Differential expression of microRNA and snoRNA of normal mucosa in patients with solitary and synchronous primary colorectal cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Wen-Jian Meng
PROVIDER: E-GEOD-67895 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We evaluated the expression profile of miRNA and snoRNA of normal mucosa in five patients with synchronous CRCs and seven patients with solitary CRCs using the Affymetrix GeneChip miRNA 1.0 array. We found that global dysregulated miRNAs and snoRNAs in normal mucosa between solitary and synchronous CRC. Our findings represent the first comprehensive miRNA and snoRNA expression signatures in normal mucosa between solitary and synchronous CRC, which increases the understanding of the molecular basis of synchronous CRC, and firstly implicates the difference of genetic background in patients with solitary and synchronous CRC.
2015-08-01 | GSE67895 | GEO
Project description:We evaluated the profile of miRNA and snoRNA expression in 7 solitary CRC and matched normal colorectal tissues using the Affymetrix GeneChip miRNA 1.0 array. We found that global dysregulated miRNAs and snoRNAs between cancer tissue and normal mucosa in solitary CRC. Our findings firstly implicates that dysregulation of snoRNAs and miRNA may play important role in the cancinogenesis and present therapeutic targets for solitary CRC. Examination of microRNA and snoRNA expression in cancer and matched normal tissues of solitary CRC
2015-08-01 | E-GEOD-68377 | biostudies-arrayexpress
Project description:We evaluated the profile of miRNA and snoRNA expression in 5 synchronous CRC and matched normal colorectal tissues using the Affymetrix GeneChip miRNA 1.0 array. A total of 24 miRNA differential expressed transcripts which represent 27 mature miRNAs, including an oncogenic miR-17-92a and oncosuppressive miR-143-145 cluster, and a global up-regulation of snoRNAs were revealed in cancer tissues compared with matched normal tissues. Global miRNA expression could distinguish synchronous cancer from normal mucosa. Our findings represent the first comprehensive miRNA and snoRNA expression signatures for synchronous CRC, which increase the understanding of the molecular basis of synchronous CRC, and firstly implicate that dysregulation of snoRNAs and miRNA clusters may present therapeutic targets for synchronous CRC. Examination of microRNA and snoRNA expression in synchronous CRC and matched normal colorectal tissues
2015-08-01 | E-GEOD-54632 | biostudies-arrayexpress
Project description:We evaluated the profile of miRNA and snoRNA expression in 7 solitary CRC and matched normal colorectal tissues using the Affymetrix GeneChip miRNA 1.0 array. We found that global dysregulated miRNAs and snoRNAs between cancer tissue and normal mucosa in solitary CRC. Our findings firstly implicates that dysregulation of snoRNAs and miRNA may play important role in the cancinogenesis and present therapeutic targets for solitary CRC.
2015-08-01 | GSE68377 | GEO
Project description:We evaluated the profile of miRNA and snoRNA expression in 5 synchronous CRC and matched normal colorectal tissues using the Affymetrix GeneChip miRNA 1.0 array. A total of 24 miRNA differential expressed transcripts which represent 27 mature miRNAs, including an oncogenic miR-17-92a and oncosuppressive miR-143-145 cluster, and a global up-regulation of snoRNAs were revealed in cancer tissues compared with matched normal tissues. Global miRNA expression could distinguish synchronous cancer from normal mucosa. Our findings represent the first comprehensive miRNA and snoRNA expression signatures for synchronous CRC, which increase the understanding of the molecular basis of synchronous CRC, and firstly implicate that dysregulation of snoRNAs and miRNA clusters may present therapeutic targets for synchronous CRC.
2015-08-01 | GSE54632 | GEO
Project description:Background an Aim: Epigenetics are thought to play a major role in the carcinogenesis of patients that develop multiple colorectal cancers (CRC) in the non-hereditary setting. Previous studies have suggested concordant DNA hypermethylation between tumor pairs. However, only a few methylation markers have been analyzed. This study was aimed at describing the underlying epigenetic signature that differentiates multiple from solitary colorectal cancer tumors using a genome-scale DNA methylation profiling. Patients and Methods: We used a population-based cohort (EPICOLON II) of 12 patients with synchronous CRC and 29 age- sex- and tumor location-paired solitary CRC patients. DNA methylation profiling was performed using the Illumina Infinium HM27 DNA methylation assay. The most significantly hypermethylated CpG sites results were validated by Methylight. Tumors samples were also analyzed for the CpG Island Methylator Phenotype (CIMP) using the Infinium DNA methylation data; KRAS and BRAF mutations; microsatellite instability; and immunohistochemistry for MLH1/MSH2/MSH6/PMS2. Functional annotation clustering of differentially methylated genes between multiple and solitary CRCs was performed. Results: We identified 102 CpG sites that showed significant DNA hypermethylation in multiple versus solitary tumors (difference in M-NM-2 value >0.1 and p<0.05). Methylight assays validated the array results for 4 selected significantly hypermethylated genes (MAP1B, HTRA1, ALOX15, TIMP3) identified in the profiling (p=0.0002). Based on the Infinium data, 8/12 (66.6%) of multiple tumors were classified as CIMP-high, as compared to 5/29 (17%) solitary tumors (p=0.004). CIMP-high tumors displayed significant hypermethylation in 301 CpG sites (difference in M-NM-2 value >0.1; p value <0.05). Interestingly, 76/102 (74.5%) of the hypermethylated CpG sites found in multiple vs. solitary tumors were also seen to be hypermethylated in CIMP-H tumors. Functional analysis of hypermethylated genes found in multiple vs. solitary tumors showed the presence and enrichment of genes involved in different tumorigenic functions. Conclusions: Multiple colorectal cancers are associated with a distinct methylation phenotype, with a close association between tumor multiplicity and CIMP-high. Our results may be important to unravel the underlying mechanism of tumor multiplicity in the non-hereditary scenario, and provide novel potential biomarkers for identifying high-risk patients and tailoring surveillance strategies. We used a population-based cohort (EPICOLON II) of 12 patients with synchronous CRC and 29 solitary CRC patients. DNA methylation profiling was performed using the Illumina Infinium HM27 DNA methylation assay.
2014-09-01 | E-GEOD-52573 | biostudies-arrayexpress
Project description:Differential expression of microRNA and snoRNA of normal mucosa in patients with solitary and synchronous primary colorectal cancer
| PRJNA281137 | ENA
Project description:Dysregulated miRNA in human colorectal cancer (CRC) were identified through comparison between 4 CRC tumors and their adjacent normal tissues by miRNA array. Histologically-confirmed CRC were included in this study. CRC tissues and paired adjacent normal tissues were obtained from the resected surgical specimens. The adjacent normal tissue is composed of normal colonic mucosa located at approximately 10 cm away from the cancer tissue. miRNA profiling of 754 human miRNAs was performed using TaqMan Human MiRNA Array Set v3.0. Quantitative real-time polymerase chain reaction (Q-PCR) was performed using Applied Biosystems 7900HT Real-Time PCR System (Applied Biosystems). Results were analyzed by the SDS RQ Manager 1.2 software (Applied Biosystems). 4 CRC tissues and 4 adjacent normal tissues were subjucted to qPCR based miRNA expression profiling. Equal amount of total RNA were used for analysis.
2013-03-20 | E-GEOD-45349 | biostudies-arrayexpress
Project description:Background an Aim: Epigenetics are thought to play a major role in the carcinogenesis of patients that develop multiple colorectal cancers (CRC) in the non-hereditary setting. Previous studies have suggested concordant DNA hypermethylation between tumor pairs. However, only a few methylation markers have been analyzed. This study was aimed at describing the underlying epigenetic signature that differentiates multiple from solitary colorectal cancer tumors using a genome-scale DNA methylation profiling. Patients and Methods: We used a population-based cohort (EPICOLON II) of 12 patients with synchronous CRC and 29 age- sex- and tumor location-paired solitary CRC patients. DNA methylation profiling was performed using the Illumina Infinium HM27 DNA methylation assay. The most significantly hypermethylated CpG sites results were validated by Methylight. Tumors samples were also analyzed for the CpG Island Methylator Phenotype (CIMP) using the Infinium DNA methylation data; KRAS and BRAF mutations; microsatellite instability; and immunohistochemistry for MLH1/MSH2/MSH6/PMS2. Functional annotation clustering of differentially methylated genes between multiple and solitary CRCs was performed. Results: We identified 102 CpG sites that showed significant DNA hypermethylation in multiple versus solitary tumors (difference in β value >0.1 and p<0.05). Methylight assays validated the array results for 4 selected significantly hypermethylated genes (MAP1B, HTRA1, ALOX15, TIMP3) identified in the profiling (p=0.0002). Based on the Infinium data, 8/12 (66.6%) of multiple tumors were classified as CIMP-high, as compared to 5/29 (17%) solitary tumors (p=0.004). CIMP-high tumors displayed significant hypermethylation in 301 CpG sites (difference in β value >0.1; p value <0.05). Interestingly, 76/102 (74.5%) of the hypermethylated CpG sites found in multiple vs. solitary tumors were also seen to be hypermethylated in CIMP-H tumors. Functional analysis of hypermethylated genes found in multiple vs. solitary tumors showed the presence and enrichment of genes involved in different tumorigenic functions. Conclusions: Multiple colorectal cancers are associated with a distinct methylation phenotype, with a close association between tumor multiplicity and CIMP-high. Our results may be important to unravel the underlying mechanism of tumor multiplicity in the non-hereditary scenario, and provide novel potential biomarkers for identifying high-risk patients and tailoring surveillance strategies.
2014-09-01 | GSE52573 | GEO
Project description:To determine the pattern of copy number alterations that characterizes Crohn’s disease associated colorectal carcinomas (CD-CRCs), we performed array-based comparative genomic hybridization (aCGH) of CD-CRCs. As control group, we used histomorphologically similar sporadic mucinous colorectal adenocarcinomas. To gain insight into the dynamics of copy number alterations in CD associated colorectal tumor development, we additionally analyzed non-dysplastic, i.e., normal or inflamed, mucosa samples and dysplastic lesions from CD-CRC patients by aCGH. This revealed the gain of chromosome arm 5p as a distinctive feature of CD related colorectal carcinogenesis, while the overall pattern of copy number changes in CD-CRC was similar to sporadic mucinous CRC, including gains of chromosomes and chromosome arms 7, 8, 13 and 20q, and losses of 5q, 8p, 17p and 18q.
2018-06-30 | GSE113015 | GEO