Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA87749 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional Profiling of the Transition from Normal Intestine to Adenoma in the APC(Min/+) Mouse. Tissue was from male 91-days old APC(Min/+) mouse (an animal model for human colon cancer). RNA was purified using Trizol and labeled for hybridization to high density oligonucleotide Affymetrix MG_U74Av2 arrays, using manufacturer protocol. We measured the relative expression level of >12000 genes and ESTs. ----------------------------------------- Samples used in analysis: * GSM12501: Normal intestine diet #1 sample C1_0112 Dnmt+/- Min/+ * GSM12502: Tumor diet #1 sample T1_0112 Dnmt+/- Min/+ * GSM12503: Normal intestine diet #1 sample C2_0112 Dnmt+/+ Min/+ * GSM12504: Tumor diet #1 sample T2_0112 Dnmt+/+ Min/+ * GSM12505: Normal intestine diet #2 sample C1_003 Dnmt+/- Min/+ * GSM12506: Tumor diet #2 sample T1_003 Dnmt+/- Min/+ * GSM12507: Normal intestine diet #2 sample C2_003 Dnmt+/+ Min/+ * GSM12508: Tumor diet #2 sample T2_003 Dnmt+/+ Min/+ * GSM12509: Normal intestine diet #3 sample C1_005 Dnmt+/- Min/+ * GSM12510: Tumor diet #3 sample T1_005 Dnmt+/- Min/+ * GSM12511: Normal intestine diet #3 sample C2_005 Dnmt+/+ Min/+ * GSM12512: Tumor diet #3 sample T2_005 Dnmt+/+ Min/+ - - - - - - - - - - - - - - - - - - - - - Comparisons were performed as described in Chen Z, Ge B, Hudson TJ and Rozen R. Gene Expression Patterns 1, 89-93, 2002. Comparing Normal intestine vs Adenoma. - - - - - - - - - - - - - - - - - - - - - This resulted in the identification of differentially expressed transcripts. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx WEB portal (www.Affymetrix.com) and literature. Keywords = Mouse Keywords = Min Keywords = normal Keywords = intestine Keywords = tumor Keywords = tumour Keywords = colon cancer Keywords = gene expression Keywords = beta-catenin Keywords = high density oligonucleotide microarrays Keywords = familial adenomatous polyposis Keywords = FAP Keywords = colorectal cancer Keywords = Affymetrix MGU74Av2 GeneChip probe array Keywords = mouse model Keywords = APC Keywords = adenomatous polyposis coli Keywords: ordered
2004-10-18 | GSE784 | GEO
Project description:Transcriptional Profiling of the Transition from Normal Intestine to Adenoma in the APC(Min/+) Mouse. Tissue was from male 91-days old APC(Min/+) mouse (an animal model for human colon cancer). RNA was purified using Trizol and labeled for hybridization to high density oligonucleotide Affymetrix MG_U74Av2 arrays, using manufacturer protocol. We measured the relative expression level of >12000 genes and ESTs. -----------------------------------------; Samples used in analysis:; * GSM12501: Normal intestine diet #1 sample C1_0112 Dnmt+/- Min/+; * GSM12502: Tumor diet #1 sample T1_0112 Dnmt+/- Min/+; * GSM12503: Normal intestine diet #1 sample C2_0112 Dnmt+/+ Min/+; * GSM12504: Tumor diet #1 sample T2_0112 Dnmt+/+ Min/+; * GSM12505: Normal intestine diet #2 sample C1_003 Dnmt+/- Min/+; * GSM12506: Tumor diet #2 sample T1_003 Dnmt+/- Min/+; * GSM12507: Normal intestine diet #2 sample C2_003 Dnmt+/+ Min/+; * GSM12508: Tumor diet #2 sample T2_003 Dnmt+/+ Min/+; * GSM12509: Normal intestine diet #3 sample C1_005 Dnmt+/- Min/+; * GSM12510: Tumor diet #3 sample T1_005 Dnmt+/- Min/+; * GSM12511: Normal intestine diet #3 sample C2_005 Dnmt+/+ Min/+; * GSM12512: Tumor diet #3 sample T2_005 Dnmt+/+ Min/+; - - - - - - - - - - - - - - - - - - - - -; Comparisons were performed as described in Chen Z, Ge B, Hudson TJ and Rozen R. Gene Expression Patterns 1, 89-93, 2002. Comparing Normal intestine vs Adenoma. - - - - - - - - - - - - - - - - - - - - -; This resulted in the identification of differentially expressed transcripts. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx WEB portal (www.Affymetrix.com) and literature.
2008-06-15 | E-GEOD-784 | biostudies-arrayexpress
Project description:Aberrant CpG methylation is a universal trait of cancer cell genomes and can result in epigenetic modulation of gene activity; however, at which stages tumour-specific epigenetic patterns arise is unknown. Here, we analyse the methylome of APCM in mouse intestinal adenoma as a model of intestinal cancer initiation, and inventory a map of over 13,000 adenoma-specific recurrent differentially methylated regions (DMRs). We find that multiple genes coding for Polycomb proteins are upregulated in adenoma, and concomitantly, hypermethylated DMRs form preferentially at Polycomb target sites. We establish that DMRs are absent from proliferating intestinal epithelial cells or intestinal stem cells, and thus arise de novo after loss of APC. Importantly, a core set of DMRs is conserved in human colon cancer, defining a class of early epigenetic alterations that are distinct from known sets of epigenetically silenced tumour suppressors. The data presented suggests a sequence of events that leads to an altered methylome of colon cancer cells, and may allow more specific selection of clinical epigenetic biomarkers. Analysis of the methylome and RNA expression in adenoma of Apc-Min/+ mutant mice and of normal intestine in Apc-Min/+ and Apc-+/+ wild type mice.
2013-04-03 | E-GEOD-38983 | biostudies-arrayexpress
Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis:; * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples; * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice; * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice; Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing WT vs Adenoma (n=6 x n=5; 83.3% concordance); WT vs Carcinoma (n=5 x n=5; 84% concordance); Adenoma vs Carcinoma (n=5 x n=5; 84% concordance). This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix).
2007-11-06 | E-GEOD-422 | biostudies-arrayexpress
Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis: * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing: * WT vs Adenoma (n=6 x n=5; 83.3% concordance) * WT vs Carcinoma (n=5 x n=5; 84% concordance) * Adenoma vs Carcinoma (n=5 x n=5; 84% concordance) This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix). Keywords = colon cancer Keywords = gene expression Keywords = DNA microarrays Keywords = beta-catenin Keywords = familial adenomatous polyposis Keywords: ordered
2003-09-12 | GSE422 | GEO
Project description:Somatic mutations in APC or CTNNB1 genes lead to aberrant Wnt signaling and colorectal cancer (CRC) initiation and progression. Activation of Wnt pathway leads to the formation of beta-catenin-T-cell factor/Lymphoid enhancer binding factor 1 (Tcf/Lef1) complexes that activate transcription of oncogenic target genes. Lef1 is the only member of the Tcf gene family that is not expressed in the normal intestine, but is induced during intestinal tumorigenesis. Thus, we wanted to assess the role of Lef1 using genetic mouse models of intestinal adenomas and scRNA-seq technology. Tumorigenesis was initiated by inducing Apc mutation in Lgr5+ stem cells. Intestinal EpCAM+ epithelial cells of Lgr5-CreERT;Apc fl/fl (LApc) mouse and Lgr5-CreERT;Apc fl/fl; Lef1 fl/fl (LApcL) mouse were used to analyze the effects of Lef1 deletion in intestinal adenoma cells. We used WT mice as a control to distinguish adenoma cells.
2021-12-10 | GSE179483 | GEO
Project description:colonic adenoma and adjacent normal from Lrig1-creERT2;Apc-fl/+ mouse
2018-10-23 | GSE117615 | GEO
Project description:Patients with germline APC mutations are recognized by hundreds of adenoma polyps in colon, which will give rise to adenocarcinoma inevitably. Over 700 germline APC mutations have been reported to be the leading cause of adenomatous polyposis. However, the underlying mechanism of APC mutation triggered colonic cancer remains mysterious. Here, using a modified STRT-seq protocol, we analyzed over 4000 single cells from the four matching adenomatous polyposis, adenocarcinoma, adjacent normal colon tissue and one lymphatic metastasis from four adenomatous polyposis patients with APC mutations. We identified the main cell types existed in human intestine such as B cells, mast cells, T cells, macrophage cells, endothelial cells, stromal cells and epithelial cells. And the proportional changes of various cell types during the development of adenoma were showed. The transcriptomic similarities and differences between adenoma, adenocarcinoma and adjacent normal tissue were comprehensively investigated. For better understanding the tumor progression process, we also take advantage of other genomic signatures, such as SNV and CNV. We found that the gene expression signatures of adenoma and adenocarcinoma were largely similar when compared with adjacent normal tissue. But the mutation accumulation was indeed observed during the progression from adenoma to adenocarcinoma. To summarized, our work will help us accurately investigate the pathogenic mechanism and heterogeneity of APC inactive mutation triggered colonic cancer, which will also help us better understand the non-familial colorectal cancers
2019-10-25 | GSE109308 | GEO
Project description:Tumor Associated Calcium Signal Transducer 2 (TACSTD2) is one of the cancer-related genes whose overexpression correlates with tumor progression and invasiveness in human colorectal cancer. TACSTD2 gene encodes for a transmembrane glycoprotein TROP2, which is implicated in altered expression of epithelial-mesenchymal transition (EMT) markers and may play a role in metastasis formation. To determine how TROP2 affects aberrant tumor cell signaling, we isolated early adenoma cells from the mouse small intestine 6 weeks after disruption of the Adenomatous polyposis coli (Apc) gene, one of the first steps in the development of colorectal cancer in human. We performed expression profiling of Trop2+ and Trop2- tumor cells and, in addition, non-tumor cells of the intestinal epithelium, including predominantly differentiated cells.
2022-11-29 | E-MTAB-11382 | biostudies-arrayexpress
Project description:Apc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set.
2017-02-01 | GSE81441 | GEO