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Links from GEO DataSets

Items: 20

1.
Full record GDS389

Colon cancer

Examination of transition from normal intestinal epithelia to adenomas and carcinomas in the multiple intestinal neoplasia adenomatous polyposis coli mutant mouse, APC(Min/+).
Organism:
Mus musculus
Type:
Expression profiling by array, count, 3 disease state, 2 strain sets
Platform:
GPL81
Series:
GSE422
16 Samples
Download data
DataSet
Accession:
GDS389
ID:
389
2.

Epithelium transition profile

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS389
Platform:
GPL81
16 Samples
Download data
Series
Accession:
GSE422
ID:
200000422
3.

Global gene expression analysis in Stat3deltaIEC APCMin/+ mice

(Submitter supplied) Background and aims: The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers. Methods: We investigated the role of Stat3 in intestinal tumors using mice with conditional ablation of Stat3 in intestinal epithelial cells (Stat3deltaIEC). Results: In the APCmin mouse model of intestinal cancer, genetic ablation of Stat3 reduced the multiplicity of early adenomas. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
18 Samples
Download data: CEL
Series
Accession:
GSE17841
ID:
200017841
4.

Transcriptional Profiling of the Transition from Normal Intestine to Adenoma in the APC(Min/+) Mouse

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL81
12 Samples
Download data
Series
Accession:
GSE784
ID:
200000784
5.

Transcriptome profile of human colorectal adenomas.

(Submitter supplied) Background: Colorectal cancers are believed to arise predominantly from adenomas. Although these precancerous lesions have been subjected to extensive clinical, pathological, and molecular analyses, little is currently known about the global gene expression changes accompanying their formation. Results: To characterize the molecular processes underlying the transformation of normal colonic epithelium, we compared the transcriptomes of 32 prospectively collected adenomas with those of normal mucosa from the same individuals. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS2947
Platform:
GPL570
64 Samples
Download data: CEL, CHP
Series
Accession:
GSE8671
ID:
200008671
6.
Full record GDS2947

Colorectal adenoma formation

Analysis of colorectal adenomas and normal mucosas from 32 patients. Results provide insight into the molecular mechanisms underlying the formation of colorectal adenomas.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state, 32 individual sets
Platform:
GPL570
Series:
GSE8671
64 Samples
Download data: CEL, CHP
DataSet
Accession:
GDS2947
ID:
2947
7.

Mutant K-ras promotes carcinogen-induced murine colorectal tumourigenesis, but does not alter tumour chromosome stability

(Submitter supplied) K-ras mutations are observed in around 40% human colorectal adenomas and carcinomas and contribute to the pathogenesis of human and rodent colorectal tumour formation. Previously, we developed and characterised a strain of transgenic mice with inducible intestinal epithelial expression of K-rasVal12 via a Cre/LoxP system. To evaluate the influence of mutant K-ras on carcinogen-induced colorectal tumourigenesis, we induced neoplastic alterations in the large intestines of wild-type and K-rasVal12 mice using the colon-selective carcinogen 1, 2-dimethylhydrazine (DMH), which has been widely used to study chemically induced colorectal tumours that are histopathologically similar to those observed in humans. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6481
7 Samples
Download data: TXT
Series
Accession:
GSE24010
ID:
200024010
8.

Altered interactions between the gut microbiome and colonic mucosa precede polyposis in APCMin/+ mice

(Submitter supplied) Mutation of the adenomatous polyposis coli (APC gene), an early event in the adenoma-carcinoma sequence, is present in 70-80% of sporadic human colorectal adenomas and carcinomas. To test the hypothesis that mutation of the APC gene alters microbial interactions with host intestinal mucosa prior to the development of polyposis, culture-independent methods (targeted qPCR assays and Illumina sequencing of the 16S rRNA gene V1V2 hypervariable region) were used to compare the intestinal microbial composition of 30 six-week old C57BL/6 APCMin/+ and 30 congenic wild type (WT) mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16417
12 Samples
Download data: TXT
Series
Accession:
GSE67634
ID:
200067634
9.

Non-tumor/tumor intestinal tissue of control or intestine-specific HAI-1 deficient Apc(Min/+) mice

(Submitter supplied) To analyse roles of HAI-1/Spint1 in intestinal tumorigenesis, we examined the effect of intestine-specific deletion of Spint1 gene on Apc(Min/+) mice. The loss of Hai-1/Spint1 significantly accelerated tumor formation in ApcMin/+ mice and shortened their survival periods. Mouse small intestine tumor tissue or background mucosa lacking macroscopically visible tumors were proceeded to RNA extraction and hybridization on microarrays (Affymetrix Mouse Genome 430 2.0 Array).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL, CHP
Series
Accession:
GSE40856
ID:
200040856
10.

Analysis of colorectal tissue from APC- and MYH-associated polyposis patients

(Submitter supplied) Expression profiling is a well established tool for the genome-wide analysis of the transcriptional activity of human neoplasia. However, the high sensitivity of this approach combined with the well-known cellular and molecular heterogeneity of cancer often result in extremely complex and extended expression signatures of difficult functional interpretation. The majority of sporadic colorectal cancer cases are triggered by mutations in the APC tumor suppressor gene leading to constitutive activation of the Wnt/b-catenin signaling pathway and adenoma formation. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3408
78 Samples
Download data: GPR
Series
Accession:
GSE9689
ID:
200009689
11.

Apc1638N intestinal tumors vs WT intestinal mucosa

(Submitter supplied) The majority of sporadic colorectal cancer cases are initiated by mutations in the APC tumor suppressor gene leading to constitutive activation of the Wnt/b-catenin signaling pathway and adenoma formation. Several pre-clinical models carrying germline mutations in the endogenous mouse Apc tumor supressor gene have been generated and their phenotype characterized. The predisposition of these mouse models to multiple intestinal adenomas closely resembles the FAP phenotype at the molecular, cellular and phenotypic level and may prove valuable to elucidate the molecular and cellular mechanisms underlying colorectal tumorigenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL339
5 Samples
Download data: CEL
Series
Accession:
GSE9580
ID:
200009580
12.

Hepatocyte-nuclear-factor-4a promotes gut neoplasia in mice and protects against the production of reactive oxygen species

(Submitter supplied) Hepatocyte-nuclear-factor-4α (Hnf4α) is a transcription factor that controls epithelial cell polarity and maturation during embryogenesis. Hnf4α conditional deletion during post-natal development results in minor consequences on intestinal epithelium integrity but promotes activation of the Wnt/β-catenin pathway. Here we show that Hnf4α does not act as a tumor suppressor gene but is crucial to promote gut tumorigenesis in mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE20968
ID:
200020968
13.

Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL21103 GPL6887
38 Samples
Download data
Series
Accession:
GSE121145
ID:
200121145
14.

Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (RNA-Seq)

(Submitter supplied) We assessed differential gene expression using RNAseq in intestinal adenomas between Apc loss-of-function (Apcmin) mice, or by Apc1322T mice encoding a partially-functional Apc truncation commonly found in colorectal carcinomas.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: TXT
Series
Accession:
GSE121142
ID:
200121142
15.

Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (Illumina Beadchip)

(Submitter supplied) Bcl9 and Pygo function within the Wnt enhanceosome to effect β-catenin-dependent transcription. Whether they also mediate β-catenin-dependent neoplasia is unclear. Here we assess their roles in intestinal tumorigenesis initiated by Apc loss-of-function (ApcMin). Gene expression profiling revealed that loss-of-Bcl9 synergizes with loss-of-Pygo to shift gene expression within Apc-mutant adenomas from stem cell-like to differentiation along Notch-regulated secretory lineages.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
32 Samples
Download data: TXT
Series
Accession:
GSE121130
ID:
200121130
16.

AP4 regulates stem and Paneth cell homeostasis and promotes adenoma initiation in the intestine (adenoma)

(Submitter supplied) AP4 is frequently expressed in primary CRCs. However, the in vivo relevance of AP4 for development of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of AP4 were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional AP4 were compared.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE99437
ID:
200099437
17.

AP4 regulates stem and Paneth cell homeostasis and promotes adenoma initiation in the intestine (small intestinal organoid)

(Submitter supplied) AP4 is frequently expressed in primary CRCs. However, the in vivo relevance of AP4 for development of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of AP4 were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional AP4 were compared.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE99434
ID:
200099434
18.

RSPO1 suppresses growth of mouse intestinal adenomas

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
7 Samples
Download data: MTX, TSV
Series
Accession:
GSE146139
ID:
200146139
19.

Single cell changes in AAV-Ctrl or AAV-RSPO1-Fc treated intestinal adenoma cells from ApcMin/+ mice

(Submitter supplied) We constructed AAV-vectors for systemic expression of a soluble RSPO1 protein in ApcMin/+ mice. We found that the RSPO1-Fc fusion protein suppresses the Wnt/ß-catenin signaling activity in intestinal adenomas and in adenoma-derived intestinal organoids ex vivo, but not in normal intestinal epithelial cells. In the Apc mutant cells, the RSPO1-Fc fusion protein activated the TGFß/SMAD signaling pathway to suppress several Wnt target genes and adenoma growth, which effect was rescued suppressed by the TGFß receptor kinase inhibitor SB-431542. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
5 Samples
Download data: MTX, RDATA, TSV
Series
Accession:
GSE146138
ID:
200146138
20.

Single cell changes in RSPO1-Fc treated intestinal adenoma organoids from ApcMin/+ mice

(Submitter supplied) We constructed AAV-vectors for systemic expression of a soluble RSPO1 protein in ApcMin/+ mice. We found that the RSPO1-Fc fusion protein suppresses the Wnt/ß-catenin signaling activity in intestinal adenomas and in adenoma-derived intestinal organoids ex vivo, but not in normal intestinal epithelial cells. In the Apc mutant cells, the RSPO1-Fc fusion protein activated the TGFß/SMAD signaling pathway to suppress several Wnt target genes and adenoma growth, which effect was rescued suppressed by the TGFß receptor kinase inhibitor SB-431542. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: MTX, RDATA, TSV
Series
Accession:
GSE146099
ID:
200146099
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