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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data for 52 microsatellite stable (MSS) primary tumors from patients with proximal colon cancer.

ABSTRACT: Samples were taken from surgically resected tumor specimens from patients with proximal colon cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. APC gene mutation status was determined using Sanger sequencing. A classifier for APC mutation status was trained using these expression data. 52 microsatellite stable (MSS) proximal colon cancers samples were analyzed. 17 samples were APC wild-type and 35 had APC protein-truncating mutations.

ORGANISM(S): Homo sapiens

SUBMITTER: Oliver Sieber

PROVIDER: E-GEOD-63624 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Wild-type APC predicts poor prognosis in microsatellite-stable proximal colon cancer.

Jorissen Robert N RN Christie Michael M Mouradov Dmitri D Sakthianandeswaren Anuratha A Li Shan S Love Christopher C Xu Zheng-Zhou ZZ Molloy Peter L PL Jones Ian T IT McLaughlin Stephen S Ward Robyn L RL Hawkins Nicholas J NJ Ruszkiewicz Andrew R AR Moore James J Burgess Antony W AW Busam Dana D Zhao Qi Q Strausberg Robert L RL Lipton Lara L Desai Jayesh J Gibbs Peter P Sieber Oliver M OM

British journal of cancer 20150825 6

<h4>Background</h4>APC mutations (APC-mt) occur in ∼70% of colorectal cancers (CRCs), but their relationship to prognosis is unclear.<h4>Methods</h4>APC prognostic value was evaluated in 746 stage I-IV CRC patients, stratifying for tumour location and microsatellite instability (MSI). Microarrays were used to identify a gene signature that could classify APC mutation status, and classifier ability to predict prognosis was examined in an independent cohort.<h4>Results</h4>Wild-type APC microsatel ...[more]

PMID: 26305864

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Expression data for 52 microsatellite stable (MSS) primary tumors from patients with proximal colon cancer.

Project description:Samples were taken from surgically resected tumor specimens from patients with proximal colon cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. APC gene mutation status was determined using Sanger sequencing. A classifier for APC mutation status was trained using these expression data.

2016-03-02 | GSE63624 | GEO

Genomic Fingerprints of DC Subsets in the Human Vaginal Mucosa, Skin, and Blood

Project description:Dendritic cells (DC) localize throughout the body, where they sense and capture invading pathogens to induce protective immune responses. Hence, harnessing the biology of tissue-resident DC is crucial for the rational design of vaccines against pathogens. Herein, we characterized the transcriptomes of four antigen presenting cell (APC) subsets from the human vagina (vLC, vCD14- DC, vCD14+ DC, vMM-NM-&) and compared them to those of three skin DC (sDC) subsets and blood myeloid DC. We find that APC genomic fingerprints are significantly influenced by the tissue of origin as well as by individual APC subsets. Nonetheless, CD14+ APC from both vagina and skin are geared towards innate immunity and pro-inflammatory responses, whereas CD14- DC, particularly sLC, vLC, and vCD14- DC, display both Th2-inducing and regulatory phenotypes. We also identified vAPC subset-specific cellular and functional biomarkers that will guide the design of mucosal vaccines against sexually transmitted pathogens. Vaginal and skin tissues were obtained from female patients who underwent pelvic or cosmetic surgeries under protocols approved by the Institutional Review Board (IRB) of Baylor Research Institute (BRI). Patients were not infected with HIV, HCV or TB and did not display inflammation in the tissues. No other diagnosis information was available. Blood from healthy female volunteers was obtained under a protocol approved by the IRB of BRI. 87 total samples. 6 Blood mDC; 16 Dermal CD1c+CD14-; 10 Epidermal LC; 12 Vaginal CD1c+CD14-; 13 Vaginal CD1c+CD14+; 7 Vaginal HLADR- w/ 2 replicates (Vaginal HLADR-_VM610 and Vaginal HLADR-_VM611); 9Vaginal LC; 14 Vaginal Macrophage.

2014-12-17 | E-GEOD-54480 | biostudies-arrayexpress

APC colon stage II

Project description:Analysis of expression profiles in stage II colon cancer according to the APC gene status

2011-01-28 | GSE26906 | GEO

High levels of canonical Wnt signaling lead to loss of stemness and increased differentiation in hematopoietic stem cells

Project description:Canonical Wnt signalling regulates the self-renewal of most if not all stem cell systems. In the blood system, the role of Wnt signalling has been subject of much debate, with positive and negative roles of Wnt signalling proposed for hematopoietic stem cells (HSC). As we have shown previously, this controversy can be largely explained by the effects of different dosages of Wnt signalling. What remained unclear however, was why high Wnt signals would lead to loss of reconstituting capacity. To better understand this phenomenon, we have taken advantage of a series of hypomorphic mutant Apc alleles resulting in a broad range of Wnt dosages in HSCs, purified those HSCs and performed whole genome gene expression analyses. Gene expression profiling and functional studies show that HSCs with APC mutations lead to high Wnt levels , enhanced differentiation and diminished proliferation, but have no effect on apoptosis, collectively leading to loss of stemness. Thus, we provide mechanistic insight into the role of APC mutations and Wnt signalling in HSC biology. As Wnt signals are explored in various in vivo and ex vivo expansion protocols for HSCs, our findings also have clinical ramifications. To investigate the effects of Wnt signals in hematopoietic cells, mice carrying floxed Apc or hypomorphic Apc mutants were crossed, LSK cells were isolated and treated with Cre IRES GFP gamma-retrovirus ex vivo, GFP+ cells were sorted and RNA expression was determined.

2016-03-23 | E-GEOD-79495 | biostudies-arrayexpress

APC colon stage II

Project description:Analysis of expression profiles in stage II colon cancer according to the APC gene status retrospective study

2011-01-28 | E-GEOD-26906 | biostudies-arrayexpress

Global DNA methylation alterations reveal multiple pathways in the initiation and progression of colorectal cancer

Project description:Genetic and epigenetic alterations are a fundamental aspect of colorectal cancer formation. There is considerable heterogeneity between colorectal cancers regarding the mutations and methylated genes they carry, and this heterogeneity may arise early in the polyp-cancer sequence. However, our understanding of the epigenetic alterations and gene mutations in colon adenomas and their relation to colorectal cancer is incomplete. Thus, we have assessed the methylome in normal colon mucosa, tubular adenomas, and colorectal adenocarcinomas and have determined the relationship of these findings between adenomas and cancer in the colon. Genome-wide alterations in DNA methylation were found in the normal colon mucosa adjacent to colorectal cancer, tubular adenomas, and colorectal cancer. Three subgroups of CRCs and two subgroups of adenomas were identified on the basis of their DNA methylation patterns. The adenomas separated into a high-frequency methylation class (Adenoma-H) and a low-frequency methylation class. The adenoma-H polyps have a methylated DNA signature similar to non-CIMP CRCs, whereas those of the Adenoma-L class have a similar methylation pattern to normal colon mucosa. The CpGs that account for these signatures are located in intragenic/intergenic regions, which suggests that these two groups of adenomas arise from different stem cell populations. We conducted genome-wide array-based studies and comprehensive data analyses of aberrantly methylated loci in 41 normal colon samples, 42 colon adenomas, and 64 colorectal cancers. Supplementary file 'GSE48684_Matrix_signal_intensities_1.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1183439-GSM1183561. Supplementary file 'GSE48684_Matrix_signal_intensities_2.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1235135-GSM1235158.

2014-09-08 | E-GEOD-48684 | biostudies-arrayexpress

GEMM CRC collection analysis

Project description:A collection of genetically engineered mouse models (GEMM) of colorectal cancer (CRC) were created, and primary tumors from these GEMMs were analyzed. Primary CRC tumors from these GEMMs were genotyped to confirm that they contain the core genetic lesions of interest, including APC, P53, KRAS, and BRAF. Primary tumors from GEMMs with combinations of lesions of interest were analyzed by whole genome expression, and their expression profiles were compared to determine how they segregate. Signatures were then generated from GEMM tumors of interest and compared to human clinical datasets with expression and outcome data. Primary tumors from CRC GEMMs with different combinations of mutant alleles of interested were generated and analyzed. Alleles include mutant forms of APC (A), P53 (P), KRAS (K) and BRAF (B).

2014-07-01 | E-GEOD-50794 | biostudies-arrayexpress

Amplicon sequencing of the trp53 locus of DNA extracted from FFPE sections of tumors obtained from the gastrointestinal tract of APC mice

Project description:This experiment was done to analyze the p53 status in gastrointestinal tumors in the colon and small intestine in APC mice carrying either a wild type p53 or a mutant p53 (R172H) allele and compare colon and small intestine tumors.

2020-02-25 | E-MTAB-8355 | biostudies-arrayexpress

Normal mucosa of Proximal Colon (i.e. proximal to hepatic flexure) versus normal mucosa of Terminal ileum Transcriptomes (Affymetrix array U133A) in colon cancer patients

Project description:Proximal Colon (i.e. proximal to hepatic flexure) versus Terminal ileum Transcriptomes (Affymetrix array U133A). All subjects were operated on for proximal-colon tumor (biopsies of proximal-colon normal mucosa were made at more than 5 cm from the site of the tumor).

2021-03-03 | E-MTAB-10164 | biostudies-arrayexpress

TGFÎ² signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype [organoids]

Project description:The aim of this study was to determine the effects of TGFÎ² at the premalignant stage of CRC development. Organoid cultures were isolated from normal colon and from tubular adenomas. One normal colon culture was genetically engineered using the CRISPR-Cas9 system to carry the BRAFV600E mutation. Organoid cultures of three different tubular adenomas and two normal colon samples, and one BRAFV600E-mutant organoid culture received TGFÎ² or control treatment after which gene expression was analyzed by microarray (Affymetrix U133+ PM Genechip Array).

2016-06-01 | E-GEOD-79461 | biostudies-arrayexpress

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