A study of the effects of bisphenol A on dog obesity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA856337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20007134_1.fastq.gz | Fastqsanger.gz | |||
| SRR20007134_2.fastq.gz | Fastqsanger.gz | |||
| SRR20007135_1.fastq.gz | Fastqsanger.gz | |||
| SRR20007135_2.fastq.gz | Fastqsanger.gz | |||
| SRR20007136_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The transcriptomic changes caused by BPA on canine adipose-derived stem cells (cADSCs) during differentiation were investigated in this study. The transcriptomic profiles were investigated using RNA-sequencing.
2024-11-04 | GSE207623 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE28351: Effects of bisphenol A on ovarian gene expression in fathead minnows and zebrafish [ZF data set] GSE28353: Effects of bisphenol A on ovarian gene expression in fathead minnows and zebrafish [FHM data set] Refer to individual Series
2012-01-01 | E-GEOD-28354 | biostudies-arrayexpress
Project description:We studied alterations in gene expression profiles of the MCF7 human breast cancer cells caused by bisphenol A, bisphenol AF and glyphosate using Illumina RNA sequencing platform.
2017-07-14 | GSE87701 | GEO
Project description:Bisphenol A (BPA) analogs, bisphenol B (BPB) and bisphenol AF (BPAF) have been widely detected in the environment and human products with increasing frequency. However, uterine health risks caused by BPBBisphenol A (BPA) analogs, bisphenol B (BPB) and bisphenol AF (BPAF) have been widely detected in the environment and human products with increasing frequency. However, uterine health risks caused by BPB and BPAF exposure need to be further elucidated. The study aimed to explore whether BPB or BPAF exposure will induce adverse outcomes in uterus. We then performed gene expression profiling using data obtained from mouse uterus exposed to BPB and BPAF at 28 days.
2023-05-12 | GSE223464 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related mortality among adults in developed countries. The discovery of the most common genetic alterations as well as the development of organoids models of pancreatic cancer have provided insight into the fundamental pathways driving the progression from normal cell, to non-invasive precursor lesion, to widely metastatic disease, offering new opportunities for the discovery of key activated pathways along cancer progression. Obesity is one of the most serious public health challenges of the 21st century. Several epidemiological studies have shown the positive association between obesity and cancer-related morbidity/mortality, as well as poor prognosis and poorer treatment outcome. Despite strong evidence indicates a link between obesity and cancer incidence, the molecular basis of the initiating events remains largely elusive. This is mainly due to the lack of an accurate and reliable model of pancreatic carcinogenesis that mimics human obesity-associated PDAC, making data interpretation difficult and often confusing. Here we propose, to our knowledge, the best suitable and manageable preclinical tool, based on next-generation cell culture models, to study the effects of obesity on pancreatic carcinogenesis. Therefore we tracked the effects of obesity on the natural evolution of PDAC in a genetically-defined transplantable model of syngeneic murine pancreatic preneoplastic lesion (mP) and tumor (mT) derived organoids that recapitulates the progression of human disease from early preinvasive lesions to metastatic disease. Our models indicated that both genetic- and diet-induced obesity promoted incidence engraftment rate and growth of both preneoplastic and neoplastic organoids, favoring pancreatic cancer progression and distant metastases dissemination. Our obesity models of carcinogenesis mimic the evolution of human pancreatic cancer pathology, promoting carcinogenesis and concomitant accumulation of a myeloid infiltrate. These changes in cancer immune infiltrate were also associated to a specific pattern of anti-inflammatory Th2 signature. Moreover, gene expression profile analysis revealed a change in gene expression programs that addresses cells to different pancreatic subtypes and stromal conditions. Our results suggest that organoid-derived transplants in obese mice represent a suitable system to study early step of carcinogenesis and support the hypothesis that inflammation induced by obesity stimulates tumor progression and metastatization during pancreatic carcinogenesis.
2020-05-26 | PXD018362 | Pride
Project description:Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related mortality among adults in developed countries. The discovery of the most common genetic alterations as well as the development of organoids models’ of pancreatic cancer has provided insight into the fundamental pathways driving tumour progression from a normal cell, to non-invasive precursor lesion, to widely metastatic disease, offering new opportunities for identifying the key driver of cancer evolution. Obesity is one of the most serious public health challenges of the 21st century. Several epidemiological studies have shown the positive association between obesity and cancer-related morbidity/mortality, as well as poor prognosis and poorer treatment outcome. Despite strong evidence indicates a link between obesity and cancer incidence, the molecular basis of the initiating events remains largely elusive. This is mainly due to the lack of an accurate and reliable model of pancreatic carcinogenesis that mimics human obesity-associated PDAC, making data interpretation difficult and often confusing. Here we propose a suitable and manageable preclinical tool, organoids-based, to study the effects of obesity on pancreatic carcinogenesis. Therefore, we tracked the effects of obesity on the natural evolution of PDAC in a genetically defined transplantable model of the syngeneic murine pancreatic preneoplastic lesion (mP) and tumour (mT) derived-organoids that recapitulates the progression of human disease from early preinvasive lesions to metastatic disease. Our results suggest that organoid-derived transplants in obese mice represent a suitable system to study early steps of pancreatic carcinogenesis and support the hypothesis that inflammation induced by obesity stimulates tumour progression and metastatization during pancreatic carcinogenesis.
2020-04-07 | GSE148135 | GEO
Project description:Bisphenol A (BPA), widely used in plastics and resins, raised health concerns for its endocrine-disrupting effects. BPA analogues like bisphenol S (BPS) and bisphenol F (BPF) emerged as alternatives but were found to exhibit similar risks. Despite many countries have implemented BPA regulations, alternatives remain insufficiently regulated Although the safety of BPS and BPF has not been sufficiently verified, they have already been detected in various surrounding environments and human urine, raising serious concerns Bisphenols are expected to have various adverse effects, but research on this is lacking. This study explores the adverse effects of bisphenol mixtures on rats from fetus to young adulthood, analyzing transcriptomes by tissue and gender to identify key genes impacted by bisphenol exposure. Dams were orally administered test substances from gestational day 6 to lactation day 6. F1 pups received the same substances at half the concentration from postnatal day 7 to day 63. The tissues collected from the pups were subjected to transcriptome analysis, and core genes were identified through integrated analysis. The study identifies core genes associated with high-density lipoprotein and hormone secretion. These genes provide insights into the mechanisms through which BPA may cause hormonal imbalances. Furthermore, the study suggests that a complex exposure of BPA, BPS, and BPF can exerts different effects than BPA alone, pronounced effects on the thyroid and reproductive organs, even though individual concentrations were below the no-observed-adverse-effect-level. It highlights the potential cumulative impact of endocrine disrupting chemicals in the body.
2024-03-08 | GSE259227 | GEO
Project description:In this study, beta-TCP was implanted in dog mandibles, after which the gene expression profiles and signaling pathways were monitored using microarray and Ingenuity Pathways Analysis (IPA). Following the extraction of premolars and subsequent bone healing, betaâTCP was implanted into the artificial osseous defect. Total RNA was isolated from bone tissues and gene expression profiles were examined using microarray analysis. We used microarrays to detail the global programme of gene expression and identified distinct classes of up- and down- regulated genes during this process. Waiting 3 months healing after tooth extraction from beagle dog mandibles, we drilled the holes in the dog mandibles, and implanted without and with beta-TCP. And these dog mandibles were selected for RNA extraction and hybridization on Affymetrix microarrays. After implanting beta-TCP in the dog mandibles 4, 7, 14 days, we selected sample at 3 time points: Control_4d, beta-TCP_4d, Control_7d, beta-TCP_7d, Control_14d, beta-TCP_14d.
2010-10-19 | E-GEOD-24756 | biostudies-arrayexpress