 24 hours, 5 times per week. However, during the therapy intrinsic and acquired tumor radioresistance may result in treatment failures. Comprehensive mechanisms of the resistance to irradiation as well as mechanisms of cellular response to fractionated dose IR remain unclear. Therefore, in the present study we evaluated global gene expression changes in murine Lewis lung carcinoma LLC1 cells following X-ray irradiation of single 2 Gy or 10 Gy and 2 Gy x 5 fractionated doses. Total RNA was harvested from mouse Lewis lung carcinoma cells 4h after treatment of single (2 Gy or 10 Gy) or fractionated (5x2 Gy) ionizing radiation dose.
2016-07-07 | E-GEOD-84108 | biostudies-arrayexpress