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Acute high dose X-irradiation-induced genomic changes in a lung tumor cell line

ABSTRACT: Accidents with ionizing radiation (IR) often involve acute high dose exposures that can lead to acute radiation syndrome and late effects. IR can induce genomic lesions, cell death or carcinogenesis. Here, we investigated acute IR-induced cellular genomic signatures at the genome wide level. After exposing the adenocarcinoma cell line A549 to an acute 6 Gy 240 kV X-Ray dose, four surviving clonogenic cells were recovered by minimal dilution and further expanded and analyzed by cytogenetics, chromosome painting and tiling-path array CGH, with the non-irradiated clone0 serving as control. It was found that acute X-ray exposure induced changes in modal chromosome number and specific translocations in the four irradiation surviving clones. Furthermore, clone4 displayed an increased radiosensitivity at D > 5 Gy. Array CGH disclosed unique and recurrent genomic changes, predominantly gains, and disclosed fragile sites FRA3B and FRA16D as preferential regions of genomic alterations in all irradiated clones, which likely relates to irradiation-induced genomic stress. Gene expression analysis revealed a specific profile of 364 genes in clone4, of which p53 pathway genes may contribute to its increased radiosensitivity. IR-induced genomic changes AND fragile site expression highlight the capacity of a single acute radiation exposure to resculpture the genome of tumor cells by inflicting genomic stress.

ORGANISM(S): Homo sapiens

PROVIDER: GSE24876 | GEO | 2011/02/04

SECONDARY ACCESSION(S): PRJNA132019

REPOSITORIES: GEO

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Acute high dose X-irradiation-induced genomic changes in a lung tumor cell line

Project description:Accidents with ionizing radiation (IR) often involve acute high dose exposures that can lead to acute radiation syndrome and late effects. IR can induce genomic lesions, cell death or carcinogenesis. Here, we investigated acute IR-induced cellular genomic signatures at the genome wide level. After exposing the adenocarcinoma cell line A549 to an acute 6 Gy 240 kV X-Ray dose, four surviving clonogenic cells were recovered by minimal dilution and further expanded and analyzed by cytogenetics, chromosome painting and tiling-path array CGH, with the non-irradiated clone0 serving as control. It was found that acute X-ray exposure induced changes in modal chromosome number and specific translocations in the four irradiation surviving clones. Furthermore, clone4 displayed an increased radiosensitivity at D > 5 Gy. Array CGH disclosed unique and recurrent genomic changes, predominantly gains, and disclosed fragile sites FRA3B and FRA16D as preferential regions of genomic alterations in all irradiated clones, which likely relates to irradiation-induced genomic stress. Gene expression analysis revealed a specific profile of 364 genes in clone4, of which p53 pathway genes may contribute to its increased radiosensitivity. IR-induced genomic changes AND fragile site expression highlight the capacity of a single acute radiation exposure to resculpture the genome of tumor cells by inflicting genomic stress. Gene expression in A549 cell line was analysed after exposure to 6Gy X-rays at a dose rate of 1Gy/min.

2011-02-04 | E-GEOD-24876 | biostudies-arrayexpress

Copy Number Variation data from non-trasformed human fibroblasts

Project description:The search for biomarkers to predict radiosensitivity is important not only to individualize radiotherapy of cancer patients but also to forecast radiation exposure risks. The aim of this study was to devise a machine learning method to stratify radiosensitivity and to investigate its association with copy number variations (CNVs) as markers of sensitivity to ionizing radiation. We used the Affymetrix CytoScan HD microarrays to for CNV estimation. Celluar radiosensitivity was measured by the clonogenic surviving fraction at 2 Gy (SF2).

2023-05-08 | GSE231621 | GEO

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

miRNA expression profile of 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. Different gene expression patterns may be partially influenced by short ~22 nt non-coding RNA molecules called microRNAs (miRNAs) via translational regulation or RNA degradation mechanisms. Therefore, in the present study we evaluated global miRNA 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 enriched in small noncoding RNAs was isolated 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-84109 | biostudies-arrayexpress

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

2016-07-07 | GSE84108 | GEO

Senescence gene signature of radiation fibrosis

Project description:Radiation lung injury is characterized by early inflammation and late fibrosis. The causes underlying the chronic, progressive nature of radiation injury are poorly understood. Here, we report that the gene expression of irradiated lung tissue correlates with that observed in the lungs in aged animals. We demonstrate that NOX4 expression and superoxide elaboration is increased in irradiated lungs and pneumocytes in a dose dependent fashion. We used microarrays to detail the global programme of gene expression and report that irradiated lung tissue correlates with that observed in the lungs in aged animals. Female C57Bl/Ncr mice, aged 10 weeks were treated with/ without radiation to the thorax with a X-RAD 320 x-ray irradiator at a dose rate of 2.61 Gy/minute. An age-matched cohort of mice received no IR while additional cohorts received 5 Gy in a single dose, 17.5 Gy in a single dose. RNA was extracted and hybridization done on Affymetrix Mouse430_2 microarrays.

2013-11-01 | E-GEOD-41789 | biostudies-arrayexpress

miRNA expression profile of 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. Different gene expression patterns may be partially influenced by short ~22 nt non-coding RNA molecules called microRNAs (miRNAs) via translational regulation or RNA degradation mechanisms. Therefore, in the present study we evaluated global miRNA 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.

2016-07-07 | GSE84109 | GEO

The response to ionizing radiation at the exon level

Project description:Humans are exposed to ionizing radiation (IR) from background radiation, medical treatments, occupational and accidental exposures. IR causes profound changes in transcription. Transcription is a primary process where protein amount and function can be regulated. One aspect of the transcriptional IR response that little is known about on a whole genome basis is alternative transcription. These investigations focus on the response to IR at the exon level in human cells but also at the whole gene level. Whole genome exon arrays were utilized to comprehensively characterize radiation-induced transcriptional expression products in two human cell types, namely EBV-transformed lymphoblast and primary fibroblast cell lines. 12 human primary fibroblast cell lines and 12 primary lymphoblast cell line samples were used for two doses (0 and 10 Gy) and two time points (0 and 4hr). Additional doses ( 1 Gy, 2 Gy, 5 Gy, and 20 Gy) and time points ( 1hr, 2hr, 8hr, 24hr and 48hr) were assessed in four lymphoblast cell lines and four primary fibroblasts.

2011-05-02 | E-GEOD-26841 | biostudies-arrayexpress

ATM-dependent Transcriptional Responses to 1.5 Gy Gamma Radiation in Human Lymphocytes

Project description:Ataxia telangiectasia (AT) is an autosomal recessive disorder characterized by neuronal degeneration, telangiectasias, acute cancer predisposition, and hypersensitivity to ionizing radiation (IR). The gene defective in AT, ATM (for AT-mutated), encodes a protein, pATM that has been found to have IR-inducible kinase activity. Cells from individuals with AT exhibit severely attenuated cell cycle checkpoints in response to gamma radiation exposure. pATM has been hypothesized to act as part of a complex that senses DNA damage, in particular, DNA double strand breaks. We are studying the pATM-dependent gene expression responses to a dose of 1.5 Gy radiation in lymphoblastoid cell lines from multiple individuals with either wild type or mutated ATM. The gene expression analyses were performed on Agilent Human 1A Oligo chips containing approximately 16,000 60mer probes. We identified a set of genes whose gene expression changes are ATM-dependent following exposure to 1.5 Gy IR. This set of genes was tested by real time quantitative PCR analysis.

2013-12-02 | GSE19287 | GEO

A radiation-induced gene expression signature as a tool to predict acute radiotherapy-induced adverse side effects

Project description:The majority of patients tolerate radiotherapy well, but some of them suffer from severe side effects. To find genes possibly predictive for radiosensitivity, mRNA profiles were generated before and 6 h after in vitro irradiation with 5 Gy. We analyzed lymphocytes from four head and neck and eight breast cancer patients with strong acute radiation toxicity and from 12 matching normal reacting patients in a blind study. In peripheral blood lymphocytes of all patients, 153 genes were identified which were statistically significantly altered by a fold change of more than 50% by irradiation. Pathway analysis revealed genes involved in p53 signalling, cell cycle control and apoptosis in response to radiation in primary lymphocytes. In these cells, a set of 67 radiation-induced genes was identified capable of differentiating between severe radiosensitive and normal reacting patients. More than one third of such classifying genes belong to the group of apoptosis or cell cycle regulating genes. Total RNA obtained from lymphocytes of cancer patients with strong acute radiation toxicity and from matching normal reacting patients were compared 6 hours after in vitro irradiation with 5 Gy.

2012-09-06 | E-GEOD-40640 | biostudies-arrayexpress

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