Identification of an intermediate signature that marks the initial phases of colorectal adenoma-carcinoma transition
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE22242 | GEO | 2010/08/29
SECONDARY ACCESSION(S): PRJNA127727
REPOSITORIES: GEO
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Project description:We evaluated the profile of miRNA expression in 6 colorectal adenoma (CRA), 6 colorectal adenocarcinoma (CRC) and 6 matched normal mucosa (NOR) using the Exiqon miRCURY LNA microRNA array,7th generation. We found that global dysregulated miRNAs between colorectal lesions and normal mucosa. Our findings implicates that dysregulation of miRNAs may play important role in the carcinogenesis and present therapeutic targets for CRC.
2018-08-23 | GSE72281 | GEO
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:In the carcinogenesis of colorectal cancer (CRC), the stepwise progression from adenoma to carcinoma is marked by a series of specific genetic alterations of known oncogenes and tumor suppressor genes. However, many patient-matched features of the transcriptome involved in the adenoma-carcinoma sequence remain unidentified. The aim of this study was to identify genes associated with the process of CRC formation by analyzing the characteristics of the transcriptome during tumor formation. Six dynamic expression patterns specific to tumor formation were characterized for the first time. Dysregulation of metabolic pathways, suppression of the immune system, and activation of canonical pathways related to cancer were associated with the adenoma-carcinoma sequence. Among a cluster of genes positively correlated with tumor formation, TPD52L1 was identified as a gene that induced oncologic behaviors and a biomarker for poor prognosis.
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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.
2015-10-16 | GSE41657 | GEO
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.
2015-10-16 | GSE41655 | GEO
Project description:Background: The change of cellular energy metabolism in colorectal carcinogenesis is poorly understood. It is widely accepted tht most, if not all, colorectal cancers (CRCs) arise from adenomatous polyps (APs). Our aim was to characterize the mitochondrial and bioenergetic alternations in the adenoma-carcinoma sequence. Results: Two glycolysis-related genes, aldolase B (ALDOB) and solute carrier family 16 member 4 (SLC16A4), were upregulated in polyps. This result was further confirmed by the real-time PCR analysis showing that the both ALDOB and SLC16A4 mRNA expressions were higher in the polyps with villous component compared with their adjacent normal mucosa.
2017-05-23 | GSE81804 | GEO
Project description:Background. Most colorectal cancers (CRC) arise in a progression through adenoma to carcinoma phenotypes as a consequence of altered genetic information. Clinical progression of CRC may occur in parallel with distinctive signaling alterations. We designed multidirectional analyses integrating microarray-based data with biostatistics and bioinformatics to elucidate the signaling and metabolic alterations underlying CRC development in the adenoma-carcinoma sequence. Methodology/Principal Findings. Studies were performed on normal mucosa, adenoma, and CRC samples obtained during surgery or colonoscopy. Collections of cryostat sections prepared from the tissue samples were evaluated by a pathologist to control the relative cell type content. RNA was isolated from 105 macro- and 40 microdissected specimens. The measurements were done using Affymetrix GeneChip HG-U133plus2, and probe set data were generated using two normalization algorithms: MAS5 and GCRMA with LVS. The data were evaluated using pair-wise comparisons and data decomposition into SVD modes. The method selected for the functional analysis used the Kolmogorov-Smirnov test. Based on a consensus of the results obtained by two tissue handling procedures, two normalization algorithms, and two probe set sorting criteria, we identified six KEGG signaling and metabolic pathways (cell cycle, DNA replication, p53 signaling pathway, purine metabolism, pyrimidine metabolism, and RNA polymerase) that are significantly altered in both macro- and microdissected tumor samples compared to normal colon. On the other hand, pathways altered between benign and malignant tumors were identified only in the macrodissected tissues. Conclusion/Significance. Multidirectional analyses of microarray data allow the identification of essential signaling alterations underlying CRC development. Although the proposed strategy is computationally complex and labor–intensive, it may reduce the number of false results. Gene expression profiles of 40 tissue samples representing distant full-thickness normal colon, normal colon mucosa dissected from tumor, adenoma, and carcinoma. Gene expression profiles of 105 tissue samples representing colon carcinomas, adenocarcinomas, and normal colon samples.
2010-08-01 | E-GEOD-20916 | biostudies-arrayexpress
Project description:Most of the carcinogenesis of colorectal cancer (CRC) follows the normal-adenoma-carcinoma (N-A-C) sequence. We aimed to identify the key proteins in the N-A-C sequence and describe the proteomic pattern of tubular adenoma, tubulovillous adenoma and high-grade neoplasia. This study used high-resolution liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS), in combination with quantitative 5-plex tandem mass tag labeling, to profile protein changes in normal epithelium, tubular adenoma, tubulovillous adenoma, high-grade neoplasia, cancer tissues in colorectum.
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