{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314325/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Other"],"species":["Mus musculus"," synthetic construct"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314325"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Inflammatory Monocytes Constrain YAP-Induced Cell Proliferation [MERFISH]","description":"YAP and its paralog, TAZ are transcriptional co-activators of the Hippo pathway that regulate cell growth. Their structural distinctiveness suggests important independent functional differences. To investigate this further, we generated YAP- and TAZ-predominant clones in the liver and followed their long-term behavior. YAP clones rapidly de-differentiate cells into a stem cell-like state with inflammatory immune cell recruitment followed by their clearance. In contrast, TAZ clones promote an anti-inflammatory immune environment resulting in their long-term maintenance, massive organ growth and increased mortality. YAP clones recruit inflammatory blood-derived monocytes, which if inhibited permits YAP clonal growth. Consistent with these results, YAPHigh colorectal cancer (CRC) patients had a 67% 5-year survival rate, while TAZHigh CRC patients did not survive to 5 years. Similar trends were seen in hepatocellular carcinoma patients. These findings underscore the importance of understanding the intrinsic differences in YAP and TAZ biology as independent drivers of disease.","dates":{"publication":"2026/07/01"},"accession":"GSE314325","cross_references":{"GSM":["GSM9393663","GSM9393664","GSM9393661","GSM9393662","GSM9393660","GSM9393658","GSM9393659"],"GPL":["31217"],"GSE":["314325"],"taxon":["Mus musculus"," synthetic construct"],"PMID":["[42341114]"]}}