Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA100123 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Total mesorectal excision (TME) is the standard treatment for rectal cancer, while transanal endoscopic microsurgery (TEM) is a recently introduced surgical approach for the treatment of rectal adenomas. Incorrect preoperative staging before TEM is a problem. To identify genetic changes that might correlate with tumour stage and could lead to optimized treatment selection we performed a genome-wide chromosomal instability search in a homogeneous, clinical cohort of rectal tumours. 78 rectal tumours during different clinical stages were analysed with 10K single nucleotide polymorphism (SNP) arrays. Logistic regression was performed to build a quantitative model of specific chromosomal aberrations. Overall, most cases (95%) had one or more chromosomal aberrations. We observed a clear correlation between the total number of aberrations and the different tumour stages. Specifically, the chromosomal events: gain of 8q22–24, 13q and 20q, and loss of 17p and 18q12–22, were far more abundant in carcinoma than in adenoma. In adenoma fractions from cases with a carcinoma (infiltrating at least in the submucosa), twice the amount of such ‘malignant aberrations’ was observed, compared to pure adenomas. Furthermore, combined aberrations such as gain of 13q and loss of 18q were only found in adenomatous fractions of carcinomas and not in benign lesions. Based on these five genomic events associated with carcinoma, a clear distinction between adenoma and carcinoma tissue could be made. These data should be validated further in order that they may be used in preoperative staging of rectal tumours. Keywords: SNP array copy number and LOH study
2007-05-30 | GSE7946 | GEO
Project description:Total mesorectal excision (TME) is the standard treatment for rectal cancer, while transanal endoscopic microsurgery (TEM) is a recently introduced surgical approach for the treatment of rectal adenomas. Incorrect preoperative staging before TEM is a problem. To identify genetic changes that might correlate with tumour stage and could lead to optimized treatment selection we performed a genome-wide chromosomal instability search in a homogeneous, clinical cohort of rectal tumours. 78 rectal tumours during different clinical stages were analysed with 10K single nucleotide polymorphism (SNP) arrays. Logistic regression was performed to build a quantitative model of specific chromosomal aberrations. Overall, most cases (95%) had one or more chromosomal aberrations. We observed a clear correlation between the total number of aberrations and the different tumour stages. Specifically, the chromosomal events: gain of 8q22â24, 13q and 20q, and loss of 17p and 18q12â22, were far more abundant in carcinoma than in adenoma. In adenoma fractions from cases with a carcinoma (infiltrating at least in the submucosa), twice the amount of such âmalignant aberrationsâ was observed, compared to pure adenomas. Furthermore, combined aberrations such as gain of 13q and loss of 18q were only found in adenomatous fractions of carcinomas and not in benign lesions. Based on these five genomic events associated with carcinoma, a clear distinction between adenoma and carcinoma tissue could be made. These data should be validated further in order that they may be used in preoperative staging of rectal tumours. Experiment Overall Design: 78 tumor samples and 19 reference normal samples
2008-06-17 | E-GEOD-7946 | biostudies-arrayexpress
Project description:Genomic profiling of human rectal adenoma and carcinoma by array-based comparative genomic hybridization Two group experiment, rectal adenoma vs. rectal carcinoma. Biological replicates: 8 adenomas vs. 8 carcinomas
2011-12-20 | E-GEOD-34472 | biostudies-arrayexpress
Project description:SNP array data from 127 hepatocellular adenomas and carcinomas were used to detect recurrent copy number alterations.
2013-12-18 | GSE43092 | 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: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:Accurate staging of rectal tumors is essential for making the correct treatment choice. In a previous study, we found that loss of 17p, 18q and gain of 8q, 13q and 20q could distinguish adenoma from carcinoma tissue and that loss of 1q was related to lymph node metastasis. In order to find markers for tumor staging, we searched for candidate genes on these specific chromosomes. We performed gene expression microarray analysis on 79 rectal tumors and integrated these data with genomic data from the same sample series (Series GSE7946, Samples GSM194994-GSM195028). We performed supervised analysis to find candidate genes on affected chromosomes and validated the results with qRT-PCR and immunohistochemistry. Approximately 8% of the genes were significantly different between adenomas and carcinomas; the most differently expressed genes were involved in cell adhesion and cell cycle processes. Integration of gene expression and chromosomal instability data revealed a significant genome-wide correlation between these two data types. Supervised analysis identified up-regulation of EFNA1 in cases with 1q gain, and EFNA1 expression was correlated with the expression of a target gene (VEGF). The BOP1 gene, involved in ribosome biogenesis and related to chromosomal instability, was over-expressed in cases with 8q gain. SMAD2 was the most down-regulated gene on 18q, and on 20q, STMN3 and TGIF2 were highly up-regulated. Immunohistochemistry for SMAD4 correlated with SMAD2 gene expression and 18q loss. This study showed a good correlation between chromosomal aberrations and gene expression data. In the near future, specific genes identified by such integrative methods could be of additional value for explaining rectal tumorigenesis. Keywords: disease state analysis Samples GSM307294-GSM307372: 79 Tumor RNAs were hybridised, all against a common reference sample, consisting of a mixture of cell line and normal colon RNA. 9 replicates (primarily duplicates) were performed (tumor samples: 217, 544, 608, 609, TME1344, TME625, TME884, TME947).
2008-10-21 | E-GEOD-12225 | biostudies-arrayexpress
Project description:Accurate staging of rectal tumors is essential for making the correct treatment choice. In a previous study, we found that loss of 17p, 18q and gain of 8q, 13q and 20q could distinguish adenoma from carcinoma tissue and that loss of 1q was related to lymph node metastasis. In order to find markers for tumor staging, we searched for candidate genes on these specific chromosomes. We performed gene expression microarray analysis on 79 rectal tumors and integrated these data with genomic data from the same sample series (Series GSE7946, Samples GSM194994-GSM195028). We performed supervised analysis to find candidate genes on affected chromosomes and validated the results with qRT-PCR and immunohistochemistry. Approximately 8% of the genes were significantly different between adenomas and carcinomas; the most differently expressed genes were involved in cell adhesion and cell cycle processes. Integration of gene expression and chromosomal instability data revealed a significant genome-wide correlation between these two data types. Supervised analysis identified up-regulation of EFNA1 in cases with 1q gain, and EFNA1 expression was correlated with the expression of a target gene (VEGF). The BOP1 gene, involved in ribosome biogenesis and related to chromosomal instability, was over-expressed in cases with 8q gain. SMAD2 was the most down-regulated gene on 18q, and on 20q, STMN3 and TGIF2 were highly up-regulated. Immunohistochemistry for SMAD4 correlated with SMAD2 gene expression and 18q loss. This study showed a good correlation between chromosomal aberrations and gene expression data. In the near future, specific genes identified by such integrative methods could be of additional value for explaining rectal tumorigenesis. Keywords: disease state analysis
2008-10-21 | GSE12225 | GEO
Project description:SNP array data from 127 hepatocellular adenomas and carcinomas were used to detect recurrent copy number alterations. 48 tumors were analyzed with Illumina HumanCNV370-Duo v1.0 chips. 79 tumors were analyzed with Illumina HumanOmniExpress BeadChip.
2013-12-18 | E-GEOD-43092 | biostudies-arrayexpress
Project description:SNP data from 126 hepatocellular adenomas and carcinomas
| PRJNA185184 | ENA