{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu YT"],"funding":["NIH National Eye Institute","NEI NIH HHS","National Cancer Institute","NCI NIH HHS","Cancer Prevention and Research Institute of Texas"],"pagination":["1854-1866"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6726575"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(9)"],"pubmed_abstract":["Disruption of the <i>CDKN2A</i> (<i>INK4A/ARF</i>) and <i>B</i> (<i>INK4B</i>) genes, which encode three function-independent tumor suppressors, is one of the most common events in human cancer. Because their relative importance in tumor prevention appears to be species- and context-specific, studying their regulation can shed light on mechanisms by which they are bypassed in malignant transformation. We previously unveiled a new pathway in which TGFβ selectively induces <i>Arf</i> at mouse <i>Cdkn2a</i> in eye development and cultured fibroblasts. As TGFβ signaling is often derailed in cancer development or progression, we investigated its control of <i>CDKN2A/B</i> in human cancer. Computational analyses of sequencing and array data from nearly 11,000 patients with cancer in TCGA showed "],"journal":["Molecular cancer research : MCR"],"pubmed_title":["Identification of <i>De Novo</i> Enhancers Activated by TGFβ to Drive Expression of <i>CDKN2A</i> and <i>B</i> in HeLa Cells."],"pmcid":["PMC6726575"],"funding_grant_id":["R01 EY019942","CA142543","RP120685-P2","RP180319","P30 CA142543"],"pubmed_authors":["Xu L","Skapek SX","Liu J","Liem P","Zheng Y","Hooks JC","Zhou Q","Bennett L","Liu YT"],"additional_accession":[]},"is_claimable":false,"name":"Identification of <i>De Novo</i> Enhancers Activated by TGFβ to Drive Expression of <i>CDKN2A</i> and <i>B</i> in HeLa Cells.","description":"Disruption of the <i>CDKN2A</i> (<i>INK4A/ARF</i>) and <i>B</i> (<i>INK4B</i>) genes, which encode three function-independent tumor suppressors, is one of the most common events in human cancer. Because their relative importance in tumor prevention appears to be species- and context-specific, studying their regulation can shed light on mechanisms by which they are bypassed in malignant transformation. We previously unveiled a new pathway in which TGFβ selectively induces <i>Arf</i> at mouse <i>Cdkn2a</i> in eye development and cultured fibroblasts. As TGFβ signaling is often derailed in cancer development or progression, we investigated its control of <i>CDKN2A/B</i> in human cancer. Computational analyses of sequencing and array data from nearly 11,000 patients with cancer in TCGA showed ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Sep","modification":"2026-05-04T10:08:50.899Z","creation":"2020-05-22T11:28:10Z"},"accession":"S-EPMC6726575","cross_references":{"pubmed":["31189690"],"doi":["10.1158/1541-7786.mcr-19-0289","10.1158/1541-7786.MCR-19-0289"]}}