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Gene expression profiling study by RNA-seq in colorectal cancer

ABSTRACT: The objective of this study is to identify a prognostic signature in colorectal cancer (CRC) patients with diverse progression and heterogeneity of CRCs. We generated RNA-seq data of 54 samples (normal colon, primary CRC, and liver metastasis) from 18 CRC patients and, from the RNA-seq data, identified significant genes associated with aggressiveness of CRC. Through diverse statistical methods including generalized linear model likelihood ratio test, two significantly activated regulators were identified. In the validation cohorts, two activated regulators were independent risk factors and potential chemotherapy-sensitive agenets in colorectal cancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE50760 | GEO | 2014/08/31

SECONDARY ACCESSION(S): PRJNA218851

REPOSITORIES: GEO

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Gene expression profiling study by RNA-seq in colorectal cancer

Project description:The objective of this study is to identify a prognostic signature in colorectal cancer (CRC) patients with diverse progression and heterogeneity of CRCs. We generated RNA-seq data of 54 samples (normal colon, primary CRC, and liver metastasis) from 18 CRC patients and, from the RNA-seq data, identified significant genes associated with aggressiveness of CRC. Through diverse statistical methods including generalized linear model likelihood ratio test, two significantly activated regulators were identified. In the validation cohorts, two activated regulators were independent risk factors and potential chemotherapy-sensitive agenets in colorectal cancers. RNA-seq data of 54 samples (normal colon, primary CRC, and liver metastasis) were generated from 18 CRC patients. Total RNA was isolated by RNeasy Mini Kit (Qiagen, CA, USA), according to the manufacturer's protocol. The quality and integrity of the RNA were confirmed by agarose gel electrophoresis and ethidium bromide staining, followed by visual examination under ultraviolet light. Sequencing library was prepared using TruSeq RNA Sample Preparation kit v2 (Illumina, CA, USA) according to the manufacturer’s protocols. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads, fragmented, and converted into cDNAs. Then, adapters were ligated and the fragments were amplified on a PCR. Sequencing was performed in paired end reads (2x100 bp) using Hiseq-2000 (Illumina).

2014-08-31 | E-GEOD-50760 | biostudies-arrayexpress

Gene expression profiling study to identify key markers associated with disease recurrence in colorectal cancers.

Project description:The objective of this study is to identify a gene set to predict recurrence of colorectal cancer (CRC) patients. We generated RNA-seq data of 110 primary CRC samples and identified significant genes associated with recurrence of CRC. Through diverse statistical methods including generalized linear model likelihood ratio test, significant 10 genes were identified. In the validation cohorts, a risk classifier consisting of the 10 genes was an independent risk factor in colorectal cancers.

2019-10-29 | GSE107422 | GEO

Transcription profiling by array of microsatellite stable stage III Colorectal Adenocarcinoma (MSS-CRC) with wild type or mutant p53 to study the prognostic significance of the mutation

Project description:Clinical Significance: Understanding the differences in colorectal cancer (CRC) aggressiveness and clinical outcomes in relation to tumor stage and different molecular subsets is at most important for designing treatment regimens. However, molecular signatures for specific phenotypic subsets that predict the aggressiveness and clinical outcomes of CRC, specifically in advanced disease stage are lacking. Therefore, for the first time, the current study has identified a set of molecular markers that are associated with aggressive Stage III CRCs that exhibited microsatellite stable and mutant p53 phenotypic features. These findings might aid in designing aggressive treatment regimens and help to provide insights into the development of novel therapeutic targets. Results: Increased incidence of p53 mutations in MSS CRCs (58%) was associated with higher CRC-specific mortality than MSS-p53 wild-type phenotypes (log-rank, P=0.025; and hazard ratio, 2.52; 95% confidence interval, 1.25-5.08). Of 49 down-regulated genes, LPAR6, PDLIM3 and PLAT and of 35 up-regulated genes, TRIM29, FUT3, IQGAP3, and SLC6A8, were confirmed by qNPA, qRT-PCR, and IHC platforms. Conclusions: p53 mutations are associated with poor prognosis of Stage III microsatellite stable CRCs. p53 wild type vs. mutant tumor samples

2012-01-26 | E-GEOD-27157 | biostudies-arrayexpress

microRNA profiles for lymph node metastasis in T1-stage colorectal cancers.

Project description:If we can more accurately predict the likelihood of regional lymph node metastasis (LNM) for endoscopically resected T1-stage colorectal cancers (CRC), the number of unnecessary additional surgeries can be reduced. We aimed of identify miRNA markers that can predict LNM-positive tumors among T1-stage CRCs and we also developed a miRNA classifier set for facilitating the accuracy and applicability.

2015-09-30 | GSE70574 | GEO

Prognostic Significance and Gene Expression Profiles of p53 Mutations in Microsatellite Stable Stage III Colorectal Adenocarcinoma

2012-01-26 | GSE27157 | GEO

Gene expression comparison of colorectal cancer samples from patients diagnosed at a young and elderly age

Project description:Colorectal cancer (CRC) incidence increases with age and early onset of the disease is an indication of genetic predisposition, estimated to cause up to 30 % of all CRC cases. To identify genes associated with an increased risk for CRC, genome-wide gene expression levels of CRCs from patients diagnosed at an early age and CRCs from patients diagnosed at higher age were investigated. Patients with known hereditary predisposition syndromes were excluded from the study.

2011-09-07 | GSE25071 | GEO

Molecular Disparities in Colorectal Cancers of White Americans, Alabama African Americans, and Oklahoma American Indians

Project description:In the US, the majority of cancer samples analyzed are from white people, leading to biases in racial and ethnic treatment outcomes. Colorectal cancer (CRC) incidence and mortality rates are high in Alabama African Americans (AAs) and Oklahoma American Indians (AIs). We hypothesized that differences between racial groups may partially explain these disparities. Thus, we compared transcriptomic profiles of CRCs of Alabama AAs, Oklahoma AIs, and white people from both states. Compared to CRCs of white people, CRCs of AAs showed (a) higher expression of cytokines and vesicle trafficking toward modulated antitumor-immune activity, and (b) lower expression of the ID1/BMP/SMAD axis, IL22RA1, APOBEC3, and Mucins; and AIs had (c) higher expression of PTGS2/COX2 (an NSAID target/pro-oncogenic inflammation) and splicing regulators, and (d) lower tumor suppressor activities (e.g., TOB2, PCGF2, BAP1). Therefore, targeting strategies designed for white CRC patients may be less effective for AAs/AIs. These findings illustrate needs to develop optimized interventions to overcome racial CRC disparities.

2023-08-23 | GSE237684 | GEO

Classification of serrated colorectal tumors

Project description:Serrated adenocarcinomas are morphologically different from conventional adenocarcinomas. The serrated pathway has recently been proposed to represent a novel mechanism of colorectal cancer (CRC) formation. However, whether they are biologically different and truly form a distinct subclass of CRC, is not known. This study shows that the gene expression profile of serrated and conventional CRCs differs from each others and that serrated CRCs are not only morphologically novel, but also biologically distinct subclass of CRC. Keywords: molecular classification

2006-07-28 | GSE4045 | GEO

Dynamics of genome alterations in Crohn’s disease associated colorectal carcinogenesis

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

A Molecular Profile of Colorectal Cancer to Guide Therapy [PDCCEs]

Project description:The ability to dissect heterogeneity in colorectal cancer (CRC) is a critical step in developing predictive biomarkers. The goal of this study was to develop a gene expression based molecular subgrouping model, which predicts the likelihood that patients will respond to specific therapies. Using microarray data compiled from 848 CRC patients, we developed a subgrouping model based on 23 activated oncogenic pathway expression signatures. Stability of the model was validated in two independent data sets. To test the capacity of our model to predict patient response to specific targeted therapies and to determine the sensitivity of the subgroups to chemotherapy in vivo, we treated patient-derived colorectal cancer explants (PDCCEs) predicted to have high mTOR pathway activity with everolimus or oxaliplatin. Results: A molecular profile of the discovery dataset revealed 8 molecular subgroups of colorectal cancer (MSCC). Both validation sets also exhibited 8 MSCC and demonstrated significant similarities to the discovery dataset. MSCC predicted to have active mTOR pathway signaling were more sensitive to everolimus compared to MSCC predicted to have low mTOR pathway activity (p=0.016). Furthermore, MSCCs displayed differential sensitivities to oxaliplatin (p<0.05). The ability to predict oncogenic signaling pathway activation is a powerful tool that may be used to sub-classify CRCs into clinically relevant MSCCs. Patterns of pathway activation may be used to target specific therapies in CRC patients and identification of sensitivities of MSCC to specific drugs can be a powerful approach to guide therapy for CRC patients.

2016-12-31 | GSE41568 | GEO

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