Histology and histopathology最新文献

{"title":"Comparative insights into miRNA-mediated repair across nervous system injuries: Implications for histology and regenerative medicine.","authors":"Yueru Shen, Bing Hu","doi":"10.14670/HH-25-136","DOIUrl":"https://doi.org/10.14670/HH-25-136","url":null,"abstract":"<p><p>Neural regeneration in the adult mammalian central nervous system (CNS) is severely restricted by both intrinsic neuronal limitations and an inhibitory post-injury microenvironment. In contrast, the peripheral nervous system (PNS) retains a greater capacity for spontaneous repair. MicroRNAs (miRNAs), a class of small non-coding RNAs, have emerged as key epigenetic regulators of neural regeneration by coordinately modulating multiple genes and signaling pathways involved in axonal growth, neuroinflammation, glial responses, and tissue remodeling. This review summarizes current advances in miRNA-mediated neural repair across both the CNS and PNS, with particular emphasis on their dual roles in regulating intrinsic neuronal growth programs and the extrinsic injury microenvironment. We compare distinct miRNA expression patterns and regenerative mechanisms following neural injury in mammalian and regenerative model systems, highlighting their contributions to axonal regeneration, immune modulation, angiogenesis, and Schwann cell-mediated repair. We further discuss emerging delivery strategies, including exosome-based systems, functionalized nanomaterials, and scaffold-assisted platforms, which improve miRNA stability, targeting efficiency, and therapeutic efficacy. Finally, we examine the major challenges limiting clinical translation, including RNA instability, blood-brain barrier penetration, delivery specificity, and potential off-target effects. Collectively, current evidence suggests that miRNA-based interventions represent a promising therapeutic avenue for neural regeneration and provide new opportunities for developing precision regenerative strategies for nervous system injuries.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25136"},"PeriodicalIF":2.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989884","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":"Cathelicidin LL-37 inhibits angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signaling.","authors":"Hui Luo, Shan Li, Heng Du, Weimin Yang, Lijuan You, Dujuan Mao","doi":"10.14670/HH-25-135","DOIUrl":"https://doi.org/10.14670/HH-25-135","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, often diagnosed at advanced stages with limited therapeutic options. Cathelicidin LL-37, an antimicrobial peptide, has demonstrated context-dependent roles in cancer progression. This study aimed to elucidate the function and underlying mechanism of LL-37 in GC, with a focus on angiogenesis and metastasis.</p><p><strong>Methods: </strong>The effects of LL-37 were investigated in GC cell lines (HGC27, MKN74, AGS, HSC-39, NCI-N87) and mouse models. <i>In vitro</i> assays included the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, wound healing assay, Transwell assay, tube formation assay, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (RT-qPCR), western blot, immunofluorescence staining, and chromatin immunoprecipitation (ChIP). Metastasis and xenograft models were established in nude mice to assess the anti-tumor efficacy of LL-37 <i>in vivo</i>.</p><p><strong>Results: </strong>LL-37 significantly suppressed the viability of multiple GC cell lines and downregulated the expression of interleukin-6 (IL-6) and vascular endothelial growth factor A (VEGFA). Functionally, LL-37 inhibited angiogenesis, migration, and invasion of GC cells, and attenuated transforming growth factor (TGF)-β-induced pro-metastatic effects. These inhibitory effects were reversed by IL-6 overexpression. Mechanistically, LL-37 inactivated the nuclear factor-κB (NF-κB) pathway, as evidenced by reduced p65 phosphorylation, impaired nuclear translocation, and decreased binding to the IL-6 promoter. The NF-κB inhibitor BAY 11-7082 mimicked the suppressive effects of LL-37. <i>In vivo</i>, LL-37 administration markedly reduced lung metastasis and decreased the levels of IL-6, VEGFA, and phospho-p65 in xenograft tumors.</p><p><strong>Conclusion: </strong>LL-37 inhibits angiogenesis, migration, and invasion in GC by suppressing the NF-κB/IL-6 signaling axis. This work provides a rationale for considering LL-37 as a potential therapeutic candidate.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25135"},"PeriodicalIF":2.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976729","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":"Protective effects of <i>Abelmoschus manihot</i> flower extracts against blue light-emitting diode light-induced retinal photoreceptor cell damage <i>in vivo</i> and <i>in vitro</i>.","authors":"Li Ling Wu, Szu-Yu Lung, Wei-Hao Peng","doi":"10.14670/HH-25-052","DOIUrl":"10.14670/HH-25-052","url":null,"abstract":"<p><strong>Background: </strong>Excessive exposure to blue light (BL) from light-emitting diodes (LEDs) induces oxidative stress and photoreceptor degeneration, contributing to retinal damage. <i>Abelmoschus manihot</i> flower extract (AME), rich in flavonoids, possesses antioxidant and anti-inflammatory properties; however, its protective effects on the retina have not been fully elucidated.</p><p><strong>Methods: </strong>We investigated the protective effects of AME <i>in vivo</i> using a BL-induced retinal damage model in C57BL/6J mice and <i>in vitro</i> using hydrogen peroxide (H₂O₂)-induced oxidative stress in 661W photoreceptor cells. Retinal morphology, synaptic integrity, and oxidative stress markers were assessed through histology, immunohistochemistry, and transmission electron microscopy. <i>In vitro</i> analyses included cell viability assays, TUNEL staining, reactive oxygen species (ROS) measurement, and evaluation of nuclear factor erythroid 2-related factor 2 (Nrf2) expression and localization.</p><p><strong>Results: </strong>AME pretreatment preserved the structural integrity of the photoreceptor layer, maintained outer segment and synaptic ribbon architecture, and reduced 8-hydroxy-2'-deoxyguanosine (8-OHdG) accumulation in BL-exposed retinas. In 661W cells, AME enhanced cell viability, decreased apoptosis, and attenuated ROS production. Furthermore, AME upregulated Nrf2 expression and promoted its nuclear translocation, suggesting activation of the antioxidant response pathway.</p><p><strong>Conclusions: </strong>AME exerts protective effects against BL-induced retinal degeneration and oxidative stress-induced photoreceptor apoptosis, potentially through activation of the Nrf2 pathway. These findings highlight the therapeutic potential of AME in preventing or mitigating retinal damage associated with oxidative stress.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1569-1584"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305190","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":"Urolithin A mitigates doxorubicin-induced myocardial injury via suppression of ROS-driven apoptotic signaling.","authors":"Wei Song, Mei Chen, Lin Pang, Jincheng Wu, Xianxing Zhao, Tianyao Ma, Pu Zhang, Hong Yang, Xianjun Wang","doi":"10.14670/HH-25-054","DOIUrl":"10.14670/HH-25-054","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin (DOX), as a broad-spectrum antitumor drug, achieved great success in the clinic. Nevertheless, severe adverse effects, in particular cardiac toxicity, significantly restrict its clinical utilization. Urolithin A (UA), a metabolite produced by the metabolic activity of intestinal microorganisms on pomegranates, exerts novel protective potential against cardiovascular disease. However, the inhibitory effect of UA against DOX-mediated cardiotoxicity has not been fully explored. Herein, the protective effect and mechanism of UA against DOX-induced cardiotoxicity <i>in vitro</i> and <i>in vivo</i> were investigated.</p><p><strong>Methods: </strong>The effects of UA and DOX on cell activity and cell apoptosis were assessed by cell counting Kit-8 (CCK-8), flow cytometry, and Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) staining. Reactive oxygen species (ROS) were examined by fluorescent probes. Protein expression was detected by western blotting. A cardiotoxicity rat model was established via injection of DOX to evaluate the <i>in vivo</i> protective mechanism.</p><p><strong>Results: </strong>DOX induced obvious ROS-mediated oxidative damage and ultimately led to H9c2 cell apoptosis <i>in vitro</i> and myocardial dysfunction <i>in vivo</i>. However, UA-cotreatment effectively mitigated DOX-induced oxidative damage and apoptosis by regulating the Nrf2 pathway and Bcl-2 family expression, inhibiting ROS, superoxide anions, and MDA generation, enhancing GSH content, and downregulating the ATR-p53 pathway <i>in vitro</i>. Furthermore, UA administration also promoted eNOS activity, inhibited myocardial abnormal proliferation and fibrosis, and improved myocardial function <i>in vivo</i>.</p><p><strong>Conclusion: </strong>Our findings validated the rational design that UA has the potential to mitigate DOX-induced myocardial injury <i>in vitro</i> and <i>in vivo</i> by inhibiting ROS-driven apoptosis, which yields significant insights for combating DOX-mediated myocardial injury.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1585-1596"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348115","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":"Advances and challenges in developing expandable human hepatocytes for regenerative medicine.","authors":"Saaya Yamane, Masaki Nishikawa, Yasuyuki Sakai, Takeshi Katsuda","doi":"10.14670/HH-25-051","DOIUrl":"10.14670/HH-25-051","url":null,"abstract":"<p><p>Liver transplantation remains the only effective treatment for severe liver disease, but donor shortages pose a serious challenge, underscoring the need for alternative therapeutic strategies. Hepatocyte transplantation has been proposed as a promising alternative; however, the lack of expandable cell sources remains a major obstacle. Considerable efforts have been made to establish culture systems that can preserve both the proliferative capacity and functional properties of hepatocytes. Recent advances in expandable hepatocytes and organoid technologies have shown partial success in repopulating injured mouse livers. However, achieving both sufficient cell numbers and robust repopulation efficiency has remained difficult, preventing clinical translation. Furthermore, when cells are transplanted, the engraftment success and replacement efficiency significantly influence the extent of repopulation. In this review, we first revisit the history of hepatocyte transplantation, then summarize recent progress in hepatocyte expansion technologies, and finally discuss the remaining challenges toward clinical application.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1471-1481"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283447","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":"Inverted urothelial papilloma: Diagnostic challenges, molecular insights, and clinical implications.","authors":"Keiichiro Kitahama, Kentaro Inamura","doi":"10.14670/HH-25-058","DOIUrl":"10.14670/HH-25-058","url":null,"abstract":"<p><p>Inverted urothelial papilloma (IUP) is a rare benign tumor of the urinary tract, most commonly arising in the bladder and characterized by an endophytic growth pattern. IUP primarily affects middle-aged and older men and typically presents with painless hematuria. IUP was first described in 1927 and recognized as an independent entity by the World Health Organization in 1973. It can be difficult to distinguish from urothelial carcinoma (UC), which can result in misdiagnosis and overtreatment. Genetic analyses have confirmed the benign nature of IUP. Activating mutations in RAS family genes (<i>HRAS, KRAS, NRAS</i>) are frequent in IUP, whereas mutations typical of UC, such as <i>FGFR3, TP53,</i> and <i>TERT</i> promoter alterations, are rare. Macroscopically, lesions are generally small, solitary, and broad-based. Histologically, IUP exhibits two architectural patterns: trabecular and glandular, which both show minimal atypia and low mitotic activity. Differentiating IUP from UC with inverted growth and benign mimickers, such as florid von Brunn's nests or cystitis cystica/glandularis, is challenging, particularly when specimen size is limited. Immunohistochemistry (KRT20, TP53, and Ki-67) may support the diagnosis but does not reliably distinguish IUP from UC in difficult cases. The standard treatment is complete transurethral resection, and recurrence rates are low. The superficial urothelial cells overlying IUP may also harbor <i>RAS</i> mutations, challenging the long-held assumption that these cells are morphologically and genetically normal. Future studies should investigate whether similar genetic alterations in morphologically normal urothelium occur in other urothelial tumors. This could refine understanding of early tumorigenesis and guide improved detection and risk assessment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1483-1491"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389921","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":"Mechanism and experimental validation of a network pharmacology-based approach of Huoluo Yinao formula in treating chronic cerebral hypoperfusion.","authors":"Song Yang, Junpeng Li, Wen Nie, Sen Chen, Haitao Song, Dewen Song, Bo Zhao","doi":"10.14670/HH-25-055","DOIUrl":"10.14670/HH-25-055","url":null,"abstract":"<p><p>Chronic cerebral hypoperfusion (CCH) is a cerebral dysfunction caused by insufficient cerebral perfusion, and Huoluo Yinao (HLYN) formula is a traditional Chinese medicinal formula used for CCH treatment. We investigated the specific mechanism of HLYN formula on CCH through network pharmacological analysis and <i>in vivo</i> experiments. The active ingredients and drug targets of HLYN formula obtained through network pharmacological analysis were subjected to molecular docking with disease targets of CCH. Wistar male rats (six weeks) were used to establish a CCH rat model by the two-vessel occlusion (2VO) method. The rats were treated with HLYN alone or in combination with the HSP90AA1 overexpression vector before behavior tests. The groups were as follows: Sham group, CCH group, CCH+HLYN group, CCH+HLYN+oe-NC group, and CCH+HLYN+oe-HSP90AA1 group, with six rats in each group. The hippocampal tissues were assessed after Hematoxylin and eosin (H&E) and Nissl stainings. Autophagosomes were observed using immunofluorescence and transmission electron microscopy. There were 83 active ingredients and 1339 potential pharmacological targets in HLYN formula, while 3175 genes were found associated with CCH. A total of 235 overlapped genes were obtained. Rats in the CCH+HLYN group showed shortened escaping latency, increased times in the target quadrant, and increased number of platform crossings, along with attenuated tissue injury, elevated Nissl-positive neurons and less apoptosis. In addition, inflammation and oxidative stress (OS) were decreased in the CCH+HLYN group, evidenced by reduced malondialdehyde (MDA), Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-6 and IL-1β, and increased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), and IL-10 expression. HLYN formula led to suppressed HSP90AA1 expression and autophagy, along with increased p-PI3K/p-AKT/p-mTOR protein expression. The phenotypes in the CCH+HLYN group can be reversed by further treatment with HSP90AA1 overexpression. HLYN formula can inhibit HSP90AA1 expression to inhibit autophagy, inflammation, and OS, which in turn contributes to attenuating cognitive impairment in CCH rats.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1597-1612"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354805","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":"Regulation of G Protein Signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway.","authors":"Gang Zhou, Changquan Wang, Wenyi Bai, Ju Gao, Yugao Liao, Lei Wang, Xiangbo Wu, Yu Tian, Guanglin Wang, Guangming Xia, Jinhua Wang","doi":"10.14670/HH-25-018","DOIUrl":"10.14670/HH-25-018","url":null,"abstract":"<p><strong>Background: </strong>Stroke is a crucial cause of morbidity and mortality worldwide. The regulator of G protein signaling 14 (RGS14) plays important roles in mediating multiple signaling pathways and various pathophysiological processes. However, the function of RGS14 in cerebral ischemic reperfusion injury (CIRI) remains unknown.</p><p><strong>Methods and results: </strong>In this study, the roles of RGS14 during CIRI were studied in terms of gain- and loss-of-function experiments. Using RT-PCR, western blot, and TCC, HE, TUNEL, immunofluorescence, immunohistochemical staining, etc., we found that RGS14 significantly improved CIRI by reducing inflammation and apoptosis in both a mouse model of transient middle cerebral artery occlusion (t/MCAO) and a primary neuronal model of oxygen-glucose deprivation/reperfusion (OGD/R). In addition, mechanism studies have shown that RGS14 acts by inhibiting the activation of the TAK1-JNK/p38 signaling pathway, which was further confirmed using the TAK1 inhibitor (iTAK1), 5Z-7-oxyzeaenol, during OGD/R treatment of Adsh<i>RGS14</i>-infected primary neurons.</p><p><strong>Conclusions: </strong>These findings imply that RGS14 is a novel negative regulator and may serve as a potential therapeutic target for CIRI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1527-1540"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145563684","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":"Acupuncture alleviates the progression of lumbar disc herniation by regulating the autophagy level of nucleus pulposus cells through the SIRT1/Sestrin2 pathway.","authors":"Xiaoyan Wang, Jia Lu, Pengyue Zhang, Yiming Zhang, Caiyan Li, Tao Zhang, Xianzhi Chen, Hangqi Zheng, Jie Yang, Ming Jing","doi":"10.14670/HH-25-050","DOIUrl":"10.14670/HH-25-050","url":null,"abstract":"<p><strong>Background and purpose: </strong>Lumbar disc herniation (LDH) is a degenerative spine disease and the most common cause of lower back pain, with a high prevalence in younger patients. The use of acupuncture (AC) as a conservative treatment for LDH has received widespread attention at home and abroad. Therefore, the present study aimed to investigate the specific mechanism of AC in the treatment of LDH.</p><p><strong>Methods: </strong>In this study, we established an LDH rat model via autologous nucleus pulposus (NP) transplantation and treated human NP cells with 50 μM tert-butyl hydroperoxide (TBHP) for 24h to establish an LDH cell model for experimental investigation. The damage to human NP cells and the development of LDH in rats were evaluated via CCK-8, flow cytometry, H&E staining, and Safranin O-Fast Green staining, and the expression of related proteins was detected via western blotting.</p><p><strong>Results: </strong>This study revealed that AC promoted the protein expression of Collagen II, Bcl-2, LC3II/I, and Beclin1, and inhibited the protein expression of Bax, Cleaved Caspase-3, and p62, thereby improving the pathological condition of lumbar NP tissue in rats and alleviating LDH progression. In addition, SIRT1 and Sestrin2 are expressed at low levels in LDH, and the overexpression of SIRT1 or Sestrin2 can improve NP cell viability and inhibit cell apoptosis by activating autophagy. Mechanistically, AC inhibits the MDM2-mediated ubiquitination of Sestrin2 by upregulating SIRT1 expression, thereby promoting Sestrin2 expression, activating autophagy, and ultimately alleviating the development of LDH.</p><p><strong>Conclusion: </strong>AC relieves the development of LDH by activating the SIRT1/Sestrin2 autophagy pathway. Our study provides a new molecular mechanism for the AC treatment of LDH.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1555-1568"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147276117","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":"Do patterns of perineural invasion improve risk stratification in prostate cancer? A narrative review.","authors":"Hiroshi Miyamoto","doi":"10.14670/HH-25-061","DOIUrl":"10.14670/HH-25-061","url":null,"abstract":"<p><p>The presence of perineural invasion (PNI), typically defined as direct contact between cancer cells and nerves, is a well-established adverse prognostic factor following definitive treatment when identified on prostate needle core biopsy. In contrast, there are mixed data regarding the clinical significance of PNI detected in radical prostatectomy specimens. Beyond the mere presence of PNI in prostate cancer specimens, several studies have suggested that quantification of the number of PNI foci may provide additional prognostic information. Nonetheless, it remains controversial whether the patterns of PNI contribute meaningfully to the risk stratification of prostate cancer. Notably, the definition of PNI appears to remain inconsistent among pathologists, ranging from broad interpretations of focal tumor involvement in or around a nerve to strict criteria requiring complete circumferential nerve encirclement. This narrative review summarizes and discusses available data supporting or refuting the clinical impact of PNI patterns, including size, degree, or other morphologic features, in men with prostate cancer. Current evidence indicates that, at least on prostate biopsy, PNI patterns generally lack independent clinical utility, while significant data exist to support the prognostic relevance of PNI patterns in radical prostatectomy specimens (and several other types of solid tumors). Until further studies providing more solid evidence are available, it may be prudent for pathologists to document and consider any patterns as PNI, especially in prostate biopsy specimens.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1507-1514"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443626","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}