Human Transcriptome Array 2.0 (HTA) from healthy colonic, colorectal adenoma and colorectal cancer tissue
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE100179 | GEO | 2019/09/13
REPOSITORIES: GEO
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Project description:We analyzed, by HTA 2.0, colorectal adenocarcinoma samples and matched normal colonic tissues in order to determine the whole transcriptome expression levels. Three widely used colorectal cancer cell lines were also analyzed. Results provided insights into the regulation, at transcript level, of genes involved in copper homeostasis.
2017-03-31 | GSE84984 | GEO
Project description:We analyzed, by HTA 2.0, colorectal adenocarcinoma samples and matched normal colonic tissues in order to determine the whole transcriptome expression levels. Three widely used colorectal cancer cell lines were also analyzed. Results provided insights into the regulation, at transcript level, of genes involved in copper homeostasis.
2016-12-31 | GSE73360 | GEO
Project description:Whole genomic microarray analysis was performed in order to identify gene expression profile alterations focusing on the dysplastic adenoma-carcinoma transition. Our aims were to determinate characteristic transcript sets for developing diagnostic mRNA expression patterns for objective classification of benign and malignant colorectal diseases and to test the classificatory power of these markers on an independent sample set. Total RNA was extracted from colonic biopsy samples of histologically negative patients and of patients with adenoma or colorectal cancer and were hybridized on Affymetrix HGU133 Plus 2.0 microarrays
2013-01-01 | E-GEOD-37364 | biostudies-arrayexpress
Project description:Traditional serrated adenoma (TSA) remains the least understood of all the colorectal adenomas although these lesions have been associated with a significant cancer risk- twice that of the conventional adenoma (CAD) and of the sessile serrated adenoma (SSA/P). This study was performed to investigate the proteomic profiles of the different colorectal adenomas to better assess the pathogenesis of TSA. We performed a global quantitative expression profile of 44 colorectal adenomas (12 TSA, 15 CAD, 17 SSA/Ps) and 17 normal colonic mucosa, conserved as formalin-fixed paraffin-embedded samples, by the label-free quantification (LFQ) method. Unsupervised consensus hierarchical clustering applied to the whole proteomic profile of the 44 colorectal adenomas identified four subtypes. The C1 and C2 were well-individualized clusters composed of most of the CAD (14/15) and most of the SSA (13/17) respectively. This is consistent with the fact that CAD and SSA/Ps are homogeneous but distinct colorectal adenoma entities. In contrast, TSA were subdivided into C3 and C4 clusters that also contained CAD and SSA/Ps, consistent with the more heterogeneous entity of TSA at the morphological and molecular levels. The comparison of the proteome expression profile between the adenoma subtypes and normal colonic mucosa further confirmed the heterogeneous nature of TSA that merged either on CAD or SSA, while CAD and TSA formed homogeneous and distinct entities. Furthermore, we identified LEFTY1 a new potential marker for TSA that may be relevant for the TSA pathogenesis. LEFTY1 is an inhibitor of the Nodal/TGFb pathway that we found to be one of the most overexpressed proteins specifically in the TSA and confirmed by immunohistochemistry. Taken together, our study confirms that CAD and SSA form homogenous but distinct colorectal adenoma entities while TSA are an heterogeneous entity and may arise from either SSA or from normal mucosa that will evolve along the conventional adenoma pathway.
2020-01-21 | PXD014511 | Pride
Project description:Background: We tested the hypothesis that short-term supplementation with a physiological dose of folate can alter global gene expression in the colon of subjects with colorectal adenoma using a randomised double blind placebo controlled trial design. Materials and Methods: Fourteen subjects with histologically confirmed colorectal adenoma, randomised to receive folic acid (400M-BM-5g/d, n=6) or placebo (n=8) for 10 weeks, had blood samples and colonic tissue biopsies collected before and after the intervention. Blood samples were used to determine serum and red cell folate, plasma homocysteine, and genetic polymorphisms in methylenetetrahydrofolate reductase (MTHFR C677T) and methionine synthase (MS A2756G). RNA extracted from normal-appearing colonic tissue samples was used to determine global gene expression in the colon using AffymetrixM-oM-^CM-^R Microarray GeneChips. Microarray results were confirmed by quantitative real time RT-PCR. Two methods were used to analyse the microarray data: (1) differences between pre- and post-intervention gene expression values in the folic acid and placebo groups separately using paired-sample t tests; (2) differences between the folic acid and placebo groups in the ratio of post-intervention to pre-intervention gene expression values using independent sample t-tests. Results: (1) Following intervention, sixty seven genes were up-regulated and 13 genes were down-regulated in the folic acid group, while 21 genes were up-regulated and none were down-regulated in the placebo group (P<0.05, adjusted for multiple testing). (2) Thirty six genes were up-regulated and 18 genes were down-regulated in the folic acid group when compared with placebo, but none of these were statistically significant after adjustment for multiple testing. These genes are involved in multiple pathways, including cell cycle, signal transduction, cell differentiation, transport, cell division, cell motility, protein transport and immune response. There were no genes involved in 1-carbon metabolism that were altered in expression, although several genes involved in neoplasia were up-regulated. Conclusions: These results indicate that while folic acid can modify gene expression, it is difficult to separate its effects from the natural variability in gene expression in the colon. Fourteen patients with colorectal adenoma were treated with either folate supplementation (6 subjects) or a placebo (8 subjects) for 10 weeks in a randomised double-blind trial. Colonic biopsies of normal tissue were taken before and after the intervention, and analysed for gene expression.
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Project description:The whole-genome oligonucleotide microarray analysis of laser microdissected human colonic epithelial cells can contribute to determination of disease-specific expression alterations in colonic epithelial cells and to localize the origin the expression changes measured in whole biopsy samples. Keywords: whole genomic expression
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2015-01-18 | GSE57965 | GEO
Project description:The whole-genome oligonucleotide microarray analysis of laser microdissected human colonic epithelial cells can contribute to determination of disease-specific expression alterations in colonic epithelial cells and to localize the origin the expression changes measured in whole biopsy samples. Keywords: whole genomic expression Total RNA was extracted from laser microdissected human colon epithelial cells and hybridized on Affymetrix HGU133 Plus 2.0 microarrays
2010-03-15 | E-GEOD-15960 | biostudies-arrayexpress