Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bioinformation Therapy for Intestinal Cancer

ABSTRACT: The aim of this study is the synergistic effect of cancer ablation and life information rehabilitation therapy on unresectable intestinal cancer.

DISEASE(S): Intestinal Neoplasms,Advanced Intestinal Cancer

PROVIDER: 2259528 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Human intestine LC-MSMS - Transcriptional and proteomic analysis revealed a synergistic effect of aflatoxin M1 and ochratoxin A mycotoxins on intestinal epithelial integrity of differentiated human Caco-2 cells

Project description:Aflatoxin M1 (AFM1) is a common mycotoxin in dairy milk and it is typically concurrently present with other mycotoxins that may represent a threat for food safety. However, knowledge on how AFM1, alone or in combination with other mycotoxins may affect human intestinal epithelial integrity remain to be established. We employed transcriptome and proteome analysis integrated with biological validation to reveal the molecular basis underlining the effect AFM1 and/or ochratoxin A (OTA) exposure on intestinal epithelial integrity of differentiated Caco-2 cells. Exposure to 4 μg/ml of OTA was found to disrupt human gut epithelial integrity, whereas 4 μg/ml of AFM1 did not. Integrated transcriptome and proteome analysis of AFM1 and OTA, alone or in combination, indicate synergistic effect of the two mycotoxins in disrupting intestinal integrity. This effect was mechanistically linked to a broad ranges of pathways related to intestinal integrity enriched by down-regulated genes and proteins, associated to focal adhesion, adherens junction, and gap junction pathways. Furthermore, the cross–omics analysis of mixed AFM1 and OTA compared with OTA alone suggest that kinases family members, including MLCK, MAPKs, and PKC are the potential key regulators on modulating intestinal epithelial integrity. These findings provide novel insight into the synergistic detrimental role of multiple mycotoxins in disrupting intestinal integrity, and, therefore, identify potential target to improve milk safety related to human health.

2018-08-08 | PXD009437 | Pride

The effect of dietary Spirulina microalga on the intestinal function of the post-weaned piglet

Project description:The aim of this study was to characterize the metabolomic and proteomic changes in the intestinal tissue of weaned piglets fed with diets containing Spirulina as an ingredient (10% incorporation in the diet), combining such information with histomorphology data.

2022-09-20 | PXD030446 | Pride

Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Intestinal fibroblasts

Project description:Innate lymphoid cells (ILC) in the small intestine govern immune homeostasis and protect the host against gut pathogens. While distinct cell-intrinsic signals have been identified that determine ILC development and differentiation, it has remained unclear which cell population regulates ILC sustenance. Using unbiased single cell RNA transcriptomic analysis of intestinal fibroblasts, we have identified a specialized Ccl19-expressing fibroblastic reticular cell (FRC) population that underpins solitary intestinal lymphoid tissue (SILT) structures including cryptopatches and isolated lymphoid follicles. Conditional ablation of lymphotoxin-β receptor (LTβR) signalling in SILT FRC impeded the maturation of isolated lymphoid follicles and blocked ILC maintenance through the downregulation of IL-7, consequently resulting in the elevated susceptibility to bacterial infection. Moreover, specific Ltbr ablation in FRC during adulthood revealed that constant LTβR-dependent FRC-ILC interaction is required to maintain SILT structures and ILC populations. Taken together, our study unveils a critical intestinal FRC niche that secures protective gut immunity.

2022-02-12 | E-MTAB-10638 | biostudies-arrayexpress

Type I Interferons Control Proliferation and Function of Intestinal Epithelium

Project description:Wnt pathway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prevent development of cancer and barrier dysfunction. Although type 1 interferons (IFN) produced in the gut under influence of microbiota are known for their anti-proliferative effects, the role of these cytokines in regulating intestinal epithelial renewal is largely unknown. Here we report a novel role for IFN in the context of intestinal knockout of casein kinase 1Î± (CK1Î±), which controls ubiquitination and degradation of both Î²-catenin and the IFNAR1 chain of the IFN receptor. Ablation of CK1Î± leads to activation of both Î²-catenin and IFN pathway and prevents unlimited proliferation of intestinal epithelial cells despite constitutive Î²-catenin activity. IFN signaling contributes to activation of the p53 pathway and appearance of apoptotic and senescence markers in the CK1Î±-deficient gut. Concurrent genetic ablation of CK1Î± and IFNAR1 leads to intestinal hyperplasia, robust attenuation of apoptosis, and rapid and lethal loss of the barrier function. These data indicate that IFN plays an important role in controlling proliferation and function of intestinal epithelium in the context of Î²-catenin activation. Two conditions were examined, with 2 replicates for each condition, yielding 4 samples in total.

2016-01-05 | E-GEOD-76512 | biostudies-arrayexpress

The jejunal proteomic study to investigate the underlying biological effects of maternal DHA supplementation during lactation on intestinal development of weaning pups in early life by using a mice model.

Project description:Docosahexaenoic acid (DHA) is well known to promote visual and brain development while its protective effect on intestinal development in early life remains unknown. In order to understand the underlying biological effects of maternal DHA supplementation during lactation on the intestinal development of pups, we analyzed the proteomics of jejunum tissues from three groups with the DIA-MS method.

2024-06-27 | PXD052063 | Pride

Transcriptomics study of mouse and human macrophage and intestinal organoids in response to pathogen

Project description:Aim of this study is to understand the transcriptional response of macrophages and intestinal epithelial cells to pathogen challenge.These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2014-11-18 | E-ERAD-310 | biostudies-arrayexpress

Transcription profiling of human samples from intervention study with two doses of iron (as ferrous gluconate via intestinal perfusion) to study the effect on genome wide gene expression in the small intestine

Project description:Human intervention study with two doses of iron (as ferrous gluconate via intestinal perfusion) to study the effect on genome-wide gene expression in the small intestine, in order to obtain detailed information about intestinal transcriptomics in vivo.

2006-05-01 | E-MEXP-325 | biostudies-arrayexpress

Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

Project description:Here we asked whether the single early-life (pup day of life P5-P10) antibiotic pulse was sufficient to enhance Type-1 Diabetes (T1D) in Non Obese Diabetic (NOD) mice. Two sets of experimental samples were analyzed for changes in intestinal pathway expression using the NOD mouse model and Pulsed Antibiotic Therapy (PAT). NODPAT sought to describe the intestinal changes related to early life PAT treatment while the RESTORE experiment sought to restore an antibiotic-perturbed host and measure the intestinal expression changes over time. We provide evidence that maternal microbiota provides partial restoration of both the altered pup microbiota and its immunological phenotypes.

2018-08-19 | E-MTAB-6826 | biostudies-arrayexpress

Dietary suppression of MHC-II expression in intestinal epithelial cells enhances intestinal tumorigenesis

Project description:Little is known about how interactions between diet, intestinal stem cells (ISCs) and immune cells impact the early steps of intestinal tumorigenesis. Here, we show that a high fat diet (HFD) reduces the expression of the major histocompatibility complex II (MHC-II) genes in intestinal epithelial cells including ISCs. This decline in epithelial MHC-II expression in a HFD correlates with reduced diversity of the intestinal microbiome and is recapitulated in antibiotic treated and germ-free mice on a control diet. Mechanistically, pattern recognition receptor (PRR) and IFN g signaling regulate epithelial MHC-II expression where genetic ablation of these signaling pathways dampen MHC-II epithelial expression. Interestingly, upon loss of the tumor suppressor gene Apc in a HFD, MHC-II- ISCs harbor greater in vivo tumor-initiating capacity than their MHC-II+ counterparts when transplanted into immune-component hosts but not immune-deficient hosts, thus implicating a role for epithelial MHC-II-mediated immune surveillance in suppressing tumorigenesis. Finally, ISC-specific genetic ablation of MHC-II in engineered Apc-mediated intestinal tumor models increases tumor burden in a cell autonomous manner. These findings highlight how a HFD perturbs a microbiome – stem cell – immune cell crosstalk in the intestine and contributes to tumor initiation through the dampening of MHC-II expression in pre-malignant ISCs.

2021-08-16 | GSE180949 | GEO

Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Innate lymphoid cells

2022-02-12 | E-MTAB-10645 | biostudies-arrayexpress