Mapping of RNA Interactomes in Adenoma-carcinoma Sequence of Human Colorectal cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA914771 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22857434_1.fastq.gz | Fastqsanger.gz | |||
| SRR22857434_2.fastq.gz | Fastqsanger.gz | |||
| SRR22857435_1.fastq.gz | Fastqsanger.gz | |||
| SRR22857435_2.fastq.gz | Fastqsanger.gz | |||
| SRR22857436_1.fastq.gz | Fastqsanger.gz |
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Project description:To study the dynamics of RNA interactomes, RIC-seq was performed on several biological replicates of colorectal cancer patients, each including colorectal adenomas, cancerous tissues, and tissues distal to cancer
2023-03-23 | GSE221551 | GEO
Project description:The colorectal adenoma-carcinoma sequence describes the stepwise progression from normal to dysplastic epithelium and then to carcinoma; only a small proportion of colorectal adenoma (CRA) progresses to colorectal carcinoma (CRC). Presently, endoscopic intervention is used on patients with CRAs of high grade dysplasia, diameters > 1 cm, or villous components > 25% who are at higher risk than other CRA sufferers. During the process, biopsy samples were taken for conventional histological diagnosis, but poor pathomorphological sensitivity and specificity greatly limit the diagnostic accuracy. Unfortunately, there are no reliable molecular criteria available that can predict the potential development of CRA to CRC. In present study, we use microarrays to detail the global programme of gene expression underlying the gradual progress of colorectal adenoma-carcinoma sequence.
2010-08-29 | GSE22242 | GEO
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.
2021-08-31 | GSE164541 | GEO
Project description:Chromosomal instability (CIN) is the hallmark of colorectal adenoma to carcinoma progression in 85% of cases, with 20q gain as the most prominent aberration. Yet, the oncogenes at this chromosomal gain are still largely unknown. Here, we aimed to identify oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on gene expression in this amplicon. Segmentation of DNA copy number changes on 20q was performed by array CGH in 67 colorectal adenomas and carcinomas. Additionally, robust analysis of mRNA expression in these segments was performed in 68 adenomas and carcinomas. This approach revealed seven genes to be important in CIN related adenoma to carcinoma progression. These genes may both serve as highly specific biomarkers for presence of high-risk precursor lesions as well as potential targets for pharmaceutical intervention. Keywords: Integration of array CGH and expression microarrays in colorectal cancer progression
2008-10-15 | GSE8067 | GEO
Project description:Chromosomal instability (CIN) is the hallmark of colorectal adenoma to carcinoma progression in 85% of cases, with 20q gain as the most prominent aberration. Yet, the oncogenes at this chromosomal gain are still largely unknown. Here, we aimed to identify oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on gene expression in this amplicon. Segmentation of DNA copy number changes on 20q was performed by array CGH in 67 colorectal adenomas and carcinomas. Additionally, robust analysis of mRNA expression in these segments was performed in 68 adenomas and carcinomas. This approach revealed seven genes to be important in CIN related adenoma to carcinoma progression. These genes may both serve as highly specific biomarkers for presence of high-risk precursor lesions as well as potential targets for pharmaceutical intervention. Keywords: Integration of array CGH and expression microarrays in colorectal cancer progression We performed array CGH on a panel of 41 progressed adenomas, from which the adenoma and carcinoma components were separately analysed (total, 82 samples). The DNA obtained from these samples was extracted from formalin-fixed, paraffin-embedded material. Additionally we analysed a series of independent frozen adenomas and carcinomas by array CGH (34 adenomas and 33 carcinomas) and expression microarrays (37 adenomas and 31 carcinomas). For array-CGH we used as reference DNA for all samples, a pool of 10 normal individuals. For expression microarrays we used as reference a commercial available RNA (pool of different cancer cell lines), from Strategene. No replicates nor dye swaps were done.
2010-06-25 | E-GEOD-8067 | biostudies-arrayexpress
Project description:Colorectal cancer often develops slowly from adenoma. In this study, we aimed to identify the oncogenes involved in the progression of colorectal adenoma to carcinoma by Tandem Mass Tag (TMT)-based quantitative proteomics. Protein expression changes were compared by TMT-based quantitative mass spectrometry in seven paired samples of normal mucosa, adenoma and carcinoma. Moreover, a bioinformatics analysis of differential protein expression was performed to screen for oncogenes. Effects of oncogene knockdown on cell viability, proliferation, migration and invasion were analyzed in colorectal cancer cell lines. Effects of oncogene overexpression on cell viability and proliferation were analyzed in adenoma organoids. The protein UTP18 was consistently upregulated in the normal-adenoma-carcinoma sequence. UTP18 downregulation was shown to inhibit colorectal cancer cell viability, proliferation, migration and invasion. UTP18 overexpression promoted adenoma organoid viability and proliferation. UTP18 facilitated the expression of MYC and impaired expression of the tumor-suppressor p21. Our data revealed the importance of UTP18 as an effector in the progression of adenoma to carcinoma. Thus, UTP18 is implicated as a highly specific biomarker for early diagnosis of progressive adenomas.
2020-06-01 | PXD017068 |
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids.
2015-01-18 | GSE57965 | GEO
Project description:We tried to examine whether the de novo colorectal carcinomas (CRCs) without an adenoma component can be discriminated from those deriving from adenoma by DNA copy-number alteration profile. The unsupervised clustering of DNA copy-number profiles of 112 colorectal cancer samples, using large-sized (≥ 9 probes) genes, disclosed 4 clusters: Clusters 1, 3, and 4 correspond to carcinoma with an adenoma component. Cluster 2 and some samples in cluster 3 correspond to carcinoma without adenoma component. Our approach suggested that Cluster 2 may represent de novo CRCs since penetrance plots were very different between cluster 2 and the other clusters. Adenocarcinoma in cluster 3 have higher potential for lymph node metastasis than those in cluster 1 and 4 and can derive from clusters 1/4 tumors.
2019-03-19 | GSE128433 | GEO
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids. To assess the expression profiling of genome-engineered organoids, we prepared total-RNA from cultured adenoma, carcinoma and genome-engineered organoids. We produced two types of genome-engineered organoids using the CRISPR/Cas9 or lentivirus vector system. Each engineered gene and engineered methods are described as a single alphabet and method name, respectively, in the sample characteristics field. The abbreviations for the engineered genes are as follows. 1) Genome-engineered organoids with CRISPR/Cas9 A = APC deletion; K = KRAS G12V knock in; S = Smad4 deletion; T = TP53 deletion; P = PIK3CA E545K knock in. 2) Genome-engineered organoids with Lent virus vector B = CTNNB1 S33Y overexpression; K = KRAS G12V overexpression; S = Smad4 shRNA overexpression; T = TP53 shRNA overexpression; P = PIK3CA E545K overexpression.
2015-01-18 | E-GEOD-57965 | biostudies-arrayexpress
Project description:UTP18 as an oncogene promotes colorectal adenoma to carcinoma progression
| PRJNA595591 | ENA