{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ter Steege EJ"],"funding":["The Dutch Cancer Society"],"pagination":["289-299"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9825844"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["258(3)"],"pubmed_abstract":["R-spondins (RSPOs) are influential signaling molecules that promote the Wnt/β-catenin pathway and self-renewal of stem cells. Currently, RSPOs are emerging as clinically relevant oncogenes, being linked to cancer development in multiple organs. Although this has instigated the rapid development and testing of therapeutic antibodies targeting RSPOs, functional evidence that RSPO causally drives cancer has focused primarily on the intestinal tract. Here, we assess the oncogenic capacity of RSPO in breast cancer in a direct fashion by generating and characterizing a novel mouse model with conditional Rspo3 expression in the mammary gland. We also address the prevalence of RSPO gene alterations in breast cancer patients. We found that a quarter of breast cancer patients harbor RSPO2/RSPO3 copy"],"journal":["The Journal of pathology"],"pubmed_title":["R-spondin-3 is an oncogenic driver of poorly differentiated invasive breast cancer."],"pmcid":["PMC9825844"],"funding_grant_id":["10957"],"pubmed_authors":["Hilkens J","Derksen PW","Song JY","Timmer NC","Bakker ER","Ter Steege EJ","Boer M","Ammerlaan CM"],"additional_accession":[]},"is_claimable":false,"name":"R-spondin-3 is an oncogenic driver of poorly differentiated invasive breast cancer.","description":"R-spondins (RSPOs) are influential signaling molecules that promote the Wnt/β-catenin pathway and self-renewal of stem cells. Currently, RSPOs are emerging as clinically relevant oncogenes, being linked to cancer development in multiple organs. Although this has instigated the rapid development and testing of therapeutic antibodies targeting RSPOs, functional evidence that RSPO causally drives cancer has focused primarily on the intestinal tract. Here, we assess the oncogenic capacity of RSPO in breast cancer in a direct fashion by generating and characterizing a novel mouse model with conditional Rspo3 expression in the mammary gland. We also address the prevalence of RSPO gene alterations in breast cancer patients. We found that a quarter of breast cancer patients harbor RSPO2/RSPO3 copy","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2025-04-05T08:52:37.741Z","creation":"2025-04-05T08:52:37.741Z"},"accession":"S-EPMC9825844","cross_references":{"pubmed":["36106661"],"doi":["10.1002/path.5999"]}}