{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shao Q"],"funding":["U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics)","NCI NIH HHS","U.S. Department of Health &amp; Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute"],"pagination":["899-908"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11976298"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(4)"],"pubmed_abstract":["Activating mutations in STAT6 are common in Follicular Lymphoma (FL) and transformed FL and various other B cell lymphomas. Here, we report RNA-seq based gene expression data on normal human lymph node derived B lymphocytes (NBC; N = 6), and primary human FL WT (N = 11) or mutant (N = 4) for STAT6 before and after ex vivo stimulation with IL4. We found that STAT6 mutants result in broad based augmentation of IL4-induced gene expression. Unexpectedly, in FL with WT STAT6 we measured reduced baseline and IL4-induced gene expression levels when compared with NBC lymphocytes or FL with STAT6 mutations. We tracked the attenuated IL4/JAK/STAT6 response to co-existing CREBBP mutations and experimentally verified that intact CREBBP is required for the induction of many IL4-induced genes. One of th"],"journal":["Leukemia"],"pubmed_title":["STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in follicular lymphoma."],"pmcid":["PMC11976298"],"funding_grant_id":["P30 CA046592","R01CA260677","R01 CA260677"],"pubmed_authors":["Shedden K","Malek IA","Shao Q","Bedi K","Malek SN"],"additional_accession":[]},"is_claimable":false,"name":"STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in follicular lymphoma.","description":"Activating mutations in STAT6 are common in Follicular Lymphoma (FL) and transformed FL and various other B cell lymphomas. Here, we report RNA-seq based gene expression data on normal human lymph node derived B lymphocytes (NBC; N = 6), and primary human FL WT (N = 11) or mutant (N = 4) for STAT6 before and after ex vivo stimulation with IL4. We found that STAT6 mutants result in broad based augmentation of IL4-induced gene expression. Unexpectedly, in FL with WT STAT6 we measured reduced baseline and IL4-induced gene expression levels when compared with NBC lymphocytes or FL with STAT6 mutations. We tracked the attenuated IL4/JAK/STAT6 response to co-existing CREBBP mutations and experimentally verified that intact CREBBP is required for the induction of many IL4-induced genes. One of th","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-05-02T14:32:32.723Z","creation":"2025-07-06T03:04:31.289Z"},"accession":"S-EPMC11976298","cross_references":{"pubmed":["39910284"],"doi":["10.1038/s41375-025-02525-6"]}}