MedComm最新文献_第9页

RNA Modification in Metabolism 代谢中的RNA修饰

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70135

Yadi Liu, Zhongyan Sun, Dingkun Gui, Yonghua Zhao, Youhua Xu

{"title":"RNA Modification in Metabolism","authors":"Yadi Liu, Zhongyan Sun, Dingkun Gui, Yonghua Zhao, Youhua Xu","doi":"10.1002/mco2.70135","DOIUrl":"https://doi.org/10.1002/mco2.70135","url":null,"abstract":"Epigenetic regulation in disease development has been witnessed within this decade. RNA methylation is the predominant form of epigenetic regulation, and the most prevalent modification in RNA is N6-methyladenosine (m6A). Recently, RNA modification has emerged as a potential target for disease treatment. RNA modification is a posttranscriptional gene expression regulation that is involved in both physiological and pathological processes. Evidence suggests that m6A methylation significantly affects RNA metabolism, and its abnormal changes have been observed in a variety of diseases. Metabolic diseases are a series of diseases caused by abnormal metabolic processes of the body, the common metabolic diseases include diabetes mellitus, obesity, and nonalcoholic fatty liver disease, etc.; although the pathogenesis of these diseases differs from each other to the current understanding, most recent studies suggested pivotal role m6A in modulating these metabolic diseases, and m6A-based drug development has been on the agenda. This paper reviewed recent understanding of RNA modification in metabolic diseases, hoping to provide systematic information for those in this area.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581586","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

The Role of Yes-Associated Protein in Inflammatory Diseases and Cancer yes相关蛋白在炎性疾病和癌症中的作用

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70128

Bing Zhong, Jintao Du, Feng Liu, Silu Sun

{"title":"The Role of Yes-Associated Protein in Inflammatory Diseases and Cancer","authors":"Bing Zhong, Jintao Du, Feng Liu, Silu Sun","doi":"10.1002/mco2.70128","DOIUrl":"https://doi.org/10.1002/mco2.70128","url":null,"abstract":"Yes-associated protein (YAP) plays a central role in the Hippo pathway, primarily governing cell proliferation, differentiation, and apoptosis. Its significance extends to tumorigenesis and inflammatory conditions, impacting disease initiation and progression. Given the increasing relevance of YAP in inflammatory disorders and cancer, this study aims to elucidate its pathological regulatory functions in these contexts. Specifically, we aim to investigate the involvement and molecular mechanisms of YAP in various inflammatory diseases and cancers. We particularly focus on how YAP activation, whether through Hippo-dependent or independent pathways, triggers the release of inflammation and inflammatory mediators in respiratory, cardiovascular, and digestive inflammatory conditions. In cancer, YAP not only promotes tumor cell proliferation and differentiation but also modulates the tumor immune microenvironment, thereby fostering tumor metastasis and progression. Additionally, we provide an overview of current YAP-targeted therapies. By emphasizing YAP's role in inflammatory diseases and cancer, this study aims to enhance our understanding of the protein's pivotal involvement in disease processes, elucidate the intricate pathological mechanisms of related diseases, and contribute to future drug development strategies targeting YAP.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581584","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 Protein Family A Member 1A Attenuates Apoptosis and Oxidative Stress via ERK/JNK Pathway in Hyperplastic Prostate 热休克蛋白家族A成员1A通过ERK/JNK通路减轻增生性前列腺细胞凋亡和氧化应激

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70129

Huan Liu, Yongying Zhou, Zhen Wang, Daoquan Liu, Yan Li, Huan Lai, Jizhang Qiu, Shidong Shan, Feng Guo, Ping Chen, Yuming Guo, Guang Zeng, Michael E. DiSanto, Xinhua Zhang

{"title":"Heat Shock Protein Family A Member 1A Attenuates Apoptosis and Oxidative Stress via ERK/JNK Pathway in Hyperplastic Prostate","authors":"Huan Liu, Yongying Zhou, Zhen Wang, Daoquan Liu, Yan Li, Huan Lai, Jizhang Qiu, Shidong Shan, Feng Guo, Ping Chen, Yuming Guo, Guang Zeng, Michael E. DiSanto, Xinhua Zhang","doi":"10.1002/mco2.70129","DOIUrl":"https://doi.org/10.1002/mco2.70129","url":null,"abstract":"Benign prostatic hyperplasia (BPH) is a prevalent disorder in aging males. It is investigated whether heat shock protein family A member 1A (HSPA1A), a cytoprotective chaperone induced under stress, has been implicated in the development of BPH. RNA-sequencing and single-cell sequencing analyses revealed significant upregulation of HSPA1A in BPH compared to controls. In vitro experiments elucidated that HSPA1A was localized in prostatic epithelium and stroma, with upregulated expression in BPH tissues. Moreover, HSPA1A silencing augmented apoptosis and reactive oxygen species (ROS) accumulation, inhibiting proliferation via ERK/JNK activation, while overexpression reversed these effects in prostatic BPH-1 and WPMY-1 cells. Additionally, ERK1/2 suppression with U0126 rescued the effects of HSPA1A silencing. In vivo, testosterone-induced BPH (T-BPH) rat models treated with the HSPA1A antagonist KNK437 exhibited prostatic atrophy and molecular changes consistent with reduced HSPA1A activity. Finally, we conducted a tissue microarray (TMA) analysis of 139 BPH specimens from Zhongnan Hospital of Wuhan University, which revealed a positive correlation between HSPA1A expression and clinical parameters, including prostate volume (PV), tPSA, fPSA, and IPSS. In conclusion, our findings suggested that HSPA1A attenuated apoptosis and oxidative stress through the ERK/JNK signaling pathway, contributing to BPH pathogenesis.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581589","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

Sleep Disorders: Pathogenesis and Therapeutic Interventions 睡眠障碍：发病机制和治疗干预

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70130

Cheng Liu, Zhigang He, Yanqiong Wu, Yanbo Liu, Zhixiao Li, Yifan Jia, Hongbing Xiang

{"title":"Sleep Disorders: Pathogenesis and Therapeutic Interventions","authors":"Cheng Liu, Zhigang He, Yanqiong Wu, Yanbo Liu, Zhixiao Li, Yifan Jia, Hongbing Xiang","doi":"10.1002/mco2.70130","DOIUrl":"https://doi.org/10.1002/mco2.70130","url":null,"abstract":"Sleep disorder significantly disrupts the quality of life for patients. Although it is clinically acknowledged, the fundamental neuropathological mechanisms are still not understood. Recent preclinical research has been directed toward understanding the fundamental mechanisms underlying the sleep deprivation and sleep/wake dysregulation. Sleep disorder is linked to changes in the structure and function of the neural basis of cognition. We reviewed the neural circuits related to sleep disorders, along with alterations in connectivity and brain region functions, based on advancements in electrophysiology and optogenetic/chemogenetic techniques. We subsequently outline the cellular and molecular modifications linked to sleep disorders in preclinical studies, primarily involving changes in neuronal metabolism, electrophysiological activity, synaptic plasticity, and glial cells. Correspondingly, on the basis of the crosstalk between the brain and peripheral organs, we elucidate the underlying mechanisms of the involvement of celiac disease and hepatic disease in the pathogenesis of sleep disorders. In this review, we mainly discussed the pathogenesis at molecular, cellular, and neural circuit levels that contribute to sleep disorder. The review also covered potential strategies for treating sleep disorders and future research avenues.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581858","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

Fusobacterium nucleatum Promotes the Growth and Metastasis of Colorectal Cancer by Activating E-Cadherin/Krüppel-Like Factor 4/Integrin α5 Signaling in a Calcium-Dependent Manner 核梭杆菌以钙依赖的方式激活E-Cadherin/ kr<s:1> ppel样因子4/整合素α5信号，促进结直肠癌的生长和转移

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70137

Xuebing Yan, Xiao Qu, Jiaxin Wang, Ling Lu, Wenjuan Wu, Jingxian Mao, Donglin Li, Ying Wang, Qing Wei, Jianqiang Liu

{"title":"Fusobacterium nucleatum Promotes the Growth and Metastasis of Colorectal Cancer by Activating E-Cadherin/Krüppel-Like Factor 4/Integrin α5 Signaling in a Calcium-Dependent Manner","authors":"Xuebing Yan, Xiao Qu, Jiaxin Wang, Ling Lu, Wenjuan Wu, Jingxian Mao, Donglin Li, Ying Wang, Qing Wei, Jianqiang Liu","doi":"10.1002/mco2.70137","DOIUrl":"https://doi.org/10.1002/mco2.70137","url":null,"abstract":"Gut microbiota and integrins are known to contribute to colorectal cancer (CRC), but whether they interact has been unclear. Here, we provided evidence that Fusobacterium nucleatum upregulated integrin α5 (ITGA5) in CRC in both human patients and murine models. Knocking down ITGA5 in CRC cells weakened the ability of F. nucleatum to stimulate their malignant characteristics. Fusobacterium nucleatum increased intracellular Ca2+ concentration, which in turn promoted interaction between E-cadherin and Krüppel-like factor 4 (KLF4), resulting in KLF4 phosphorylation and translocation in the nucleus, where it induced ITGA5 transcription and activated the downstream signaling. Knocking down E-cadherin or chelating Ca2+ with BAPTA-AM antagonized the impact of F. nucleatum on KLF4, whereas knocking down KLF4 or chelating Ca2+ antagonized the bacteria's oncogenic role. Knocking down KLF4 or ITGA5 attenuated F. nucleatum–induced growth of patient-derived organoids, subcutaneous xenografts, and orthotopic tumors, as well as liver metastasis in nude mice. Integrin α5 antibody antagonized the oncogenic role of F. nucleatum in vitro and in vivo. These findings suggest that F. nucleatum promotes the growth and metastasis of CRC by activating E-cadherin/KLF4/integrin α5 signaling in a Ca2+-dependent manner.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70137","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581587","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 Utility of 18Fluorine-Fibroblast Activation Protein Inhibitor-04 Positron Emission Tomography/Computed Tomography in the Evaluation of Pancreatic Ductal Adenocarcinoma: Comparison With 18Fluorine-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography 18 -氟-成纤维细胞活化蛋白抑制剂-04正电子发射断层扫描/计算机断层扫描在胰腺导管腺癌评估中的临床应用：与18 -氟脱氧葡萄糖正电子发射断层扫描/计算机断层扫描的比较

IF 10.7

MedComm Pub Date : 2025-03-10 DOI: 10.1002/mco2.70136

Lili Lin, Guangfa Wang, Yafei Zhang, Guolin Wang, Kui Zhao, Xinhui Su

{"title":"Clinical Utility of 18Fluorine-Fibroblast Activation Protein Inhibitor-04 Positron Emission Tomography/Computed Tomography in the Evaluation of Pancreatic Ductal Adenocarcinoma: Comparison With 18Fluorine-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography","authors":"Lili Lin, Guangfa Wang, Yafei Zhang, Guolin Wang, Kui Zhao, Xinhui Su","doi":"10.1002/mco2.70136","DOIUrl":"https://doi.org/10.1002/mco2.70136","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is highly susceptible to metastasis, making early detection of metastases and associated risk factors crucial for effective management. This study aimed to assess the performance of 18fluorine (18F)- fibroblast activation protein inhibitor-04 (18F-FAPI-04) positron emission tomography/computed tomography (PET/CT) in detecting metastasis and predicting pathological characteristics and risk factors in 67 PDAC patients. Comparisons were made with 18F-fluorodeoxyglucose (18F-FDG) PET/CT. Lesion identifications and radiotracer uptakes were evaluated through visual inspection and semiquantitative analysis using the maximum standardized uptake value (SUVmax). We analyzed the risk factors for metastasis and observed that 18F-FAPI-04 identified more positive lesions and showed significantly higher SUVmax values than 18F-FDG in both primary tumors and metastases, leading to upstaging in several cases. In primary tumors, 18F-FAPI-04 was associated with higher levels of poorly differentiated PDAC, compared to those with moderately differentiated tumors. Notably, the SUVmax of 18F-FAPI-04 in primary tumors demonstrated a significant correlation with pathological differentiation and served as an independent prognostic factor for peritoneal metastasis, rather than lymph node or liver metastasis. Our findings suggested that 18F-FAPI-04 PET/CT offers superior tumor detectability and improved node-metastasis (NM) staging in PDAC patients, positioning it as a more effective tool than 18F-FDG PET/CT.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581825","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

The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions 病毒性肝炎向肝细胞癌的恶性转化：机制和干预措施

IF 10.7

MedComm Pub Date : 2025-03-08 DOI: 10.1002/mco2.70121

Huimin Yuan, Ruochen Xu, Senlin Li, Mengzhu Zheng, Qingyi Tong, Ming Xiang, Yonghui Zhang

{"title":"The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions","authors":"Huimin Yuan, Ruochen Xu, Senlin Li, Mengzhu Zheng, Qingyi Tong, Ming Xiang, Yonghui Zhang","doi":"10.1002/mco2.70121","DOIUrl":"https://doi.org/10.1002/mco2.70121","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality globally, predominantly associated with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. These infections drive persistent liver inflammation, culminating in cellular dysregulation, fibrosis, and cancer. Despite advancements in targeted therapies, drug resistance and the lack of reliable biomarkers for patient stratification still terribly hinder the treatment of viral HCC. To this end, the review delves into the intricate mechanisms underlying the malignant transformation of viral hepatitis to HCC, including viral integration, genomic instability, epigenetic modifications, oxidative stress, gut microbiota dysbiosis, chronic inflammation, immune escape, and abnormal signaling pathways, highlighting their complex interactions and synergies. Cutting-edge preclinical and clinical advancements in HCC management, including lifestyle modifications, drug therapies, immunotherapies, gene-based approaches, and innovative treatments, are further investigated, with particular priority given to their therapeutic potential and future applications in overcoming current limitations. By synthesizing recent scientific and clinical insights, this review aims to deepen the understanding of HCC pathogenesis in the context of chronic viral hepatitis, paving the way for novel therapeutic targets and personalized treatment strategies, ultimately improving patient outcomes.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581752","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

The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases 中性粒细胞胞外陷阱在自身免疫性和自身炎性疾病中的新作用

IF 10.7

MedComm Pub Date : 2025-03-06 DOI: 10.1002/mco2.70101

Liuting Zeng, Wang Xiang, Wei Xiao, Yang Wu, Lingyun Sun

{"title":"The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases","authors":"Liuting Zeng, Wang Xiang, Wei Xiao, Yang Wu, Lingyun Sun","doi":"10.1002/mco2.70101","DOIUrl":"https://doi.org/10.1002/mco2.70101","url":null,"abstract":"Neutrophil extracellular traps (NETs) are unique fibrous structures released by neutrophils in response to various pathogens, exhibiting both anti-inflammatory and proinflammatory effects. In autoimmune conditions, NETs serve as crucial self-antigens triggering inflammatory cascades by activating the inflammasome and complement systems, disrupting self-tolerance mechanisms and accelerating autoimmune responses. Furthermore, NETs play a pivotal role in modulating immune cell activation, affecting adaptive immune responses. This review outlines the intricate relationship between NETs and various diseases, including inflammatory arthritis, systemic autoimmune diseases, Behçet's disease, systemic lupus erythematosus, autoimmune kidney diseases, autoimmune skin conditions, systemic sclerosis, systemic vasculitis, and gouty arthritis. It highlights the potential of targeting NETs as a therapeutic strategy in autoimmune diseases. By examining the dynamic balance between NET formation and clearance in autoimmune conditions, this review offers critical insights and a theoretical foundation for future research on NET-related mechanisms. Advances in systems biology, flow cytometry, and single-cell multiomics sequencing have provided valuable tools for exploring the molecular mechanisms of neutrophils and NETs. These advancements have renewed focus on the role of neutrophils and NETs in autoimmune diseases, offering promising avenues for further investigation into their clinical implications.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143564992","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

Colorectal Cancer: Pathogenesis and Targeted Therapy 结直肠癌：发病机制和靶向治疗

IF 10.7

MedComm Pub Date : 2025-03-06 DOI: 10.1002/mco2.70127

Jingyuan Li, Jiashu Pan, Lisheng Wang, Guang Ji, Yanqi Dang

{"title":"Colorectal Cancer: Pathogenesis and Targeted Therapy","authors":"Jingyuan Li, Jiashu Pan, Lisheng Wang, Guang Ji, Yanqi Dang","doi":"10.1002/mco2.70127","DOIUrl":"https://doi.org/10.1002/mco2.70127","url":null,"abstract":"Colorectal cancer (CRC) ranks among the most prevalent malignant neoplasms globally. A growing body of evidence underscores the pivotal roles of genetic alterations and dysregulated epigenetic modifications in the pathogenesis of CRC. In recent years, the reprogramming of tumor cell metabolism has been increasingly acknowledged as a hallmark of cancer. Substantial evidence suggests a crosstalk between tumor cell metabolic reprogramming and epigenetic modifications, highlighting a complex interplay between metabolism and the epigenetic genome that warrants further investigation. Biomarkers associated with the pathogenesis and metabolic characteristics of CRC hold significant clinical implications. Nevertheless, elucidating the genetic, epigenetic, and metabolic landscapes of CRC continues to pose considerable challenges. Here, we attempt to summarize the key genes driving the onset and progression of CRC and the related epigenetic regulators, clarify the roles of gene expression and signaling pathways in tumor metabolism regulation, and explore the potential crosstalk between epigenetic events and tumor metabolic reprogramming, providing a comprehensive mechanistic explanation for the malignant progression of CRC. Finally, by integrating reliable targets from genetics, epigenetics, and metabolic processes that hold promise for translation into clinical practice, we aim to offer more strategies to overcome the bottlenecks in CRC treatment.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565068","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

PD-1/PD-L1 Inhibitors Plus Chemotherapy Versus Chemotherapy Alone as First-Line Therapy for Patients With Unfavorable Cancer of Unknown Primary: A Multicenter, Retrospective Cohort Study 一项多中心、回顾性队列研究：PD-1/PD-L1抑制剂联合化疗与单独化疗作为一线治疗原发不明的不良癌症患者

IF 10.7

MedComm Pub Date : 2025-03-06 DOI: 10.1002/mco2.70124

Riqing Huang, Haifeng Li, Shuo Li, Ditian Shu, Rishang Chen, Zhousan Zheng, Tinghua Gao, Meiting Chen, Anqi Hu, Yunjie Huang, Qiufan Zheng, Xin An, Cong Xue, Yuchen Cai, Yanxia Shi

{"title":"PD-1/PD-L1 Inhibitors Plus Chemotherapy Versus Chemotherapy Alone as First-Line Therapy for Patients With Unfavorable Cancer of Unknown Primary: A Multicenter, Retrospective Cohort Study","authors":"Riqing Huang, Haifeng Li, Shuo Li, Ditian Shu, Rishang Chen, Zhousan Zheng, Tinghua Gao, Meiting Chen, Anqi Hu, Yunjie Huang, Qiufan Zheng, Xin An, Cong Xue, Yuchen Cai, Yanxia Shi","doi":"10.1002/mco2.70124","DOIUrl":"https://doi.org/10.1002/mco2.70124","url":null,"abstract":"This multicenter study aimed to investigate the efficacy and safety of PD-1/PD-L1 inhibitors plus chemotherapy (ICI-Chemo group) versus chemotherapy alone (Chemo group) for patients with cancer of unknown primary (CUP) in the first-line setting. We included patients with unfavorable CUP across four medical centers in China. Between January 2014 and December 2023, 117 patients were enrolled: 46 patients in the ICI-Chemo group and 71 patients in the Chemo group. After a median follow-up of 28.1 months, the ICI-Chemo group exhibited a significant improvement over the Chemo group in median PFS (9.10 months vs. 6.37 months; hazard ratio [HR] 0.46; 95% CI: 0.30–0.71; p < 0.001) and OS (35.67 months vs. 10.2 months; HR 0.37; 95% CI: 0.22–0.64; p < 0.001). Similarly, among patients who received TP (taxane plus platinum)-based chemotherapies, OS and PFS benefits were observed in the ICI-Chemo group. The objective response rate was higher in the ICI-Chemo group than in the Chemo group (54.35% vs. 22.53%, p < 0.001). Grade 3 or higher drug-related adverse events occurred in 11 patients (23.91%) in the ICI-Chemo group and 28 patients (39.44%) in the Chemo group. Thus, PD-1/PD-L1 inhibitors plus chemotherapy could be the preferred first-line treatment for patients with unfavorable CUP, providing improved efficacy and manageable toxicity.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565069","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