{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ji Z"],"funding":["Howard Hughes Medical Institute","HHS | NIH | National Cancer Institute","NCI NIH HHS"],"pagination":["9453-9462"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6511065"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["116(19)"],"pubmed_abstract":["Using an inducible, inflammatory model of breast cellular transformation, we describe the transcriptional regulatory network mediated by STAT3, NF-κB, and AP-1 factors on a genomic scale. These proinflammatory regulators form transcriptional complexes that directly regulate the expression of hundreds of genes in oncogenic pathways via a positive feedback loop. This transcriptional feedback loop and associated network functions to various extents in many types of cancer cells and patient tumors, and it is the basis for a cancer inflammation index that defines cancer types by functional criteria. We identify a network of noninflammatory genes whose expression is well correlated with the cancer inflammatory index. Conversely, the cancer inflammation index is negatively correlated with the exp"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Inflammatory regulatory network mediated by the joint action of NF-kB, STAT3, and AP-1 factors is involved in many human cancers."],"pmcid":["PMC6511065"],"funding_grant_id":["R01 CA107486","K99 CA207865","K99 CA 207865","CA 107486","R00 CA207865"],"pubmed_authors":["Regev A","Ji Z","He L","Struhl K"],"additional_accession":[]},"is_claimable":false,"name":"Inflammatory regulatory network mediated by the joint action of NF-kB, STAT3, and AP-1 factors is involved in many human cancers.","description":"Using an inducible, inflammatory model of breast cellular transformation, we describe the transcriptional regulatory network mediated by STAT3, NF-κB, and AP-1 factors on a genomic scale. These proinflammatory regulators form transcriptional complexes that directly regulate the expression of hundreds of genes in oncogenic pathways via a positive feedback loop. This transcriptional feedback loop and associated network functions to various extents in many types of cancer cells and patient tumors, and it is the basis for a cancer inflammation index that defines cancer types by functional criteria. We identify a network of noninflammatory genes whose expression is well correlated with the cancer inflammatory index. Conversely, the cancer inflammation index is negatively correlated with the exp","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 May","modification":"2026-05-03T06:35:28.417Z","creation":"2025-06-01T03:26:39.793Z"},"accession":"S-EPMC6511065","cross_references":{"pubmed":["30910960"],"doi":["10.1073/pnas.1821068116"]}}