E-PROT-105
Ontology highlight
ABSTRACT:
DISEASE(S): Colon Adenoma,Normal
PROVIDER: E-PROT-105 | ExpressionAtlas | 2023-06-22
REPOSITORIES: ExpressionAtlas
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Project description:Colorectal adenomas are common precancerous lesions with the potential for malignant transformation to colorectal adenocarcinoma. Endoscopic polypectomy provides an opportunity for cancer prevention, however, recurrence rates are high. We collected formalin-fixed paraffin-embedded tissue of fourteen primary adenomas with recurrence, fourteen primary adenomas without recurrence, and fourteen matched pair samples (primary adenoma and the corresponding recurrent adenoma). These samples were analysed by array-based comparative genomic hybridisation (aCGH) to understand the dynamics of copy number alterations (CNAs) and to identify molecular markers to predict recurrence. ACGH analysis confirmed the genetic landscape specific for colorectal tumorigenesis, i.e., CNAs of chromosomes 7 (13.7%), 13q (13.7%), 18 (5.8%) and 20q (13.7%). CNAs were detected in 41/51 (80.4%) of colorectal adenomas (2N). Focal aberrations (≤10 Mbp) were mapped to chromosome bands 6p22.1-p21.33 (33.3%), 7q22.1 (31.4%) and 16q21 (29.4%). Gains of CDX2 were exclusively seen in adenomas with recurrence compared to adenomas without recurrence. However, the average number of copy alterations failed to discriminate primary adenomas with recurrence from primary adenomas without recurrence.
2018-04-01 | GSE110221 | GEO
Project description:Colorectal adenomas are benign precursor lesions of colorectal cancer (CRC) that arise from normal epithelium1. The prevalence of adenomas in the large intestine is much higher than the incidence of cancer implying that the majority of adenomas will never progress to CRC4. In clinical practice, adenomas detected during colonoscopy are completely removed, and consequently the natural history of disease disrupted. Based on the prevalence of focal cancer in endoscopically removed adenomas, it is estimated that only 5% of adenomas will eventually progress to CRC. The aim of the present study was to characterize adenomas at low and high risk of progressing to cancer by extensive molecular profiling at DNA, RNA, and protein level, allowing to examine the biological processes in which they differ and to discover putative drivers of early colorectal tumor development.
2019-08-22 | PXD012254 | Pride
Project description:Colorectal adenomas are precursor lesions of colorectal cancers and represent clonal amplifications of single cells from colonic crypts. DNA methylation patterns specify cell-type identity during cellular differentiation and therefore provide novel opportunities for the molecular analysis of tumors. We have now analyzed DNA methylation patterns in colorectal adenomas and identified three biologically defined subclasses that describe different intestinal crypt differentiation stages. Importantly, colorectal carcinomas could be classified into the same methylation subtypes, reflecting their shared cell-types of origin with adenomas. Further data analysis also revealed significantly reduced overall survival for one of the subtypes. Our results establish a novel concept for understanding the methylation patterns observed in colorectal cancer and provide opportunities for tumor subclassification and patient stratification.
2018-06-12 | E-MTAB-6450 | biostudies-arrayexpress
Project description:We showed that a lot of genes were deregulated in colorectal adenocarcinomas in comparison with colorectal adenomas. 37 colorectal adenoma and 9 colorectal adenocarcinoma samples were analyzed. We generated a comparison between adenocarcinomas and adenomas.
2013-08-27 | E-GEOD-50115 | biostudies-arrayexpress
Project description:Background & aim: Flat adenomas form a specific phenotype of colorectal adenomas that has been associated with more severe molecular changes and consequently a more aggressive clinical behavior compared to their polypoid counterparts. In the present study we set out to compare one of the molecular changes most explicitly associated with adenoma to carcinoma progression, i.e. chromosomal instability, between flat and polypoid colorectal adenomas. Methods: Consecutive series of 83 flat and 35 polypoid adenomas were analyzed for DNA copy number changes using a high resolution arrayCGH platform as well as for mutations in the adenomatous polyposis coli (APC) gene. Gene ontology on the genes located on the significantly different regions was performed. Results: Overall, flat adenomas show similar DNA copy number changes as polypoid adenomas. Patterns of DNA copy number changes differed between the two phenotypes with significantly more frequently loss of 5q14.3 and 5q15-q23.3 in flat adenomas, while loss of 1p36.32-p35.3, 10q25.2-q25.3, 17p12 and chromosome 18 were more frequent in polypoid adenomas. The 5q15-q23.3 region harbors the APC locus, therefore mutation status of APC was investigated, showing significantly less mutations in flat adenomas. Pathway analysis and datamining linked the 5q region to inflammation. Conclusion: These results provide evidence that flat and polypoid adenomas have partly overlapping DNA copy number changes, while alterations more specific to flat adenomas have associations with inflammation. Loss of 5q has been associated with aggressive behavior and this could serve as an explanation for a more aggressive clinical behavior of flat lesions.
2012-10-04 | GSE30479 | GEO
Project description:We showed that a large number of genes were deregulated in colorectal adenomas in comparison with colorectal normal mucosae. 37 colorectal adenoma and 9 colorectal normal mucosa samples were analyzed. We generated a comparison between adenomas and normal mucosae.
2013-08-27 | E-GEOD-50114 | biostudies-arrayexpress
Project description:Genetic and epigenetic alterations are a fundamental aspect of colorectal cancer formation. There is considerable heterogeneity between colorectal cancers regarding the mutations and methylated genes they carry, and this heterogeneity may arise early in the polyp-cancer sequence. However, our understanding of the epigenetic alterations and gene mutations in colon adenomas and their relation to colorectal cancer is incomplete. Thus, we have assessed the methylome in normal colon mucosa, tubular adenomas, and colorectal adenocarcinomas and have determined the relationship of these findings between adenomas and cancer in the colon. Genome-wide alterations in DNA methylation were found in the normal colon mucosa adjacent to colorectal cancer, tubular adenomas, and colorectal cancer. Three subgroups of CRCs and two subgroups of adenomas were identified on the basis of their DNA methylation patterns. The adenomas separated into a high-frequency methylation class (Adenoma-H) and a low-frequency methylation class. The adenoma-H polyps have a methylated DNA signature similar to non-CIMP CRCs, whereas those of the Adenoma-L class have a similar methylation pattern to normal colon mucosa. The CpGs that account for these signatures are located in intragenic/intergenic regions, which suggests that these two groups of adenomas arise from different stem cell populations.
2014-09-08 | GSE48684 | GEO
Project description:We showed that some microRNAs could be characteristic of the progression from adenoma to adenocarcinoma in colorectal cancer. 48 colorectal biopsy samples (28 adenomas, 15 adenocarcinomas and 5 normal mucosae) were analyzed. We generated three comparisons: adenomas versus. normal mucosae, adenocarcinomas versus. normal mucosae, and adenocarcinomas versus. adenomas.
2013-08-30 | E-GEOD-50194 | biostudies-arrayexpress
Project description:Genetic and epigenetic alterations are a fundamental aspect of colorectal cancer formation. There is considerable heterogeneity between colorectal cancers regarding the mutations and methylated genes they carry, and this heterogeneity may arise early in the polyp-cancer sequence. However, our understanding of the epigenetic alterations and gene mutations in colon adenomas and their relation to colorectal cancer is incomplete. Thus, we have assessed the methylome in normal colon mucosa, tubular adenomas, and colorectal adenocarcinomas and have determined the relationship of these findings between adenomas and cancer in the colon. Genome-wide alterations in DNA methylation were found in the normal colon mucosa adjacent to colorectal cancer, tubular adenomas, and colorectal cancer. Three subgroups of CRCs and two subgroups of adenomas were identified on the basis of their DNA methylation patterns. The adenomas separated into a high-frequency methylation class (Adenoma-H) and a low-frequency methylation class. The adenoma-H polyps have a methylated DNA signature similar to non-CIMP CRCs, whereas those of the Adenoma-L class have a similar methylation pattern to normal colon mucosa. The CpGs that account for these signatures are located in intragenic/intergenic regions, which suggests that these two groups of adenomas arise from different stem cell populations. We conducted genome-wide array-based studies and comprehensive data analyses of aberrantly methylated loci in 41 normal colon samples, 42 colon adenomas, and 64 colorectal cancers. Supplementary file 'GSE48684_Matrix_signal_intensities_1.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1183439-GSM1183561. Supplementary file 'GSE48684_Matrix_signal_intensities_2.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1235135-GSM1235158.
2014-09-08 | E-GEOD-48684 | biostudies-arrayexpress
Project description:Colorectal cancer can be divided into four consensus molecular subtypes, which might associate with distinct precursor lesions. The aim of this study was to determine the subtype affiliation of two types of colorectal adenomas: tubular adenomas (TAs) and sessile serrated adenomas (SSAs) and to determine the activity of TGFβ signaling and the role of this cytokine in subtype affiliation. Adenoma samples were collected in the Academic Medical Center (AMC), Amsterdam, The Netherlands. Tubular adenomas (TAs) were obtained from familial adenomatous polyposis (FAP) patients and sessile serrated adenomas (SSAs) were collected from serrated polyposis syndrome (SPS) patients.
2016-06-01 | GSE79460 | GEO