{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Warde KM"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute","Huntsman Cancer Institute","NCI NIH HHS","V Foundation for Cancer Research","NIH HHS"],"pagination":["846-865"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11534150"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3(7)"],"pubmed_abstract":["Aging markedly increases cancer risk, yet our mechanistic understanding of how aging influences cancer initiation is limited. Here we demonstrate that the loss of ZNRF3, an inhibitor of Wnt signaling that is frequently mutated in adrenocortical carcinoma, leads to the induction of cellular senescence that remodels the tissue microenvironment and ultimately permits metastatic adrenal cancer in old animals. The effects are sexually dimorphic, with males exhibiting earlier senescence activation and a greater innate immune response, driven in part by androgens, resulting in high myeloid cell accumulation and lower incidence of malignancy. Conversely, females present a dampened immune response and increased susceptibility to metastatic cancer. Senescence-recruited myeloid cells become depleted "],"journal":["Nature aging"],"pubmed_title":["Senescence-induced immune remodeling facilitates metastatic adrenal cancer in a sex-dimorphic manner."],"pmcid":["PMC11534150"],"funding_grant_id":["P30 CA042014","K08 CA222620","S10 OD026959","V2021-021","P30CA040214","T32 CA265782","Pathmaker Scholars Program"],"pubmed_authors":["Jones KD","Warde KM","Ammer JL","Liu L","Castaneda-Hernandez G","Ekiz HA","Giordano TJ","Hammer GD","Willett PW","Stubben CJ","Kiseljak-Vassiliades K","Lohman BK","Smith LJ","Converso-Baran K","Barry M","Basham KJ","Zhang C","Imodoye SO","Clay MR"],"additional_accession":[]},"is_claimable":false,"name":"Senescence-induced immune remodeling facilitates metastatic adrenal cancer in a sex-dimorphic manner.","description":"Aging markedly increases cancer risk, yet our mechanistic understanding of how aging influences cancer initiation is limited. Here we demonstrate that the loss of ZNRF3, an inhibitor of Wnt signaling that is frequently mutated in adrenocortical carcinoma, leads to the induction of cellular senescence that remodels the tissue microenvironment and ultimately permits metastatic adrenal cancer in old animals. The effects are sexually dimorphic, with males exhibiting earlier senescence activation and a greater innate immune response, driven in part by androgens, resulting in high myeloid cell accumulation and lower incidence of malignancy. Conversely, females present a dampened immune response and increased susceptibility to metastatic cancer. Senescence-recruited myeloid cells become depleted ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-06-03T00:07:46.413Z","creation":"2025-04-05T09:31:01.516Z"},"accession":"S-EPMC11534150","cross_references":{"pubmed":["37231196"],"doi":["10.1038/s43587-023-00420-2"]}}