Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248117 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:<p>The ~80% of individuals with classic familial adenomatous polyposis (FAP) have detectable mutations in the coding sequence of the adenomatous polyposis coli (APC) gene. To investigate the 20% of families without detectable causative mutations, we used exome sequencing and second-generation sequencing of the APC locus including non-coding regions. We identified a novel ~11kb deletion 44kb upstream of APC that was present only in affected individuals of three kindreds. SNP analysis showed that this ~11kb deletion was accompanied by silencing of one of the APC alleles in blood-derived RNA of affected individuals. </p>
| phs000904 | dbGaP
Project description:The first step in the development of colorectal cancer (CRC) is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (APC) gene encoding an essential tumor suppressor. In order to identify genes affected by Apc loss, expression profiling of intestinal epithelium isolated from mice harboring the conditional allele of the gene was performed.
2019-11-01 | E-MTAB-6915 | biostudies-arrayexpress
Project description:Vil-CreERT2 was used to drive loss of APC (Adenomatous polyposis coli) in the murine intestinal epithelium. 4 days post induction, mice were sampled and 1cm of tissue from the proximal intestine was collected into RNA later. This was compared to control (wild-type) intestine. This analysis allows investigation of transcriptional changes following APC loss (and therefore activation of the WNT signalling pathway).
2019-12-31 | GSE112226 | GEO
Project description:APCmin/+ mice develop spontaneous gastrointestinal polyposis due to a dominantly inhereited germline loss-of-function mutation in the tumor suppressor adenomatous polyposis coli (APC). Changes in intestinal immune activity have been documented to occur prior to the development of fulminate polyposis. Such changes are thought to contribute to disease development. We used microarrays to describe the changing intestinal transcriptional landscape in APCmin/+ mice. Whole transcriptome profiling from polypotic and nonpolypotic intestinal sections of APC/min+ mice were examined in the early stages of disease, and compared to normal intestinal sections from littermate matched wildtype B6 mice.
2013-08-20 | GSE49970 | GEO
Project description:Polyposis in rat colon (Pirc) model harbors an Apc mutation and mimics human Familial Adenomatous Polyposis (FAP), allowing for intervention studies (e.g., PMID: 27706811, PMID: 30643017). RNA-sequencing of adenomatous polyps and normal colon identified genes altered by dietary spinach consumption.
2021-09-22 | GSE180160 | GEO
Project description:The tumor suppressor gene adenomatous polyposis coli (APC) is mutated in most colorectal cancers (CRC) resulting in constitutive Wnt activation. To understand the Wnt-activating mechanism of APC mutation, we applied CRISPR/Cas9 technology to engineer various APC-truncated isogenic lines. We find that the β-catenin inhibitory domain (CID) in APC represents the threshold for pathological levels of Wnt activation and tumor transformation. Mechanistically, CID-deleted APC truncation promotes β-catenin deubiquitination through reverse binding of β-TrCP and USP7 to the destruction complex. USP7 depletion in APC-mutated CRC inhibits Wnt activation by restoring β-catenin ubiquitination, drives differentiation and suppresses xenograft tumor growth. Finally, the Wnt-activating role of USP7 is specific to APC mutations, thus can be used as tumor-specific therapeutic target for most CRCs.
2017-11-09 | PXD007947 | Pride
Project description:Mutant KRAS activates cancer stem cells (CSCs) contributing transformation of colorectal cancer (CRC) cells harboring adenomatous polyposis coli (APC) mutations. The factors mediating activation of CSCs by KRAS mutation were systematically investigated through a microarray analysis of the APC-mutated isogenic DLD-1 CRC cells harboring homogeneous wild-type KRAS (D-WT) or mutant KRAS (D-MT). The objective of the study was to find the factors specifically induced in the spheroids harboring both APC and KRAS mutations.
2019-10-16 | GSE119197 | GEO
Project description:The APC (Adenomatous Polyposis Coli) gene encodes a large multidomain protein that plays an integral role in the Wnt/beta-catenin signaling pathway. The loss-of-function mutation in APC is considered the earliest genetic alteration in the course of adenoma-carcinoma sequence of colorectal cancer progression, and the resulting constitutive activation of Wnt/beta-catenin signaling is required for the maintenance of advanced colorectal cancer. In order to identify genes affected by loss of Apc function, we performed transcription profiling of mouse small intestinal tissues comparing polyps with normal mucosa of Apc+/Delta716 mice. We isolated total RNA from intestinal polyps and normal intestinal mucosa from 3 individual Apc+/Delta716 mice. Total RNA samples were then employed to perform microarray analysis (Agilent Whole Mouse Genome Microarray Ver. 2.0, 4x44K).
2020-11-01 | E-MTAB-9187 | biostudies-arrayexpress
Project description:APCmin/+ mice develop spontaneous gastrointestinal polyposis due to a dominantly inhereited germline loss-of-function mutation in the tumor suppressor adenomatous polyposis coli (APC). Changes in intestinal immune activity have been documented to occur prior to the development of fulminate polyposis. Such changes are thought to contribute to disease development. We used microarrays to describe the changing intestinal transcriptional landscape in APCmin/+ mice. Whole transcriptome profiling from polypotic and nonpolypotic intestinal sections of APC/min+ mice were examined in the early stages of disease, and compared to normal intestinal sections from littermate matched wildtype B6 mice. Nonpolypotic (wildtype and APCmin/+) and Polypotic (APCmin/+) sections of terminal ileum were identified by visual inspection, and subsequently selected for RNA isolation and hydridzation to Affymetrix Mouse Genome 430A 2.0 Arrays. Interference from bacterial RNA was selected against using a probeset enriched in oligos extending into 3’-poly-A tails.
2013-08-20 | E-GEOD-49970 | biostudies-arrayexpress
Project description:The first step in the development of human colorectal cancer is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (Apc) gene encoding an essential tumor suppressor. The gene encoding transcriptional factor msh homeobox 1 (Msx1) displayed robust upregulation upon Apc inactivation in intestinal epithelium isolated in mice harboring the conditional allele of the Apc gene. To identify the gene signature in the small intestine upon Msx1 depletion, small intestinal epithelium from mice harboring conditional alleles of Apc and Msx1 was isolated and the gene expression profile was compared with control mice harboring the conditional allele of Apc only.
2019-11-01 | E-MTAB-6930 | biostudies-arrayexpress