Gene expression data of 135 patients presenting colorectal adenoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE117607 | GEO | 2018/12/01
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression profiles of 70 patients presenting with concurrent colorectal adenomas and colorectal tumors were obtained using Affymetrix U133+ arrays.
2018-12-01 | GSE117606 | GEO
Project description:Gene expression data of 135 patients presenting colorectal adenoma
| PRJNA482633 | ENA
Project description:Colorectal adenomas are benign precursor lesions of colorectal cancer (CRC) that arise from normal epithelium1. The prevalence of adenomas in the large intestine is much higher than the incidence of cancer implying that the majority of adenomas will never progress to CRC4. In clinical practice, adenomas detected during colonoscopy are completely removed, and consequently the natural history of disease disrupted. Based on the prevalence of focal cancer in endoscopically removed adenomas, it is estimated that only 5% of adenomas will eventually progress to CRC. The aim of the present study was to characterize adenomas at low and high risk of progressing to cancer by extensive molecular profiling at DNA, RNA, and protein level, allowing to examine the biological processes in which they differ and to discover putative drivers of early colorectal tumor development.
2019-08-22 | PXD012254 | Pride
Project description:We showed that a lot of genes were deregulated in colorectal adenocarcinomas in comparison with colorectal adenomas. 37 colorectal adenoma and 9 colorectal adenocarcinoma samples were analyzed. We generated a comparison between adenocarcinomas and adenomas.
2013-08-27 | E-GEOD-50115 | biostudies-arrayexpress
Project description:Approximately two decades ago, Vogelstein and Fearon proposed the adenoma-carcinoma sequence of sporadic CRC development and illustrated the accumulation of genetic alterations during the stepwise progression, thereby providing a guideline for clinical practice. Although the detection and excision of precancerous lesions could prevent colorectal cancer and reduce mortality, 6% of adenomas will ultimately develop into colorectal cancer. Thus, this genetic model for colorectal tumorigenesis may not completely reflect the complex essence of the disease and whether the mode of initiation of the events in the multistep progression affects the outcome of CRC is still unknown. In this study, mRNA and miRNA expression profiling was performed with human colorectal tissues, including normal mucosa, adenoma and adenocarcinoma. Then, an integrated approach was adopted to establish the regulatory interaction networks that were correlated with colorectal carcinogenesis. Finally, a 55-gene signature whose expression was down-regulated in precancerous lesions compared to normal tissue was identified as a potential early indicator of CRC survival. The results suggested that genes related to immunity and homeostasis played a critical role in protection against adenoma initiation and that the altered molecular events that influence colorectal cancer prognosis may be set in an early, precancerous stage. Four types of human colorectal tissues were selected by colonoscopic resection or colorectal surgery, including 12 normal mucosae, 21 low-grade adenomas (mild or moderate atypical hyperplasia), 30 high-grade adenomas (severe atypical hyperplasia or carcinoma in situ) and 25 adenocarcinomas. Gene expression profiling analysis of these samples was performed using Agilent 4x44K human whole genome gene expression microarray (G4112F).
2015-10-16 | E-GEOD-41657 | biostudies-arrayexpress
Project description:Approximately two decades ago, Vogelstein and Fearon proposed the adenoma-carcinoma sequence of sporadic CRC development and illustrated the accumulation of genetic alterations during the stepwise progression, thereby providing a guideline for clinical practice. Although the detection and excision of precancerous lesions could prevent colorectal cancer and reduce mortality, 6% of adenomas will ultimately develop into colorectal cancer. Thus, this genetic model for colorectal tumorigenesis may not completely reflect the complex essence of the disease and whether the mode of initiation of the events in the multistep progression affects the outcome of CRC is still unknown. In this study, mRNA and miRNA expression profiling was performed with human colorectal tissues, including normal mucosa, adenoma and adenocarcinoma. Then, an integrated approach was adopted to establish the regulatory interaction networks that were correlated with colorectal carcinogenesis. Finally, a 55-gene signature whose expression was down-regulated in precancerous lesions compared to normal tissue was identified as a potential early indicator of CRC survival. The results suggested that genes related to immunity and homeostasis played a critical role in protection against adenoma initiation and that the altered molecular events that influence colorectal cancer prognosis may be set in an early, precancerous stage. Four types of human colorectal tissues were selected by colonoscopic resection or colorectal surgery, including 15 normal mucosae, 39 low-grade adenomas (mild or moderate atypical hyperplasia), 20 high-grade adenomas (severe atypical hyperplasia or carcinoma in situ) and 33 adenocarcinomas. MicroRNA expression profiling analysis of these samples was performed on Agilent 8Ã16K Human miRNA Microarray V3 (G4470C).
2015-10-16 | E-GEOD-41655 | biostudies-arrayexpress
Project description:We showed that a lot of genes were deregulated in colorectal adenocarcinomas in comparison with colorectal adenomas.
2013-08-27 | GSE50115 | GEO
Project description:We showed that a large number of genes were deregulated in colorectal adenomas in comparison with colorectal normal mucosae. 37 colorectal adenoma and 9 colorectal normal mucosa samples were analyzed. We generated a comparison between adenomas and normal mucosae.
2013-08-27 | E-GEOD-50114 | biostudies-arrayexpress
Project description:Colorectal cancer often arises from adenomatous polyps. Polyps can grow and progress to cancer, but may also remain static in size, regress, or resolve. Prediciting which progress to cancer and which remain benign is difficult. We developed a long-lived murine model of colorectal cancer with tumors that can be followed by colonoscopy. Our aim was to assess whether these tumors have similar growth patterns and histologic fates to human colorectal polyps to identify features to aid in risk stratification of colonic tumors. Long-lived Apcin/+ mice were treated with 4% dextran sodium sulfate to promote colonic tumorigenesis. Tumor growth patterns were characterized by serial colonoscopy, and pathology was determined. Serial biopsies of tumors were obtained for immunohistochemistry and gene expression profiling by microarray analysis with Affymetrix Whole Genome array. Tumors (n=424) grew, remained static, regressed, or resolved over time with different relative frequencies. Newly developed tumors demonstrated dynamic growth patterns with higher rates of growth and resolution, while more established tumors tended to remain static in size. Colonic tumors were hyperplastic lesions (3%), adenomas (73%), intramucosal carcinomas (20%), or adenocarcinomas (3%). Differentially expressed genes between adenomas and intramucosal carcinomas were identified. We did not identify differentially expressed genes between early and late biopsies from the same tumor. This novel murine model of intestinal tumorigenesis develops colonic tumors that can be monitored by serial colonoscopy, mirror growth patterns seen in human colorectal polyps, and progress to colorectal cancer. Further characterization of cellular and molecular features are needed to determine which features can be used to risk-stratify polyps for progress to colorectal cancer and potentially guide prevention strategies. F1 (SWR x C57BL/6) Apcin/+ mice who had been given two treatments of 4% dextran sodium sulfate in drinking water at weaning underwent colonoscopy around 80 days of age. Those with distal colonic tumors amenable to biopsy had two biopsies taken at that time. Tumors were monitored by colonoscopy every 14 days. Every 28 days, two additional biopsies were taken of each tumor. This protocol was repeated until mice were moribund. Six tumors were removed after sacrifice. The earliest and latest biopsies of each tumor were selected for RNA extraction and Affymetrix hybridization.
2014-05-03 | E-GEOD-46626 | biostudies-arrayexpress
Project description:We showed that a large number of genes were deregulated in colorectal adenomas in comparison with colorectal normal mucosae.
2013-08-27 | GSE50114 | GEO