Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of rat footpad skin in radiation dermatitis

ABSTRACT: Radiation dermatitis is a side effect in cancer radiotherapy, where ionizing radiation is delivered to eradicate cancer. Normal tissue such as the skin is also damaged by this treatment. We report here the gene expression change in a rat footpad model of this disease.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE81907 | GEO | 2019/05/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression response to high radiation treatment in MCF7 breast cancer cell line

Project description:Intraoperative radiotherapy (IOERT) is a high radiation therapeutic technique which administers a single high dose of ionizing radiation (IR) immediately after surgical tumor removal in order to destroy the residual cancer cells in the site at high risk for recurrence. IR is able to regulate several genes and factors involved in cell-cycle progression, survival and/or cell death, DNA repair and inflammation modulating an intracellular response radiation dependent producing an imbalance in cell fate decision. In this study, we examined changes in gene expression in MCF7 breast cancer cell line exposed to 9Gy and 23Gy high single dose of IR delivered by IOERT.

2015-06-11 | GSE63667 | GEO

Gene expression response to high radiation treatment in MCF7 breast cancer cell line

2015-06-11 | E-GEOD-63667 | biostudies-arrayexpress

Ionizing Radiation-induced Acute Damage in the Salivary Gland

Project description:Ionizing radiation (IR) – induced salivary gland damage is a common adverse effect in radiotherapy for patients with head and neck cancers. Currently, there is no effective treatment for the resulting salivary gland hypofunction and xerostomia (dry mouth). Here we profiled the acute gene expression change in the mouse submandibular salivary gland, and defined its damage response patterns at the transcriptome level.

2021-09-23 | GSE184673 | GEO

Tumorgenic properties of high-dose ionizing radiation of primary cancer-associated fibroblasts

Project description:In the context of radiotherapy, the effects elicited by ionizing radiation on the supportive stroma of tumors remains understudied. Tumor infiltrating fibroblasts are abundantly found in the stromal tissue of most tumor types and are key determinants of tumor progression and metastasis. Given the clinical attention that ablative radiotherapy is gaining nowadays, and the paramount role played by CAFs in cancer sustainability, in this study the effect of high-dose ionizing radiation on primary CAF?S have been investigated. We have used high-throughput transcriptome analysis to ascertain in which degree tumor stromal fibroblast become pro-tumorigenic or anti-tumorigenic after ablative irradiation. Hence, genome-wide transcriptome analysis has been carried out on CAFs isolated from NSCLC tumors after receiving a single dose of 18 Gray. The expressions of relevant genes have been validated by real-time PCR, and transformed cellular pathways have been checked by functional assays. Overall, our data reveals profound changes in biological pathways including cellular stress, DNA damage, cell cycle, aging, apoptosis, oxidative stress, and matrix remodeling. Ablative radiation doses may exert both pro-and anti-tumorigenic effects on CAFs. The ultimate effect of such disturbances merits further investigation in more complex in vivo settings.

2012-04-16 | GSE37318 | GEO

ATR inhibition potentiates ionizing radiation-induced interferon response via cytosolic nucleic acid-sensing pathways

Project description:Mechanistic understanding of how ionizing radiation induces type I interferon signaling and how to amplify this signaling module should help to maximize the efficacy of radiotherapy. In the current study, we report that inhibitors of the DNA damage response kinase ATR can significantly potentiate ionizing radiation-induced innate immune responses. Using a series of mammalian knockout cell lines, we demonstrate that, surprisingly, both the cGAS/STING-dependent DNA-sensing pathway and the MAVS-dependent RNA-sensing pathway are responsible for type I interferon signaling induced by ionizing radiation in the presence or absence of ATR inhibitors. The relative contributions of these two pathways in type I interferon signaling depend on cell type and/or genetic background. We propose that DNA damage-elicited double-strand DNA breaks releases DNA fragments, which may either activate the cGAS/STING-dependent pathway or-especially in the case of AT-rich DNA sequences-be transcribed and initiate MAVS-dependent RNA sensing and signaling. Together, our results suggest the involvement of two distinct pathways in type I interferon signaling upon DNA damage. Moreover, radiation plus ATR inhibition may be a promising new combination therapy against cancer.

2020-05-07 | GSE150003 | GEO

Genomic profiling by SNParray of human sarcomas developed in the field of irradiation after radiotherapy

Project description:Genomic signature of the ionizing radiation effect in sarcomas developed in the field of irradiation after radiotherapy

2012-06-08 | E-MEXP-3248 | biostudies-arrayexpress

Genomic profiling by SNParray of human angiosarcomas

Project description:Genomic signature of the ionizing radiation effect in angiosarcoma developed in the field of irradiation after radiotherapy

2012-06-09 | E-MEXP-3252 | biostudies-arrayexpress

Transcription profiling by array of human sarcomas developed in the field of irradiation after radiotherapy.

Project description:Transcriptome signature of the ionizing radiation effect in sarcomas developed in the field of irradiation after radiotherapy

2011-03-31 | E-MEXP-2687 | biostudies-arrayexpress

Radiation-induced epigenetic DNA methylation modification of radiation-response pathways

Project description:Treatment of tumors with ionizing radiation for cancer therapy induces biological responses that include changes in cell cycle, activation of DNA repair mechanisms, and induction of apoptosis or senescence programs. What is not known is whether ionizing radiation induces an epigenetic DNA methylation response or whether epigenetic changes occur in genes in pathways classically associated with the radiation response. We exposed breast cancer cells to 0, 2, or 6 Gy and determined global DNA methylation at 1, 2, 4, 8, 24, 48, and 72 hours post-irradiation. We found that radiation treatment resulted in a DNA methylation response and that cell cycle, DNA repair, and apoptosis pathways were enriched in genes are were differentially-methylated. DNA methylation profiling of ionizing radiation treated cells using the Infinium HumanMethylation450 BeadChip.

2013-07-01 | E-GEOD-45958 | biostudies-arrayexpress

Gene expression profile of mouse Lewis lung carcinoma cell line treated with single or fractionated ionizing radiation doses

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data