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360 results for “carcinogenesis”
Link to dataset related to article "Sustained activation of detoxification pathways promotes liver carcinogenesis in response to chronic bile acid-mediated damage"
<p>This record contains link to raw data related to article "Sustained activation of detoxification pathways promotes liver carcinogenesis in response to chronic bile acid-mediated damage"</p> <p>Chronic inflammation promotes oncogenic transformation and tumor progression. Many inflammatory agents also generate a toxic microenvironment, implying that adaptive mechanisms must be deployed for cells to survive and undergo transformation in such unfavorable contexts. A paradigmatic case is represented by cancers occurring in pediatric patients with genetic defects of hepatocyte phosphatidylcholine transporters and in the corresponding mouse model (Mdr2-/- mice), in which impaired bile salt emulsification leads to chronic hepatocyte damage and inflammation, eventually resulting in oncogenic transformation. By combining genomics and metabolomics, we found that the transition from inflammation to cancer in Mdr2-/- mice was linked to the sustained transcriptional activation of metabolic detoxification systems and transporters by the Constitutive Androstane Receptor (CAR), a hepatocyte-specific nuclear receptor. Activation of CAR-dependent gene expression programs coincided with reduced content of toxic bile acids in cancer nodules relative to inflamed livers. Treatment of Mdr2-/- mice with a CAR inhibitor blocked cancer progression and caused a partial regression of existing tumors. These results indicate that the acquisition of resistance to endo- or xeno-biotic toxicity is critical for cancers that develop in toxic microenvironments.</p> <p>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80777 under the accession GSE80777, which comprises ChIP-seq data (GSE80775) and expression data (GSE80776).</p>
Aberrant basal cell clonal dynamics shape early lung carcinogenesis
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Dataset related to article "Neutrophils mediate protection in colitis and carcinogenesis by controlling bacterial invasion and IL-22 production by gdT cells"
<p>This record contains raw data related to article "<strong>Neutrophils mediate protection in colitis and carcinogenesis by controlling bacterial invasion and IL-22 production by gd T cells"</strong></p><p>Abstract</p><p>Neutrophils are the most abundant leukocytes in human blood and play a primary role in resistance against invading microorganisms and in the acute inflammatory response. However, their role in colitis and colitis-associated colorectal cancer is still under debate. Therefore, this study aims to dissect the role of neutrophils in these pathological contexts by using a rigorous genetic approach. Neutrophil-deficient mice (Csf3r-/- mice) were challenged with classic models of colitis and colitis-associated colorectal cancer and the role of neutrophils was assessed by histological, cellular and molecular analyses coupled with adoptive cell transfer and correlative analyses using human datasets. Csf3r-/- mice showed increased susceptibility to colitis and colitis-associated colorectal cancer compared to control Csf3r+/+ mice and adoptive transfer of neutrophils in Csf3r-/- mice reverted the phenotype. In colitis, Csf3r-/- mice showed increased bacterial invasion and reduced number of healing ulcers in the colon, indicating compromised regenerative capacity of epithelial cells. Neutrophils were essential for T cell polarization and IL-22 production. In patients with ulcerative colitis, the expression of CSF3R was positively correlated with IL-22 and IL-23 expression. Moreover, gene signatures associated with epithelial cell development, proliferation and antimicrobial response were enriched in CSF3Rhigh patients. Our data support a model where neutrophils mediate protection against intestinal inflammation and colitis-associated colorectal cancer by controlling the intestinal microbiota and driving the activation of an IL-22-dependent tissue repair pathway.</p><p> </p>
Issues Concerning the Carcinogenesis Risk and Implementation of the System of RP
<p>The ICRP’s System of radiological protection has been changing over time, and while it is robust enough, there is a need to add new knowledge and further improvement. Radiological protection is based on a combination of scientific knowledge, experience, and values; however, experience and values would be flexible and change with time and region. Radiation biology strives for universality based on biological mechanisms. At low dose and low dose rate, which is the main area of radiation protection, carcinogenesis is regarded as the main risk and its knowledge need to be elucidated. The DDREF is considered separately as LDEF and DREF nowadays. The key question is how to apply them to radiation risk inference. In terms of risk estimation by epidemiology, the paper of an extended observation period for cancer incidence for high natural radiation areas in Kerala, India, is recently published. It shows that there is no increase in cancer risk with increasing cumulative dose with greater confidence. The involvement of stem cell competition, as proposed in ICRP Publ. 131, in the dose rate effect has also been clarified by recent biological studies. On the other hand, in the implementation of the system of radiological protection, it is necessary to clearly show how to deal with uncertainty when protection measures are taken for small doses. It would be a departure from the principle of optimisation to require additional conservatism based on the precautionary principle when radiation safety standards established with sufficiently conservative assumptions are complied with. Another important issue for the application of optimisation will be waste management, which requires different actions depending on the exposure situation; although there is very little on waste management in the ICRP papers, it is necessary to discuss whether the guidance in the existing publications should be basically effective or not. The concept of waste disposal in existing exposure situations could be a point of discussion. Although, it is understandable that simplification and clarification are useful for the application of protection, due consideration should be taken to avoid misunderstanding and confusion. It is hoped that the process of reaching a decision on the basic approach and arrangements for the System of RP will be carried out with open doors involving stakeholders.</p>
Data and code for "Multi-omics Reveals Microbiome, Host Gene Expression, and Immune Landscape in Gastric Carcinogenesis" by Park et al., iScience 2022
<p>This repository is a part of the supplementary document in Park et al., "Multi-omics Reveals Microbiome, Host Gene Expression, and Immune Landscape in Gastric Carcinogenesis" published in iScience 2022.</p> <p>Abstract: To date, there has been no multi-omic analysis characterizing the intricate relationships between the intragastric microbiome and gastric mucosal gene expression in gastric carcinogenesis. Using multi-omic approaches, we provide a comprehensive view of the connections between the microbiome and host gene expression in distinct stages of gastric carcinogenesis (i.e., healthy, gastritis, cancer). We uncover associations specific to disease states. For example, uniquely in gastritis, Helicobacteraceae is highly correlated with the expression of <em>FAM3D</em>, which has been previously implicated in gastrointestinal inflammation. Additionally, in gastric cancer but not in adjacent gastritis, Lachnospiraceae is highly correlated with the expression of <em>UBD</em>, which regulates mitosis and cell cycle time. Furthermore, lower abundances of B cells in gastric cancer compared to gastritis may suggest a previously unidentified immune evasion process in gastric carcinogenesis. Our integrative analysis provides the most comprehensive description of microbial, host transcriptomic, and immune cell factors of the gastric carcinogenesis pathway.</p>
The Role of Proteomics Analysis in Carcinogenesis in a Rat Mammary Cancer Model Induced by DMBA (7,12-dimethylbenz(α)anthracene)
<p>The dataset consists of raw data on protein concentration from a Nanodrop Spectrophotometer and raw data on protein molecular weight from SDS-PAGE</p>
Dysregulation of cell state dynamics during early stages of serous endometrial carcinogenesis
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Data from: LAR1 activates NF-κB signaling pathway by binding to APOC1 mRNA and enhancing its expression: A novel mechanism underlying breast carcinogenesis
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Dataset related to article "Computer-aided assessment of the extra-cellular matrix during pancreatic carcinogenesis: a pilot study."
<p>BACKGROUND:</p> <p>A hallmark of pancreatic ductal adenocarcinoma is the desmoplastic reaction, but its impact on the tumor behavior remains controversial. Our aim was to introduce a computer -aided method to precisely quantify the amount of pancreatic collagenic extra-cellular matrix, its spatial distribution pattern, and the degradation process.</p> <p>METHODS:</p> <p>A series of normal, inflammatory and neoplastic pancreatic ductal adenocarcinoma formalin-fixed and paraffin-embedded Sirius red stained sections were automatically digitized and analyzed using a computer-aided method.</p> <p>RESULTS:</p> <p>We found a progressive increase of pancreatic collagenic extra-cellular matrix from normal to the inflammatory and pancreatic ductal adenocarcinoma. The two-dimensional fractal dimension showed a significant difference in the collagenic extra-cellular matrix spatial complexity between normal versus inflammatory and pancreatic ductal adenocarcinoma. A significant difference when comparing the number of cycles necessary to degrade the pancreatic collagenic extra-cellular matrix in normal versus inflammatory and pancreatic ductal adenocarcinoma was also found. The difference between inflammatory and pancreatic ductal adenocarcinoma was also significant. Furthermore, the mean velocity of collagenic extra-cellular matrix degradation was found to be faster in inflammatory and pancreatic ductal adenocarcinoma than in normal.</p> <p>CONCLUSION:</p> <p>These findings demonstrate that inflammatory and pancreatic ductal adenocarcinomas are characterized by an increased amount of pancreatic collagenic extra-cellular matrix and by changes in their spatial complexity and degradation. Our study defines new features about the pancreatic collagenic extra-cellular matrix, and represents a basis for further investigations into the clinical behavior of pancreatic ductal adenocarcinoma and the development of therapeutic strategies.</p>
ARRIVE checklist for 'The role of proteomics analysis in carcinogenesis in a rat mammary cancer model induced by DMBA (7,12-Dimethylbenz[a]anthracene)
<p>The ARRIVE guidelines for animal reporting: ‘The role of proteomics analysis in carcinogenesis in a rat mammary cancer model induced by DMBA (7,12-Dimethylbenz[a]anthracene)’</p>
Diet Composition, Weight Control, and Breast Carcinogenesis
ClinicalTrials.gov study NCT01315483. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study on the Carcinogenesis of Gα12 in Oral Cancer, and the Treatment of Oral Cancer Using Ga12 Inhibitor.
ClinicalTrials.gov study NCT01919580. IPD Sharing: Not stated. Countries: 1. Publications: 16.
Study on the Probiotics Regulating miRNA in H. Pylori-induced Wnt/β-catenin Gastric Carcinogenesis.
ClinicalTrials.gov study NCT05544396. IPD Sharing: NO. Countries: 1. Publications: 3.
Comparison of Expression of Carcinogenesis-related Molecular Markers in the Patients With Colon Cancer and Polyp
ClinicalTrials.gov study NCT05638542. IPD Sharing: NO. Countries: 1. Publications: 1.
Study on the Carcinogenesis of SOX-9 in Oral Cancer, and Chemopreventive Possibility for the Treatment of Oral Cancer.
ClinicalTrials.gov study NCT01919567. IPD Sharing: Not stated. Countries: 1. Publications: 21.
Processed Meat and Colon Carcinogenesis
ClinicalTrials.gov study NCT00994526. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Figure 1 from: Kachur O, Fira L, Lykhatskyі P, Fira D, Stechyshyn I (2021) The state of pro- and antioxidant systems in rats with DMH-induced colon carcinogenesis on the background of extracorporeal detoxification. Pharmacia 68(4): 941-946. https://doi.org/10.3897/pharmacia.68.e71840
Figure 1 Dynamics of the content of OMP products in the blood serum and liver homogenate of the rats with adenocarcinoma of the colon on the background of the enterosorbent AUT-M use. Note: * – significant differences in comparison to control animals; ** – significant differences between the indices of carcinogenic animals and carcinogenic animals that received enterosorbent.
The Sakakibara Health Integrative Profile of Atherosclerotic-Carcinogenesis Hypothesis (SHIP-AC)
ClinicalTrials.gov study NCT04198896. IPD Sharing: NO. Countries: 0. Publications: 1.
Chemoprevention of Gastric Carcinogenesis
ClinicalTrials.gov study NCT02794428. IPD Sharing: NO. Countries: 2. Publications: 0.
Data from: Differentially expressed mRNA targets of differentially expressed miRNAs predict changes in the TP53 axis and carcinogenesis related pathways in human keratinocytes chronically exposed to arsenic
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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.