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In the realm of marine environmental engineering, the swift and accurate detection of underwater targets is of considerable significance. Recently, methods based on Convolutional Neural Networks (CNN) have been applied to enhance the detection of such targets. However, deep neural networks usually require a large number of parameters, resulting in slow processing speed. Meanwhile, existing methods present challenges in accurate detection when facing small and densely arranged underwater targets. To address these issues, we propose a new neural network model, YOLOv8-LA, for improving the detection performance of underwater targets. First, we design a Lightweight Efficient Partial Convolution (LEPC) module to optimize spatial feature extraction by selectively processing input channels to improve efficiency and significantly reduce redundant computation and storage requirements. Second, we developed the AP-FasterNet architecture for small targets that are commonly found in underwater datasets. By integrating depth-separable convolutions with different expansion rates into FasterNet, AP-FasterNet enhances the model's ability to capture detailed features of small targets. Finally, we integrate the lightweight and efficient content-aware reorganization (CARAFE) up-sampling operation into YOLOv8 to enhance the model performance by aggregating contextual information over a large perceptual field and mitigating information loss during up-sampling.Evaluation results on the URPC2021 dataset show that the YOLOv8-LA model achieves 84.7% mean accuracy (mAP) on a single Nvidia GeForce RTX 3090 and operates at 189.3 frames per second (FPS), demonstrating that it outperforms existing state-of-the-art methods in terms of performance. This result demonstrates the model's ability to ensure high detection accuracy while maintaining real-time processing capabilities.
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BACKGROUND: Bladder cancer (BC), a prevalent malignancy in the urinary system, often poses challenges for effective treatment. Immunotherapy, harnessing the immune system, has exhibited promise in early-stage clinical trials. Mucosal associated invariant T (MAIT) cells, a subset of immune cells implicated in various diseases, including certain cancer, have yet to be explored in BC patients. We aimed to investigate the quantity, function, and anti-tumor effects of MAIT cells in BC patients. METHODS: A total of 75 newly diagnosed BC patients and 183 healthy volunteers were included. Blood samples were collected and analyzed to evaluate the quantity and function of MAIT cells. Surgical resection provided BC tissues for further analysis, and the clinical features of BC tumors were collected and their relationship with MAIT cells was explored. RESULTS: MAIT cells were identified in both healthy individuals and BC patients. The proportion of MAIT cells in the peripheral blood of BC patients did not significantly differ from that of healthy controls. However, the study revealed a correlation between the proportion of IFN-γ producing MAIT cells and tumor number and invasion in BC patients. Furthermore, MAIT cells exhibited cytotoxic effects on BC cells in vitro and in vivo. CONCLUSIONS: This study sheds light on the role of MAIT cells in BC. While the quantity of MAIT cells showed no significant change in BC patients, their functional attributes and association with tumor characteristics suggest their potential as an immunotherapy target in BC treatment.
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Células T Invariantes Asociadas a Mucosa , Neoplasias de la Vejiga Urinaria , Humanos , Neoplasias de la Vejiga Urinaria/inmunología , Neoplasias de la Vejiga Urinaria/patología , Neoplasias de la Vejiga Urinaria/terapia , Células T Invariantes Asociadas a Mucosa/inmunología , Masculino , Femenino , Persona de Mediana Edad , Anciano , Animales , Interferón gamma/metabolismo , Adulto , Línea Celular Tumoral , Inmunoterapia/métodos , Ratones , Citotoxicidad InmunológicaRESUMEN
BRCAT54 and miR-130b-3p are two recently characterized critical players in cancer biology, while their functions in prostate cancer (PC) are unknown. From preliminary sequencing analysis, we observed altered expression of BRCAT54 and miR-130b-3p in PC and an inverse correlation between them. This study was conducted to explore their involvement in PC. A total of 64 PC patients were enrolled to collect paired PC and nontumor tissues. The expression of BRCAT54 and miR-130b-3p were determined by RT-qPCR. Overexpression of BRCAT54 and miR-130b-3p was achieved in PC cells to explore their roles in regulating the expression of each other. Methylation-specific PCR (MSP) was conducted to explore the role of BRCAT54 in regulating promoter methylation of miR-130b-3p. BrdU assay was used to evaluate the role of BRCAT54 and miR-130b-3p in regulating PC cell proliferation. The results showed that PC tissues exhibited downregulation of BRCAT54 and upreglation of miR-130b-3p compared to that in nontumor tissues. They were inversely correlated across PC tissue samples. Overexpression of BRCAT54 decreased RNA accumulation of miR-130b-3p in PC cells. In addition, overexpression of BRCAT54 increased promoter methylation of miR-130b-3p. Moreover, BRCAT54 suppressed the role of miR-130b-3p in promoting PC cell proliferation. In conclusion, BRCAT54 is downregulated in PC and it may inhibit cancer cell proliferation by downregulating miR-130b-3p through methylation.
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MicroARNs , Neoplasias de la Próstata , ARN Largo no Codificante , Masculino , Humanos , MicroARNs/genética , MicroARNs/metabolismo , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Neoplasias de la Próstata/genética , Metilación , Proliferación CelularRESUMEN
Substantial progress has been made in cancer biology and treatment in recent years, but the clinical outcome of patients with renal cell carcinoma (RCC) remains unsatisfactory. The tumor microenvironment (TME) is a potential target. By analyzing single-cell RNA sequencing (sc-RNAseq) data from six RCC tumor samples, this study identified 11 different cell types in the RCC cellular microenvironment, indicating a high degree of intratumoral heterogeneity. Through re-dimensionality reduction clustering of epithelial cells, neutrophils, macrophages, and T cells, we deeply reveal differences in the RCC tumor microenvironment. By analyzing differentially expressed genes in normal epithelial cells and malignant epithelial cells, we identify RNASET2 and GATM as potential prognostic biomarkers in RCC. In addition, by transcriptional factor analysis, we found significant differences in the expression of GZMK-CD8 T cell and B cell transcription factors between cancer tissues and normal tissues. By cell correlation analysis, we found significant correlations between neutrophils and macrophages and between IL7R-CD4 T cells and T regulatory (Treg) cells in RCC, which may be involved in the formation of immune TMEs. By cell developmental trajectory analysis, we showed that macrophages may be derived from neutrophils, whereas Treg cells may be derived from IL7R-CD4 T cells. By cell communication analysis, we found a clear interaction between macrophages and endothelial cells, neutrophils, and GZMK-CD8 T cells. In addition, we found that ADGRE5 signaling was mainly derived from mast cells and GZMK-CD8 T cells, and had a significant communication effect with neutrophils. The COLLAGEN signaling pathway is mainly derived from fibroblasts and has a significant communication effect with mast cells. Finally, we verified that RNASET2, which is highly expressed in epithelial cells, promotes proliferation and migration of RCC in vitro. RNASET2 is likely to be a potential target for renal cell carcinoma therapy. The results based on sc-RNAseq data analysis help to further elucidate the cellular microenvironment of RCC and provide help for cancer heterogeneity studies. This will help to provide more accurate personalized treatment for patients in clinical diagnosis.
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Carcinoma de Células Renales , Neoplasias Renales , Humanos , Carcinoma de Células Renales/genética , Carcinoma de Células Renales/metabolismo , Carcinoma de Células Renales/patología , Neoplasias Renales/genética , Neoplasias Renales/metabolismo , Neoplasias Renales/patología , RNA-Seq , Células Endoteliales/metabolismo , Células Endoteliales/patología , Análisis de Expresión Génica de una Sola Célula , Microambiente Tumoral/genéticaRESUMEN
BACKGROUND: Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in various cancers including bladder cancer (BC). The precise expression pattern of lncRNA small nucleolar RNA host gene 18 (SNHG18) in BC and its mechanisms of action have not been fully explored. MATERIALS AND METHODS: The expression of SNHG18 was evaluated by RT-qPCR in bladder cancer clinical samples and human bladder cancer cell lines, and stable cell lines overexpressing SNHG18 were constructed. The effect of SNHG18 on the proliferation of bladder cancer cells was detected by soft agar colony formation test, ATP activity test and subcutaneous tumorigenesis model in nude mice. The specific mechanism of SNHG18 inhibition of bladder cancer proliferation was studied by flow cytometry, western blotting, dual luciferase reporter gene assay and protein degradation assay. RESULTS: We found that SNHG18 is significantly downregulated in BC tissues and cell lines. Kaplan-Meier analysis showed that SNHG18 expression is positively correlated with survival in BC patients. Ectopic overexpression of SNHG18 significantly inhibited the proliferation of BC cells in vitro and in vivo. Further mechanistic investigations demonstrated that SNHG18 inhibited c-Myc expression by modulating the ubiquitination-proteasome pathway and that c-Myc is the critical transcription factor that mediates SNHG18 inhibition of BC growth by directly binding to the p21 promoter, which was attributed with significant p21 accumulation. CONCLUSIONS: SNHG18 promotes the transcription and expression of p21 by inhibiting c-Myc expression, leading to G0-G1 arrest and inhibiting the proliferation of bladder cancer cells. These findings highlight a novel cell cycle regulatory mechanism involving the SNHG18/c-Myc/p21 pathway in BC pathogenesis and could potentially lead to new lncRNA-based diagnostics and/or therapeutics for BC.
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BACKGROUND: Emerging evidence shows that periodontal disease (PD) may increase the risk of Coronavirus disease 2019 (COVID-19) complications. Here, we undertook a two-sample Mendelian randomization (MR) study, and investigated for the first time the possible causal impact of PD on host susceptibility to COVID-19 and its severity. METHODS: Summary statistics of COVID-19 susceptibility and severity were retrieved from the COVID-19 Host Genetics Initiative and used as outcomes. Single nucleotide polymorphisms associated with PD in Genome-wide association study were included as exposure. Inverse-variance weighted (IVW) method was employed as the main approach to analyze the causal relationships between PD and COVID-19. Three additional methods were adopted, allowing the existence of horizontal pleiotropy, including MR-Egger regression, weighted median and weighted mode methods. Comprehensive sensitivity analyses were also conducted for estimating the robustness of the identified associations. RESULTS: The MR estimates showed that PD was significantly associated with significantly higher susceptibility to COVID-19 using IVW (OR = 1.024, P = 0.017, 95% CI 1.004-1.045) and weighted median method (OR = 1.029, P = 0.024, 95% CI 1.003-1.055). Furthermore, it revealed that PD was significantly linked to COVID-19 severity based on the comparison of hospitalization versus population controls (IVW, OR = 1.025, P = 0.039, 95% CI 1.001-1.049; weighted median, OR = 1.030, P = 0.027, 95% CI 1.003-1.058). No such association was observed in the cohort of highly severe cases confirmed versus those not hospitalized due to COVID-19. CONCLUSIONS: We provide evidence on the possible causality of PD accounting for the susceptibility and severity of COVID-19, highlighting the importance of oral/periodontal healthcare for general wellbeing during the pandemic and beyond.
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COVID-19 , Enfermedades Periodontales , COVID-19/genética , Estudio de Asociación del Genoma Completo , Humanos , Análisis de la Aleatorización Mendeliana , Enfermedades Periodontales/complicaciones , Enfermedades Periodontales/genética , Polimorfismo de Nucleótido SimpleRESUMEN
Metastasis of bladder cancer is a complex process and has been associated with poor clinical outcomes. However, the mechanisms of bladder cancer metastasis remain largely unknown. The present study found that the long noncoding RNA lnc00892 was significantly downregulated in bladder cancer tissues, with low lnc00892 expression associated with poor prognosis of bladder cancer patients. Lnc00892 significantly inhibited the migration, invasion, and metastasis of bladder cancer cells in vitro and in vivo. In-depth analysis showed that RhoA/C acted downstream of lnc00892 to inhibit bladder cancer metastasis. Mechanistically, lnc00892 reduces nucleolin gene transcription by competitively binding the promoter of nucleolin with c-Jun, thereby inhibiting nucleolin-mediated stabilization of RhoA/RhoC mRNA. Taken together, these findings provide novel insights into understanding the mechanisms of bladder cancer metastasis and suggest that lnc00892 can serve as a potential therapeutic target in patients with invasive bladder cancer.
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Regulación Neoplásica de la Expresión Génica , Fosfoproteínas/metabolismo , Proteínas Proto-Oncogénicas c-jun/metabolismo , ARN Largo no Codificante/metabolismo , Proteínas de Unión al ARN/metabolismo , Neoplasias de la Vejiga Urinaria/patología , Proteína de Unión al GTP rhoA/metabolismo , Proteína rhoC de Unión a GTP/metabolismo , Animales , Apoptosis , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Proliferación Celular , Femenino , Humanos , Ratones , Ratones Desnudos , Invasividad Neoplásica , Metástasis de la Neoplasia , Fosfoproteínas/genética , Proteínas Proto-Oncogénicas c-jun/genética , ARN Largo no Codificante/genética , Proteínas de Unión al ARN/genética , Células Tumorales Cultivadas , Neoplasias de la Vejiga Urinaria/genética , Neoplasias de la Vejiga Urinaria/metabolismo , Ensayos Antitumor por Modelo de Xenoinjerto , Proteína de Unión al GTP rhoA/genética , Proteína rhoC de Unión a GTP/genética , NucleolinaRESUMEN
Although MIR516A has been reported to be downregulated and act as a tumor suppressor in multiple cancers, its expression and potential contribution to human bladder cancer (BC) remain unexplored. Unexpectedly, we showed here that MIR516A was markedly upregulated in human BC tissues and cell lines, while inhibition of MIR516A expression attenuated BC cell monolayer growth in vitro and xenograft tumor growth in vivo, accompanied with increased expression of PHLPP2. Further studies showed that MIR516A was able to directly bind to the 3'-untranslated region of PHLPP2 mRNA, which was essential for its attenuating PHLPP2 expression. The knockdown of PHLPP2 expression in MIR516A-inhibited cells could reverse BC cell growth, suggesting that PHLPP2 is a MIR516A downstream mediator responsible for MIR516A oncogenic effect. PHLPP2 was able to mediate BECN1/Beclin1 stabilization indirectly, therefore promoting BECN1-dependent macroautophagy/autophagy, and inhibiting BC tumor cell growth. In addition, our results indicated that the increased autophagy by attenuating MIR516A resulted in a dramatic inhibition of xenograft tumor formation in vivo. Collectively, our results reveal that MIR516A has a novel oncogenic function in BC growth by directing binding to PHLPP2 3'-UTR and inhibiting PHLPP2 expression, in turn at least partly promoting CUL4A-mediated BECN1 protein degradation, thereby attenuating autophagy and promoting BC growth, which is a distinct function of MIR516A identified in other cancers.Abbreviation: ATG3: autophagy related 3; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG12: autophagy related 12; BAF: bafilomycin A1; BC: bladder cancer; CHX: cycloheximide; Co-IP: co-immunoprecipitation; CUL3: cullin 3; CUL4A: cullin 4A; CUL4B: cullin 4B; IF: immunofluorescence: IHC-p: immunohistochemistry-paraffin; MIR516A: microRNA 516a (microRNA 516a1 and microRNA 516a2); MS: mass spectrometry; PHLPP2: PH domain and leucine rich repeat protein phosphatase.
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Autofagia/genética , Beclina-1/metabolismo , Carcinogénesis/genética , Regulación Neoplásica de la Expresión Génica , MicroARNs/metabolismo , Fosfoproteínas Fosfatasas/genética , Neoplasias de la Vejiga Urinaria/genética , Regiones no Traducidas 3'/genética , Secuencia de Bases , Carcinogénesis/patología , Línea Celular Tumoral , Proliferación Celular/genética , Proteínas Cullin/metabolismo , Regulación hacia Abajo/genética , Humanos , Antígeno Ki-67/genética , Antígeno Ki-67/metabolismo , MicroARNs/genética , Fosfoproteínas Fosfatasas/metabolismo , Unión Proteica , Proteolisis , Neoplasias de la Vejiga Urinaria/patología , Neoplasias de la Vejiga Urinaria/ultraestructura , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
BACKGROUND: Metastasis is the leading cause of death in patients with bladder cancer (BC). However, current available treatments exert little effects on metastatic BC. Moreover, traditional grading and staging have only a limited ability to identify metastatic BC. Accumulating evidence indicates that the aberrant expression of microRNA is intimately associated with tumor progression. So far, many miRNAs have been identified as molecular targets for cancer diagnosis and therapy. This study focused on the role of miR-516a-5p (miR-516a) in BC. METHODS: MiR-516a expression and its downstream signaling pathway were detected using molecular cell biology and biochemistry approaches and techniques. Fresh clinical BC tissue was used to study the clinicopathological characteristics of patients with different miR-516a expression. The biological functions of miR-516a in BC were tested both in vivo and in vitro. RESULTS: A more invasive BC phenotype was significantly and positively correlated with miR-516a overexpression in BC patients. MiR-516a inhibition significantly decreased BC cell invasion and migration in vitro and in vivo. Furthermore, miR-516a attenuated the expression of PH domain leucine-rich repeat-containing protein phosphatase 2 protein and inhibited SMAD-specific E3 ubiquitin protein ligase 1 transcription by activating the AKT/Forkhead box O3 signaling pathway, which stabilized MMP9 and slowed down its proteasomal degradation, ultimately promoting BC motility and invasiveness. CONCLUSIONS: Our findings reveal the crucial function of miR-516a in promoting BC metastasis, and elucidate the molecular mechanism involved, suggesting that miR-516a may be a promising novel diagnostic and therapeutic target for BC.
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BACKGROUND: Numerous researches have suggested that circular RNAs (circRNAs) play critical functions in bladder cancer (BC) progression. This study aims to investigate the potential roles of circRNA_103809 in regulating BC development. METHODS: qRT-PCR was used to analyze gene expression. CCK8 and colony formation were used to analyze cell proliferation. Transwell was utilized to examine cell migration and invasion. Gemcitabine was used to analyze the effect of circRNA_103809 on the chemo-resistance of BC cells. Luciferase reporter assay was performed to detect the RNA interactions. RESULTS: circRNA_103809 was highly expressed in BC tissues and cell lines. CircRNA_103809 high expression was associated with a poor progression in BC patients. CircRNA_103809 knockdown impaired the growth and metastasis of BC cells. Furthermore, circRNA_103809 silencing increased the sensitivity of BC cells to Gemcitabine treatment. CircRNA_103809 was the sponge for miR-516a-5p and promoted FBXL18 expression via restraining miR-516a-5p activity. CONCLUSION: circRNA_103809 promotes proliferation, migration, invasion and chemo-resistance of BC cells through regulating miR-516a-5p/FBXL18 axis.
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Emerging evidence has uncovered critical regulatory roles of circular RNAs (circRNAs) function as dynamic scaffolding molecules in tumorigenesis and progression. However, the aberrant expression and clinical significance of hsa_circ_0058063 (circRNA_0058063) in bladder cancer (BC) remain poorly understood. circRNA expression was analyzed via a microarray in cancerous tissue and non-carcinoma tissues. Luciferase reporter assays and RNA immunoprecipitation (RIP) were both conducted to uncover the function of circRNA_0058063 in BC. circRNA_0058063 was overexpressed in BC tissues compared with adjacent normal tissues. Knockdown of circRNA_0058063 dramatically decreased cell proliferation and invasion, and promoted apoptosis in 5637 and BIU-87 cell lines. Furthermore, mechanistic investigations showed that circRNA_0058063 and FOXP4 could directly bind to miR-486-3p, demonstrating that circRNA_0058063 regulated FOXP4 expression by competitively binding to miR-486-3p. Taken together, circRNA_0058063 functions by sponging miR-486-3p in BC progression, which could act as a new biomarker and further developed to be a therapeutic target in BC.
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ARN Circular/genética , Neoplasias de la Vejiga Urinaria/genética , Biomarcadores de Tumor/genética , Carcinogénesis/genética , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Progresión de la Enfermedad , Factores de Transcripción Forkhead/genética , Factores de Transcripción Forkhead/metabolismo , Regulación Neoplásica de la Expresión Génica/genética , Humanos , MicroARNs/genética , MicroARNs/metabolismoRESUMEN
Because bladder cancer (BC) is one of the most common malignant cancers of the urinary system, identification of BC cell growth-associated effectors is of great significance. Cyclin-dependent kinase (CDK)6 is a member of the CDK family of cell cycle-related proteins and plays an important role in cancer cell growth. This is borne out by the fact that a CDK6 inhibitor had been approved to treat several types of cancers. Nevertheless, underlying molecular mechanisms concerning how to regulate CDK6 expression in BC remains unclear. In the present study, it was observed that miR-934 was much higher in human BCs and human BC cell lines as well. The results also revealed that miR-934 inhibition dramatically decreased human BC cell monolayer growth in vitro and xenograft tumor growth in vivo; the outcomes were accompanied by CDK6 protein down-regulation and G0-G1 cell cycle arrest. Moreover, overexpression of CDK6 reversed the inhibition of BC cell growth induced by miR-934. Further studies showed that miR-934 binds to a 3'-UTR of ubiquitin-conjugating enzyme 2N (ube2n) mRNA, down-regulated UBE2N protein expression; this, in turn, attenuated CDK6 protein degradation and led to CDK6 protein accumulation as well as the promotion of BC tumor growth. Collectively, this study not only establishes a novel regulatory axis of miR-934/UBE2N of CDK6 but also provides data suggesting that miR-934 and UBE2N may be potentially promising targets for therapeutic strategies against BC.-Yan, H., Ren, S., Lin, Q., Yu, Y., Chen, C., Hua, X., Jin, H., Lu, Y., Zhang, H., Xie, Q., Huang, C., Huang, H. Inhibition of UBE2N-dependent CDK6 protein degradation by miR-934 promotes human bladder cancer cell growth.
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Proliferación Celular/genética , Quinasa 6 Dependiente de la Ciclina/genética , MicroARNs/genética , Enzimas Ubiquitina-Conjugadoras/genética , Neoplasias de la Vejiga Urinaria/genética , Regiones no Traducidas 3'/genética , Animales , Línea Celular , Línea Celular Tumoral , Quinasa 6 Dependiente de la Ciclina/metabolismo , Regulación Neoplásica de la Expresión Génica , Humanos , Ratones Desnudos , Proteolisis , Interferencia de ARN , Tratamiento con ARN de Interferencia/métodos , Enzimas Ubiquitina-Conjugadoras/metabolismo , Neoplasias de la Vejiga Urinaria/metabolismo , Neoplasias de la Vejiga Urinaria/patología , Ensayos Antitumor por Modelo de Xenoinjerto/métodosRESUMEN
Although increasing aberrantly expressed circular RNAs (circRNAs) have been identified among many human cancer tissues, their roles in tumor progression still remain largely unknown. In bladder cancer, the function of hsa_circ_0000144 has not been reported. In our study, we found hsa_circ_0000144 as a novel oncogene in bladder cancer by bioinformatics analysis. We found that hsa_circ_0000144 expression was significantly upregulated in bladder cancer tissues compared with adjacent normal tissues, and its high expression was related with poor prognosis. Additionally, knockdown of hsa_circ_0000144 remarkably suppressed the proliferation and invasion of bladder cancer cells in vitro. Hsa_circ_0000144 silence also led to reduced tumor volumes in vivo. In mechanism, we found that hsa_circ_0000144 was a sponge of miR-217 while miR-217 targeted RUNX2. Our results indicated that the expression of miR-217 was inversely correlated with that of both hsa_circ_0000144 and RUNX2 in bladder cancer tissues. Rescue assays showed that either inhibition of miR-217 or restoration of RUNX2 reversed the suppressive effects of hsa_circ_0000144 knockdown on bladder cancer cell proliferation and invasion. Taken together, these findings demonstrated that hsa_circ_0000144 exerts oncogenic roles in bladder cancer via repressing miR-217 to facilitate RUNX2 expression.
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Subunidad alfa 1 del Factor de Unión al Sitio Principal/genética , MicroARNs/genética , ARN/genética , Neoplasias de la Vejiga Urinaria/genética , Regiones no Traducidas 3' , Animales , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Técnicas de Silenciamiento del Gen , Humanos , Ratones , Trasplante de Neoplasias , ARN CircularRESUMEN
We analyzed clinicopathologically 12 gastric schwannomas. Patient ages ranged from 41 to 79 years (mean, 52 years; median, 59 years). They variably presented with gastric discomfort, bleeding, or rarely gastric outlet obstruction and many were incidental findings during other medical procedures. The maximum tumor diameters ranged from 1.0 to 5.4 cm (mean, 3.5 cm; median 3.8 cm). The typical histologic features included spindle cells with micro-trabecular architecture, focal nuclear atypia, and peritumoral lymphoid cuff. Median mitotic count was 1/50 high-power field. No malignant variants were recognized, and follow-up did not reveal recurrences or metastases. Immunohistochemically, all tumors were positive for S100 and SOX10, and most were also GFAP positive, whereas CD34 and NF were rarely positive. All tumors were negative for cytokeratin AE1/3, HMB45, c-kit, DOG1, smooth muscle actin, desmin, and synaptophysin. None of the tumors showed gastrointestinal stromal tumor-specific KIT or PDGFRA mutations. Gastric schwannoma is a distinctive form of peripheral nerve sheath tumor and it should be distinguished from gastrointestinal stromal tumor and other mesenchymal tumors of the gastrointestinal tract, especially clear cell sarcoma and metastatic melanoma.