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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="id">2581</item><item key="factors"><item><item key="GSM967314"><item key="PAIR">pair 2</item><item key="TREATMENT">TGB-beta1 for 8h</item></item></item><item><item key="GSM967313"><item key="PAIR">pair 1</item><item key="TREATMENT">TGB-beta1 for 8h</item></item></item><item><item key="GSM967312"><item key="PAIR">pair 2</item><item key="TREATMENT">non-treated</item></item></item><item><item key="GSM9673"><item key="PAIR">pair 1</item><item key="TREATMENT">non-treated</item></item></item></item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">4</item><item key="summary_wrapped">The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis...</item><item key="pubmed_id">23153532</item><item key="geo_gse_id">E-GEOD-39394</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">2</item><item key="sample_count">4</item><item key="tags"><item>cancer</item><item>colon</item><item>colorectal cancer</item><item>disease</item><item>mucosa</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">expression-data-from-fibroblasts-treated-with-tgf</item><item key="geo_id_plat">E-GEOD-39394_A-AFFY-44</item><item key="name">Expression data from fibroblasts treated with TGF-Beta</item><item key="created">Jul.12, 2014</item><item key="summary">The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We quantified the association of TGF-beta-activated fibroblasts with disease progression. To this end, we used as surrogates the gene expression programme upregulated by addition of TGF-beta to normal colon mucosa-derived fibroblasts (CCD-Co-18) in culture. CCD-Co-18 were seeded at 60% confluence and treated with TGF-&#946;1. Gene expression profiles were measured in duplicate using HG-U133 plus 2.0. We used RMA background correction, quantile normalization and RMA summarization (Gautier et al., 2004). A TGF-&#946; response signature was obtained by selecting genes with limma P-value &lt; 0.05 and at least two fold up-regulation in TGF-&#946; treated fibroblasts.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-39394</item><item key="species">human</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-39394/samples/</item></data></biogps>
