Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA133595 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE24575: Beta-arrestin-2 deficiency effect on intestinal tumorigenesis in Apc-mutated mice GSE24576: Gene expression analysis of tumors from ApcD14/+ mice Refer to individual Series
2012-01-20 | E-GEOD-24577 | biostudies-arrayexpress
Project description:The effect of TGF-beta in Apc-mutated mouse intestinal organoids
| PRJNA156159 | ENA
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice. 16 tumors from ApcD14/+:Arrb2+/+ mice and 13 tumors from ApcD14/+:Arrb2-/- mice
2012-01-20 | E-GEOD-24575 | biostudies-arrayexpress
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice. 10 tumors from 2 different ApcD14 mice
2012-01-20 | E-GEOD-24576 | biostudies-arrayexpress
Project description:APC is mutated in the majority of colorectal cancers. Inducible deletion of Apc in intestinal epithelial cells in Apcfl//fl; Villin-CreERT2 mice recapitulates this tumor-initiating mutation resulting in expanded intestinal crypts, including stem cells. We used microarrays to analyze BEC gene expression changes during the early stages of intestinal tumorigenesis.
2022-03-29 | GSE111783 | GEO
Project description:Transcription profiling of colonic mucosa of Apc Min/+ mice fed with maslinic acid (MA) to study the underlying mechanisms by which MA inhibits intestinal tumorigenesis
2015-11-02 | E-MTAB-4007 | ExpressionAtlas
Project description:Cited-1 deficiency suppresses intestinal tumorigenesis through the repression of the Wnt pathway- evidence for the just right model of Wnt mediated tumorigenesis
2015-10-22 | E-MEXP-3202 | ExpressionAtlas
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice.
2012-01-20 | GSE24576 | GEO
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice.
2012-01-20 | GSE24575 | GEO