{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kubler K"],"funding":["G.G. is partly supported by the Paul C. Zamecnik Chair in Oncology at the Massachusetts General Hospital Cancer Center.","U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)","United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs","U.S. Department of Health & Human Services | NIH | National Cancer Institute","United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP)","U.S. Department of Defense","U.S. Department of Defense (United States Department of Defense)","NCI NIH HHS","KWF Kankerbestrijding"],"pagination":["2192-2202"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12425819"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["57(9)"],"pubmed_abstract":["Mutagenic processes and clonal selection contribute to the development of therapy-associated secondary neoplasms, a known complication of cancer treatment. The association between tamoxifen therapy and secondary uterine cancers is uncommon but well established; however, the genetic mechanisms underlying tamoxifen-driven tumorigenesis remain unclear. We find that oncogenic PIK3CA mutations, common in spontaneously arising estrogen-associated de novo uterine cancer, are significantly less frequent in tamoxifen-associated tumors. In vivo, tamoxifen-induced estrogen receptor stimulation activates phosphoinositide 3-kinase (PI3K) signaling in normal mouse uterine tissue, potentially eliminating the selective benefit of PI3K-activating mutations in tamoxifen-associated uterine cancer. Together, "],"journal":["Nature genetics"],"pubmed_title":["Tamoxifen induces PI3K activation in uterine cancer."],"pmcid":["PMC12425819"],"funding_grant_id":["W81XWH-17-1-0084","K08 CA191058","P50CA240243","5K08CA191058-05","P50 CA240243","R01 CA237414"],"pubmed_authors":["Lanfermeijer M","Feit AS","Nederlof PM","Miller M","Nardone A","Hermida-Prado F","Gibson WJ","Droog M","Cha J","Getz G","Leshchiner I","Pun M","Gao J","Radovich M","Zwart W","Cohen Feit G","Van Allen EM","Stewart C","Dackus G","van Leeuwen FE","Kubler K","Mourits MJE","Matulonis UA","Nguyen QD","Jeselsohn R","Maruvka YE","Paweletz CP","Anand S","Kuang Y","Akhshi T","Gregoricchio S","Gurevich D","Cornelissen S","Feiglin A"],"additional_accession":[]},"is_claimable":false,"name":"Tamoxifen induces PI3K activation in uterine cancer.","description":"Mutagenic processes and clonal selection contribute to the development of therapy-associated secondary neoplasms, a known complication of cancer treatment. The association between tamoxifen therapy and secondary uterine cancers is uncommon but well established; however, the genetic mechanisms underlying tamoxifen-driven tumorigenesis remain unclear. We find that oncogenic PIK3CA mutations, common in spontaneously arising estrogen-associated de novo uterine cancer, are significantly less frequent in tamoxifen-associated tumors. In vivo, tamoxifen-induced estrogen receptor stimulation activates phosphoinositide 3-kinase (PI3K) signaling in normal mouse uterine tissue, potentially eliminating the selective benefit of PI3K-activating mutations in tamoxifen-associated uterine cancer. Together, ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T02:51:29.927Z","creation":"2026-04-23T03:11:55.534Z"},"accession":"S-EPMC12425819","cross_references":{"pubmed":["40846762"],"doi":["10.1038/s41588-025-02308-w"]}}