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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Distinct tumorigenic pathways within hereditary nonpolyposis colorectal cancer

ABSTRACT: 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. RNA extracted from 132 FFPE specimens (40 FCCTX, 42 LS, 50 sporadic) were profiled for differential gene expression by the whole genome cDNA-mediated annealing, selection, extension, and ligation (WG-DASL) assay containing 18626 genes.

ORGANISM(S): Homo sapiens

SUBMITTER: Mev Dominguez

PROVIDER: E-GEOD-36335 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

HNPCC-Sys: Molecular Characterization of Lynch Syndromes

Project description:<p>Lynch Syndrome (LS) tumors are characterized by constitutional mutations in DNA mismatch-repair genes. Colorectal cancers (CRCs) are the predominant tumor type in patients with LS. Here, we have used whole-genome and transcriptome sequencing of LS- CRC to find similarities and differences of mutation and gene expression characteristics between LS-CRC and sporadic CRC (data provided by <a href="./study.cgi?study_id=phs000178">TCGA via dbGaP</a>). Furthermore, we were interested in the molecular heterogeneity of LS-CRC. We have performed a molecular characterization of LS-tumors and of matched tumor-distant reference colonic mucosa based on whole-genome DNA- and RNA-sequencing analyses. Our data indicates the existence of two subgroups of LS-CRCs, G1 and G2, where G1 tumors show a higher number of somatic mutations, higher microsatellite slippage and a different mutation spectrum.</p>

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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. Expression profiling of 34 MSI colorectal cancers and 15 normal colonic mucosas was performed in 2002. Comparison of malignant and healthy tissue.

2011-03-01 | E-GEOD-24514 | biostudies-arrayexpress

Expression data from human MSI colorectal cancer and normal colonic mucosa

2011-03-01 | GSE24514 | GEO

Genome-wide DNA methylation profiling of colorectal tumours from MLH1 epimutation carriers

Project description:Genome-wide DNA methylation analysis of colorectal tumour samples from 44 FFPE tumour and 15 FFPE normal mucosa samples was performed to invesgitate genome-wide DNA methylation signatures that can distinguish MLH1 epimutation carrier CRCs. This was further applied to resolve clinically challenging CRCs including MLH1 promoter VUS carriers and MLH1 methylated EOCRCs

2023-07-01 | GSE233854 | GEO

Rhesus Macaque Model of Mismatch Repair-Deficient Colorectal Cancer (RNA-Seq)

Project description:Colorectal cancer (CRC) remains the third most common cancer in the US, with 15% of cases displaying Microsatellite Instability (MSI) secondary to Lynch Syndrome (LS) or somatic hypermethylation of the MLH1 promoter. A cohort of rhesus macaques from our institution developed spontaneous mismatch repair deficient (MMRd) CRC with a notable fraction harboring a pathogenic germline mutation in MLH1. DNA methylation and transcriptome analysis was used to evaluate the rhesus macaque as a model organism to study carcinogenesis, develop immunotherapies and vaccines, and implement chemoprevention approaches pertinent to sporadic MSI-H and LS CRC in humans. NIH grant(s): Grant ID: 5 P30 CA016672-44 Grant title: Cancer Center Support Grant Affiliation: The University of Texas MD Anderson Cancer Center Grantor: NCI

2022-03-31 | GSE178381 | GEO

Rhesus Macaque Model of Mismatch Repair-Deficient Colorectal Cancer (RRBS)

Project description:Colorectal cancer (CRC) remains the third most common cancer in the US, with 15% of cases displaying Microsatellite Instability (MSI) secondary to Lynch Syndrome (LS) or somatic hypermethylation of the MLH1 promoter. A cohort of rhesus macaques from our institution developed spontaneous mismatch repair deficient (MMRd) CRC with a notable fraction harboring a pathogenic germline mutation in MLH1. DNA methylation and transcriptome analysis was performed to evaluate the rhesus macaque as a model organism to study carcinogenesis, develop immunotherapies and vaccines, and implement chemoprevention approaches pertinent to sporadic MSI-H and LS CRC in humans. NIH grant(s): Grant ID: 5 P30 CA016672-44 Grant title: Cancer Center Support Grant Affiliation: The University of Texas MD Anderson Cancer Center Grantor: NCI

2022-03-31 | GSE178377 | GEO

Copy Number Abnormalities in Sporadic Canine Colorectal Cancers

Project description:Human colorectal cancer (CRC) is one of the better-understood systems for studying the genetics of cancer initiation and progression. To develop a cross-species comparison strategy for identifying CRC causative gene or genomic alterations, we performed array comparative genomic hybridization (aCGH) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported for human CRCs, in 10 spontaneously occurring canine CRCs. The results revealed for the first time a strong degree of genetic homology between sporadic canine and human CRCs. First, we saw that between 5 and 22% of the canine genome was amplified/deleted in these tumors, and that, reminiscent of human CRCs, the total altered sequences directly correlated to the tumorâs progression stage, origin, and likely microsatellite instability status. Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted that the canine orthologs of genes participating in known human CRC pathways were recurrently disrupted, indicating that these pathways might be altered in the canine CRCs as well. Lastly, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from the two species were clustered according to the tumor subtypes but not the species. Significantly, compared with the shared CNAs, we found that species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that harbor more segmental duplications and interspecies genomic rearrangement breakpoints. These findings indicate that CNAs recurrent between human and dog CRCs may have a higher probability of being cancer-causative, compared with CNAs found in one species only Comparison of human and dog colon cancer CNAs

2010-05-15 | E-GEOD-19318 | biostudies-arrayexpress

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

Colorectal cancers with microsatellite instability display unique miRNA profiles

Project description:Analysis of microRNA expression of tumoral and non-tumoral colonic tissues. The aim of this study was to analyze the global miRNA signatures in various groups of well-characterized CRCs based on the presence of microsatellite instability (MSI). Total RNA from formalin-fixed paraffin-embedded tissue blocks from 4 different groups (normal colonic mucosa, Lynch syndrome tumors, sporadic MSI tumors and MSS tumors) was isolated using the RecoverAll Total Nucleic Acid Isolation Kit (Ambion) according to manufacturer instructions. MiRNA expression profiles were analyzed using miRNA microarray platform.

2011-11-22 | E-GEOD-30454 | biostudies-arrayexpress

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