Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-18216
PROVIDER: PRJNA119587 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Low dose ionizing radiation treated lymphoblastoid cells
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Project description:The risk of breast cancer increases decades after ionizing radiation exposure, thereby linking aging intrinsically to the evolution of cancer. We hypothesized that radiation accelerates aging and carcinogenesis through similar pathways, specifically low-grade systemic inflammation. Here, we used the radiation-genetic mammary chimera model to examine the differential expression of 532 plasma proteins in BALB/c female mice between radiation exposure and experiment termination at 18 months. Mice were sham-irradiated or irradiated with 50 cGy prior to being orthotopically transplanted with syngeneic Trp53 null mammary epithelium and half were treated for 6 months with anti-inflammatory low-dose aspirin. Plasma was collected at 4, 8, and 18 months from non-tumor-bearing mice and from those that had developed tumors between 12 and 18 months. Plasma quantitative proteomic analysis identified significant alterations in proteins involved in the inflammatory response in irradiated mice as a function of age. Levels of C4b-binding protein were decreased at 4 months in irradiated mice compared to controls, which was blocked in aspirin-treated irradiated mice. Notable differences in the expression of proteins associated with the inflammation were evident in tumor-bearing versus similarly aged mice. Complement components C1qA, C1qB, and C1qC were significantly increased in tumor-bearing mice that had been irradiated, whereas similarly aged mice without tumors displayed a decline in complement system activity. The specific changes in the complement system, which mediates adaptive immune function, following radiation exposure may contribute to cancer progression as a function of age.
2025-07-15 | PXD064950 | Pride
Project description:DNA methylation biomarkers for evaluating cardiovascular disease risk from epigenome profiles altered by low-dose ionizing radiation
2025-10-23 | GSE246076 | GEO
Project description:The effects of high-dose ionizing radiation (HDIR) exposure on the immune system are largely understood with consensus, yet there remains a fragmented understanding of the impact of low-dose ionizing radiation (LDIR) on immune homeostasis, especially in sustained exposure conditions. This study investigates the effects of continuous LDIR exposure on the murine immune system, focusing on transcriptomic responses and cellular perturbations following low-dose-rate whole-body -radiation. Female 18-week-old C57BL/6 mice were continuously exposed to low-dose-rate 60Co radiation over a period of 7 days, resulting in cumulative absorbed doses of 10 mGy and 100 mGy. Our findings indicate that the LDIR exposure induced, at most, only minimal transcriptomic perturbations to the immune system in C57BL/6 mice. These results suggest a preservation of immune cell homeostasis under the sustained low-dose-rate exposure conditions studied. It contributes to a broader understanding of radiation biology, emphasizing that the effects of LDIR on the immune system can be limited at low-dose-rates in mice.
2026-04-14 | GSE296450 | GEO
Project description:Response to low dose ionizing radiation in male mouse
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Project description:Effect of low dose ionizing radiation on gene expression profile in human lymphocytes.
2013-05-11 | E-MEXP-2918 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) are emerging as key regulators of diverse cell functions and processes. However, the relevance of lncRNAs in the cell and tissue response to ionizing radiation has not yet been characterized. Here we used microarray profiling to determine lncRNA and mRNA expression in mammary glands of BALB/c and SPRET/EiJ mice after low-dose ionizing radiation (LDIR) exposure. We found that unirradiated mammary tissues of these strains differed significantly in baseline expressions of 290 lncRNAs. LDIR exposure (10 cGy) induced a significant change in the expression of many lncRNAs. For BALB/c mice, a total of 357, 480, and 335 lncRNAs and 550, 911, and 389 coding RNAs were identified at 2, 4, and 8 weeks post-irradiation, respectively, while for SPRET/EiJ, a total of 327 lncRNAs and 424 mRNAs were identified at 4 weeks post-irradiation.
2014-12-01 | GSE62662 | GEO
Project description:Thyroid gland is among the most sensitive organs to ionizing radiation. Whether low-dose radiation-induced papillary thyroid cancer (PTC) differs from sporadic PTC is yet unknown. We used microarrays to identify gene signature of radiation-induced papillary thyroid carcinomas
2015-12-31 | GSE35570 | GEO