{"entity": "journal", "iuid": "baf56f5c5cb140149845b468288ce098", "timestamp": "2026-08-20T21:18:39.932Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Endocr%20Soc.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Endocr%20Soc"}}, "title": "J Endocr Soc", "issn": "2472-1972", "issn-l": null, "publications_count": 3, "publications": [{"entity": "publication", "iuid": "2269fb4442624060ae1eb3eb1d817ae6", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2269fb4442624060ae1eb3eb1d817ae6.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2269fb4442624060ae1eb3eb1d817ae6"}}, "title": "Transcriptome Analysis Reveals Distinct Patterns Between the Invasive and Noninvasive Pituitary Neuroendocrine Tumors.", "authors": [{"family": "Jotanovic", "given": "Jelena", "initials": "J", "orcid": "0009-0007-9064-0384", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e96cfb7e0be04f56ab125f984fc31268.json"}}, {"family": "Tebani", "given": "Abdellah", "initials": "A"}, {"family": "Hekmati", "given": "Neda", "initials": "N"}, {"family": "Sivertsson", "given": "\u00c5sa", "initials": "\u00c5"}, {"family": "Lindskog", "given": "Cecilia", "initials": "C"}, {"family": "Uhl\u00e8n", "given": "Mathias", "initials": "M"}, {"family": "Gudjonsson", "given": "Olafur", "initials": "O"}, {"family": "Tsatsaris", "given": "Erika", "initials": "E"}, {"family": "Engstr\u00f6m", "given": "Britt Ed\u00e9n", "initials": "BE"}, {"family": "Wikstr\u00f6m", "given": "Johan", "initials": "J"}, {"family": "Pont\u00e9n", "given": "Fredrik", "initials": "F"}, {"family": "Casar-Borota", "given": "Olivera", "initials": "O", "orcid": "0000-0001-7376-7331", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/be2f108c23f24ce6b661c0446eeb3134.json"}}], "type": "journal article", "published": "2024-03-12", "journal": {"title": "J Endocr Soc", "issn": "2472-1972", "volume": "8", "issue": "5", "pages": "bvae040", "issn-l": null}, "abstract": "Although most pituitary neuroendocrine tumors (PitNETs)/pituitary adenomas remain intrasellar, a significant proportion of tumors show parasellar invasive growth and 6% to 8% infiltrate the bone structures, thus affecting the prognosis. There is an unmet need to identify novel markers that can predict the parasellar growth of PitNETs. Furthermore, mechanisms that regulate bone invasiveness of PitNETs and factors related to tumor vascularization are largely unknown. We used genome-wide mRNA analysis in a cohort of 77 patients with PitNETs of different types to explore the differences in gene expression patterns between invasive and noninvasive tumors with respect to the parasellar growth and regarding the rare phenomenon of bone invasiveness. Additionally, we studied the genes correlated to the contrast enhancement quotient, a novel radiological parameter of tumor vascularization. Most of the genes differentially expressed related to the parasellar growth were genes involved in tumor invasiveness. Differentially expressed genes associated with bone invasiveness are involved in NF-\u03baB pathway and antitumoral immune response. Lack of clear clustering regarding the parasellar and bone invasiveness may be explained by the influence of the cell lineage-related genes in this heterogeneous cohort of PitNETs. Our transcriptomics analysis revealed differences in the molecular fingerprints between invasive, including bone invasive, and noninvasive PitNETs, although without clear clustering. The contrast enhancement quotient emerged as a radiological parameter of tumor vascularization, correlating with several angiogenesis-related genes. Several of the top genes related to the PitNET invasiveness and vascularization have potential prognostic and therapeutic application requiring further research.", "doi": "10.1210/jendso/bvae040", "pmid": "38505563", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC10949357"}, {"db": "pii", "key": "bvae040"}], "notes": [], "created": "2026-08-20T12:38:04.199Z", "modified": "2026-08-20T12:38:04.327Z"}, {"entity": "publication", "iuid": "9c28b188cadf4552899402edb0a046ca", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/9c28b188cadf4552899402edb0a046ca.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/9c28b188cadf4552899402edb0a046ca"}}, "title": "Investigating the Effect of Estradiol Levels on the Risk of Breast, Endometrial, and Ovarian Cancer.", "authors": [{"family": "Johansson", "given": "\u00c5sa", "initials": "\u00c5", "orcid": "0000-0002-2915-4498", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a0bac3e1e64949fcbac4b4d839e1144d.json"}}, {"family": "Schmitz", "given": "Daniel", "initials": "D", "orcid": "0000-0003-4480-891X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/30e1b982f81a4c11ba59043beab3e4df.json"}}, {"family": "H\u00f6glund", "given": "Julia", "initials": "J", "orcid": "0000-0001-8061-3947", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bca098a65a67444899762a18f654f447.json"}}, {"family": "Hadizadeh", "given": "Fatemeh", "initials": "F"}, {"family": "Karlsson", "given": "Torgny", "initials": "T", "orcid": "0000-0001-8095-6149", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c8b2bb8ecf4545ad946ae2203c870282.json"}}, {"family": "Ek", "given": "Weronica E", "initials": "WE", "orcid": "0000-0003-2194-496X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8172f56f87554938a75cef7505f8603e.json"}}], "type": "journal article", "published": "2022-08-01", "journal": {"title": "J Endocr Soc", "issn": "2472-1972", "volume": "6", "issue": "8", "pages": "bvac100", "issn-l": null}, "abstract": "High levels of estrogen are associated with increased risk of breast and endometrial cancer and have been suggested to also play a role in the development of ovarian cancer. Cancerogenic effects of estradiol, the most prominent form of estrogen, have been highlighted as a side effect of estrogen-only menopausal hormone therapy. However, whether high levels of endogenous estrogens, produced within the body, promote cancer development, has not been fully established.\n\nWe aimed to examine causal effects of estradiol on breast, endometrial, and ovarian cancer.\n\nHere we performed a two-sample Mendelian randomization (MR) to estimate the effect of endogenous estradiol on the risk of developing breast, endometrial, and ovarian cancer, using the UK Biobank as well as 3 independent cancer cohorts.\n\nUsing 3 independent instrumental variables, we showed that higher estradiol levels significantly increase the risk for ovarian cancer (OR = 3.18 [95% CI, 1.47-6.87], P = 0.003). We also identified a nominally significant effect for ER-positive breast cancer (OR = 2.16 [95% CI, 1.09-4.26], P = 0.027). However, we could not establish a clear link to the risk of endometrial cancer (OR = 1.93 [95% CI, 0.77-4.80], P = 0.160).\n\nOur results suggest that high estradiol levels promote the development of ovarian and ER-positive breast cancer.", "doi": "10.1210/jendso/bvac100", "pmid": "35822202", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9265484"}, {"db": "pii", "key": "bvac100"}], "notes": [], "created": "2026-08-20T12:38:02.155Z", "modified": "2026-08-20T12:38:02.276Z"}, {"entity": "publication", "iuid": "d001de3cfeec44d9b818769dbbf3e9fa", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d001de3cfeec44d9b818769dbbf3e9fa.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d001de3cfeec44d9b818769dbbf3e9fa"}}, "title": "Reproductive and Behavior Dysfunction Induced by Maternal Androgen Exposure and Obesity Is Likely Not Gut Microbiome-Mediated.", "authors": [{"family": "Lindheim", "given": "Lisa", "initials": "L", "orcid": "0000-0001-7732-3869", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/175ecb54dd0346a99c78b3a6cf880734.json"}}, {"family": "Manti", "given": "Maria", "initials": "M"}, {"family": "Fornes", "given": "Romina", "initials": "R"}, {"family": "Bashir", "given": "Mina", "initials": "M"}, {"family": "Czarnewski", "given": "Paulo", "initials": "P", "orcid": "0000-0001-8150-4021", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/501677a1262c438aa4077b205bb39a72.json"}}, {"family": "Diaz", "given": "Oscar E", "initials": "OE", "orcid": "0000-0001-7622-7832", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/29eecafe74864c759129278a48114c4a.json"}}, {"family": "Seifert", "given": "Maike", "initials": "M"}, {"family": "Engstrand", "given": "Lars", "initials": "L", "orcid": "0000-0002-7713-2373", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/02d8684df81e42169e613de803446fbf.json"}}, {"family": "Villablanca", "given": "Eduardo J", "initials": "EJ", "orcid": "0000-0001-9522-9729", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c90ee0c3d1904ae0933efe3631a651e0.json"}}, {"family": "Obermayer-Pietsch", "given": "Barbara", "initials": "B", "orcid": "0000-0003-3543-1807", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4fb8e7388e6e417c9df0f48759c2b314.json"}}, {"family": "Stener-Victorin", "given": "Elisabet", "initials": "E", "orcid": "0000-0002-3424-1502", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ad1ced271f514141ae3c89e90184c88e.json"}}], "type": "journal article", "published": "2018-12-01", "journal": {"title": "J Endocr Soc", "issn": "2472-1972", "volume": "2", "issue": "12", "pages": "1363-1380", "issn-l": null}, "abstract": "Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder of unclear etiology in women and is characterized by androgen excess, insulin resistance, and mood disorders. The gut microbiome is known to influence conditions closely related with PCOS, and several recent studies have observed changes in the stool microbiome of women with PCOS. The mechanism by which the gut microbiome interacts with PCOS is still unknown. We used a mouse model to investigate if diet-induced maternal obesity and maternal DHT exposure, mimicking the lean and obese PCOS women, cause lasting changes in the gut microbiome of offspring. Fecal microbiome profiles were assessed using Illumina paired-end sequencing of 16S rRNA gene V4 amplicons. We found sex-specific effects of maternal and offspring diet, and maternal DHT exposure on fecal bacterial richness and taxonomic composition. Female offspring exposed to maternal obesity and DHT displayed reproductive dysfunction and anxietylike behavior. Fecal microbiota transplantation from DHT and diet-induced obesity exposed female offspring to wild-type mice did not transfer reproductive dysfunction and did not cause the expected increase in anxietylike behavior in recipients. Maternal obesity and androgen exposure affect the gut microbiome of offspring, but the disrupted estrous cycles and anxietylike behavior are likely not microbiome-mediated.", "doi": "10.1210/js.2018-00266", "pmid": "30534630", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC6280317"}, {"db": "pii", "key": "js_201800266"}, {"db": "Dryad", "key": "10.5061/dryad.7h4338m"}], "notes": [], "created": "2026-08-20T12:38:06.284Z", "modified": "2026-08-20T12:38:06.499Z"}], "created": "2026-08-20T12:38:02.243Z", "modified": "2026-08-20T12:38:02.243Z"}