{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cipolat S"],"funding":["Cancer Research UK","European Union","Medical Research Council","Wellcome Trust"],"pagination":["e01888"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4007207"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3"],"pubmed_abstract":["Atopic dermatitis can result from loss of structural proteins in the outermost epidermal layers, leading to a defective epidermal barrier. To test whether this influences tumour formation, we chemically induced tumours in EPI-/- mice, which lack three barrier proteins-Envoplakin, Periplakin, and Involucrin. EPI-/- mice were highly resistant to developing benign tumours when treated with 7,12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). The DMBA response was normal, but EPI-/- skin exhibited an exaggerated atopic response to TPA, characterised by abnormal epidermal differentiation, a complex immune infiltrate and elevated serum thymic stromal lymphopoietin (TSLP). The exacerbated TPA response could be normalised by blocking TSLP or the immunoreceptor NKG2"],"journal":["eLife"],"pubmed_title":["Epidermal barrier defects link atopic dermatitis with altered skin cancer susceptibility."],"pmcid":["PMC4007207"],"funding_grant_id":["096540"],"pubmed_authors":["Watt FM","Natsuga K","Cipolat S","Hoste E","Quist SR"],"additional_accession":[]},"is_claimable":false,"name":"Epidermal barrier defects link atopic dermatitis with altered skin cancer susceptibility.","description":"Atopic dermatitis can result from loss of structural proteins in the outermost epidermal layers, leading to a defective epidermal barrier. To test whether this influences tumour formation, we chemically induced tumours in EPI-/- mice, which lack three barrier proteins-Envoplakin, Periplakin, and Involucrin. EPI-/- mice were highly resistant to developing benign tumours when treated with 7,12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). The DMBA response was normal, but EPI-/- skin exhibited an exaggerated atopic response to TPA, characterised by abnormal epidermal differentiation, a complex immune infiltrate and elevated serum thymic stromal lymphopoietin (TSLP). The exacerbated TPA response could be normalised by blocking TSLP or the immunoreceptor NKG2","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 May","modification":"2025-04-21T18:56:46.691Z","creation":"2019-03-27T01:27:26Z"},"accession":"S-EPMC4007207","cross_references":{"pubmed":["24843010"],"doi":["10.7554/eLife.01888"]}}