Histology and histopathology最新文献

{"title":"Prognostic significance of ACADL and MCM2 in meningiomas: Current evidence and clinical implications.","authors":"Alberto Pietrantoni, Fabio Agistri, Valeria Barresi","doi":"10.14670/HH-25-046","DOIUrl":"10.14670/HH-25-046","url":null,"abstract":"<p><p>This review summarizes the current evidence on the expression and prognostic significance of acyl-CoA dehydrogenase long-chain (ACADL) and minichromosome maintenance 2 (MCM2) in meningiomas. Meningiomas, which comprise approximately 41% of intracranial tumors, are classified by the World Health Organization into 15 histological subtypes and three grades of malignancy. However, owing to the biological heterogeneity within tumors of the same grade, alternative classifications based on molecular features have been proposed. One of these classifies meningiomas into four prognostically relevant molecular groups: immunogenic, benign <i>NF2</i>-wildtype, hypermetabolic, and proliferative. The latter two groups have the worst clinical outcomes and are enriched in ACADL and MCM2 expression, suggesting their potential as immunohistochemical surrogates. The revision of the current literature on the expression of these markers in meningiomas indicates their likely unsuitability as surrogates for molecular groups. However, MCM2 expression was consistently associated with aggressive histopathological features and reduced recurrence-free survival, emerging as a promising independent prognostic marker. ACADL also showed negative prognostic relevance, but with limited data, predominantly in grade 2 meningiomas. Both markers correlated with higher WHO grades but lacked standardized assessment criteria, limiting their clinical application. While ACADL and MCM2 immunoexpression does not reliably substitute molecular classification, MCM2, in particular, holds potential for routine prognostic use pending further validation and standardization of immunohistochemical protocols.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1349-1355"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asiatic acid alleviates dexamethasone-induced muscle atrophy through regulating the Sirt1/PGC-1α/FOXO3 pathway.","authors":"Dongfang Ji, Mingxin Cui, Chao Tian, Kaili Chen, Jing Shao","doi":"10.14670/HH-18-991","DOIUrl":"10.14670/HH-18-991","url":null,"abstract":"<p><strong>Background: </strong>Skeletal muscle atrophy, which results in muscular dysfunction and weakness, is associated with various factors, including aging, sepsis, chronic diseases, and long-term glucocorticoid therapy. Although asiatic acid exhibits multiple biological activities and can activate the Sirt1 signaling pathway, an important regulator of skeletal muscle function,itsrole in muscle atrophy remains unclear.</p><p><strong>Methods: </strong>C2C12 myotubes were treated with 10 μM dexamethasone,with or without designated concentrations of asiatic acid. Subsequently, cell viability, apoptosis, differentiation markers (MyHC and myogenin), levels of atrophy-related proteins (MAFbx, MuRF1), and the Sirt1/PGC-1α/FOXO3 pathway were analyzed. Moreover,the underlyingmechanismswere further explored through inhibition of Sirt1 using the selective inhibitor EX-527 or short hairpin RNA <i>in vitro</i>. <i>In vivo</i>, muscle atrophy was induced via intraperitoneal injections of 20 mg/kg dexamethasone, and 50 mg/kg asiatic acid was administered by oral gavage. Body weight, muscle strength, gastrocnemius muscle mass, histological changes, and atrophy- and Sirt1/PGC-1α/FOXO3 pathway-associated proteins were assessed.</p><p><strong>Results: </strong>Asiatic acid elevated cellviability, inhibited apoptosis, increased MyHC and myogeninprotein contents, and suppressed MAFbx and MuRF1 proteinlevels in dexamethasone-treated C2C12 myotubes. Moreover, asiatic acid activated the Sirt1/PGC-1αp athwayand inactivated FOXO3. Inhibition of Sirt1 attenuated the influence of asiatic acid in a muscle atrophy cell model. <i>In vivo</i>, asiatic acid increased body weight and gastrocnemius muscle mass, improved muscle strength and structural damage of gastrocnemius muscles, suppressed MAFbx and MuRF1 protein contents, and regulated the Sirt1/PGC-1α/FOXO3 pathway.</p><p><strong>Conclusions: </strong>Asiatic acid can improve dexamethasone-induced muscle atrophy via regulating the Sirt1/PGC-1α/FOXO3 pathway. Therefore, asiatic acid might be a potential therapeutic agent for muscle atrophy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1387-1397"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD34⁺ cells contribute to cardiac remodeling during disease development.","authors":"Hanwei Jin, Kai Chen, Qingbo Xu, Xiangyuan Pu","doi":"10.14670/HH-25-042","DOIUrl":"10.14670/HH-25-042","url":null,"abstract":"<p><p>CD34, once considered solely a hematopoietic stem cell marker, is now recognized as a lineage interface identifying distinct tissue-resident progenitor populations that critically influence cardiac homeostasis and pathological remodeling. It has been applied clinically for CD34-targeted therapies, such as cell-capture stents, G-CSF mobilization, and unselected CD34⁺ cell transplantation. However, they fail to discriminate between reparative and pathogenic subsets. Recent advances in lineage tracing, single-cell genomics, and human tissue studies have made major progress in this research field. It has been reported that (1) non-bone marrow-derived endothelial progenitor cells (EPCs) sustain vascular integrity and promote neovascularization; (2) hematopoietic progenitors give rise to inflammatory monocytes, neutrophils, and dendritic cells, orchestrating immune responses after injury; and (3) resident fibroblast progenitor cells (FPCs) differentiate into myofibroblasts and drive interstitial and perivascular fibrosis. During cardiac remodeling, it seems that all types of CD34⁺ cells were involved. In this Review, we integrate histological, mechanistic, and clinical evidence to delineate the diverse CD34⁺ lineages in cardiac remodeling. We discuss how to refine surface-marker panels for isolating endothelial-committed progenitors and exclusion of inflammatory and fibrogenic subsets during cardiac repair. We propose a paradigm shift from generic CD34⁺ cell enrichment toward lineage-specific therapeutic strategies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1357-1366"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunohistological parathormone production changes and angiogenesis in normal and adenomatous human parathyroid glands.","authors":"Teruyuki Sato, Yutaka Tateda, Kazue Ise, Hiroki Shimada, Yusuke Ishida, Takahiro Suzuki, Muneharu Yamazaki, Yasuhiro Nakamura, Nobuo Ohta","doi":"10.14670/HH-25-048","DOIUrl":"10.14670/HH-25-048","url":null,"abstract":"<p><strong>Introduction: </strong>Parathyroid tumor function is not always positively correlated with tumor size, complicating the disease picture. Here, we compared parathormone (PTH) and vascular endothelial growth factor (VEGF)-A expression intensities in normal and adenomatous parathyroid glands, as well as the number of vessels, as determined by CD31 expression.</p><p><strong>Methods: </strong>Eight adenomatous and six normal samples were compared for the expression intensities of PTH and VEGF-A, expression granule area of VEGF-A per unit area (/900 μm²), and number of blood vessels. We then examined relationships between the expression intensities of PTH and VEGF-A and the number of blood vessels.</p><p><strong>Results: </strong>The mean (SD) expression intensities of PTH and VEGF-A were 179.7 (27.5) and 100.6 (13.9) bits, respectively, in the normal group-significantly higher than the 99.0 (37.6) and 73.5 (19.5) bits in the adenoma group (<i>p</i><0.01). The mean (SD) expression granule area of VEGF-A was 86.0 (41.2) μm²/900 μm² in the normal group-significantly higher than the 13.7 (11.5) μm² in the adenoma group (<i>p</i><0.001). The mean (SD) number of blood vessels by CD31 expression was 26.0 (6.9) in the normal group-significantly higher than the 13.9 (8.7) in the adenoma group (<i>p</i><0.05). The mean expression intensity of PTH was positively correlated with the number of blood vessels in the adenoma group (R=0.802, <i>p</i><0.05).</p><p><strong>Conclusion: </strong>Normal parathyroid tissue exhibits significantly higher expression levels of PTH and VEGF-A, along with more blood vessels per unit area, compared with adenomatous tissue.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1367-1375"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide adenine dinucleotide phosphate hydrogen oxidase 2 exacerbates abdominal aortic aneurysm formation by inducing oxidative stress through autophagy inhibition.","authors":"Xiaoliang Yin, Dehai Lang, Songjie Hu","doi":"10.14670/HH-25-049","DOIUrl":"10.14670/HH-25-049","url":null,"abstract":"<p><p>Abdominal aortic aneurysm (AAA) has high mortality and enhanced oxidative stress; autophagy inhibition accelerates its formation. Nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase 2 (NOX2) is responsible for generating reactive oxygen species (ROS). The aim is to clarify the mechanism of NOX2-mediated autophagy in AAA. Subcutaneous angiotensin II (AngII) infusion in ApoE^-/- mice with a high-fat diet was performed to construct an AAA animal model. NOX2 inhibitor GSK2795039 was administered. Following detection of the aortic diameter, HE, Verhoeff's Van Gieson, and MASSON staining were performed to assess pathological damage, elastin, and collagen deposition of the aorta. Immunofluorescence for alpha smooth muscle actin (α-SMA) and light chain 3 (LC3), ELISA for oxidative stress-indicators, and western blot were conducted. <i>In vitro</i>, primary mouse vascular smooth muscle cells (VSMCs) were randomly divided into Control, AngII, AngII+GSK2795039, AngII+rapamycin (autophagy agonist, RA), and AngII+GSK2795039+RA groups. EDU assay, cell scratch assay, and mRFP-GFP-LC3 detection were conducted. ROS was measured by dihydroethidium staining. In AAA mice, aortic diameter, pathological damage, ROS, and NOX2 expression increased, and LC3 expression decreased, which were reversed by GSK2795039. Additionally, AAA mice showed enhanced collagen deposition, osteopontin, malondialdehyde, and p62 expression, and reduced elastin, α-SMA, glutathione peroxidase (GSH-PX), GSH, superoxide dismutase, LC3II/LC3I, and Beclin-1 expression. Notably, in AngII-treated VSMCs, both GSK2795039 and RA decreased cell proliferation, migration, and ROS, and increased the number of autophagosomes and autophagolysosomes. NOX2 inhibitor GSK2795039 decelerated AAA progression by mitigating oxidative stress via the activation of autophagy, providing new potential targets for therapeutic strategies in AAA.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1435-1449"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147270797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naoluotong granules inhibit necroptosis of neural cells and improve cerebral ischemia-reperfusion injury by regulating the RIP1/NIK/IKKα/NF-κB pathway.","authors":"Yajun Li, Wei Dong, Liangyong Li, Wenming Yang","doi":"10.14670/HH-25-035","DOIUrl":"10.14670/HH-25-035","url":null,"abstract":"<p><strong>Background: </strong>Cerebral ischemia-reperfusion can cause structural changes in brain tissue and disrupt physiological functions. Naoluotong granules (NLT) exhibit significant neuroprotective effects on brain nerve cells and are widely utilized in treating cerebral ischemia-reperfusion injury (CIRI). However, the underlying molecular mechanisms remain elusive.</p><p><strong>Methods: </strong>The CIRI model was established <i>in vivo</i>, with rats assigned to four groups. 2,3,5-triphenyltetrazolium chloride (TTC), hematoxylin and eosin (H&E), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were used to evaluate the effects of NLT and AST-IV on neurological function and pathological injury after cerebral ischemia-reperfusion. immunofluorescence, real-time PCR, and Western-blot assays were performed to explore the effects of NLT and AST-IV on the RIP1/NIK/IKKα/NF-κB pathway. The micro-enzyme immunoassay method was applied to examine the expression levels of various factors in each group. To verify the neuroprotective effects of NLT and AST-IV <i>in vitro</i>, an oxygen-glucose deprivation/reoxygenation (OGD/R) PC12 cell model was established and treated with the drug-containing serum of NLT and AST-IV.</p><p><strong>Results: </strong>Necroptosis plays a significant role in the onset and progression of ischemia-reperfusion-induced neural injury. <i>In vivo</i> studies have shown that both NLT and AST-IV improve neurological function scores, reduce infarct volume, and enhance pathological features following MCAO/R. They significantly inhibited the expression of the RIP1/NIK/IKKα/NF-κB pathway, thereby reducing neuronal cell necroptosis. <i>In vitro</i> studies also showed that NLT and AST-IV reduced OGD/R-induced necroptosis.</p><p><strong>Conclusions: </strong>This study confirms that the significant neuroprotective effects of NLT and AST-IV in alleviating CIRI are related to inhibiting necrosis by suppressing the RIP1/NIK/IKKα/NF-κB pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1415-1426"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Approach and nomenclature problems of extracutaneous basaloid neoplasias of visceral organs with three cases of basaloid carcinoma described for the first time in the urinary bladder.","authors":"Yeşim Sağlıcan, Yaşar Ünlü, Kemal Behzatoğlu","doi":"10.14670/HH-25-060","DOIUrl":"10.14670/HH-25-060","url":null,"abstract":"<p><p>Pure basal cell carcinomas/basaloid carcinomas (BCC/BC) from only basal cells in the urinary bladder have not been reported so far. Our aim in this study was to present three BC cases showing distinct pilomatrixoma-like keratinization (matrixial) and sebaceous differentiation in the bladder in transurethral resection material, without urothelial and squamous carcinoma components, and to discuss the concept of BCC/BC in visceral organs. In three cases, it invaded the muscularis propria. Immunohistochemically, Keratin-7 and EMA were almost completely negative, while GATA3 was positive in very few cells. p63, keratin-5,6 and bcl2 were positive in all three tumors. Adipophilin was positive in areas of sebaceous differentiation. BCC/BC are very rare in visceral organs and had different nomenclatures. These show different patterns and variants, and have different nomenclature depending on the histological diversity/embryological development of the organ in which they are localized. We also noticed that adenoid cystic carcinoma and basaloid carcinoma have similar histology and are transitional to each other in many organs, necessitating a common nomenclature.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1377-1385"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147432557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Squamous papilloma of the external ear in Southwest China: A large case series highlighting predominant HPV subtypes, pathologic features, and unique epidemiologic factors.","authors":"Jun Zhou, Tianming Yang, Wenjuan Cheng, Youquan Zhao","doi":"10.14670/HH-25-044","DOIUrl":"10.14670/HH-25-044","url":null,"abstract":"<p><p>Squamous papilloma (SP) of the external ear is a rare benign neoplasm, with limited research on its associated human papillomavirus (HPV) infections and pathologic features. This study aims to provide a comprehensive analysis of the largest case series of external ear SP from Southwest China. We retrospectively collected 88 cases diagnosed with SP in the external ear canal, of which 85 (97%) were located in the external auditory canal and 3 (3%) on the auricle. We investigated the clinical, pathological, and HPV-typing characteristics using Polymerase chain reaction (PCR) and reverse dot blot (RDB) hybridization. Our series included 74 males and 14 females, with a median age of 62.5 years (range: 5-91 years). The predominant HPV type was HPV-6 (59/62, 95.2%), followed by high-risk types HPV-16 (4/62, 6.5%), HPV-52 (2/62, 3.2%), and HPV-58 (1/62, 1.6%). Histologically, all cases demonstrated typical features of SP, including koilocytes, hyperkeratosis, and basal/parabasal hyperplasia. Additionally, co-infection with multiple HPV types was observed in four cases. Notably, high-risk HPV types were detected in seven cases, all of which were completely excised with no recurrence during follow-up. This study suggests regional variations in HPV-subtype distribution and highlights potential environmental factors contributing to the prevalence of SP in Southwest China.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1427-1434"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial distribution of LGR5 expression in normal, ectopic, and neoplastic human endometrium.","authors":"Hyesung Kim, Cheol Lee, Bogun Jang","doi":"10.14670/HH-25-134","DOIUrl":"10.14670/HH-25-134","url":null,"abstract":"<p><strong>Background: </strong>Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) is a well-established stem cell marker in multiple epithelial tissues. However, its spatial distribution and biological relevance in normal and pathological human endometrium remain incompletely defined.</p><p><strong>Materials and methods: </strong>We analyzed LGR5 expression in normal proliferative and secretory endometrium, adenomyosis, endometriosis, endometrial hyperplasia, and endometrioid carcinoma using RNA in situ hybridization on tissue microarrays. Associations with ARID1A loss, β-catenin nuclear expression, and mismatch repair deficiency were evaluated by immunohistochemistry.</p><p><strong>Results: </strong>In normal endometrium, LGR5 expression was spatially compartmentalized, showing consistent enrichment in the luminal epithelium with decreasing expression toward functional and basal glandular regions across menstrual phases. This gradient was preserved in both proliferative and secretory endometrium. In adenomyosis and ovarian endometriosis, LGR5 remained highly expressed in luminal-type epithelial linings, recapitulating the topographic pattern observed in ectopic endometrium. In endometrial hyperplasia and endometrioid carcinoma, LGR5 expression demonstrated inter-sample variability but showed no significant differences compared with normal luminal epithelium. Furthermore, LGR5 expression was not associated with ARID1A loss, β-catenin dysregulation, or mismatch repair deficiency.</p><p><strong>Conclusions: </strong>LGR5 expression in the human endometrium shows a consistent spatial distribution, with enrichment in the luminal epithelial compartment across normal, ectopic, and neoplastic conditions. No clear association was identified between LGR5 expression and key molecular alterations in endometrioid carcinoma. These findings support a descriptive role for LGR5 as a compartment-associated epithelial marker and provide a basis for future functional studies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25134"},"PeriodicalIF":2.2,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights into solitary bronchial mucosal neuroma: A case report and literature review.","authors":"Dan Gao, Lei Han, Guijie Guan, Weijia Han, Li Shi, Yunshuang Liu, Ying Wu","doi":"10.14670/HH-25-132","DOIUrl":"https://doi.org/10.14670/HH-25-132","url":null,"abstract":"<p><p>Solitary bronchial mucosal neuroma is an exceptionally rare benign neurogenic tumor, with only four cases reported to date. Its etiology remains unclear, and histologically it resembles a traumatic neuroma despite arising in the absence of prior injury or surgery. Here, we present the fourth reported case of solitary bronchial mucosal neuroma and review all documented cases to better characterize its clinicopathological features and pathogenesis. Case Presentation. A 58-year-old man with a history of pulmonary tuberculosis presented with cough, purulent sputum, and hemoptysis. Imaging and bronchoscopy revealed a yellowish-white endobronchial lesion causing luminal stenosis. Histological examination of biopsy specimens demonstrated disorganized nerve bundles beneath the mucosa, comprising S-100-positive Schwann cells and neurofilament-positive axons, with variable epithelial membrane antigen-positive perineurial cells. Screening for multiple endocrine neoplasia type 2B (MEN2B) and other syndromic associations was negative. Wedge resection additionally revealed an incidental 2 mm carcinoid tumorlet. Conclusion. Solitary bronchial mucosal neuroma predominantly affects middle-aged to elderly individuals, often in the context of chronic inflammatory lung disease. It likely represents a traumatic neuroma of autonomic origin, with chronic inflammation playing a contributory role. Solitary bronchial mucosal neuroma should be considered in the differential diagnosis of endobronchial lesions and may coexist with carcinoid tumors. The lesion follows a benign course and is curable with complete resection. Further studies are needed to elucidate its pathogenesis and clinical spectrum.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25132"},"PeriodicalIF":2.2,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148602423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}