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Links from GEO DataSets

Items: 20

1.

TISSUE-LOCATION SPECIFIC TRANSCRIPTIONAL PROGRAMS IN COLON DETERMINE MOLECULAR DEPENDENCIES FOR TUMOR INITIATION [ChIP-Seq]

(Submitter supplied) It is not known why cancers arising in anatomically distinct locations but within the same tissue type can exhibit stark differences in molecular, pathological and clinical features. Cancers arising in proximal and distal sites of the colon are emblematic of these above differences as the proximal and distal colon cancers harbor differences in key molecular features, with BRAFV600E oncogene predominantly occurring in proximal colon cancers in the context of the increased promoter DNA methylation phenotype (CIMP-high), while distal colon cancers lack these molecular features. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
24 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE218479
ID:
200218479
2.

TISSUE-LOCATION SPECIFIC TRANSCRIPTIONAL PROGRAMS IN COLON DETERMINE MOLECULAR DEPENDENCIES FOR TUMOR INITIATION

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL24247
40 Samples
Download data: BW, CSV, NARROWPEAK
Series
Accession:
GSE218482
ID:
200218482
3.

TISSUE-LOCATION SPECIFIC TRANSCRIPTIONAL PROGRAMS IN COLON DETERMINE MOLECULAR DEPENDENCIES FOR TUMOR INITIATION [RNA-Seq]

(Submitter supplied) It is not known why cancers arising in anatomically distinct locations but within the same tissue type can exhibit stark differences in molecular, pathological and clinical features. Cancers arising in proximal and distal sites of the colon are emblematic of these above differences as the proximal and distal colon cancers harbor differences in key molecular features, with BRAFV600E oncogene predominantly occurring in proximal colon cancers in the context of the increased promoter DNA methylation phenotype (CIMP-high), while distal colon cancers lack these molecular features. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: CSV
Series
Accession:
GSE218480
ID:
200218480
4.

Colon tumor samples from mice with Braf V600E, Cdx2-/-, or both, as well as control colon, and tumors from Apc-/- mice.

(Submitter supplied) We tamoxifen treated 8-12 week old mice that had floxed alleles of the following: 1) both Apc alleles (giving rise to Apc truncation/inactivation); 2) both Cdx2 alleles (giving rise to Cdx2 inactivation; 3) one Braf allele, that upon Cre-mediated recombination gives a Braf V600E mutant allele (details below), and 4) the combination of both the Cdx2 alleles and the BrafV600E allele. All four of those groups also had a CDX2P-CreERT2 transgene that expresses Cre recombinase fused to a tamoxifen-regulated fragment of the estrogen receptor ligand binding domain. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
15 Samples
Download data: CEL, TXT, XLSX
Series
Accession:
GSE84650
ID:
200084650
5.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [Colo320 cell line]

(Submitter supplied) Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL23976
4 Samples
Download data: IDAT, TXT
Series
Accession:
GSE124915
ID:
200124915
6.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [BrafV637E knock-in ]

(Submitter supplied) Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. more...
Organism:
Mus musculus
Type:
Methylation profiling by genome tiling array
Platform:
GPL16446
6 Samples
Download data: PAIR, TXT
Series
Accession:
GSE108606
ID:
200108606
7.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by genome tiling array; Methylation profiling by array
4 related Platforms
33 Samples
Download data: IDAT, PAIR
Series
Accession:
GSE98534
ID:
200098534
8.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [Caco2 cell line]

(Submitter supplied) Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
4 Samples
Download data: TXT
Series
Accession:
GSE98533
ID:
200098533
9.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [3 cell lines]

(Submitter supplied) Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
3 Samples
Download data: TXT
Series
Accession:
GSE98532
ID:
200098532
10.

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [tumor, paired normal]

(Submitter supplied) Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array; Methylation profiling by array
Platform:
GPL8490
16 Samples
Download data: TXT
Series
Accession:
GSE98531
ID:
200098531
11.

DNA methylation profiling in colon cancer

(Submitter supplied) Profiling of CpG island methylation in 19 primary colon cancer and paired normal samples
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL9767
40 Samples
Download data: TXT
Series
Accession:
GSE39334
ID:
200039334
12.

Leukemogenesis by CDX2 involves KLF4 repression and deregulated PPARgamma signaling.

(Submitter supplied) Aberrant expression of the homeodomain transcription factor CDX2 occurs in most cases of acute myeloid leukemia (AML) and promotes leukemogenesis, making CDX2, in principle, an attractive therapeutic target. Conversely, CDX2 acts as a tumor suppressor in colonic epithelium. The effectors mediating the leukemogenic activity of CDX2 and the mechanism underlying its context-dependent properties are poorly characterized, and strategies for interfering with CDX2 function in AML remain elusive. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL
Series
Accession:
GSE40939
ID:
200040939
13.

Transcriptome of sessile serrated adenoma/polyps shows a relation with MSI-high colorectal cancer and decrease of CDX2

(Submitter supplied) The objective of this study was to elucidate the molecular background of sessile serrated adenoma/polyp (SSA/P) endoscopically resected with comprehensive gene expression analysis. Gene expression profiling was performed for 10 tumor-normal pairs of SSA/P. Cluster analysis, gene set enrichment analysis (GSEA), and consensus molecular subtype (CMS) classification of colorectal cancer (CRC) were applied to our transcriptome analysis. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL21185
20 Samples
Download data: TXT
Series
Accession:
GSE198692
ID:
200198692
14.

Reduction of DNA methylation suppresses colon carcinogenesis through induction of tumor cell differentiation

(Submitter supplied) In this study, we analyzed global gene expressions of colon tumors from DNA hypomethylated and the control mice. We found that DNA hypomethylated tumors express significantly higher levels of intestinal differentiation-related genes when compared with the control tumors. These results suggest that DNA methylation may play a role in the maintenance of undifferentiated state of colon tumor cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE60620
ID:
200060620
15.

Degree of Tissue Differentiation Dictates Susceptibility to BRAF-driven Colorectal Cancer

(Submitter supplied) In murine models, we find that oncogenic BRAF paradoxically suppresses stem cell renewal and instead promotes differentiation and senescence. This corresponds to inefficient tumor formation in oncogenic BRAF mouse models of colon cancer. By reducing levels of differentiation in the gut via genetic manipulation of either of two distinct differentiation-promoting factors (Smad4 or Cdx2), stem cell activity is restored in BRAFV600E intestines, and the oncogenic capacity of mutant BRAF is amplified. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE106330
ID:
200106330
16.

Colorectal Cancer Cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome variation profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array; Genome variation profiling by SNP array
5 related Platforms
35 Samples
Download data: CEL, CNCHP, TXT
Series
Accession:
GSE30475
ID:
200030475
17.

COLO320 DNA copy number analysis

(Submitter supplied) Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platform:
GPL6801
1 Sample
Download data: CEL, CNCHP
Series
Accession:
GSE30182
ID:
200030182
18.

COLO320 cells: siCDX2 vs. non-targeting control

(Submitter supplied) Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
2 Samples
Download data: TXT
Series
Accession:
GSE30181
ID:
200030181
19.

CDX2 ChIP-seq

(Submitter supplied) Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
3 Samples
Download data: TXT
Series
Accession:
GSE30026
ID:
200030026
20.

Colorectal Cancer Cell Lines aCGH

(Submitter supplied) Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by array
Platforms:
GPL7780 GPL9073
29 Samples
Download data
Series
Accession:
GSE29953
ID:
200029953
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