Genomic profiling of gastric carcinoma in situ and gastric adenomas by array-based comparative genomic hybridization
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ABSTRACT: This SuperSeries is composed of the following subset Series: GSE19566: Genomic profiling of gastric carcinoma in situ by array-based comparative genomic hybridization GSE19574: Genomic profiling of gastric adenomas by array-based comparative genomic hybridization Refer to individual Series
Project description:In this study, we investigated CNAs of 20 gastric CIS (Vienna category 4.2) and 20 adenomas, including 7 low-grade adenomas (LGA; Vienna category 3) and 13 high-grade adenomas (HGA; Vienna category 4.1), by 244k oligonucleotide-based array comparative genomic hybridization (array CGH). 20 gastric carcinoma in situ (CIS) vs. 20 controls. The supplementary file 'GSE19566_aberrations.txt' file contains a summary of the aberrations in the gastric CISs as determined by the ADM-2 algorithm.
Project description:In this study, we investigated CNAs of 20 gastric CIS (Vienna category 4.2) and 20 adenomas, including 7 low-grade adenomas (LGA; Vienna category 3) and 13 high-grade adenomas (HGA; Vienna category 4.1), by 244k oligonucleotide-based array comparative genomic hybridization (array CGH). 20 gastric adenomas vs. 20 controls. The supplementary file 'GSE19574_aberrations.txt' file contains a summary of the aberrations in the gastric adenomas as determined by the ADM-2 algorithm.
Project description:In this study, 19 tumor samples from patients with renal cell carcinoma (RCC)-end-stage renal disease (ESRD) were analyzed by array comparative genomic hybridization (array CGH) using the Agilent Whole Human Genome 4× Array. 19 cystic disease samples from patients with RCC-ESRD
Project description:In this study, we investigated CNAs of 59 tumor samples from 27 patients with submucosal-invasive gastric cancers (SMGC) by 44k oligonucleotide-based array comparative genomic hybridization (array CGH). 23 mucosal portion of SMGC vs 23 paired submucosal (SM) portion of SMGC, 9 SM portion vs 9 paired lymph node (LN) metastasis, 12 SMGC with LN metastasis vs 15 SMGC without LN metastasis
Project description:Genomic copy number aberrations of 11 gastric cancer cell lines were analyzed by 244k CGH array from Agilent Technologies. Based on this results, we separated the 11 cell lines into 2 groups, with and without copy number increase at chromosome 20q13 We performed array comparative genomic hybridization to detect genomic copy number aberrations in 11 gastric cancer cell lines. Microarray images were analyzed by using Feature Extraction and DNA analytics softwares.
Project description:In this study, eighty tumor samples from 63 patients with renal cell carcinoma (RCC)-end-stage renal disease (ESRD) were analyzed by array comparative genomic hybridization (array CGH) using the Agilent Whole Human Genome 4×44K Oligo Micro Array. 79 tumor samples from 63 patients with RCC-ESRD
Project description:In this study, we investigated CNAs of 4 tumor samples from 2 patients, including conventioanl chromophobe renal cell carcinoma(ChRCC), ChRCC with neuroendocrine differentiation and no-tumor region by 44k oligonucleotide-based array comparative genomic hybridization (array CGH). 2 cases of ChRCC(NOS) vs ChRCC with neuroendocrine differentiation
Project description:Background & Aims. Resection of hepatocellular carcinoma (HCC) tumors by partial hepatectomy (PHx) is associated with promoting hepatocarcinogenesis. We have previously reported that PHx promotes hepatocarcinogenesis in the Mdr2-knockout (Mdr2-KO) mouse, a model for inflammation-mediated HCC. Now, we explored the molecular mechanisms underlying the tumor-promoting effect of PHx in these mice. Methods. Using microarrays-based techniques, we compared genomic and transcriptomic profiles of HCC tumors developing in the Mdr2-KO mice either spontaneously or following PHx. Results. PHx accelerated HCC development in these mice by four months. PHx-induced tumors had only amplifications affecting multiple chromosomes and locating mainly near the acrocentric centromeres of murine chromosomes. Four different chromosomal regions were amplified each in at least three tumors. All tumors of untreated mice had chromosomal aberrations, including both deletions and amplifications. Comparison of gene expression profiles revealed a significantly enriched expression of oncogenes, chromosomal instability markers and E2F1 targets in the post-PHx compared to spontaneous tumors. Both tumor groups shared the same frequent amplification at chromosome 18. Here, we demonstrated that one of the regulatory genes encoded by this amplified region, Crem, was over-expressed in the nuclei of murine and human HCC cells in vivo, and that it stimulated proliferation of human HCC cells in vitro. Conclusions: PHx of a chronically inflamed liver directed tumor development to a discrete pathway characterized by amplification of specific chromosomal regions and expression of specific tumor-promoting genes. Crem is a new candidate HCC oncogene frequently amplified in this model and frequently over-expressed in human HCC. To explore the mechanisms of the accelerated HCC development by PHx, we compared liver tumors and their matched non-tumor liver tissues between 9-month-old hepatectomized and 13-14-month-old untreated Mdr2-KO mice.
Project description:In this study, we investigated CNAs of 20 primary clear cell renal cell caricinomas (ccRCCs), 20 corresponding metastases and another subsets of 30 primary ccRCCs by 44k oligonucleotide-based array comparative genomic hybridization (array CGH). 20 primary ccRCCs, 20 corresponding metastases and another subsets of 30 primary ccRCCs.