{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yokomoto-Umakoshi M"],"funding":["The MEXT Cooperative Research Project Program","JST-Moonshot","Secom Science and Technology Foundation (SSTF)","The Uehara Memorial Foundation","JSPS KAKENHI","The Nakatomi Foundation","Medical Research Center Initiative for High Depth Omics","Japan Foundation for Applied Enzymology","Grant of The Clinical Research Promotion Foundation","JST A-STEP","AMED-BINDS","Secom Science and Technology Foundation","Joint Research Program of Institute for Genetic Medicine, Hokkaido University","Takeda Science Foundation","JES Grant for Promising Investigator","Takeda Science Foundation (TSF)","CURE","Ono Medical Research Foundation"],"pagination":["e2421489122"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11892633"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122(9)"],"pubmed_abstract":["Aldosterone-producing adenomas (APA), a major endocrine tumor and leading subtype of primary aldosteronism, cause secondary hypertension with high cardiometabolic risks. Despite potentially producing multiple steroid hormones, detailed cellular mechanisms in APA remain insufficiently studied. Our multiomics analysis focusing on APA with <i>KCNJ5</i> mutations, which represent the most common genetic form, revealed marked cellular heterogeneity. Tumor cell reprogramming initiated from stress-responsive cells to aldosterone-producing or cortisol-producing cells, with the latter progressing to proliferative stromal-like cells. These cell subtypes showed spatial segregation, and APA exhibited genomic intratumor heterogeneity. Among the nonparenchymal cells, lipid-associated macrophages, which "],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Multiomics analysis unveils the cellular ecosystem with clinical relevance in aldosterone-producing adenomas with &lt;i&gt;KCNJ5&lt;/i&gt; mutations."],"pmcid":["PMC11892633"],"funding_grant_id":["JPMJTR204J","NA","JP24ama121055","JP22H04993","JP22K08627","JP23K15392","JP21K14472","JPMJMS2011-62","JPMXP1323015486","JP22H05185","JP24K23476"],"pubmed_authors":["Izumi Y","Fujita M","Kawamura N","Yokomoto-Umakoshi M","Shimma S","Ogasawara T","Oda Y","Umakoshi H","Haji S","Bamba T","Fukumoto T","Eto M","Iwahashi N","Ogawa Y","Kaneko H","Nakao H","Suzuki Y","Nakatani K","Ogawa S","Seki M"],"additional_accession":[]},"is_claimable":false,"name":"Multiomics analysis unveils the cellular ecosystem with clinical relevance in aldosterone-producing adenomas with &lt;i&gt;KCNJ5&lt;/i&gt; mutations.","description":"Aldosterone-producing adenomas (APA), a major endocrine tumor and leading subtype of primary aldosteronism, cause secondary hypertension with high cardiometabolic risks. Despite potentially producing multiple steroid hormones, detailed cellular mechanisms in APA remain insufficiently studied. Our multiomics analysis focusing on APA with <i>KCNJ5</i> mutations, which represent the most common genetic form, revealed marked cellular heterogeneity. Tumor cell reprogramming initiated from stress-responsive cells to aldosterone-producing or cortisol-producing cells, with the latter progressing to proliferative stromal-like cells. These cell subtypes showed spatial segregation, and APA exhibited genomic intratumor heterogeneity. Among the nonparenchymal cells, lipid-associated macrophages, which ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-05-09T10:36:58.323Z","creation":"2026-04-08T00:48:22.104Z"},"accession":"S-EPMC11892633","cross_references":{"pubmed":["40009643"],"doi":["10.1073/pnas.2421489122"]}}