Neuroendocrinology最新文献

{"title":"Clinical Impact of Molecular Tumor Board Inclusion on Treatment Outcomes in Neuroendocrine Neoplasms.","authors":"Maryam Barsch, Linda Gräßel, Patrick Metzger, Alexander von Werder, Johanna Ganz, Lioba Klaas, Lisanne Schulz, Annegrit Decker, Anna Dammer, Patrick Wenzel, Mathias Friedrich, Julia Falkenstein, Henriette Bertemes, Julia Kuehn, Cornelius Miething, Alisa Martina Lörsch, Johannes Jung, Anna Lena Illert, Atsuko Kasajima, Yasmin Dorusch, Elaine-Pashupati Dopfer, Anne Maria Schultheis, Silke Lassmann, Marianne Pavel, Martin Werner, Melanie Boerries, Justus Duyster, Roland M Schmid, Carolin Mogler, Nicole Pfarr, Heiko Becker, Robert Thimme, Michael Quante, Sebastian Lange","doi":"10.1159/000552650","DOIUrl":"10.1159/000552650","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroendocrine neoplasms (NENs) are rare and biologically heterogeneous tumors with limited evidence-based systemic treatment options, particularly in advanced disease stages. Molecular Tumor Boards (MTBs) offer an interdisciplinary framework for interpreting genomic alterations and identifying personalized treatment strategies.</p><p><strong>Methods: </strong>We conducted a retrospective two-center analysis of patients with NENs discussed at the MTBs of the University Medical Center Freiburg and the Technical University of Munich between 2019 and 2024. Clinical characteristics, molecular profiling results, MTB-based therapy recommendations, treatment implementation, and outcomes were evaluated. Overall survival (OS) was analyzed using a predefined 6-month landmark approach to account for immortal time bias. Treatment efficacy was further assessed using progression-free survival (PFS) and PFS2/PFS1 ratio.</p><p><strong>Results: </strong>A total of 87 patients were discussed at both MTBs, 74 of whom underwent molecular profiling. Actionable therapy recommendations were issued for 58 patients, and 20 patients ultimately received MTB-guided therapy. Molecular alterations frequently involved DNA damage repair pathways, immune-related biomarkers, and signaling cascades relevant to targeted therapy. 6-month landmark OS analysis demonstrated significantly improved OS for patients receiving MTB-guided therapy. At the individual level, 8 of 20 treated patients achieved a PFS2/PFS1 ratio >1.3.</p><p><strong>Conclusion: </strong>Molecular-guided precision oncology can provide clinically meaningful benefit for selected patients with NENs, despite limited overall implementation rates. Earlier integration of molecular profiling may increase the feasibility and impact of personalized treatment approaches in these rare tumor entities.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"353-367"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory Signaling and Emotional Symptoms in Hashimoto's Thyroiditis beyond Thyroid Function Status.","authors":"Simiao Yao, Xingyu Zhu, Xin Apos Ai Li, Xinying Si, Qian Zhang, Zhiguo Ding, Junhui Wang","doi":"10.1159/000553087","DOIUrl":"10.1159/000553087","url":null,"abstract":"<p><p><p>Introduction: Patients with Hashimoto's thyroiditis (HT) frequently report persistent emotional and cognitive symptoms even when thyroid hormone levels are within the reference range. The mechanisms underlying these symptoms beyond thyroid function status remain incompletely understood. This study aimed to characterize the symptom profile of HT patients with thyroid hormone levels within the reference ranges and to investigate whether peripheral inflammatory signaling is associated with emotional symptoms independent of thyroid-related factors.</p><p><strong>Methods: </strong>Clinical data were analyzed from 80 patients with HT whose free triiodothyronine and free thyroxine levels were within the reference ranges and who did not have suppressed thyroid-stimulating hormone (TSH). Thyroid-related quality of life was assessed using the Thyroid Patient-Reported Outcome-39 (ThyPRO-39). Serum interleukin-6 (IL-6) and interleukin-17 (IL-17) levels were measured by enzyme-linked immunosorbent assay. Associations between symptom dimensions, thyroid-related factors, and inflammatory markers were evaluated using multivariable linear regression models with log-transformed cytokine levels, adjusting for age, sex, elevated TSH, current levothyroxine sodium use, and thyroid autoantibodies.</p><p><strong>Results: </strong>Symptom profiling revealed that fatigue and emotional dimensions, including emotional susceptibility, anxiety, and depressivity, were the most prominently affected domains, whereas thyroid-related somatic and social functioning domains were relatively preserved. Neither elevated TSH, current levothyroxine sodium use, nor thyroid autoantibody levels showed significant independent associations with emotional symptom scores. In contrast, higher peripheral IL-6 levels were independently associated with increased emotional susceptibility, anxiety, and depressivity after adjustment for thyroid-related parameters. No consistent independent associations were observed between IL-17 levels and emotional symptom dimensions.</p><p><strong>Conclusion: </strong>In patients with HT whose thyroid hormone levels are within the reference ranges, emotional symptoms are common and cannot be fully explained by TSH status, levothyroxine sodium use, or thyroid autoantibody levels. Peripheral inflammatory signaling, particularly IL-6, may be associated with emotional symptom burden beyond classical thyroid-related mechanisms, highlighting a potential neuroimmune pathway underlying persistent symptoms in HT. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"380-391"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13441259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiotherapeutic Strategies and Advances in the Management of Pituitary Adenomas.","authors":"Neil D Almeida, Jeff F Zhang, Harshini K Cheruvu, David Shen, Rohil Shekher, Victor Goulenko, Venkatesh S Madhugiri, Hanna Algattas, David J Park, Tony J C Wang, Dheerendra Prasad","doi":"10.1159/000549316","DOIUrl":"10.1159/000549316","url":null,"abstract":"<p><p><p>Background: Pituitary adenomas are benign brain tumors that develop from hormone-producing cells in the anterior pituitary gland and account for 10-20% of all intracranial tumors. However, pituitary adenomas can have significant morbidity due to local invasion and changes to hormonal secretion. Though radiotherapy can result in side effects ranging from hypopituitarism to visual changes, radiation therapy remains an important tool due to its long-term benefits and high tumor control rates. Summary: Standard treatment for pituitary adenomas often includes surgical resection followed by radiation therapy. Recent developments in radiation delivery methods and techniques include external beam radiotherapy, stereotactic radiosurgery, proton therapy, and peptide receptor radionuclide therapy, which have improved precision while minimizing damage to healthy tissues. These advancements have continued to improve patient safety and long-term outcomes in cases of both functioning and nonfunctioning pituitary adenomas. Key Messages: Pituitary adenomas, while benign, can have significant clinical consequences. Advances in radiation therapy have expanded the therapeutic landscape to offer safer, more effective and more precise treatment options. Modern radiotherapy techniques have enhanced long-term outcomes and quality of life for patients with pituitary adenomas. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"88-96"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12734409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145459131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between Patterns of Neuroendocrine Liver Metastatic Burden and Outcomes after Liver-Directed Therapy, Systemic Chemotherapy, and Peptide Receptor Radionuclide Therapy.","authors":"Cathal O Apos Leary, David J Tischfield, Rony Avritscher, Ghassan El-Haddad, Ricardo Garcia-Monaco, Nicholas Fidelman, Namrata Vijayvergia, Pamela L Kunz, Nicholas J Seewald, Michael C Soulen","doi":"10.1159/000551977","DOIUrl":"10.1159/000551977","url":null,"abstract":"<p><strong>Introduction: </strong>Treatment selection is a challenge for liver-dominant metastatic neuroendocrine tumors (NETs). Post hoc analysis of NETTER-1 suggested that tumor size but not tumor burden predicted progression-free survival (PFS), contrary to prior publications. Analysis of imaging datasets from capecitabine-temozolomide (CapTem), liver-directed therapy (LDT), and peptide receptor radionuclide therapy (PRRT) cohorts was performed to investigate whether imaging features of liver metastatic disease may guide treatment selection.</p><p><strong>Methods: </strong>Patients with measurable liver-dominant metastatic NET were identified from imaging datasets from two completed multicenter prospective clinical trials, the capecitabine-temozolomide (CapTem) arm of ECOG-ACRIN 2211 (EA2211) and Randomized Embolization Trial for NeuroEndocrine Tumors (RETNET). A retrospective institutional cohort of consecutive patients treated with PRRT was reviewed for comparison. Extent of liver metastases was categorized by number, maximum diameter, and tumor burden as a fraction of liver volume. These categories were correlated with response category, the primary endpoint, objective response rate (ORR), and PFS by RECIST criteria. Descriptive and graphical analyses were followed by multivariable modeling to test treatment-by-stratum interaction.</p><p><strong>Results: </strong>A total of 220 patients were included: CapTem (67), LDT (77), and PRRT (76). Pancreatic (62%, 137/220) and bowel primaries predominated (27%, 59/220). Imaging features were not associated with ORR or PFS in any cohort nor the overall population. The ORR for LDT, PRRT, and CapTem were 65%, 38%, and 25%, respectively (p < 0.001). The respective median PFS were LDT 18.9 months (95% CI: 16.3-24), PRRT 21.6 (95% CI: 14.3-26.9), and 16.6 (95% CI: 11.5-29) for CapTem (p = 0.99).</p><p><strong>Conclusion: </strong>In a review of three distinct cohorts of neuroendocrine tumor patients, no imaging features were identified that predicted treatment outcomes or could inform treatment selection. Further comparative analyses are required prior to using these imaging features to guide treatment selection.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"275-287"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural Innervation of Adipose Tissue: Current Understanding and Future Perspective.","authors":"Chun-Ning Wang, Chun Yang","doi":"10.1159/000551952","DOIUrl":"10.1159/000551952","url":null,"abstract":"<p><strong>Background: </strong>Adipose tissue plays a pivotal role in metabolic homeostasis regulation. It is predominantly innervated by sympathetic efferent and sensory afferent nerves, forming a bidirectional communication network. Although the sympathetic innervation of adipose tissue has been extensively studied before, several novel insights have been provided recently. In contrast, the functional significance of sensory innervation in adipose tissue remains underexplored.</p><p><strong>Summary: </strong>This review summarized recent advances between adipocytes and nerve innervation in metabolic regulation. Furthermore, we demonstrated the interplay between immune cells and nerve fibers within adipose tissue, as well as the crosstalk between sympathetic efferent and sensory afferent nerves in metabolic processes. Our review suggests targeting zinc/Mg supplementation, the calsyntenin-3β-S100b, and the leptin-brain-derived neurotrophic factor axis have become promising therapies to treat obesity and other metabolic diseases. Of note, the sympathetic innervation is vital for adipose adaptation to long-term metabolic challenges with different energy demands, and it remains to be explored whether sensory nerves have similar capacity upon different energy challenges, particularly in different strains of rodents as well as across species.</p><p><strong>Key messages: </strong>The crosstalk in adipose tissue microenvironment plays an essential role in metabolic homeostasis regulation. The functions and mechanisms of sensory afferent nerves and the dynamic interplay between sympathetic efferent and sensory afferent nerves in adipose tissue represent a critical frontier for more detailed research.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"332-348"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"","doi":"10.1159/000552319","DOIUrl":"10.1159/000552319","url":null,"abstract":"&lt;p&gt;&lt;p&gt;In the article \"Expanded Targeted-Exome Sequencing and Functional Validation Improve Molecular Diagnosis and Refine Genotype-Phenotype Correlations in Congenital Hypogonadotropic Hypogonadism\" [Neuroendocrinology. 2026;116(1):1-17; https://doi.org/10.1159/000548348] by Fausto et al., the authors identified an error in the nomenclature of the protein variant associated with the genetic variant.The authors note that the variant affects the stop codon (Ter / *) at position 139, converting it to a Trp codon (a no-stop variant) and resulting in a C-terminal extension of the protein. Translation continues for seven amino acids beyond the original termination site before reaching a new stop codon (Ter / *) at position 7 of the added sequence. Accordingly, the protein change should be corrected from p.*139Trpext*41 to p.*139Trpext*7, following the recommendations of the Human Genome Variation Society (HGVS) protein extension nomenclature guidelines (https://hgvs-nomenclature.org/stable/recommendations/protein/extension/).The corrected Table 2 is shown here.Table 2.Novel and known pathogenic/likely pathogenic variants and VUS identified by the 52-gene CHH exome panel in our cohort of 35 patients with CHHIDFamilial historyGeneVariantTypeZygosityMAF (GnomAD/AbraOM)ACGMReference1sporadicSPRY4c.19A&gt;Gmissensehtz&lt;0.005/NRVUS (PM2, BP4)Novelp.Thr7Ala2sporadicIL17RDc.1705C&gt;Tmissensehtz&lt;0.02/NRVUS (PM2, BS2, BP1, BP4)Novel (RCV:004212115.1)p.Pro569Ser3sporadicWDR11c.1303G&gt;Amissensehtz&lt;0.015/NRPathogenic (PS1, PS3)[42]p.Ala435Thr4sporadicANOS1c.1369C&gt;TnonsensehmNR/NRPathogenic (PVS1, PS1)[43]p.Arg457*5sporadicCHD7c.2978A&gt;Tmissensehtz&lt;0.007/NRVUS (PM1-PM2-PP3)Novelp.Asp993ValPCSK1c.239G&gt;Amissensehtz&lt;0.007/NRLikely pathogenic (PS1, PM2, PM5)[44]p.Arg80Gln6familialKISS1c.417delAnostop (stoploss)htz&lt;0.001/0.206VUS (PM2, PM4)Novel (RCV: 001730690.2)p.*139Trpext*77sporadicTACR3c.1115G&gt;Amissensehtz&lt;0.004/NRVUS (PM2, PP2, PP5)Novelp.Arg372His8familialPROKR2c.802C&gt;Tmissensehtz&lt;0.01/0.009VUS (PS3)[61]p.Arg268Cys9sporadicIGSF10c.467G&gt;Tmissensehtz&lt;0.005/0.002VUS (PM1, PM2, PP5, BP1)Novelp.Arg156Leu10sporadicPROKR2c.868C&gt;Tmissensehtz&lt;0.01/NRPathogenic (PS1, PM1, PM2, PP2, PP3, PP5)[15, 45, 47]p.Pro290Ser11familialGNRHRc.806C&gt;Tmissensehm&lt;0.0002/NRPathogenic[21, 48]CHD7p.Thr269Metmissensehtz&lt;0.001/NRVUS (PM2,BP4)Novel (RCV: 000819615.6)GHSRc.577A&gt;Gmissensehtz0.003/0.0016VUS (PM2, BP4)Novel (RCV: 001149557.4)KISS1p.Met193Valmissensehtz0.01/0.006VUS (PP3)Novel (RCV: 003730668.1)MSX1c.10 72G&gt;Amissensehtz0.001/NRVUS (PM2, PP3)Novel (RCV: 000983935.6)SEMA3Ap.Ala358Thrmissensehm0.01/0.008VUS (PP3)Novel (RCV: 002489291.1)c.268C&gt;Tp.His90Aspc.821C&gt;Tp.Ala274Valc.1000A&gt;Gp.Ile334Val12familialKISS1Rc.608C&gt;Amissensehm&lt;0.007/NRLikely pathogenic (PS3, PM1, PM2, PP2)present studyp.Ala203Asp13sporadicANOS1c.712C&gt;TnonsensehtzNR/NRPathogenic (PVS1, PM2, PP3)Novelp.Gln238*14sporadicOTUD4c.910G&gt;Amissensehtz&lt;0.003/0.0008VUS (PM2, BP4)NovelSPRY4p.Thr349Promissensehtz&lt;0.004/NRLikely pathogenic (PS1","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"349-352"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Potential Neural Nuclei and Circuits Underlying Asthma: A Comprehensive Review.","authors":"Ziteng Wang, Zhenchun Shi, Jingyu Xian, Zengxun Liu, Jinhao Sun","doi":"10.1159/000551836","DOIUrl":"10.1159/000551836","url":null,"abstract":"<p><strong>Background: </strong>Asthma is a common chronic inflammatory airway disease, characterized clinically by recurrent wheezing, shortness of breath, chest tightness, and cough. The roles of inflammatory cells such as T cells, eosinophils, and basophils in asthma are now well established. Recent studies have further revealed that the nervous system is not merely a \"bystander\" to the inflammatory response. Consequently, the peripheral nerves and the neural nuclei involved in asthma have attracted increasing research interest.</p><p><strong>Summary: </strong>This review summarizes the currently identified peripheral and central nerves implicated in transmitting airway inflammatory signals in asthma. It describes the principal mechanisms through which various brain nuclei - including nucleus tractus solitarius, paraventricular nucleus, and amygdala - participate in asthma regulation. We also discuss whether these nuclei interact to form specific neural circuits that modulate the disease. First-line anti-inflammatory medications remain ineffective for a subset of patients, and current pharmacological interventions targeting neural pathways show limited clinical efficacy.</p><p><strong>Key messages: </strong>A clear elucidation of the neural circuits regulating asthma would advance our understanding of its pathogenesis, offer new directions and targets for drug development, and raise the possibility of treating asthma through direct central nervous system interventions.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"244-260"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of [¹¹¹In]octreotide Scintigraphy and [⁶⁸Ga]DOTATOC PET in Gastroenteropancreatic Neuroendocrine Tumors: Concordance of Krenning Scores and Implications for Peptide Receptor Radionuclide Therapy Eligibility.","authors":"Roberto Fedrigo, Sara Harsini, Luke Murtha, Joao Paulo Solar Vasconcelos, Carlos Uribe, Don Wilson, Francois Benard, Ian Alberts, Patrick Martineau, Jonathan M Loree","doi":"10.1159/000552968","DOIUrl":"10.1159/000552968","url":null,"abstract":"<p><strong>Background: </strong>Peptide receptor radionuclide therapy (PRRT) is an established treatment for somatostatin receptor (SSTR)-positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs), with eligibility determined by the Krenning score. While SSTR PET provides greater sensitivity than octreotide scintigraphy, its impact on PRRT eligibility remains unclear. We compared Krenning scores between [111In]octreotide scintigraphy and [68Ga]DOTATOC PET and assessed eligibility under NETTER-1 and NETTER-2 criteria.</p><p><strong>Methods: </strong>We retrospectively assessed tumor Krenning scores in 115 patients with well-differentiated GEP-NETs who underwent both [111In]octreotide scintigraphy and [68Ga]DOTATOC PET. PRRT eligibility was defined according to NETTER-1 (Krenning ≥2) and NETTER-2 (Krenning ≥3) criteria. Logistic regression identified predictors of Krenning ≥3 on SSTR PET. Quantitative PET analysis was performed for patients with positive baseline [68Ga]DOTATOC PET scans.</p><p><strong>Results: </strong>Median Krenning scores were higher with SSTR PET than planar imaging (3 [IQR 3-4] vs. 2 [IQR 0-3], p < 10-8). NETTER-1 eligibility increased from 59.1% with planar imaging to 81.7% with PET (p < 10-3), and NETTER-2 from 48.7% to 76.5% (p < 10-4). Among patients eligible on planar imaging, 95.6% (NETTER-1) and 98.2% (NETTER-2) had concordant PET findings. Conversely, 61.7% (NETTER-1) and 55.9% (NETTER-2) of patients ineligible on planar imaging were reclassified as eligible with PET. Metastatic disease was associated with higher SSTR PET uptake (odds ratio 9.5 [95% confidence interval: 2.7-32.8], p < 10-3). SUV_max discriminated patients with Krenning ≥3 using an optimal threshold of 9.2 (AUC 0.93).</p><p><strong>Conclusions: </strong>[68Ga]DOTATOC PET yields higher Krenning scores and increases PRRT eligibility compared with [111In]octreotide scintigraphy. PET may be unnecessary for clearly positive planar studies but identifies additional candidates with borderline or negative planar results.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"299-306"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aggressive Pituitary Tumors and Pituitary Carcinomas: A Narrative Review of Clinical Features and Management.","authors":"Barbara Buchalska, Jacek Kunicki","doi":"10.1159/000551557","DOIUrl":"10.1159/000551557","url":null,"abstract":"<p><strong>Background: </strong>Aggressive pituitary tumors (APTs) are commonly defined as invasive neoplasms refractory to treatment with early recurrences, while pituitary carcinomas (PCs) represent a subset of APTs that have developed metastases. However, the diagnostic criteria for APTs remain poorly standardized, and many different classifications of these tumors currently exist. Early and accurate identification of APTs is essential, as these tumors frequently recur and are associated with significant therapeutic challenges.</p><p><strong>Summary: </strong>In this review we provide an overview of different classifications of APTs and summarize the key characteristics and treatment methods for these tumors. Proposed criteria of APTs include histopathological features (such as high Ki-67 index, increased mitotic activity, aggressive histopathological subtypes), genetic alterations (most commonly involving TP53 and ATRX), radiological findings (like invasive behavior, multilobulated morphology, microcystic changes, low signal intensity on T2-weighted magnetic resonance imaging), and clinical characteristics (including rapid growth, early recurrences, resistance to standard therapies). Treatment of APTs typically requires a multimodal approach. Most patients undergo at least one surgical resection, followed by radiotherapy, and in selected cases, pharmacological treatment with temozolomide. Other drugs like immunotherapeutics or cytotoxic agents are also used. In this review we provide an overview of different classifications of APTs and summarize the key characteristics and treatment methods for these tumors.</p><p><strong>Key messages: </strong>Early identification of APTs and PCs may be achieved by integrating histopathological, genetic, radiological, and clinical features.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"307-320"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147458688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Soyasaponin Aa prevents obesity-related precocious puberty by inhibiting hypothalamic-pituitary-gonadal axis in female Sprague-Dawley rats.","authors":"Yunfei Jiang, Wen Xie, Dani Qin, Qiuju Zheng, Huiping Shen, Yong Lei","doi":"10.1159/000550176","DOIUrl":"10.1159/000550176","url":null,"abstract":"<p><strong>Objective: </strong>Early-onset puberty is a major reason for pediatric endocrinology clinics, particularly among girls. Obesity is linked to disruptions in the hypothalamic-pituitary-gonadal (HPG) axis, thereby leading to early-onset puberty. This study was designed to investigate the regulatory effects of soyasaponin Aa in an animal model of obesity-associated precocious puberty.</p><p><strong>Study design: </strong>A rat model of obesity-induced precocious puberty was established through high-fat diet (HFD) feeding, which closely mimics the condition in children caused by excessive caloric intake. Obesity was assessed through body weight, serum lipid levels, and gonadal fat mass. Western blotting was performed to assess key adipogenesis regulators (PPARγ and C/EBPα) in gonadal white adipose tissues. ELISA was used to analyze serum levels of hormones (LH, FSH, and GnRH). The mRNA expression of HPG axis-related genes in the hypothalamus, pituitary gland, and ovary were detected by RT-qPCR. Histopathological changes in ovarian and uterine tissues were examined using hematoxylin and eosin staining.</p><p><strong>Results: </strong>Soyasaponin Aa significantly reduced body weight gain in HFD-fed rats and suppressed increases in serum lipid levels and gonadal white adipose tissue mass. It inhibited HFD-induced lipogenesis, as indicated by reduced expression of PPARγ and C/EBPα. Soyasaponin Aa effectively delayed puberty onset in female rats, as evidenced by prolonged vaginal opening and first estrous cycle, reduced endometrium thickness, and lower uterine and ovarian weights, along with suppressed follicular maturation. The HFD group showed elevated serum LH and FSH levels and increased hypothalamic GnRH secretion, all of which were significantly counteracted by soyasaponin Aa. Moreover, soyasaponin Aa downregulated HPG axis-related gene expression.</p><p><strong>Conclusion: </strong>Soyasaponin Aa protects against obesity-induced precocious puberty by suppressing the activation of HPG axis.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"1-16"},"PeriodicalIF":2.8,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}