Cells最新文献

{"title":"Extracellular Vesicles in the Crosstalk of Autophagy and Apoptosis: A Role for Lipid Rafts.","authors":"Agostina Longo, Valeria Manganelli, Roberta Misasi, Gloria Riitano, Tuba Rana Caglar, Elena Fasciolo, Serena Recalchi, Maurizio Sorice, Tina Garofalo","doi":"10.3390/cells14100749","DOIUrl":"10.3390/cells14100749","url":null,"abstract":"<p><p>Autophagy and apoptosis are two essential mechanisms regulating cell fate. Although distinct, their signaling pathways are closely interconnected through various crosstalk mechanisms. Lipid rafts are described to act as both physical and functional platforms during the early stages of autophagic and apoptotic processes. Only recently has a role for lipid raft-associated molecules in regulating EV biogenesis and release begun to emerge. In particular, lipids of EV membranes are essential components in conferring stability to these vesicles in different extracellular environments and/or to facilitate binding or uptake into recipient cells. In this review we highlight these aspects, focusing on the role of lipid molecules during apoptosis and secretory autophagy pathways. We describe the molecular machinery that connects autophagy and apoptosis with vesicular trafficking and lipid metabolism during the release of EVs, and how their alterations contribute to the development of various diseases, including autoimmune disorders and cancer. Overall, these findings emphasize the complexity of autophagy/apoptosis crosstalk and its key role in cellular dynamics, supporting the role of lipid rafts as new therapeutic targets.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All-Trans Retinoic Acid Induces Differentiation and Downregulates Stemness Markers and MGMT Expression in Glioblastoma Stem Cells.","authors":"Justin Tang, Raymond Yang","doi":"10.3390/cells14100746","DOIUrl":"10.3390/cells14100746","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) remains almost uniformly fatal, owing in part to therapy-resistant cancer stem-like cells (CSCs) and to temozolomide (TMZ) resistance driven by O⁶-methylguanine-DNA methyltransferase (MGMT). Differentiation therapy with all-trans retinoic acid (ATRA) has the potential to attenuate stemness and sensitize GBM to TMZ. We therefore asked whether ATRA reduces expression of key CSC markers and MGMT in established GBM lines.</p><p><strong>Methods: </strong>Two established human GBM cell lines, U87-MG and A172, were cultured under neurosphere-promoting conditions to enrich for potential stem-like subpopulations. Cells were treated with either 1 µM ATRA or vehicle control (DMSO) for 5 days. Total RNA was extracted, and cDNA was synthesized. Quantitative Real-Time PCR (qPCR) assessed relative mRNA expression levels of key stemness transcription factors (SOX2, NES) and the DNA repair gene MGMT and corresponding protein levels were measured by an Enzyme-Linked Immunosorbent Assay (ELISA). Gene expression was normalized to the geometric mean of two validated housekeeping genes (GAPDH, ACTB). Relative quantification was calculated using the ΔΔCt method, and statistical significance was determined using Student's <i>t</i>-tests.</p><p><strong>Results: </strong>ATRA markedly suppressed stemness and MGMT in both lines. In U87-MG, SOX2 mRNA fell 3.7-fold (<i>p</i> = 0.0008) and protein 2.99-fold (148.3 ± 6.0 → 49.7 ± 2.7 pg µg^-1; <i>p</i> = 0.0002); Nestin dropped 4.1-fold (<i>p</i> = 0.0005) and 3.51-fold (450.0 ± 17.3 → 128.3 ± 4.4 pg µg^-1; <i>p</i> = 0.00008). MGMT decreased 2.6-fold at transcript level (<i>p</i> = 0.0065) and 2.11-fold at protein level (81.7 ± 4.4 → 38.7 ± 1.8 pg µg^-1; <i>p</i> = 0.0005). In A172, SOX2 was reduced 2.9-fold (<i>p</i> = 0.0041) and 2.31-fold (<i>p</i> = 0.0007); Nestin 3.3-fold (<i>p</i> = 0.0028) and 2.79-fold (<i>p</i> = 0.00009). MGMT declined 2.2-fold (<i>p</i> = 0.0132) and 1.82-fold (<i>p</i> = 0.0015), respectively.</p><p><strong>Conclusions: </strong>Five-day exposure to ATRA diminishes SOX2, Nestin, and MGMT at both mRNA and protein levels in stem-enriched GBM cultures, supporting the premise that ATRA-induced differentiation can concurrently blunt CSC traits and TMZ-resistance mechanisms. These data provide a molecular rationale for testing ATRA in combination regimens aimed at improving GBM therapy.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MvfR Shapes <i>Pseudomonas aeruginosa</i> Interactions in Polymicrobial Contexts: Implications for Targeted Quorum-Sensing Inhibition.","authors":"Kelsey M Wheeler, Myung Whan Oh, Julianna Fusco, Aishlinn Mershon, Erin Kim, Antonia De Oliveira, Laurence G Rahme","doi":"10.3390/cells14100744","DOIUrl":"10.3390/cells14100744","url":null,"abstract":"<p><p>Infections often occur in complex niches consisting of multiple bacteria. Despite the increasing awareness, there is a fundamental gap in understanding which interactions govern microbial community composition. <i>Pseudomonas aeruginosa</i> is frequently isolated from monomicrobial and polymicrobial human infections. This pathogen forms polymicrobial infections with other ESKAPEE pathogens and defies eradication by conventional therapies. By analyzing the competition within co-cultures of <i>P. aeruginosa</i> and representative secondary pathogens that commonly co-infect patients, we demonstrate the antagonism of <i>P. aeruginosa</i> against other ESKAPEE pathogens and the contribution of this pathogen's multiple quorum-sensing (QS) systems in these interactions. QS is a highly conserved bacterial cell-to-cell communication mechanism that coordinates collective gene expressions at the population level, and it is also involved in <i>P. aeruginosa</i> virulence. Using a collection of <i>P. aeruginosa</i> QS mutants of the three major systems, LasR/LasI, MvfR/PqsABCDE, and RhlR/RhlI, and mutants of several QS-regulated functions, we reveal that MvfR and, to a lesser extent, LasR and RhlR, control competition between <i>P. aeruginosa</i> and other microbes, possibly through their positive impact on pyoverdine, pyochelin, and phenazine genes. We show that MvfR inhibition alters competitive interspecies interactions and preserves the coexistence of <i>P. aeruginosa</i> with the ESKAPEE pathogens tested while disarming the pathogens' ability to form biofilm and adhere to lung epithelial cells. Our results highlight the role of MvfR inhibition in modulating microbial competitive interactions across multiple species, while simultaneously attenuating virulence traits. These findings reveal the complexity and importance of QS in interspecies interactions and underscore the impact of the anti-virulence approach in microbial ecology and its importance for treating polymicrobial infections.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Complement in the Pathogenesis and Treatment of Myasthenia Gravis.","authors":"Armando Martinez Salazar, Sepideh Mokhtari, Edwin Peguero, Muhammad Jaffer","doi":"10.3390/cells14100739","DOIUrl":"10.3390/cells14100739","url":null,"abstract":"<p><p>Myasthenia gravis is an antibody-mediated autoimmune condition characterized by defects in cholinergic transmission at the neuromuscular junction. In AchR antibody-positive patients, complement activation plays a prominent role in the disease process, which appears to be mediated by the activation of the membrane attack complex. Since IgG4 is not a good complement activator, the role of complement in MuSK antibody-positive myasthenia gravis patients is negligible. Experimental animal models of myasthenia gravis have shown promise with the antagonism of different elements of the complement cascade, with positive clinical outcomes. This has led to the development of the first C5 inhibitors approved for myasthenia gravis with AchR antibodies: eculizumab, ravulizumab, and zilucoplan. Other clinical trials are currently in progress, investigating the potential therapeutic role of other targets, including the Factor B inhibition or hepatic synthesis of the C5 protein. Other proposed potential targets that have not yet been clinically tested are also discussed in this review article.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor-Associated Macrophages: Polarization, Immunoregulation, and Immunotherapy.","authors":"Abdullah Farhan Saeed","doi":"10.3390/cells14100741","DOIUrl":"10.3390/cells14100741","url":null,"abstract":"<p><p>Tumor-associated macrophages' (TAMs) origin, polarization, and dynamic interaction in the tumor microenvironment (TME) influence cancer development. They are essential for homeostasis, monitoring, and immune protection. Cells from bone marrow or embryonic progenitors dynamically polarize into pro- or anti-tumor M2 or M1 phenotypes based on cytokines and metabolic signals. Recent advances in TAM heterogeneity, polarization, characterization, immunological responses, and therapy are described here. The manuscript details TAM functions and their role in resistance to PD-1/PD-L1 blockade. Similarly, TAM-targeted approaches, such as CSF-1R inhibition or PI3Kγ-driven reprogramming, are discussed to address anti-tumor immunity suppression. Furthermore, innovative biomarkers and combination therapy may enhance TAM-centric cancer therapies. It also stresses the relevance of this distinct immune cell in human health and disease, which could impact future research and therapies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activated Immune and Complement C3 Are Potential Contributors in MASH via Stimulating Neutrophil Extracellular Traps.","authors":"Ao Liu, Xiaoling Deng, Shuhui Hou, Yuwen Xi, Keshu Xu","doi":"10.3390/cells14100740","DOIUrl":"10.3390/cells14100740","url":null,"abstract":"<p><p>The number of metabolic dysfunction-associated steatotic liver disease (MASLD) patients is increasing rapidly. More attention has been paid to the relationship between immunity and MASLD. This study explored the roles of serum autoantibodies, immunoglobulins, and complements in MASLD. A total of 182 MASLD patients were investigated and grouped by autoantibody or NAS scores. Correlation between immunology and clinical features was assessed. In addition, metabolic dysfunction-associated steatohepatitis (MASH) models were constructed to verify the findings. Neutrophils were isolated from mice and treated with complement C3 to investigate the association between C3 and neutrophil extracellular traps (NETs). IgG, IgM, and NAS scores in the autoantibody positive group were significantly higher than those in the autoantibody negative group. Antinuclear antibodies (ANA), IgA, IgE, IgG, C3, C4, ALT, and AST were related to MASH. Meanwhile, IgA and C3 correlated with the severity of MASLD. The ROC curve showed that IgA > 2.990 g/L or C3 > 1.115 g/L predicted the presence of MASH. More importantly, IgG, activated C3, and NETs were increased in MASH. C3 stimulation directly induced NET formation in the neutrophils. Immunity systems were activated in MASH and elevated IgG activated C3 to stimulate the production of NETs, thus exacerbating MASH.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effects of Neuronal <i>Fyn</i> Knockdown in the Hippocampus in the Rat Kainate Model of Temporal Lobe Epilepsy.","authors":"Nikhil S Rao, Marson Putra, Christina Meyer, Sirisha Parameswaran, Thimmasettappa Thippeswamy","doi":"10.3390/cells14100743","DOIUrl":"10.3390/cells14100743","url":null,"abstract":"<p><p>Previous studies have demonstrated neuronal and microglial Fyn, a Src family kinase (SFK), and how its interactions with tau contribute to epileptogenesis. Saracatinib, a Fyn/SFK inhibitor, modifies disease progression in rat kainate (KA) epilepsy models. In this study, we investigated neuronal-specific <i>fyn</i> knockdown effects on Fyn-tau signaling, neurodegeneration, and gliosis using a calcium/calmodulin-dependent protein kinase II (CaMKII)-promoter-driven adeno-associated viral vector (AAV9)-mediated <i>fyn</i>-shRNA injection in the rat hippocampus. Eight days following AAV administration, rats received repeated low-dose KA injections intraperitoneally to induce <i>status epilepticus</i> (SE). Both <i>fyn</i>-shRNA and control groups showed comparable SE severity, indicating inadequate neuronal <i>fyn</i> knockdown at this timepoint. Two weeks post <i>fyn</i>-shRNA injection, hippocampal Fyn significantly decreased, alongside reductions in NR2B, pNR2B^Y1472, PSD95, and total tau. There was also a compensatory activation of SFK (pSFK^Y416:Fyn) and tau hyperphosphorylation (AT8:total tau), negatively correlating with NeuN expression. Proximity ligation assay indicated unchanged Fyn-tau interactions, suggesting tau interactions with alternative SH3 domain proteins. Persistent neuronal loss, astrogliosis, and microgliosis suggested limited effectiveness of neuronal-specific <i>fyn</i> knockdown at this timepoint. An extended-duration <i>fyn</i> knockdown study, or using broad SFK inhibitors such as saracatinib or tau-SH3 blocking peptides, may effectively prevent SE-induced epileptogenesis.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endometriosis Cell Spheroids Undergo Mesothelial Clearance in a Similar Manner to Ovarian Cancer Cell Spheroids.","authors":"Allison A Kloeckner, Sarah R Walker","doi":"10.3390/cells14100742","DOIUrl":"10.3390/cells14100742","url":null,"abstract":"<p><p>Endometriosis is a gynecological disease characterized by the presence of endometrium-like cells located outside the uterus. The most widely accepted theory for endometriosis development, retrograde menstruation, does not account for extra-pelvic lesions or ones found on other organs in the peritoneal cavity. Similar to ovarian cancer, endometriosis cells can interact with the mesothelial cells of the peritoneal cavity. In ovarian cancer metastasis, ovarian cancer cell spheroids attach and push away the mesothelial cells lining the peritoneal cavity, clearing the mesothelial layer. Since endometriosis cells are known to interact with the mesothelium, we hypothesized that endometriosis cells would be able to form spheroids capable of undergoing mesothelial clearance. To test this, we designed an in vitro mesothelial clearance assay using endometriosis spheroids and a mesothelial cell monolayer. Our results demonstrate that normal and endometriotic epithelial cell spheroids can perform mesothelial clearance similar to ovarian cancer spheroids, though normal endometrial cells do not clear as well as endometriosis cells. Additionally, we demonstrated that our mesothelial clearance assay can test potential pharmacological therapies for endometriosis prior to clinical trials. These results give insight into the development of endometriosis lesions, but further research is needed to determine the mechanisms behind mesothelial clearance in endometriosis.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiological Oxygen Levels in the Microenvironment Program Ex Vivo-Generated Conventional Dendritic Cells Toward a Tolerogenic Phenotype.","authors":"Antonia Peter, Morgane Vermeulen, Mats Van Delen, Amber Dams, Stefanie Peeters, Hans De Reu, Waleed F A Marei, Zwi N Berneman, Nathalie Cools","doi":"10.3390/cells14100736","DOIUrl":"10.3390/cells14100736","url":null,"abstract":"<p><p>Dendritic cells (DCs) are critical regulators of immune homeostasis, balancing tolerance and immunity through antigen presentation and T cell modulation. While the influence of hypoxia (<2% O₂) on DC function in pathological settings is well-documented, the impact of physiological O₂ levels remains underexplored. This study investigates the role of physioxia (4% O₂) in programming mature DCs toward a tolerogenic phenotype compared to atmospheric conditions (21% O₂) typically present in in vitro assays. DC cultures generated under 4% O₂ exhibited a reduced monocyte-to-DC transformation rate, increased lactate production, a semi-mature surface marker profile, and increased surface expression of the tolerance-associated marker ILT4. T cell priming was altered only when atmospheric DCs were co-cultured under physioxia, suggesting an O₂-dependent threshold for immunostimulatory capacity. These findings highlight the complexity of O₂-dependent mechanisms in DC-T cell interactions, revealing a delicate balance between tolerance and immunogenicity. Our results underscore the need for physiologically relevant O₂ conditions in DC research to better reflect in vivo behavior and inform immunotherapy design. Overall, this study advances understanding of how microenvironmental cues shape DC biology, with implications for immune tolerance, autoimmunity, and cancer immunotherapy.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recognizing Epithelial Cells in Prostatic Glands Using Deep Learning.","authors":"Liton Devnath, Puneet Arora, Anita Carraro, Jagoda Korbelik, Mira Keyes, Gang Wang, Martial Guillaud, Calum MacAulay","doi":"10.3390/cells14100737","DOIUrl":"10.3390/cells14100737","url":null,"abstract":"<p><p>Artificial intelligence (AI) is becoming an integral part of pathological assessment and diagnostic procedures in modern pathology. As most prostate cancers (PCa) arise from glandular epithelial tissue, an AI-based methodology has been developed to recognize glandular epithelial nuclei in prostate biopsy tissue. An integrated machine-learning network, named GlandNet, was developed to correctly recognize the epithelial cells within prostate glands using cell-centric patches selected from the core biopsy specimens. Feulgen-Thionin (a DNA stoichiometric label) was used to stain biopsy sections (4-7 µm in thickness) from 82 active surveillance patients diagnosed with PCa. Images of these sections were human-annotated, and the resultant dataset consisted of 1,264,772 segmented, cell-centric nuclei patches, of which 449,879 were centered on epithelial gland nuclei from 110 needle biopsies (training set: <i>n</i> = 66; validation set: <i>n</i> = 22; and test set: <i>n</i> = 22). The training of GlandNet used semi-supervised machine-learning knowledge of the training and validation cohorts and integrated both human and AI predictions to enhance its performance on the test cohort. The performance was evaluated against a consensus deliberation from three observers. The GlandNet demonstrated an average accuracy, sensitivity, specificity, and F1-score of 94.1%, 95.7%, 87.8%, and 95.2%, respectively, when tested on the 20,735 glandular cells found in the three needle biopsies with the visually best consensus predictions. Conversely, the average accuracy, sensitivity, specificity, and F1-score were 90.9%, 86.4%, 94.0%, and 89.7% when assessed on 57,217 cells found in the three needle biopsies with the visually worst consensus predictions. GlandNet is a first-generation AI with an excellent ability to differentiate between epithelial and stromal nuclei in core biopsies from patients with early prostate cancer.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}