E-GEOD-48522
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA210424
PROVIDER: E-GEOD-48522 | ExpressionAtlas | 2015-07-16
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-48522-analysis-methods.tsv | Tabular | |||
| E-GEOD-48522-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-48522-configuration.xml | Xml | |||
| E-GEOD-48522-percentile-ranks.tsv | Tabular | |||
| E-GEOD-48522.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 53 |
Similar Datasets
Project description:Akt signalling leads to stem cell activation and promotes tumour development in epidermis.
| PRJNA210424 | ENA
Project description:Loss-of-parkin function enhances cyclin D1 expression and AKT signalling and promotes glioblastoma cell proliferation
2025-01-24 | E-GEOD-29494 | ExpressionAtlas
Project description:Activation of auxin signalling counteracts photorespiratory hydrogen peroxide dependent cell death
2015-05-08 | E-GEOD-52013 | ExpressionAtlas
Project description:The specific ablation of Rb1 gene in epidermis (RbF/F;K14cre) promotes proliferation and altered differentiation but does not produce spontaneous tumour development. These phenotypic changes are associated with increased expression of E2F members and E2F-dependent transcriptional activity. Here, we have focused on the possible dependence on E2F1 gene function. We have generated mice that lack Rb1 in epidermis in an inducible manner (RbF/F;K14creERTM). These mice are indistinguishable from those lacking pRb in this tissue in a constitutive manner (RbF/F;K14cre). In an E2F1-null background (RbF/F;K14creERTM; E2F1-/- mice), the phenotype due to acute Rb1 loss is not ameliorated by E2F1 loss, but rather exacerbated, indicating that pRb functions in epidermis do not rely solely on E2F1. On the other hand, RbF/F;K14creERTM;E2F1-/- mice develope spontaneous epidermal tumours of hair follicle origin with high incidence. These tumours, which retain a functional p19arf/p53 axis, also show aberrant activation of βcatenin/Wnt pathway. Gene expression studies revealed that these tumours display relevant similarities with specific human tumours. These data demonstrate that the Rb/E2F1 axis exerts essential functions not only in maintaining epidermal homeostasis, but also in suppressing tumour development in epidermis, and that the disruption of this pathway may induce tumour progression through specific alteration of developmental programs. Gene expression was compared between normal mouse skin, skin from transgenic RbF/F;K14creERTM; E2F1-/- , E2F1-/-, and RbF/F;K14creERTM; E2F1-/- mouse, and carcinomas arising in the skin of RbF/F;K14creERTM; E2F1-/- mouse. All mice were treated with tamoxifen.
2012-08-20 | E-GEOD-38048 | biostudies-arrayexpress
Project description:Crosstalk between deregulated hepatocyte metabolism and cells within the tumour microenvironment, and consequent effects on liver tumourigenesis, are incompletely understood. We show here that hepatocyte specific loss of the gluconeogenic enzyme fructose 1,6-bisphosphatase 1 (FBP1) disrupts liver metabolic homeostasis and promotes tumour progression. FBP1 is universally silenced in both human and murine liver tumours, and hepatocyte-specific Fbp1 deletion results in steatosis, concomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phenotype (SASP). Depleting senescent HSCs by senolytic treatment with dasatinib/quercetin or ABT-263 inhibits tumour progression. We further demonstrate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; blocking its release with the small molecule inflachromene limits FBP1-dependent HSC activation, subsequent SASP development, and tumour progression. Collectively, these findings provide genetic evidence for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical link between hepatocyte metabolism and HSC senescence that promotes tumour growth.
2020-03-02 | MSV000085045 | MassIVE
Project description:Stem cell factor programs the mast cell activation phenotype
2014-07-03 | E-GEOD-35332 | ExpressionAtlas
Project description:Transcription profiling by array of Arabidopsis after infection with Agrobacterium tumefaciens and tumour development
2014-10-08 | E-GEOD-13927 | ExpressionAtlas
Project description:Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]
2015-07-27 | E-GEOD-51786 | ExpressionAtlas
Project description:The specific ablation of Rb1 gene in epidermis (RbF/F;K14cre) promotes proliferation and altered differentiation but does not produce spontaneous tumour development. These phenotypic changes are associated with increased expression of E2F members and E2F-dependent transcriptional activity. Here, we have focused on the possible dependence on E2F1 gene function. We have generated mice that lack Rb1 in epidermis in an inducible manner (RbF/F;K14creERTM). These mice are indistinguishable from those lacking pRb in this tissue in a constitutive manner (RbF/F;K14cre). In an E2F1-null background (RbF/F;K14creERTM; E2F1-/- mice), the phenotype due to acute Rb1 loss is not ameliorated by E2F1 loss, but rather exacerbated, indicating that pRb functions in epidermis do not rely solely on E2F1. On the other hand, RbF/F;K14creERTM;E2F1-/- mice develope spontaneous epidermal tumours of hair follicle origin with high incidence. These tumours, which retain a functional p19arf/p53 axis, also show aberrant activation of βcatenin/Wnt pathway. Gene expression studies revealed that these tumours display relevant similarities with specific human tumours. These data demonstrate that the Rb/E2F1 axis exerts essential functions not only in maintaining epidermal homeostasis, but also in suppressing tumour development in epidermis, and that the disruption of this pathway may induce tumour progression through specific alteration of developmental programs.
2012-08-20 | GSE38048 | GEO
Project description:To identify the regulatory mechanisms and signalling pathways involved in colorectal cancer (CRC) development, we compared the transcriptome of patient-derived tumor-initiating cells (TICs) with their normal stem cell counterparts of the same patient. This study demonstrates the relevance of AKT-signalling in colonic TIC proliferation and survival. Functional testing uncovered the selective AKT-inhibitor MK-2206 as a potential therapeutic for TIC-directed therapy in CRC. Gene expression profiling of tumor and normal tissues from 5 patients.
2016-07-06 | E-GEOD-70018 | biostudies-arrayexpress