Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from human MSI colorectal cancer and normal colonic mucosa

ABSTRACT: Microsatellite instability (MSI), caused by defective mismatch repair, is observed in a subset of colorectal cancers (CRCs). We evaluated somatic mutations in microsatellite repeats of genes chosen based on reduced expression in MSI CRC and existence of a coding mononucleotide repeat. Expression profiling of 34 MSI colorectal cancers and 15 normal colonic mucosas was performed in 2002. Comparison of malignant and healthy tissue.

ORGANISM(S): Homo sapiens

SUBMITTER: Pia Vahteristo

PROVIDER: E-GEOD-24514 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Candidate driver genes in microsatellite-unstable colorectal cancer.

Alhopuro Pia P Sammalkorpi Heli H Niittymäki Iina I Biström Mia M Raitila Anniina A Saharinen Juha J Nousiainen Kari K Lehtonen Heli J HJ Heliövaara Elina E Puhakka Jani J Tuupanen Sari S Sousa Sónia S Seruca Raquel R Ferreira Ana M AM Hofstra Robert M W RM Mecklin Jukka-Pekka JP Järvinen Heikki H Ristimäki Ari A Orntoft Torben F TF Hautaniemi Sampsa S Arango Diego D Karhu Auli A Aaltonen Lauri A LA

International journal of cancer 20110803 7

Defects in the mismatch repair system lead to microsatellite instability (MSI), a feature observed in ∼ 15% of all colorectal cancers (CRCs). Microsatellite mutations that drive tumourigenesis, typically inactivation of tumour suppressors, are selected for and are frequently detected in MSI cancers. Here, we evaluated somatic mutations in microsatellite repeats of 790 genes chosen based on reduced expression in MSI CRC and existence of a coding mononucleotide repeat of 6-10 bp in length. All the ...[more]

PMID: 21544814

Similar Datasets

Expression data from human MSI colorectal cancer and normal colonic mucosa

Project description:Microsatellite instability (MSI), caused by defective mismatch repair, is observed in a subset of colorectal cancers (CRCs). We evaluated somatic mutations in microsatellite repeats of genes chosen based on reduced expression in MSI CRC and existence of a coding mononucleotide repeat.

2011-03-01 | GSE24514 | GEO

Dickkopf 1 Impairs Sensitivity to PD-1 Blockade through CD8+ T Cell Inactivation in dMMR/MSI Colorectal Cancer

Project description:Dickkopf 1 (DKK1) could promote tumor progression by suppressing immunity. Therefore, we investigated whether DKK1 influence prognosis and sensitivity to PD-1 blockade in colorectal cancers (CRCs) with defective DNA mismatch repair genes (dMMR) or microsatellite instability (MSI). We found that elevated DKK1 expression was associated with recurrence and dismissed CD8+ T cell infiltrations, and patients with high serum DKK1 had poor anti-PD-1 response. RNA interference or neutralization of DKK1 in CRCs enhanced CD8+ T cell cytotoxicity, and down-regulation of T-bet and E2F1 following GSK3β activation was detected in DKK1-treated CD8+ T cells. In organoid-lymphocyte co-culture model, apoptosis proportions were elevated after individual neutralization of both PD-1 and DKK1, and the combined neutralization resulted in further increases. In conclusion, DKK1 suppresses tumor immunity in dMMR/MSI CRCs by inactivating CD8+ T cells through GSK3β/E2F1/T-bet axis. DKK1 neutralization may improve the sensitivity to PD-1 blockade in dMMR/MSI CRCs.

2021-04-07 | GSE149206 | GEO

Distinct tumorigenic pathways within hereditary nonpolyposis colorectal cancer

Project description:Gene expression profiling has discriminated between sporadic microsatellite instable (MSI) and microsatellite stable (MSS) colorectal cancers (CRCs), whereas the expression pattern of familial colorectal cancer type X (FCCTX) and Lynch syndrome (LS) associated CRCs remain largely unknown. The purpose of this study is to use gene expression profiling of formalin-fixed paraffin-embedded (FFPE) tumor specimens from FCCTX, LS and sporadic CRC as a control to detect expression patterns and to identify signaling pathways differing between FCCTX and LS tumors.

2012-03-08 | GSE36335 | GEO

Distinct tumorigenic pathways within hereditary nonpolyposis colorectal cancer

2012-03-08 | E-GEOD-36335 | biostudies-arrayexpress

Expression data from primary gastric tumors (MSI and MSS) and adjacent normal samples

2008-12-18 | GSE13911 | GEO

Synthetical lethality of Werner helicase and mismatch repair deficiency is mediated by p53 and PUMA in colon cancer

Project description:Synthetic lethality is a powerful approach for targeting oncogenic drivers in cancer. Recent studies revealed that cancer cells with microsatellite instability (MSI) require Werner (WRN) helicase for survival; however, the underlying mechanism remains unclear. In this study, we found that WRN depletion strongly induced p53 and its downstream apoptotic target PUMA in MSI colorectal cancer (CRC) cells. p53 or PUMA deletion abolished apoptosis induced by WRN depletion in MSI CRC cells. Importantly, correction of MSI abrogated the activation of p53/PUMA and cell killing, while induction of MSI led to sensitivity in isogenic CRC cells. Rare p53-mutant MSI CRC cells are resistant to WRN depletion due to lack of PUMA induction, which could be restored by wildtype p53 knock-in or reconstitution. WRN depletion or treatment with the RecQ helicase inhibitor ML216 suppressed in vitro and in vivo growth of MSI CRCs in a p53/PUMA_x0002_dependent manner. ML216 treatment was efficacious in MSI CRC patient-derived xenografts (PDX). Interestingly, p53 gene remains wildtype in the majority of MSI CRCs. These results indicate a critical role of p53/PUMA-mediated apoptosis in the vulnerability of MSI CRCs to WRN loss, and support WRN as a promising therapeutic target in p53-wildtype MSI CRCs.

2022-10-26 | GSE216455 | GEO

Expression profiles of a panel of MSS and MSI colon cancer cell lines

Project description:Expression profiling was used to identify genes differentially expressed in MSS (microsatellite stable) and MSI (microsatellite unstable) colon cancer cell lines. Data submitted in support of manuscript entitled Villin expression is frequently lost in poorly differentiated colon cancer, Diego Arango, Sheren Al-Obaidi, David S. Williams, Jose Dopeso, Rocco Mazzolini, Georgia Corner, Do-Sun Byun, Carmel Murone, Lars Tögel, Nikolajs Zeps, Lauri A. Aaltonen, Barry Iacopetta and John M. Mariadason, American Journal of Pathology, 2012. 5 microsatellite stable (MSS) and 5 microsatellite unstable (MSI) colon cancer cell lines profiled. Each cell line grown and arrayed in duplicate, and the duplicates averaged for each cell line before calculating means for MSS and MSI lines.

2012-02-07 | E-GEOD-35566 | biostudies-arrayexpress

SILAC-Based Quantification of TGFBR2-Dependent Protein Expression in Extracellular Vesicles of Microsatellite Unstable Colorectal Cancers

Project description:Microsatellite unstable (MSI) colorectal cancers (CRCs) are characterized by Transforming Growth Factor Beta Receptor Type 2 (TGFBR2) deficiency. TGFBR2-deficient CRCs present altered target gene and protein expression. Such cellular alterations modulate the content of CRC-derived extracellular vesicles (EVs). EVs function as couriers of proteins, nucleic acids, and lipids in intercellular communication. At a qualitative level, we have previously shown that TGFBR2 deficiency can cause overall alterations in the EV protein content. To deepen the basic understanding of altered protein dynamics, this work aimed to quantify EV protein signatures in a TGFBR2-dependent manner. Using a SILAC approach for mass spectrometry-based quantification, 48 proteins that appeared to be regulated by cellular TGFBR2 expression were identified in MSI-derived EVs. TGFBR2-primed EVs were enriched in proteasome-associated proteins, whereas TGFBR2 deficiency led to upregulation of EV proteins related to the extracellular matrix and nucleosome. Altogether, the present study emphasizes the general overlap of proteins between EVs and their parental CRC cells and highlights the pathological role of the MSI tumor driver mutation affecting TGFBR2 by altering protein landscapes of EVs. From a clinical perspective, TGFBR2-regulated quantitative differences of protein expression in EVs might nominate novel biomarkers for liquid biopsy-based MSI typing in the future.

2019-09-04 | PXD013980 | Pride

Transcription profiling of human primary gastric tumors (MSI and MSS) and adjacent normal samples

Project description:Gastric cancers with mismatch repair (MMR) inactivation are characterised by microsatellite instability (MSI). In this study, the transcriptional profile of 38 gastric cancers with and without MSI was analysed. Unsupervised analysis showed that the immune and apoptotic gene networks efficiently discriminated these two cancer types. Hierarchical clustering analysis revealed numerous gene expression changes associated with the MSI phenotype. Amongst these, the p53-responsive genes maspin and 14-3-3 sigma were significantly more expressed in tumours with than without MSI. A tight immunosurveillance coupled with a functional p53 gene response is consistent with the better prognosis of MSI cancers. Frequent silencing of MLH1 and downregulation of MMR target genes, such as MRE11 and MBD4, characterised MSI tumours. The downregulation of SMUG1 was also a typical feature of these tumours. The DNA repair gene expression profile of gastric cancer with MSI is of relevance for therapy response. Experiment Overall Design: Genes differentially expressed between MSI and MSS tumours were identified as follows: (i) gene probe sets were pre-selected for being flagged as ‘PRESENT’ in at least 10 tumour samples (21,324 probe sets); (ii) the probe set signal values on the pre-selected probe sets were used to run a t-test between the two types of tumour samples; (iii) the false discovery rate (FDR) method was applied to the t-test calculated p-values to correct for multiple testing and (iv) a false discovery rate <0.05 and a t-test p-value < 0.01 were chosen as threshold criteria to identify the genes differentially expressed in tumours with and without MSI

2009-01-03 | E-GEOD-13911 | biostudies-arrayexpress

Microsatellite stable (n=38) and instable-high (n=13) human colorectal tumors assayed with Affymetrix HuGeneFL arrays.

Project description:mRNA assays were performed on 51 samples of human colorectal tumors using Affymetrix HuGeneFL arrays containing 7129 probe-sets. We compared 38 microsatelite stable (MSS) tumors with 13 microsatellite instable-high (MSI) tumors to form a list of genes differing between the two types. In order to identify molecular signatures characterizing MSI tumors, we examined only MSI-high cancers and not MSI-low ones. Keywords: disease state analysis Human samples of 38 microsatellie stable and 13 microsatellite instable-high colorectal tumors, each from a separate patient, had mRNA assays performed using Affymetrix HuGeneFL arrays, with 7129 probe-sets. A supplementary Excel file (Colon_HuFL_logs.xls) is attached below that gives the log-transformed probe-set values. It also gives the p-values from T-tests comparing these values between MSS and MSI samples, as well as an estimated average fold-difference, for which the mathematical functions are explicitly given.

2009-04-10 | E-GEOD-11543 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data