Human rectal adenoma (8 cases) vs. rectal carcinoma (8 cases)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Ming-Rong Wang
PROVIDER: E-GEOD-34472 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Genomic profiling of human rectal adenoma and carcinoma by array-based comparative genomic hybridization
2011-12-20 | GSE34472 | GEO
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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:A patient-derived epithelium-only colon rectal organoid, also referred to as a colonoid, was generated from an adenoma (associated with a resection surgery of an invasive moderately differentiated colorectal adenocarcinoma) as part of the development of an on-going organoid biobank at the Michigan Medicine Translational Tissue Modeling Laboratory (TTML, www.UmichTTML.org). The genomic variant signature of this adenoma colonoid was characterized using whole exome sequencing in order to access genomic concordance between the source patient tissue (adenoma and histologically normal tissue 10 cm from lesion) and the in vitro culture, as well as to access genomic stability of the culture over time at 2 and 6.5 months in culture.
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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).
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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
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Project description:Copy number variation analysis between BJ cells and BJ cells derived iPS cells which were established by using non-transmissible measles virus vector DNA derived from BJ cell and iPS cells were extracted and analysis using CGH array
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Project description:Whole genome profiling of DNA methylation in Ciliary derived stem/progenitor cells and differentiated cells 6 samples total, 3 with CPE derived neurospheres and 3 with CPE derived differentiated progeny.
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Project description:DNA from four 29 cases, 38 tumor samples (23 PB, 12 LN, 1 Tonsil, 1 colonic biopsy, 1 spleen) and 29 normal DNA from the same patients were analyzed with Affymetrix SNP 6.0 platform for copy number alterations study. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from blood samples, lymph nodes and other tissues like spleen, tonsil and colonic biopsy Copy number analysis of Affymetrix SNP 6.0 arrays was performed for 29 MCL cases samples and their respective matched non-tumor DNA, which were used as references for copy number inference.
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