EGAS00001000778-sc-20160302 - samples
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ABSTRACT:
PROVIDER: EGAD00001001934 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Pilot study for mutagen exposure work to be carried out as part of mutational signatures project.
| EGAS00001000778 | EGA
Project description:Analysis of mutational signatures caused by exposure to known mutagens in human induced pluripotent stem (iPS) cells. A reference human iPS cell-line will be exposed to 100 chemicals known or proposed to be mutagenic. Following exposure to mutagen, cells will undergo a period of recovery before sub clones are generated and sequenced. The progenitor "parental" IPS cell-line will be used to generate reference sequence data, in order to determine the mutational signatures acquired as a result of exposure to different mutagens.
| EGAD00001005351 | EGA
Project description:Analysis of mutational signatures caused by exposure to known mutagens in human induced pluripotent stem (iPS) cells. A reference human iPS cell-line will be exposed to 100 chemicals known or proposed to be mutagenic. Following exposure to mutagen, cells will undergo a period of recovery before sub clones are generated and sequenced. The progenitor “parental” IPS cell-line will be used to generate reference sequence data, in order to determine the mutational signatures acquired as a result of exposure to different mutagens.
| EGAS00001002060 | EGA
Project description:These analyses set out to evaluate changes in microRNA signatures in the mouse plasma in response to simulated wildland fire exposure conditions. These exposure conditions were based on smoke condensate consisting of particulate matter and semivolative organic compounds resulting from the burning of two biomass fuels; namely , peat and red oak. These biomasses were evaluated under two burn conditions: flaming and smoldering. Saline exposures were also carried out as negative controls.
2022-09-01 | GSE173561 | GEO
Project description:Aflatoxin B1 (AFB1) is a mutagen and IARC (International Agency for Research on Cancer) Group 1 carcinogen that causes hepatocellular carcinoma (HCC). Here we present the first whole genome data on the mutational signatures of AFB1 exposure from a total of > 40,000 mutations in four experimental systems: two different human cell lines, and in liver tumors in wild-type mice and in mice that carried a hepatitis B surface antigen transgene – this to model the multiplicative effects of aflatoxin exposure and hepatitis B in causing HCC. AFB1 mutational signatures from all four experimental systems were remarkably similar. We integrated the experimental mutational signatures with data from newly-sequenced HCCs from Qidong County, China, a region of well-studied aflatoxin exposure. This indicated that COSMIC mutational signature 24, previously hypothesized to stem from aflatoxin exposure, indeed likely represents AFB1 exposure, possibly combined with other exposures. Among published somatic mutation data, we found evidence of AFB1 exposure in 0.7% of HCCs treated in North America, 1% of HCCs from Japan, but 16% of HCCs from Hong Kong. Thus, aflatoxin exposure apparently remains a substantial public health issue in some areas. This aspect of our study exemplifies the promise of future widespread resequencing of tumor genomes in providing new insights into the contribution of mutagenic exposures to cancer incidence.
| EGAS00001002490 | EGA
Project description:Whole-genome-sequencing (WGS) of human tumours has revealed distinct mutation patterns that hint at the causative origins of cancer. We examined mutational-signatures in 324 WGS of human induced pluripotent stem cells (iPSCs) following exposure to known or suspected environmental carcinogens. 79 agents were tested with or without metabolic activation at concentrations that produced measurable cytotoxicity; 41 yielded characteristic substitution mutational signatures. Some exhibit similarity with signatures found in human tumours. Additionally, 6 agents produced double-substitution signatures and 8 produced indel signatures. Investigating mutation asymmetries across genome topography reveals fully functional mismatch and transcription-coupled repair pathways in iPSCs. Primary adducts induced by environmental carcinogens can be resolved by disparate repair/replicative pathways, resulting in an assortment of signature outcomes even for a single mutagen. This compendium of experimentally-induced mutational-signatures permits further exploration of roles of environmental agents in cancer aetiology, and underscores how human stem cell DNA is directly vulnerable to environmental agents.
| EGAD00001004583 | EGA
Project description:This was a pilot project carried out by Dr Wojciech Majeran to determine the maize pollen proteome harvested from field-grown W22 (T43) plants in plots on the Musgrave Research Farm (Cornell CALS) in Aurora (NY). To enhance proteome coverage, the pollen were separated into soluble and membrane bound protein fractions, and separated by SDS-PAGE followed by in-gel digestion and shot-gun proteomics using a nanoLC-Orbitrap system.
2023-09-11 | PXD045274 | Pride
Project description:Mutational signatures can reveal properties of underlying mutational processes and are important when assessing signals of selection in cancer. Here we describe the sequence characteristics of mutations induced by ultraviolet (UV) light, a major mutagen in several human cancers, in terms of extended (longer than trinucleotide) patterns as well as variability of the signature across chromatin states. Promoter regions display a distinct UV signature with reduced TCG>TTG transitions, and genome-wide mapping of UVB-induced DNA photoproducts (pyrimidine dimers) showed that this may be explained by decreased damage formation at hypomethylated promoter CpG sites. Further, an extended signature model encompassing additional information from longer contextual patterns improves modeling of UV mutations, which may enhance discrimination between drivers and passenger events. Our study presents a refined picture of the UV signature and underscores that the characteristics of a single mutational process may vary across the genome.
2019-09-11 | GSE127966 | GEO
Project description:The uncovering of genes involved in susceptibility to the sporadic cancer types is a great challenge. It is well established that the way in which an individual deals with DNA damage is related to the chance to develop cancer. Mutagen sensitivity is a phenotype that reflects an individual’s susceptibility to the major sporadic cancer types, including colon, lung and head and neck cancer. A standard test for mutagen sensitivity is measuring the number of chromatid breaks in lymphocytes after exposure to bleomycin. The aim of the present study was to search for the pathways involved in mutagen sensitivity. Lymphoblastoid cell lines of seven individuals with a low mutagen sensitivity were compared with seven with a high score. RNA was isolated from cells exposed to bleomycin (4 hr) and unexposed cells. Micro-array analysis (19K) was used to compare gene expression of insensitive and sensitive cells. The profile of most altered genes after bleomycin exposure, analyzed in all fourteen cell lines, included genes involved in multiple processes, most prominent in cell proliferation and DNA repair. When comparing the insensitive and sensitive individuals other differentially expressed genes were found, that were involved in proliferation (e.g. BUB1) and signal transduction (e.g. DUSP4). This difference in expression profiles between mutagen sensitive and insensitive individuals justifies further studies aiming to elucidate the genes responsible for the development of sporadic cancers. Keywords: exposure to dna damaging agent, comparison of phenotypic response to dna damaging agent
2006-01-01 | GSE3598 | GEO