{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T07:56:25Z","timestamp":1793087785864,"version":"4.5.0"},"reference-count":62,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T00:00:00Z","timestamp":1771286400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,2,17]]},"abstract":"\n BACKGROUND:<\/jats:title>\n \n Pulmonary arterial hypertension (PAH) and breast cancer disproportionately affect women.\n BMPR2<\/jats:italic>\n (bone morphogenetic protein receptor type 2) mutations, the most common genetic cause of heritable PAH, also exert tumor-suppressive functions, but their role in linking these diseases remains unclear.\n <\/jats:p>\n <\/jats:sec>\n \n METHODS:<\/jats:title>\n \n We combined bioinformatic, epidemiologic, and experimental approaches. Public cancer datasets were mined for\n BMPR2<\/jats:italic>\n alterations. In vivo, mammary tumor development and pulmonary hemodynamics were assessed in female\n Bmpr2<\/jats:italic>\n +\/\u039471<\/jats:sup>\n rats with or without carcinogen (7,12-dimethylbenz[a]anthracene) exposure. Pulmonary arterial smooth muscle cells were exposed to tumor-conditioned media to test inflammatory proliferation. Finally, associations between breast cancer and PAH were examined in the French National Healthcare Database (9964 patients with PAH).\n <\/jats:p>\n <\/jats:sec>\n \n RESULTS:<\/jats:title>\n \n BMPR2<\/jats:italic>\n expression was markedly reduced in human breast tumors, with recurrent somatic variants and deep deletions identified.\n Bmpr2<\/jats:italic>\n \n +\/\u039471<\/jats:italic>\n <\/jats:sup>\n rats exhibited spontaneous mammary tumors and, following 7,12-dimethylbenz[a]anthracene exposure, developed exacerbated pulmonary hypertension with increased vascular remodeling and inflammation. Tumor-bearing\n Bmpr2<\/jats:italic>\n \n +\/\u039471<\/jats:italic>\n <\/jats:sup>\n rats showed elevated lung IL-1\u03b2 and NF-\u03baB activation. In vitro, conditioned media from\n Bmpr2<\/jats:italic>\n \n +\/\u039471<\/jats:italic>\n <\/jats:sup>\n tumors induced proliferation of\n Bmpr2<\/jats:italic>\n \n +\/\u039471<\/jats:italic>\n <\/jats:sup>\n pulmonary arterial smooth muscle cells via IL-1\u03b2\u2013dependent signaling, while neutralization of IL-1\u03b2 attenuated this effect. Human pulmonary arterial smooth muscle cells carrying\n BMPR2<\/jats:italic>\n mutations similarly displayed heightened IL-1\u03b2\u2013induced proliferation. Epidemiologically, breast cancer incidence was more than doubled in patients with PAH compared with the general population, and PAH incidence was increased nearly 9-fold among patients with breast cancer, indicating a bidirectional relationship.\n <\/jats:p>\n <\/jats:sec>\n \n CONCLUSIONS:<\/jats:title>\n \n These findings identify a reciprocal association between breast cancer and PAH mediated by defective\n BMPR2<\/jats:italic>\n signaling and tumor-associated inflammation. Breast cancer may act as a \u201csecond hit,\u201d unmasking\n BMPR2<\/jats:italic>\n -related susceptibility to PAH, underscoring BMPR2 as a shared molecular vulnerability with implications for surveillance of at-risk populations.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/circulationaha.125.079067","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T10:00:32Z","timestamp":1769594432000},"page":"516-533","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Breast Cancer Reveals Latent\n BMPR2<\/i>\n -Related Susceptibility to Pulmonary Hypertension"],"prefix":"10.1161","volume":"153","author":[{"given":"Victoria","family":"Toro","sequence":"first","affiliation":[{"name":"Centre de Recherche de l\u2019Institut Universitaire de Cardiologie et de Pneumologie de Qu\u00e9bec, Qu\u00e9bec, QC, Canada (V.T., M.M., C.A.G., R.E.K., C. Bilodeau, Y.G., S.M., S.B.-B., A.A.-S., O.B., S.P., S.B., F.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-2821-7345","authenticated-orcid":true,"given":"Manon","family":"Mougin","sequence":"additional","affiliation":[{"name":"Centre de Recherche de l\u2019Institut Universitaire de Cardiologie et de Pneumologie de Qu\u00e9bec, Qu\u00e9bec, QC, Canada (V.T., M.M., C.A.G., R.E.K., C. Bilodeau, Y.G., S.M., S.B.-B., A.A.-S., O.B., S.P., S.B., F.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-6333-5674","authenticated-orcid":true,"given":"Coline","family":"Brossat","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Grenoble Alpes, INSERM U1300, HP2, and INSERM CIC1406, Grenoble, France (C. Brossat, CJ.-B., A.H.)."},{"name":"Pharmacovigilance Unit, CHU Grenoble Alpes, Grenoble, France (C. 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