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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="species">mouse</item><item key="factors"><item><item key="GSM889563"><item key="GENOTYPE">in vitro deletion of RBP-Jk in mouse fibroblasts</item><item key="GENETIC BACKGROUND">C57BL/6</item></item></item><item><item key="GSM889564"><item key="GENOTYPE">control for in vitro deletion of RBP-Jk in mouse</item><item key="GENETIC BACKGROUND">C57BL/6fibroblasts</item></item></item><item><item key="GSM889565"><item key="GENOTYPE">in vivo deletion of RBP-Jk in mouse fibroblasts</item><item key="GENETIC BACKGROUND">C57BL/6</item></item></item><item><item key="GSM889566"><item key="GENOTYPE">control for in vivo deletion of RBP-Jk in mouse fibroblasts</item><item key="GENETIC BACKGROUND">C57BL/6</item></item></item></item><item key="id">6805</item><item key="pop_total">0</item><item key="platform">6</item><item key="summary_wrapped">It is currently unclear whether tissue changes surrounding multifocal epithelial tumors are a cause or consequence of cancer. Here, we...</item><item key="pubmed_id">22682244</item><item key="geo_gse_id">E-GEOD-36359</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>actinic keratosis</item><item>cancer</item><item>cell</item><item>keratosis</item><item>notch</item><item>skin</item><item>skin cancer</item><item>squamous</item><item>squamous cell</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-36359_A-AFFY-45</item><item key="slug">global-changes-in-gene-expression-in-dermal-fibrob</item><item key="geo_gds_id"/><item key="name">Global changes in gene expression in dermal fibroblasts with in vivo and in vitro deletion of the RBP-Jk gene</item><item key="created">Nov.12, 2014</item><item key="summary">It is currently unclear whether tissue changes surrounding multifocal epithelial tumors are a cause or consequence of cancer. Here, we provide evidence that loss of mesenchymal Notch/CSL signaling causes tissue alterations, including stromal atrophy and inflammation, which precede and are potent triggers for epithelial tumors. Mice carrying a mesenchymal-specific deletion of CSL/RBP-JK, a key Notch effector, exhibit spontaneous multifocal keratinocyte tumors that develop after dermal atrophy and inflammation. CSL-deficient dermal fibroblasts promote increased tumor cell proliferation through up-regulation of c-Jun and c-Fos expression and consequently higher levels of diffusible growth factors, inflammatory cytokines, and matrix remodeling enzymes. In human skin samples, stromal fields adjacent to cutaneous squamous cell carcinomas and multifocal premalignant actinic keratosis lesions exhibit decreased Notch/CSL signaling and associated molecular changes. Importantly, these changes in gene expression are also induced by UVA, a known environmental cause of cutaneous field cancerization and skin cancer. We used microarrays to detail the global changes in gene expression in dermal fibroblasts with in vivo and in vitro deletion of the RBP-Jk gene, compared to corresponding controls Global changes in gene expression in dermal fibroblasts with in vivo and in vitro deletion of the RBP-Jk gene were assessed, in parallel with the corresponding controls</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-36359</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-36359/samples/</item></data></biogps>
