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360
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ShareScore release 0.9.0
Dataset results
360 results for “carcinogenesis”
Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis
GEO Series GSE247995. Mus musculus. 33 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
A distinct mechanism of epigenetic reprogramming silences PAX2 and initiates endometrial carcinogenesis
GEO Series GSE275345. Homo sapiens. 15 samples. Type: Expression profiling by high throughput sequencing.
Invasive Escherichia coli contributes to colon carcinogenesis by suppressing epithelial autophagy: application of phage therapy
GEO Series GSE144719. Mus musculus. 12 samples. Type: Expression profiling by array.
Non-targeted effects of low dose ionizing radiation act via TGF-beta to promote mammary carcinogenesis
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.
Age and Space Irradiation Modulate Tumor Progression: Implications for Carcinogenesis Risk
Age plays a major role in tumor incidence and is an important consideration when modeling the carcinogenesis process or estimating cancer risks. Epidemiological data show that from adolescence through middle age, cancer incidence increases with age. This effect is commonly attributed to a lifetime accumulation of cellular, particularly DNA, damage. However, during middle-age, the incidence begins to decelerate and, for many tumor sites, it actually decreases at sufficiently advanced ages. We investigated if the observed deceleration and potential decrease in incidence could be attributed to a decreased capacity of older hosts to support tumor progression, and whether HZE (high atomic number (Z), high energy (E)) radiation differentially modulates tumor progression in young versus middle-age hosts, issues relevant to estimating carcinogenesis risk for astronauts. Lewis lung carcinoma (LLC) cells were injected into syngeneic mice (143 and 551 days old), which were then subject to whole-body 56Fe irradiation (1GeV/amu). Three findings emerged: 1) among unirradiated animals, substantial inhibition of tumor progression and significantly decreased tumor growth rates were seen for middle-aged mice compared to young mice; 2) whole-body 56Fe irradiation (1GeV/amu) inhibited tumor progression in both young and in middle-aged mice (with greater suppression seen in case of young animals), with little effect on tumor growth rates; and 3) 56Fe irradiation (1GeV/amu) suppressed tumor progression in young mice, to a degree not significantly different than transiting from young to middle-aged. Thus, 56Fe irradiation (1GeV/amu) acted similar to aging with respect to tumor progression. We further investigated the molecular underpinnings driving the radiation modulation of tumor dynamics in young and middle-aged mice. Through global gene expression analysis, the key players, FASN, AKT1, and the CXCL12/CXCR4 complex, were determined to be contributory. In sum, these findings demonstrate a reduced capacity of middle-aged hosts to support the progression phase of carcinogenesis and identify molecular factors contributory to HZE radiation modulation of tumor progression as a function of age. For genome-wide expression profiling of tumor tissue, Mouse WG-6 BeadArray chips (Illumina, San Diego, CA) were used. Total RNA was amplified with the Ambion Illumina TotalPrep Amplification Kit (Ambion, Austin, TX) and labeled from all replicate biological samples for each condition. The number of tumor sample replicates used from each condition is as follows: 10 samples from young unirradiated mice, 8 samples from young irradiated mice, 7 samples from middle-aged unirradiated mice, 5 samples from middle-aged irradiated mice. Total RNA was isolated and purified using Trizol (Invitrogen) or RNeasy (Qiagen), quantified and qualified using Agilent Bioanalyzer (Agilent) and samples were deemed suitable for amplification and hybridization if they had O.D. 260/280 = 1.7 - 2.1, 28s/18s = 2:1, RIN (RNA integrity number) >7. Total RNA of 500ng per sample was amplified using Ambion TotalPrep (Ambion), and 1.5ug of the product was loaded onto the chips. Following hybridization at 55C, the chips were washed and then scanned using the Illumina iScan (Illumina), and the data were analyzed using GenomeStudio (Illumina). Data were first analyzed for gene expression and then culled for present genes (genes that meet the criteria of detection p-value < 0.05). Expression above background was included in an expressed genes working data set for further analyses. Rank variant normalization was applied to the data before extensive analysis. Differential gene expression analysis was used to compare to the reference group, young unirradiated mice, and genes were then evaluated and validated.
The Enterotoxigenic Bacteroides fragilis (ETBF) in intestinal inflammation and colorectal carcinogenesis [whole cell RNA]
GEO Series GSE161047. Homo sapiens. 8 samples. Type: Non-coding RNA profiling by high throughput sequencing.
miR-135b exerts metastatic activity in the ErbB2 driven mammary carcinogenesis
GEO Series GSE28949. Mus musculus. 16 samples. Type: Expression profiling by array.
Aberrant expression of miRNAs in the liver carcinogenesis from NASH
GEO Series GSE52822. Homo sapiens; Mus musculus. 9 samples. Type: Non-coding RNA profiling by array.
An organoid-based transplantation model reveals genetic interactions potentiating niche-independent gastric carcinogenesis
GEO Series GSE192604. Mus musculus. 8 samples. Type: Expression profiling by array.
HIP1 mediates prostate carcinogenesis and progression through STAT3 signalling
GEO Series GSE35211. Homo sapiens. 24 samples. Type: Expression profiling by array.
Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment
GEO Series GSE43453. Mus musculus. 16 samples. Type: Expression profiling by array.
The underlying mechanism by which ZCCHC7 exerted carcinogenesis and its potential targets in CRC
GEO Series GSE234581. Homo sapiens. 4 samples. Type: Other.
Genome-wide DNA methylation analysis of livers obtained from 2-stage carcinogenesis model in rats
GEO Series GSE53518. Rattus norvegicus. 70 samples. Type: Methylation profiling by high throughput sequencing.
Translatomics coupled with transcriptomics reveals a novel mechanism of oral carcinogenesis [RNA-seq]
GEO Series GSE185249. Homo sapiens. 5 samples. Type: Expression profiling by high throughput sequencing.
The effect of 5-ASA on colitis-associated carcinogenesis
GEO Series GSE185599. Mus musculus. 15 samples. Type: Expression profiling by array.
MAdCAM-1 targeting strategy can prevent colitic cancer carcinogenesis and progression via suppression of immune cell infiltration and inflammatory signals
GEO Series GSE236524. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Hepatitis B/C viruses manipulate TNNT1 expression to induce epithelial-mesenchymal transition and hepatocellular carcinogenesis
GEO Series GSE233441. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Site-Specific HPV18 Integration Facilitates Cervical Carcinogenesis through metabolic reprogramming-Induced dysfunction of the SpHK1/S1P/S1PR1 pathway-part2
GEO Series GSE285796. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs
GEO Series GSE165285. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
The Enterotoxigenic Bacteroides fragilis (ETBF) in intestinal inflammation and colorectal carcinogenesis [exosomes]
GEO Series GSE161048. Homo sapiens. 6 samples. Type: Non-coding RNA profiling by high throughput sequencing.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.