MedComm最新文献

{"title":"Correction to \"AMPK-upregulated microRNA-708 Plays as a Suppressor of Cellular Senescence and Aging via Downregulating Disabled-2 and mTORC1 Activation\".","authors":"","doi":"10.1002/mco2.71077","DOIUrl":"https://doi.org/10.1002/mco2.71077","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1002/mco2.475.].</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71077"},"PeriodicalIF":14.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocellular Carcinoma Targeted Thermosensitive Cu²⁺ Liposomes Based on the Cuproptosis Mechanism.","authors":"Hao Yang, Hui Hou, Hong Li, Xianglong Wang, Wei Zhang, Mengsi Yin, Fuyu Zhang, Faxin Zhang, Mingyuan Li, Xiangcheng Wang, Xianggao Zhu","doi":"10.1002/mco2.71068","DOIUrl":"https://doi.org/10.1002/mco2.71068","url":null,"abstract":"<p><p>Cuproptosis is characterized by elevated intracellular copper concentrations that disrupt copper homeostasis and impair the tricarboxylic acid cycle, ultimately causing cell death. However, the lack of targeted intervention for intracellular copper may induce systemic side effects, hindering the application of cuproptosis in tumor therapy. Herein, we constructed a targeted copper ion delivery system (Cu-Lip-Gal(H)) based on galactose-modified thermosensitive liposomes, combined with local tumor hyperthermia targeted copper delivery into hepatocellular carcinoma (HCC) cells. Cu-Lip-Gal showed excellent physicochemical properties and 42°C thermosensitive release, with 64.67% ± 2.52% cumulative release within 0.5 h. The Cu-Lip-Gal(H) group reduced HepG2 and Huh7 cell viability to 24.48% ± 3.31% and 18.00% ± 3.18%, respectively; it exhibited 5.8-fold higher intracellular copper concentration in HepG2 cells and 5.2-fold higher in Huh7 cells. In nude mouse xenografts, Cu-Lip-Gal(H) achieved a tumor inhibition rate of 86.7% ± 1.9% without obvious histopathological changes in major organs but significantly increased necrotic cells in tumors along with the highest FDX1 expression levels observed in this study. These findings provide new insights into cuproptosis-based copper ion delivery systems for HCC treatment.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71068"},"PeriodicalIF":14.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An LCK/PPARG/SCD Lipid Metabolism Axis Promotes Invasion in Human Oral Cancer.","authors":"Jonas Pyko, Tamara Tomin, Markus Glaß, Lisa Müller, Jana Macho, Matthias Schittmayer, Monika Haemmerle, Ruth Birner-Gruenberger, Tony Gutschner","doi":"10.1002/mco2.71060","DOIUrl":"https://doi.org/10.1002/mco2.71060","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) frequently metastasizes to regional lymph nodes, yet the metabolic adaptations that enable invasive dissemination remain incompletely understood. Although lipid metabolic reprogramming has emerged as a hallmark of metastatic dissemination, the upstream signaling pathways coordinating these processes remain poorly defined. Here, we combined transcriptomic, epigenomic, and lipidomic analyses with genetic and pharmacological perturbation of lymphocyte cell-specific protein tyrosine kinase (LCK) and peroxisome proliferator-activated receptor gamma (PPARG) to define the signaling network linking oncogenic kinase activity to lipid metabolism. We identify PPARG as a critical downstream effector of LCK that promotes invasion by reprogramming lipid metabolism. Mechanistically, LCK maintained PPARG expression, which induced stearoyl-CoA desaturase (SCD), increased monounsaturated fatty acid synthesis, and limited lipid peroxide accumulation. Pharmacological inhibition of SCD suppressed cancer cell invasion, impaired viability, and sensitized PPARG-activated cells to ferroptosis-associated cell death. Together, these findings establish an LCK/PPARG/SCD signaling axis that couples oncogenic signaling to lipid metabolic plasticity during OSCC invasion. Our study identifies SCD as a potential therapeutic vulnerability and suggests that therapeutic activation of PPARG signaling should be approached with caution in patients with established oral cancer and carefully evaluated in biomarker-guided clinical studies.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71060"},"PeriodicalIF":14.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149187267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Multi-Time-Point ¹⁸F-FAPI PET/CT and Immune Histopathology for Predicting Pathological Complete Response in Microsatellite-Stable Locally Advanced Rectal Cancer Treated With Neoadjuvant Radiotherapy, Chemotherapy, and Immunotherapy.","authors":"Minyi He, Huiting Yang, Yunxing Shi, Rongqin Zhang, Taixuan Wan, Xiaolin Pang, Zhanwen Zhang, Liang Huang","doi":"10.1002/mco2.71072","DOIUrl":"https://doi.org/10.1002/mco2.71072","url":null,"abstract":"<p><p>Predicting pathological complete response (pCR) after neoadjuvant short-course radiotherapy combined with immunotherapy and chemotherapy remains challenging in microsatellite-stable (MSS) locally advanced rectal cancer. In this prospective exploratory study (ClinicalTrials.gov identifier: NCT06608537), 49 patients received short-course radiotherapy followed by sintilimab plus CAPOX and subsequently underwent radical surgery. We investigated whether treatment response could be better characterized by integrating two complementary biological dimensions: baseline immune organization and treatment-related stromal remodeling captured by multi-time-point ¹ ⁸F-FAPI PET/CT. The pCR rate was 49.0% (24/49), and serial ¹ ⁸F-FAPI imaging revealed distinct stromal kinetic patterns between response groups. Integration of intratumoral tertiary lymphoid structure (iTLS) count, B-cell density, preoperative tumor-to-iliacus muscle ratio (TIMR) at 30 min, and the delayed TIMR retention index from 90 to 120 min (RI₃₄) yielded a four-variable model with a mean AUC of 0.874 in repeated nested cross-validation. Complementary preclinical experiments provided functional support for a CAF-TGFβ-B-cell/TLS axis linking stromal regulation, immune organization, and treatment resistance. These findings highlight the complementary value of spatial immune organization and dynamic FAPI-defined stromal kinetics and provide a biologically informed framework for post-neoadjuvant, preoperative response stratification, pending prospective multicenter validation.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71072"},"PeriodicalIF":14.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropathic Pain: From Mechanisms to Therapeutic Interventions.","authors":"Yaling Dai, Mengquan Tan, Man Yuan, Huixian Zhou, Qin Xie, Jiling Zeng, Yixin Yang, Xinran He, Siyuan Song","doi":"10.1002/mco2.71061","DOIUrl":"https://doi.org/10.1002/mco2.71061","url":null,"abstract":"<p><p>Neuropathic pain is caused by injury or disease of the somatosensory system. It involves peripheral nerve injury, central sensitization, transmitter imbalance, glial activation, and large-scale network remodeling. Despite substantial advances in pain biology, clinical assessment continues to rely predominantly on patient-reported symptoms, sensory examination, and conventional neurophysiological testing, approaches that often fail to delineate the predominant biological mechanisms underlying pain in individual patients. Recent advances in sensory phenotyping and multimodal imaging have enabled in vivo characterization of abnormalities at the receptor, neuroinflammatory, and circuit levels, thereby providing a foundation for mechanism-based stratification and more individualized therapeutic decision-making. This review summarizes neuropathic pain from clinical stratification to mechanism-based imaging and therapeutic intervention. We describe key clinical dimensions, including sensory gain, sensory loss, peripheral and central pain generators, mixed nociceptive-neuropathic pain, central sensitization, and autonomic or small-fiber modifiers. These dimensions help explain why patients with the same diagnosis may show different symptoms and treatment responses. We also review major molecular mechanisms, including glutamatergic overactivity, GABAergic and glycinergic disinhibition, monoaminergic remodeling, and neuroimmune modulation. These changes reshape spinal, thalamocortical, limbic, salience, reward, cerebellar, and descending control circuits. Peripheral nerve ultrasound and MR neurography can help identify structural peripheral pain generators. PET, MRS, MRI, DTI, fMRI, EEG, and multimodal imaging can assess receptor availability, neurotransmitter balance, neuroinflammation, white matter integrity, and network connectivity. These imaging tools may link clinical phenotypes with biological mechanisms and help define mechanism-based subtypes. Imaging biomarkers may also support treatment selection, treatment monitoring, neuromodulation targeting, and translational trial design. This framework supports a shift from symptom-based assessment to mechanism-guided precision care for neuropathic pain.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71061"},"PeriodicalIF":14.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149187056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acid-Stable Nitrofuran Triple Therapy With Rabeprazole and Amoxicillin Targeting <i>Helicobacter pylori</i> Infection.","authors":"Nagendran Tharmalingam, Kulandaisamy Arulsamy, Shaolei Lu, Sadhna Dhingra, Scott Goodrich, Joseph St Laurent, Gerald Jones, Eleftherios Mylonakis","doi":"10.1002/mco2.71057","DOIUrl":"https://doi.org/10.1002/mco2.71057","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> is an emerging antibiotic-resistant and carcinogenic gastric pathogen. We developed nitrofuran derivatives with anti-<i>H. pylori</i> activity and found the analog CLI-19-009 (2-nitro-6,7-dihydrobenzofuran-4-one N-(cinnamoyl)hydrazone) inhibited <i>H. pylori</i> growth at 0.25 mg/L. Notably, CLI-19-009 contains a non-conjugated hydrazone side chain, which may influence nitroreductive activation compared with classical nitrofurans and retain activity under acidic conditions. CLI-19-009 exhibited an additive effect with clinical antibiotics and proton pump inhibitors, cleared <i>H. pylori</i> on gastric epithelial cells, reduced bacterial motility, and decreased vacuolation. CLI-19-009 also showed low cytotoxicity (IC₅₀>64 mg/L) and significantly improved survival of <i>H. pylori</i>-infected wax moth larvae compared with untreated controls (<i>p = </i>0.0002). Host-cell RNA sequencing revealed that CLI-19-009 treatment downregulated inflammatory genes (IL1B, IL18, IL23A, MAPK1, NFKB1, TNF, and IRAK1) during host-pathogen interactions. Long-term exposure generated CLI-19-009-resistant clones harboring a single-nucleotide polymorphism in <i>rdxA</i> in both lineages, demonstrated using whole-genome sequencing; this finding suggests alterations in nitroreductive activation. CLI-19-009 showed in vitro synergy with rabeprazole and additive activity with amoxicillin, and these combinations reduced gastric inflammation and colonization compared with untreated mice when tested in a murine infection model (<i>p</i> < 0.0001). These findings support further development of CLI-19-009 as an anti-<i>H. pylori</i> therapeutic alternative to clarithromycin-based regimens.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71057"},"PeriodicalIF":14.1,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149187221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"O-GlcNAcylation Stimulation Modulates Na+/K+ ATPase and Improves Outcomes in Hemorrhagic Shock.","authors":"Thomas Dupas, Amandine Vergnaud, Virginie Aillerie, Martin Bouaud, Angélique Erraud, Thomas Pelé, Antoine Persello, Barbara Ribeiro de Oliveira, Jérôme Montnach, Aurore Girardeau, Jules Lecomte, Nolwenn Tessier, Mathilde Guyon, Angélique Blangy-Letheule, Matthieu Rivière, Jacques Lebreton, Arnaud Tessier, Edith Bigot-Corbel, Aurélia A Leroux, Michel De Waard, Nicolas J Prat, Bertrand Rozec, Manon Denis, Benjamin Lauzier","doi":"10.1002/mco2.71056","DOIUrl":"https://doi.org/10.1002/mco2.71056","url":null,"abstract":"<p><p>Hemorrhagic shock (HS), caused by blood loss leading to inadequate organ perfusion, remains a major cause of death worldwide, with 1.9 million fatalities annually. It triggers severe disturbances in cardiovascular, neurohormonal, and metabolic homeostasis with ionic imbalance notably due to Na⁺/K⁺-ATPase dysfunction. O-GlcNAcylation, a post-translational modification essential for cellular protection under stress, has emerged as a promising therapeutic target in ischemia-reperfusion and septic shock. This study aimed to determine the effects of stimulating O-GlcNAcylation during HS and to clarify the related molecular mechanisms. Adult male rats were subjected to controlled HS and received either NButGT (2 injections of 10 mg/kg) to enhance O-GlcNAcylation or saline. Hemodynamic parameters and plasmatic markers of organ injury were assessed after 24 h. O-GlcNAcylation levels, protein expression, and Na⁺/K⁺-ATPase O-GlcNAcylation were analyzed via Western blot and immunofluorescence, while Na⁺/K⁺-ATPase activity was measured by colorimetry. NButGT increased cardiac and renal O-GlcNAcylation levels, improved hemodynamic and reduced organ damage. HS disrupts electrolyte homeostasis with decreased bicarbonate and sodium levels and elevated potassium concentration. NButGT administration restored ionic balance and renal Na⁺/K⁺-ATPase expression. Treatment with NButGT elevated Na⁺/K⁺-ATPase activity. These results demonstrate that acute O-GlcNAcylation stimulation supports physiological recovery in HS by promoting ionic homeostasis and Na⁺/K⁺-ATPase function.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71056"},"PeriodicalIF":14.1,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149187082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myelination and Remyelination in Peripheral Nerve Injury: Mechanisms, Regulation, and Therapeutic Perspectives.","authors":"Li-Xin Huang, Tao Sun, Yi-Bo Zhao, Zhi-Min Wu, Jun Sun, Ming-Yang Li, Qing-Yi Huo, Yun-Mou Ou, Qing-Tian Liang, Cong Ling, Bao-Yu Zhang, Chuan Chen, Ying Guo, Hui Wang","doi":"10.1002/mco2.71019","DOIUrl":"https://doi.org/10.1002/mco2.71019","url":null,"abstract":"<p><p>Peripheral nerve injury (PNI) affects 13-23 individuals per 100,000 annually, and functional recovery hinges on faithful remyelination of regenerating axons by Schwann cells (SCs). This review integrates the complete molecular logic governing the transition from injury-induced SC plasticity to mature myelin regeneration. The hierarchical transcriptional program-from SOX10 pioneer factor engagement through OCT6-mediated promyelinating transition to KROX20/EGR2-driven activation of compact myelin genes-and the instructive role of axonal Neuregulin-1 Type III signaling are dissected. Wallerian degeneration via the NMNAT2-SARM1-mediated axon degeneration cascade, c-JUN-dependent SC reprogramming, and the epigenetic and noncoding RNA mechanisms that re-engage myelination are examined. The immune microenvironment is considered as a temporally layered network in which macrophage polarization, macrophage-to-myofibroblast transition, and regulatory T cell activity coordinate the transition from inflammation to repair. Finally, this review critically evaluates emerging therapeutic strategies-including Neuregulin-1 supplementation, SC transplantation, nerve guidance conduits, electrical stimulation, and senolytic clearance of aged SCs-and argues that rationally sequenced combination therapies will be required to achieve transformative improvements in functional recovery after severe PNI. This review provides a mechanistic roadmap for designing next-generation regenerative strategies aimed at restoring saltatory conduction.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71019"},"PeriodicalIF":14.1,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fumarate and Its Esters: Physiology, Pathology, Molecular Mechanisms, Diseases, and Therapy.","authors":"Peng Zhu, Mengling You, Yi Zeng, Jinglin Zhang, Si Chen, Rong Rong, Xiaobo Xia","doi":"10.1002/mco2.71059","DOIUrl":"https://doi.org/10.1002/mco2.71059","url":null,"abstract":"<p><p>Fumarate is a critical intermediate of the tricarboxylic acid cycle that, beyond its metabolic role, has emerged as an important regulator of cellular signaling. Fumaric acid esters (FAEs), including dimethyl fumarate and monomethyl fumarate, have been utilized as therapeutic agents for immune-mediated diseases and are being explored for broader applications. Accumulating evidence indicates that both fumarate and FAEs modulate diverse biological processes through mechanisms such as protein succination and metabolic reprogramming. In this review, we discuss the current understanding of fumarate and FAEs in health and disease, integrating evidence from various clinical and preclinical research. We conclude that protein succination represents an important mechanism for many of their biological activities, whereas differences in electrophilicity, cell permeability, intracellular distribution, and the metabolic context dictate distinct molecular targets and functional outcomes. We further evaluate the opportunities and limitations of current research, highlighting key technical challenges that complicate mechanistic interpretation and clinical translation. By bridging and differentiating the biology of endogenous fumarate and the pharmacology of FAEs, this review provides a conceptual framework for interpreting existing studies and outlines future directions for developing more precise fumarate-targeted interventions in diseases.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71059"},"PeriodicalIF":14.1,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transformer-Based Preoperative Invasiveness Identification and Postoperative Recurrence Risk Stratification in Stage T1N0M0 Lung Adenocarcinoma: A Multi-Center Cohort Study.","authors":"Xueyun Tan, Hui Xia, Delong Li, Meifang Wang, Na Zhan, Yan Huang, Mengyuan Liang, Pei Ma, Xiao Wang, Yaqi Cao, Linpeng Shi, Liang Zhang, Xiaoling Liu, Lian Yang, Quan Kong, Sufei Wang, Yang Jin","doi":"10.1002/mco2.71055","DOIUrl":"https://doi.org/10.1002/mco2.71055","url":null,"abstract":"<p><p>Surgery is the primary curative treatment for early-stage lung adenocarcinoma (LUAD), with accurate identification of tumor invasiveness critical for determining pulmonary resection extent. Due to significant variability in postoperative recurrence among early-stage LUAD patients with aggressive tumors, a more effective risk stratification system is urgently needed to improve prognosis. This study developed the T1LUT system, a transformer-based tool for T1N0M0 LUAD management, covering preoperative tumor invasiveness identification and postoperative recurrence risk stratification. Preoperatively, a 3D Vision Transformer (ViT) with extra learnable tokens analyzes CT images. It outperforms 3D ViT with only CLS tokens, 2D ViT, and 3D ResNet across three independent test centers (Center D: 0.896 vs. 0.892, 0.879, 0.836; Center E: 0.906 vs. 0.837, 0.837, 0.835; Center F: 0.884 vs. 0.884, 0.881, 0.861), achieving higher mean AUROC to accurately assess invasiveness and guide surgical resection extent. Postoperatively, the multimodal IAC-PR model integrates CT images, reports, pathological data, and clinical/demographic information. It stratifies invasive adenocarcinoma (IAC) patients into low-, medium-, or high-risk groups with an AUROC of 0.807 in testing-significantly better than single/partial-modal models. Validated via large-scale multicenter research, this system overcomes traditional assessment limitations, offering a robust tool for precise early LUAD treatment and improved prognosis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":"e71055"},"PeriodicalIF":14.1,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149187126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}