IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70997

Lujun Shen, Letao Lin, Shuanggang Chen, Chen Li, Ruizhi Tang, Lin Xie, Yujia Wang, Yunpeng Li, Hongliang Zou, Dandan Li, Xiaoshi Zhang, Weijun Fan

{"title":"Efficacy and Safety of Co-Ablation Combined With Aintilimab for Metastatic Melanoma to the Liver (CryoCheck-001): A Phase II Trial","authors":"Lujun Shen, Letao Lin, Shuanggang Chen, Chen Li, Ruizhi Tang, Lin Xie, Yujia Wang, Yunpeng Li, Hongliang Zou, Dandan Li, Xiaoshi Zhang, Weijun Fan","doi":"10.1002/mco2.70997","DOIUrl":"https://doi.org/10.1002/mco2.70997","url":null,"abstract":"Liver metastasis is a key driver of immune tolerance in melanoma, limiting immune checkpoint inhibitor efficacy. This prospective single-arm phase II trial investigated the efficacy and safety of co-ablation combined with sintilimab for liver-metastatic melanoma (ChiCTR2200061591). Eligible patients received sintilimab (anti-PD-1, 200 mg every 3 weeks) for up to eight cycles alongside co-ablation. The primary endpoint was a 6-month progression-free survival (PFS) rate per Response Evaluation Criteria in Solid Tumors v1.1. Secondary endpoints included overall survival (OS), PFS time, and overall response rate (ORR). Between June 2022 and July 2025, 16 patients were enrolled. Three patients achieved a partial response (ORR 18.75%). The 6-month PFS rate was 31.25% (95% confidence interval [CI]: 15.1–64.6), with a median PFS of 3.94 months (95% CI: 2.77–14.30). The 12- and 24-month OS rates were 53.8% (95% CI: 33.7–86.0) and 28.7% (10.3–80.1), respectively; median OS was 16.67 months (95% CI: 7.50–NR). Grade ≥ 3 treatment-related adverse events occurred in 14 of 16 patients (87.5%), the most common being elevated liver enzyme levels. Co-ablation combined with sintilimab demonstrates a manageable safety profile and encouraging antitumor activity in patients with liver-metastatic melanoma, meriting further evaluation.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70997","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962646","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}

引用次数: 0

Cancer Neuroscience: From Local Neuro-Immune Microenvironments to Systemic Brain-Body Circuitry. 癌症神经科学：从局部神经免疫微环境到全身脑-体回路。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.71025

Mingxuan Xie, Yu Zhao, Xinruo Xing, Yuqiang Liu, Jungang Zhao, Maojin Yao, Jun Tang, Jianzhu Zhao

{"title":"Cancer Neuroscience: From Local Neuro-Immune Microenvironments to Systemic Brain-Body Circuitry.","authors":"Mingxuan Xie, Yu Zhao, Xinruo Xing, Yuqiang Liu, Jungang Zhao, Maojin Yao, Jun Tang, Jianzhu Zhao","doi":"10.1002/mco2.71025","DOIUrl":"10.1002/mco2.71025","url":null,"abstract":"Classic oncological models have largely restricted cancer pathogenesis to autonomous genetic mutations within localized cells. Current research, however, reframes solid tumors as structurally integrated \"pseudo-organs\" that rely on host neural networks for survival. This review examines the reciprocal signaling networks connecting nervous, immune, and malignant cells within the tumor microenvironment. At the tissue level, we outline how tumors construct de novo neural architecture via axonogenesis, cellular plasticity, and the assembly of functional neuro-neoplastic synapses. Expanding beyond the local niche, we describe the systemic brain-body circuitry. We specifically address how central nervous system pathways respond to tumor-derived cues and how chronic stress signaling disrupts physiological homeostasis. To explain the associated immune evasion, we analyze how sensory neuropeptides, particularly CGRP and, more broadly, Substance P-NK1R signaling, contribute to immune dysfunction, tumor-promoting inflammation, and therapeutic resistance. Finally, we discuss the clinical implications of these pathways. Rather than relying on nonspecific structural denervation, future therapeutic strategies should focus on targeted \"neural reprogramming\" to uncouple tumors from their neural dependencies and restore antitumor immunity while minimizing neurotoxicity. Ultimately, this review conceptualizes solid tumors as systemically integrated entities, establishing a framework for precision neural reprogramming to overcome immune evasion and therapeutic resistance.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e71025"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148956942","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}

引用次数: 0

Heat Shock Proteins in Cancer: Mechanisms and Therapeutic Targeting. 热休克蛋白在癌症中的作用：机制和治疗靶向。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70966

Sheng Ma, Chen-Qian Liu, Si-Yang Ma, Shao-Gang Wang, Qi-Dong Xia, Meng-Yao Xu

{"title":"Heat Shock Proteins in Cancer: Mechanisms and Therapeutic Targeting.","authors":"Sheng Ma, Chen-Qian Liu, Si-Yang Ma, Shao-Gang Wang, Qi-Dong Xia, Meng-Yao Xu","doi":"10.1002/mco2.70966","DOIUrl":"10.1002/mco2.70966","url":null,"abstract":"Heat shock proteins (HSPs) are molecular chaperones that couple proteostasis to cancer metabolic reprogramming under oncogenic and microenvironmental stress. This Review integrates structural, biochemical, preclinical, and clinical evidence on HSP90, HSP70, HSP60, HSP40, HSP110, and small HSPs. We explain how ATPase cycles, chaperonin cages, co-chaperone networks, and organelle-specific localization stabilize metabolic enzymes, glucose transporters, hypoxia-responsive factors, and electron-transport-chain components, thereby coordinating glycolysis, mitochondrial bioenergetics, redox homeostasis, lipid metabolism, and metabolic plasticity. These mechanisms enable tumor survival and therapy resistance but also create context-dependent vulnerabilities. We critically evaluate pan-HSP and isoform-selective inhibitors, disruption of chaperone-client or co-chaperone interfaces, HSP-directed immunotherapies, and biomarker-guided combinations with metabolic or immune therapies. Clinical translation remains limited by systemic toxicity, compensatory heat-shock responses, tumor-type heterogeneity, and the absence of validated predictive biomarkers. We also assess circulating HSPs, cryo-EM analysis of chaperone complexes, and AI-assisted ligand design as routes for biomarker development and selective drug discovery. By linking chaperone architecture and client specificity to metabolic outputs and cancer phenotypes, this Review establishes a framework for differentiating actionable HSP dependencies from observational associations. It further defines priorities for patient stratification and precision oncology, supporting the development of selective and tractable strategies that target proteostasis-metabolism coupling.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e70966"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957583","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}

引用次数: 0

SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3. SKP2通过p27介导的FOXN3降解调控细菌感染引发的肺部炎性损伤。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70963

Jinjin Yu, Xinghong Hu, Huanhuan Wang, Jingyu Yu, Lele Jin, Yingke Li, Jihong Zhou, Xinxing Zhu, Emmanuel Jairaj Moses, Chunfu Zheng, Yong Zhang, Wei Li

{"title":"SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.","authors":"Jinjin Yu, Xinghong Hu, Huanhuan Wang, Jingyu Yu, Lele Jin, Yingke Li, Jihong Zhou, Xinxing Zhu, Emmanuel Jairaj Moses, Chunfu Zheng, Yong Zhang, Wei Li","doi":"10.1002/mco2.70963","DOIUrl":"10.1002/mco2.70963","url":null,"abstract":"Excessive inflammatory responses are a primary driver of acute lung injury, yet the underlying molecular mechanisms remain incompletely understood. In this study, we identify SKP2, an E3 ubiquitin ligase, as a critical negative regulator of pulmonary inflammation during methicillin-resistant Staphylococcus aureus (MRSA) infection. Mechanistically, SKP2 promotes the degradation of its direct substrate p27kip1 (p27), which functions as an activator of a noncanonical NF-κB signaling pathway. We further demonstrate that p27 facilitates the recruitment of p38 kinase to heterogeneous nuclear ribonucleoprotein-U (hnRNPU), leading to direct phosphorylation of the transcriptional repressor FOXN3 at serine residues 83 and 85. This dual phosphorylation event triggers subsequent proteasomal degradation of FOXN3, thereby relieving transcriptional repression and enabling NF-κB-driven activation of pro-inflammatory genes. In vivo, genetic ablation of Skp2 worsens pulmonary inflammatory injury, elevates neutrophil infiltration, and significantly reduces survival in MRSA-infected mice, and these effects are greatly rescued by concurrent p27 depletion. Collectively, our findings uncover the SKP2-p27-FOXN3 axis as a pivotal regulatory module in pulmonary inflammation and suggest that targeting this axis may offer a promising therapeutic strategy for bacterial infection-induced lung injury.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e70963"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957689","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}

引用次数: 0

Diagnostic Performance of a Novel Optical Coherence Tomography-Derived Fractional Flow Reserve: A Prospective Multicenter Study. 一种新型光学相干层析衍生的分流储备的诊断性能：一项前瞻性的多中心研究。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.71015

Junyan Jin, Delong Chen, Xuebo Liu, Hao Zhou, Xueqiang Guan, Pengcheng Li, Jiniu Huang, Chenyun Zhang, Abuduwufuer Yidilisi, Yuxuan Zhang, Jiacheng Fang, Yiyue Zheng, Qiyue Gao, Haibo Chen, Qiyuan Xu, Jianan Wang, Jun Jiang

{"title":"Diagnostic Performance of a Novel Optical Coherence Tomography-Derived Fractional Flow Reserve: A Prospective Multicenter Study.","authors":"Junyan Jin, Delong Chen, Xuebo Liu, Hao Zhou, Xueqiang Guan, Pengcheng Li, Jiniu Huang, Chenyun Zhang, Abuduwufuer Yidilisi, Yuxuan Zhang, Jiacheng Fang, Yiyue Zheng, Qiyue Gao, Haibo Chen, Qiyuan Xu, Jianan Wang, Jun Jiang","doi":"10.1002/mco2.71015","DOIUrl":"10.1002/mco2.71015","url":null,"abstract":"Optical coherence tomography-derived fractional flow reserve (OCT-FFR) offers a combined assessment of anatomical and physiological lesions. However, its diagnostic accuracy needs improvement. In this prospective, multicenter, single-arm study, 210 patients across four centers with indications for percutaneous coronary intervention underwent simultaneous FFR and OCT-FFR assessments. OCT-FFR was computed using a novel multitask learning algorithm that integrated lumen segmentation and bifurcation detection, enabling fluid dynamics-based modeling of pressure gradients across coronary lesions. The primary outcome was the diagnostic accuracy of OCT-FFR. The per-protocol analysis included 200 lesions in 200 patients. The mean stenosis diameter was 67.43 ± 9.01%, and mean FFR was 0.85 ± 0.08. Using FFR ≤ 0.80 as the reference, OCT-FFR showed an accuracy of 98.0%, sensitivity of 93.6%, specificity of 99.3%, and positive predictive value of 97.8%. It showed strong correlation (r = 0.95, p < 0.001) and agreement (mean difference: -0.001 ± 0.026) with FFR. Furthermore, it demonstrated superior diagnostic accuracy compared with previous methods without patient-specific blood pressure (98.0% vs. 90.0%) or minimal lumen area optimization (98.0% vs. 93.0%) (both p < 0.01). The new algorithm exhibits excellent diagnostic performance and strong concordance with invasive FFR, potentially optimizing revascularization strategies. However, larger prospective cohorts are needed to validate these findings and confirm generalizability.Trial registration: ChiCTR2500098052.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e71015"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957616","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}

引用次数: 0

Tissue-Resident Macrophage in Inflammation and Cancer. 组织巨噬细胞在炎症和癌症中的作用。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70970

Siyuan Huang, Jiangbo Fan, Wenyi Liu, Di Liu, Rui Wang, Yuanyang Wang, Jianhui Sun, Huacai Zhang, Qingli Cai, Zhe Xu, Fang Xu, Jianxin Jiang, Zhen Wang, Ling Zeng

{"title":"Tissue-Resident Macrophage in Inflammation and Cancer.","authors":"Siyuan Huang, Jiangbo Fan, Wenyi Liu, Di Liu, Rui Wang, Yuanyang Wang, Jianhui Sun, Huacai Zhang, Qingli Cai, Zhe Xu, Fang Xu, Jianxin Jiang, Zhen Wang, Ling Zeng","doi":"10.1002/mco2.70970","DOIUrl":"10.1002/mco2.70970","url":null,"abstract":"Tissue-resident macrophages (TRMs) are long-lived immune cells strategically distributed across organs, where their functional plasticity enables both homeostatic maintenance and pathological dysfunction. This review provides a comprehensive analysis of TRM biology in inflammation and cancer. We first delineate the heterogeneity and developmental origins of TRM subsets across organs, highlighting how organ-specific niche signals create distinct vulnerability patterns. We then dissect macrophage dysfunction during sepsis, tracing their trajectory from protective anti-infectious immunity through critical tipping points to immunoparalysis. Next, we examine additional inflammatory contexts, including sterile inflammation, autoimmune inflammation, Type 2 inflammation, and metabolic inflammation, each revealing distinct facets of macrophage functional plasticity. In parallel, we examine how the tumor microenvironment chronically co-opts TRMs, transforming them into tumor-associated macrophages that promote angiogenesis, suppress antitumor immunity, facilitate metastasis, and support cancer stem cells (CSCs). Then, a systematic cross-disease comparison reveals shared mechanisms that underlie the opposing functional outputs of macrophages in inflammation and cancer. Finally, we evaluate emerging therapeutic strategies and propose a paradigm shift from functional blockade toward precise recalibration of macrophage function to restore immune balance across both disease categories. Together, this review highlights the therapeutic potential of targeting shared macrophage regulatory nodes to restore immune balance across inflammation and cancer.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e70970"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957702","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}

引用次数: 0

Microbial Signals in Cancer: Dissecting Host-Microbiota-Tumor Interactions and Potential Therapeutic Strategy. 肿瘤中的微生物信号：剖析宿主-微生物-肿瘤的相互作用和潜在的治疗策略。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70994

Juan Lu, Mengjuan Xuan, Liang Yu, Zhongyang Xie, Qingfei Chu, Shihui Wei, Tuokai Wang, Chen Xue, Lanjuan Li

{"title":"Microbial Signals in Cancer: Dissecting Host-Microbiota-Tumor Interactions and Potential Therapeutic Strategy.","authors":"Juan Lu, Mengjuan Xuan, Liang Yu, Zhongyang Xie, Qingfei Chu, Shihui Wei, Tuokai Wang, Chen Xue, Lanjuan Li","doi":"10.1002/mco2.70994","DOIUrl":"10.1002/mco2.70994","url":null,"abstract":"Cancers develop within a host ecosystem in which kinds of factors such as gut and tumor-resident microbiota influence the tumor microenvironment (TME) and therapeutic response. High-throughput sequencing has revealed the presence of low-biomass bacteria, fungi, and viruses across diverse malignancies, establishing the intratumoral microbiota as a fundamental TME component. However, evidence remains fragmented across descriptive associations, unclear mechanisms, and early clinical interventions, limiting casual interpretation and clinical translation. This review dissects the host-microbiota-tumor axis from intratumoral origins and colonization to pattern-recognition signaling, including TLR-NF-κB and cGAS-STING, and oncogenic networks such as Wnt/β-catenin, JAK-STAT, and PI3K-AKT. Moreover, it also discusses how microbial metabolites like short-chain fatty acids, secondary bile acids, and tryptophan derivatives reshape immune cell phenotypes and tumor cell metabolism. We then synthesize evidence linking microbiota to immune checkpoint blockade, chemotherapy resistance, radiotherapy toxicity, diagnosis, and prognosis. Finally, we compare translational strategies, including fecal microbiota transplantation (FMT), engineered bacteria, oncolytic viruses, and bacteriophages, together with their safety and standardization barriers. By connecting molecular mechanisms with preclinical and clinical evidence, this review comprehensively provides a framework for causal, biomarker-guided microbiota interventions.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e70994"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957708","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}

引用次数: 0

Clinical Heterogeneity of Refractory Ascites After Pediatric Liver Transplantation Modulates Allograft Rejection Risk. 小儿肝移植术后难治性腹水的临床异质性调节同种异体移植排斥风险。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.71002

Bingran Wang, Yunmu Gao, Jiaqi Song, Qi Pan, Aiwei Zhou, Hongyuan Liu, Wanglong Xiao, Zhicong Zhao, Taihua Yang, Chen Chen, Zhipeng Zong, Tao Zhou, Yi Luo, Yongbo Liu, Yuan Liu, Qiang Xia

{"title":"Clinical Heterogeneity of Refractory Ascites After Pediatric Liver Transplantation Modulates Allograft Rejection Risk.","authors":"Bingran Wang, Yunmu Gao, Jiaqi Song, Qi Pan, Aiwei Zhou, Hongyuan Liu, Wanglong Xiao, Zhicong Zhao, Taihua Yang, Chen Chen, Zhipeng Zong, Tao Zhou, Yi Luo, Yongbo Liu, Yuan Liu, Qiang Xia","doi":"10.1002/mco2.71002","DOIUrl":"10.1002/mco2.71002","url":null,"abstract":"Refractory ascites (RA) is a severe complication that impedes long-term survival after pediatric liver transplantation (LT), but its etiology remains complex and heterogeneous. To systematically evaluate the prognostic impact, clinical risk factors, and immunological features of RA, we retrospectively analyzed 1455 pediatric recipients who received LT in Renji Hospital between October 2016 and December 2021. RA was associated with increased mortality and graft loss after pediatric LT. Univariate analysis identified 13 clinical factors associated with RA, whereas a preliminary multivariable model showed only moderate discrimination, suggesting substantial heterogeneity among RA patients. Based on unsupervised clustering of clinical parameters, RA individuals were classified into two subgroups. Type I ascites was mainly associated with low graft-to-recipient weight ratio, decreased preoperative white blood cell count, and platelet count, indicating the involvement of persistent portal hypertension. In contrast, type II ascites was characterized by ABO incompatibility, elevated early postoperative soluble IL-2 receptor, and increased risk of T-cell-mediated rejection, suggesting excessive alloimmune activation. These findings indicate that RA after pediatric LT comprises distinct clinical entities with different pathogenic implications. Prudent graft selection and close monitoring of immune status may help prevent RA and improve post-transplant outcomes.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e71002"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957275","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}

引用次数: 0

Effects of Daratumumab Treatment on a Case of Overlapping Autoimmunity With Sjögren's Disease and Linear IgA Dermatosis. 达拉单抗治疗自身免疫叠加Sjögren病和线性IgA皮肤病1例疗效观察

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70881

Carlijn Hut, Rob J Volkering, Gwenny M Verstappen, Jaap A van Doesum, Frans G M Kroese, Barbara Horváth, Hendrika Bootsma, Tobit D Steinmetz

引用次数: 0

Immunotherapy With Anti-PD-1 Versus Anti-PD-L1 in SCLC: A Comprehensive Retrospective Analysis. 抗pd -1与抗pd - l1免疫治疗SCLC：一项全面的回顾性分析。

IF 14.1

MedComm Pub Date : 2026-09-11 eCollection Date: 2026-09-01 DOI: 10.1002/mco2.70872

Ruiyuan Yang, Jiadi Gan, Lan Yang, Bojiang Chen, Weimin Li

{"title":"Immunotherapy With Anti-PD-1 Versus Anti-PD-L1 in SCLC: A Comprehensive Retrospective Analysis.","authors":"Ruiyuan Yang, Jiadi Gan, Lan Yang, Bojiang Chen, Weimin Li","doi":"10.1002/mco2.70872","DOIUrl":"10.1002/mco2.70872","url":null,"abstract":"Small cell lung cancer (SCLC) is a highly malignant tumor characterized by strong invasiveness and poor prognosis. Immune checkpoint inhibitors have provided new therapeutic options for SCLC, but their comparative clinical benefit remains unclear. This retrospective study enrolled 171 patients with SCLC treated between January 2016 and June 2023, with follow-up through June 30, 2024, to compare survival and safety profiles between anti-programmed death-1 (anti-PD-1) and anti-programmed death-ligand 1 (anti-PD-L1) inhibitors. Among the 119 patients (69.6%) who received immunotherapy plus chemoradiotherapy, the median overall survival (OS) was 48.3 months, compared with 25.2 months in those who did not receive radiotherapy. Multivariable Cox regression confirmed that liver metastasis and radiotherapy status were independently associated with OS and progression-free survival (PFS). Subgroup analyses revealed that patients younger than 65 years who underwent radiotherapy, particularly those without liver metastasis, achieved longer OS with anti-PD-1 agents. In conclusion, both anti-PD-1 and anti-PD-L1 inhibitors improved the prognosis of SCLC. Patients younger than 65 years receiving radiotherapy and those with limited-stage SCLC may represent populations more likely to benefit from anti-PD-1 therapy.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 9","pages":"e70872"},"PeriodicalIF":14.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957629","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}

引用次数: 0

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