Project description:To reveal mechanisms for acquired imatinib resistance in gastrointestinal stromal tumor (GIST), we have analyzed several cell lines with resistance to imatinib.
Project description:This SuperSeries is composed of the following subset Series: GSE19396: ETV1 knockdown in GIST cell lines GSE22433: Imatinib Treatment of GIST882 GSE22441: Mapping of ETV1 genomic binding sites in gastrointestinal stromal tumor (GIST). Refer to individual Series
Project description:Gastrointestinal stromal tumors (GIST) are phenotypically and clinically heterogeneous mesenchymal tumors. Using the cDNA array technique, we analyzed the gene expression profiles of 22 GIST and 7 non-neoplastic gastrointestinal smooth muscle specimens, in order to detect molecular differences between GIST and non-neoplastic tissue, and to detect differences between GIST of various phenotypic and clinical subgroups. As a result, we found 796 differentially expressed genes and ESTs between GIST and smooth muscle tissue, including promising new candidate genes for the pathogenesis of GIST. Furthermore, we identified differences in gene expression between GIST of different site, size, and immunohistochemical expression of CD34 and SMA. Our data show that alterations in gene expression are associated with morphologically and clinically detectable features of GIST and provide new aspects for the understanding of these tumors. Keywords = Gastrointestinal Stromal Tumor (GIST)
Project description:Silencing of the adaptor SH3BP2 impairs Gastrointestinal stromal tumors growth through miRNAs We dissected SH3BP2 pathway in Gastrointestinal Stromal Tumor cells (GIST) performing a miRNA array in SH3BP2-silenced GIST cells
Project description:Gastrointestinal stromal tumors (GIST) are phenotypically and clinically heterogeneous mesenchymal tumors. Using the cDNA array technique, we analyzed the gene expression profiles of 22 GIST and 7 non-neoplastic gastrointestinal smooth muscle specimens, in order to detect molecular differences between GIST and non-neoplastic tissue, and to detect differences between GIST of various phenotypic and clinical subgroups. As a result, we found 796 differentially expressed genes and ESTs between GIST and smooth muscle tissue, including promising new candidate genes for the pathogenesis of GIST. Furthermore, we identified differences in gene expression between GIST of different site, size, and immunohistochemical expression of CD34 and SMA. Our data show that alterations in gene expression are associated with morphologically and clinically detectable features of GIST and provide new aspects for the understanding of these tumors. Keywords = Gastrointestinal Stromal Tumor (GIST) Keywords: other
Project description:GIST (gastrointestinal stromal tumor) is the most prominent mesenchymal neoplasms of the gastrointestinal tract, and liver is the most common metastasis site for GIST. The molecular mechanism leading to liver metastasis of GIST is currently unclear. With the goal of revealing the underlying mechanism, we performed whole-genome gene expression profiling in 18 pairs of RNA samples comprised of liver metastasis tissues and corresponding non-tumor tissues. To reveal the underlying mechanism leading to liver metastasis of GIST
