{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Harro CM"],"funding":["American Cancer Society","National Cancer Institute","NCI NIH HHS"],"pagination":["135711"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7843215"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["131(3)"],"pubmed_abstract":["Cutaneous T cell lymphoma (CTCL) has a poorly understood etiology and no known cure. Using conditional knockout mice, we found that ablation of the genomic organizer special AT-rich sequence-binding protein 1 (Satb1) caused malignant transformation of mature, skin-homing, Notch-activated CD4+ and CD8+ T cells into progressively fatal lymphoma. Mechanistically, Satb1 restrained Stat5 phosphorylation and the expression of skin-homing chemokine receptors in mature T cells. Notably, methyltransferase-dependent epigenetic repression of SATB1 was universally found in human Sézary syndrome, but not in other peripheral T cell malignancies. H3K27 and H3K9 trimethylation occluded the SATB1 promoter in Sézary cells, while inhibition of SUV39H1/2 methyltransferases (unlike EZH2 inhibition) restored pr"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Methyltransferase inhibitors restore SATB1 protective activity against cutaneous T cell lymphoma in mice."],"pmcid":["PMC7843215"],"funding_grant_id":["T32CA009140","T32 CA009140","P30 CA010815","P30-CA076292","R01 CA157664","R01CA240434,R01CA157664,R01CA124515,) CA076292","R01 CA240434","U01 CA200495","R01 CA124515","P30 CA076292","R01 CA184185"],"pubmed_authors":["Pinilla-Ibarz J","Showe LC","Chaurio RA","Biswas S","Liu K","Harro CM","Mandal G","Conejo-Garcia JR","Anadon CM","Sprenger KB","Mine JA","Payne KK","Rigolizzo KE","Rodriguez PC","Perez-Sanz J","Costich TL","Yu X","Sokol L"],"additional_accession":[]},"is_claimable":false,"name":"Methyltransferase inhibitors restore SATB1 protective activity against cutaneous T cell lymphoma in mice.","description":"Cutaneous T cell lymphoma (CTCL) has a poorly understood etiology and no known cure. Using conditional knockout mice, we found that ablation of the genomic organizer special AT-rich sequence-binding protein 1 (Satb1) caused malignant transformation of mature, skin-homing, Notch-activated CD4+ and CD8+ T cells into progressively fatal lymphoma. Mechanistically, Satb1 restrained Stat5 phosphorylation and the expression of skin-homing chemokine receptors in mature T cells. Notably, methyltransferase-dependent epigenetic repression of SATB1 was universally found in human Sézary syndrome, but not in other peripheral T cell malignancies. H3K27 and H3K9 trimethylation occluded the SATB1 promoter in Sézary cells, while inhibition of SUV39H1/2 methyltransferases (unlike EZH2 inhibition) restored pr","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2026-06-04T03:13:14.768Z","creation":"2022-02-09T18:06:47.843Z"},"accession":"S-EPMC7843215","cross_references":{"pubmed":["33270606"],"doi":["10.1172/JCI135711","10.1172/jci135711"]}}