MedComm最新文献

{"title":"The Long Noncoding RNA LINC02820 Promotes Tumor Growth and Metastasis Through Regulating MYH9 Expression in Esophageal Squamous Cell Carcinoma","authors":"Xiaomin Xu,&nbsp;Xinting Mao,&nbsp;Wenrong Liu,&nbsp;Yue Ming,&nbsp;Tingting Zhang,&nbsp;Yang Yang,&nbsp;A-Lai Gu-Ha,&nbsp;Yi-Dan Lin,&nbsp;Yong Peng","doi":"10.1002/mco2.70218","DOIUrl":"https://doi.org/10.1002/mco2.70218","url":null,"abstract":"<p>Long noncoding RNAs (lncRNAs) play important roles in tumorigenesis, but their biological functions and mechanisms in esophageal squamous cell carcinoma (ESCC) remain poorly understood. In this study, we employed high-throughput sequencing and bioinformatics analyses to identify the differentially expressed lncRNAs between ESCC tumors and adjacent normal tissues, among which LINC02820 is significantly upregulated in ESCC. Rapid amplification of cDNA ends assays determined the transcription initiation and termination sites of LINC02820, confirming it as a novel transcript variant localized in both the nucleus and cytoplasm of ESCC cells. Functional studies demonstrated that LINC02820 promotes cell proliferation and migration in vitro and enhances tumor growth and metastasis in vivo. Mechanistically, LINC02820 interacts with Myosin-9 protein and prevent it from ubiquitination-mediated proteasomal degradation. Additionally, the RNA-binding protein insulin-like growth factor 2 mRNA-binding protein 2 binds to LINC02820 and increase its RNA stability in ESCC cells, thus upregulating LINC02820 expression. Therefore, these findings indicate LINC02820 as an oncogenic lncRNA in ESCC progression and suggest its potential as a therapeutic target.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144117923","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":"DLGAP5 mutations Disrupt Normal Chromosome Segregation and Spindle Formation of human Oocyte Meiosis and Lead to Female Infertility","authors":"Meng Wang,&nbsp;Zhou Li,&nbsp;Juepu Zhou,&nbsp;Rui Long,&nbsp;Qingsong Xi,&nbsp;Hong Gao,&nbsp;Youzhu Li,&nbsp;Lei Jin,&nbsp;Lixia Zhu","doi":"10.1002/mco2.70224","DOIUrl":"https://doi.org/10.1002/mco2.70224","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;&lt;p&gt;Nowadays, approximately one out of six couples of reproductive age are confronted with infertility. Assisted reproductive technology (ART) constitutes one of the most effective measures to address this issue; however, in certain instances, ART fails [&lt;span&gt;1&lt;/span&gt;]. Moreover, some patients experience recurrent ART failure with a uniform phenotype, suggesting a genetic component to their condition [&lt;span&gt;2&lt;/span&gt;]. Recently, the advent of whole-exome sequencing (WES) has led to the identification of an increasing number of genetic causes of human infertility [&lt;span&gt;3&lt;/span&gt;]. However, the genetic underpinnings of a significant proportion of cases remain enigmatic [&lt;span&gt;3&lt;/span&gt;]. Consequently, it is imperative to elucidate the potential genetic determinants of ART failure and to identify novel genetic etiologies for genetic counseling, as well as for the diagnosis and treatment of infertility patients.&lt;/p&gt;&lt;p&gt;In this study, we observed a pair of sisters who were undergoing ART. Both of the sisters were diagnosed with unexplained primary infertility. Following numerous in vitro fertilization (IVF) and/or intracytoplasmic sperm injection (ICSI) cycles, they failed to conceive, and the majority of their oocytes were immature. Subsequent genetic analysis identified a homozygous nonsense mutation c.1101C&gt;G (p.Tyr367*) in &lt;i&gt;DLGAP5&lt;/i&gt; in both sisters. The parents of the sisters are known to be from a consanguineous marriage family (family 1). The father was a heterozygous carrier, and the mother had already passed away (Figure 1A). This mutation is not indexed in the gnomAD (v4.1) database, and the affected amino acids were found to be highly evolutionarily conserved in different species. In the further expansion of screening, the same homozygous mutation c.1101C&gt;G (p.Tyr367*) in &lt;i&gt;DLGAP5&lt;/i&gt; was also identified in another patient suffering from primary infertility. Her mother was found to be a heterozygous carrier of the mutation (Figure 1A). She has undergone three fresh IVF cycles, and the majority of oocytes retrieved were also immature (Table S1). Consequently, no embryos were available, and the cycles had to be terminated.&lt;/p&gt;&lt;p&gt;Discs large-associated protein 5 (DLGAP5), also known as hepatoma upregulated protein (HURP), has been initially found to be upregulated in hepatocellular carcinoma cells [&lt;span&gt;4&lt;/span&gt;]. It has been demonstrated to play a role in cell division and cancer biology [&lt;span&gt;5&lt;/span&gt;]. Research has shown that DLGAP5 is a microtubule-associated protein that contributes to chromosome movement and alignment by stabilizing mitotic microtubules and regulating microtubule dynamics to ensure proper chromosome segregation during cell division [&lt;span&gt;6-8&lt;/span&gt;]. In addition, female &lt;i&gt;Dlgap5&lt;/i&gt; knockout mice are infertile [&lt;span&gt;9&lt;/span&gt;]. These animals have been observed to exhibit implantation failure due to defects in endometrial mesenchymal proliferation [&lt;span&gt;9&lt;/span&gt;], as well as aneuploid embryo","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118120","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":"A Novel Intravascular Lithotripsy System in Severely Calcified Coronary Lesions: The Prospective COronary CAlcified Lesion Lithotripsy Procedure (COCALP) Study","authors":"Xin Deng,&nbsp;Yiqing Hu,&nbsp;Guosheng Fu,&nbsp;Genshan Ma,&nbsp;Xuebo Liu,&nbsp;Bei Shi,&nbsp;Jianfang Luo,&nbsp;Jingfeng Wang,&nbsp;Zhixiong Zhong,&nbsp;Hanbin Cui,&nbsp;Likun Ma,&nbsp;Juying Qian,&nbsp;Jian'an Wang,&nbsp;Hao Lu,&nbsp;Junbo Ge","doi":"10.1002/mco2.70208","DOIUrl":"https://doi.org/10.1002/mco2.70208","url":null,"abstract":"<p>Intravascular lithotripsy (IVL) is a promising therapy for calcified coronary lesions. This study evaluated the safety and effectiveness of a novel IVL system. The <b>CO</b>ronary <b>CA</b>lcified Lesion <b>L</b>ithotripsy <b>P</b>rocedure (COCALP) study (No. ChiCTR2300073280) was a prospective, multicenter, single-arm trial involving 266 patients with severely calcified coronary lesions. The primary endpoint was procedural success, defined as successful stent implantation with ≤30% residual stenosis and no in-hospital major adverse cardiovascular events (MACE). In a subgroup, calcium morphology was evaluated by optical coherence tomography (OCT) assessment. A total of 266 patients were included. The procedural success rate was 97.4% (95% confidence interval [CI]: 0.947–0.989), with the lower limit of the CI exceeding the prespecified performance goal (<i>p</i> &lt; 0.001). No MACE occurred intraoperatively. During hospitalization, MACE occurred in five patients (1.9%), all of which were myocardial infarctions. MACE rates at 1 and 6 months were 2.3 and 3.4%, respectively. In the OCT subgroup (<i>n</i> = 76), IVL induced a 76.8% rate of calcification fracture. The minimal lumen area increased from 1.77 ± 0.72 to 2.59 ± 1.11 mm² following IVL (<i>p </i>&lt; 0.001), and further expanded to 5.22 ± 1.69 mm² poststenting (<i>p </i>&lt; 0.001). The novel IVL system demonstrated high effectiveness and safety, supporting its use for treating severely calcified coronary lesions and enhancing stent implantation success.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70208","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144100526","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":"Synergistic PD-1/LAG-3 Inhibition: Mechanistic Insights and Implications for Enhanced Tumor Immunotherapy","authors":"Jianqiao Shentu,&nbsp;Hening Xu,&nbsp;Shiwei Duan","doi":"10.1002/mco2.70216","DOIUrl":"https://doi.org/10.1002/mco2.70216","url":null,"abstract":"&lt;p&gt;In the August issue of &lt;i&gt;Cell&lt;/i&gt; 2024, three pivotal studies published in &lt;i&gt;Cell&lt;/i&gt; by the Vignali and Wherry research teams advanced our understanding of programmed cell death protein 1 (PD-1)/lymphocyte activation gene 3 (LAG-3) synergy in T cell exhaustion [&lt;span&gt;1-3&lt;/span&gt;]. This provides new therapeutic strategies for clinical guidance in anti-infection and antitumor treatments.&lt;/p&gt;&lt;p&gt;PD-1 and LAG-3 are both key inhibitory receptors (IRs). In the context of tumors and chronic viral infections, their expression on CD8&lt;sup&gt;+&lt;/sup&gt; T cells increase, hampering the immune system's ability to eliminate these threats. Research indicates that PD-1 and LAG-3 jointly contribute to T cell exhaustion, diminishing effector functions and weakening antitumor immunity. Clinically, the combination of PD-1 and LAG-3 inhibitors has shown remarkable success—particularly in the RELATIVITY-047 melanoma trial—improving progression-free survival (PFS) and demonstrating superior efficacy in neoadjuvant settings compared to PD-1 monotherapy, while maintaining a favorable toxicity profile. However, mechanistic uncertainties persist [&lt;span&gt;4&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;In the first study, the Vignali team utilized mouse models and clinical data to explore the synergistic effects of PD-1 and LAG-3 on T cell function and antitumor immunity [&lt;span&gt;2&lt;/span&gt;]. In a melanoma mouse model, CD8&lt;sup&gt;+&lt;/sup&gt; T cells deficient in both PD-1 and LAG-3 exhibited enhanced tumor clearance and improved survival rates. Transcriptomic analysis revealed that the absence of PD-1 and LAG-3 led to increased T-cell receptor (TCR) clonality and upregulation of effector-like and interferon-responsive genes. These transcriptional changes boosted IFN-γ secretion and enhanced T cell antitumor efficacy. The study discovered that the increase in IFN-γ does not directly drive antitumor immunity by regulating tumor cells or other cells within the tumor microenvironment. Instead, it acts on CD8&lt;sup&gt;+&lt;/sup&gt; T cells themselves in an intracellular and autocrine manner to enhance their function. Particularly, the upregulation of CCL5 may play a crucial role in this process, although CCL5 might have diverse functions in different environments. Further studies have demonstrated that PD-1 and LAG-3 jointly promote the exhaustion of CD8&lt;sup&gt;+&lt;/sup&gt; T cells and restrict their proliferation and effector functions. This process is closely associated with the regulation of the transcription factor TOX. Specifically, the loss of PD-1 and LAG-3 significantly reduces the expression level of TOX, indicating that these two receptors have a synergistic effect in regulating the development of T cell exhaustion. Especially in regulating TOX expression, LAG-3 exhibits a more significant dominant role. Additionally, the study also found that in the context of PD-1 and LAG-3 loss, the expression pattern of natural killer group 2 member A (NKG2A) shows interesting inconsistencies in monoclonal and polyclonal systems. This difference","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144100527","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":"Aptamers: Design, Theory, and Applications to Diagnosis and Therapy for Diseases","authors":"Sepideh Hassibian,&nbsp;Mahsa Amin,&nbsp;Seyed Mohammad Taghdisi,&nbsp;Elham Sameiyan,&nbsp;Reza Ghaffari,&nbsp;Mona Alibolandi,&nbsp;Mohammad Ramezani,&nbsp;Khalil Abnous,&nbsp;Seyed Mohsen Dehnavi","doi":"10.1002/mco2.70180","DOIUrl":"https://doi.org/10.1002/mco2.70180","url":null,"abstract":"<p>Single-stranded DNA or RNA entities referred to as aptamers exhibit a strong affinity and specificity for attaching to specific targets. Owing to their special properties, which include simplicity of synthesis, low immunogenicity, and adaptability in targeting a variety of substances, these synthetic oligonucleotides have garnered a lot of interest. The function of aptamers can be altered by combining them with complementary oligonucleotides “antidotes,” which are antisense to a particular aptamer sequence. Antidotes play an important role in several fields by specifically targeting the corresponding section of the aptamer. Nevertheless, even with their promising capabilities, the creation of antidotes to regulate or inhibit aptamer function continues to be a relatively unexamined field, constraining their secure and efficient application in medical environments. The review explores experimental methodologies for creating antidotes, the systematic design strategies for managing antidotes in aptamer-based therapies, and their therapeutic efficacy in counteracting disease biomarkers. Additionally, it highlights their diagnostic applications in biosensing and imaging, offering a promising alternative to traditional antibodies. It also investigates the progress, latest innovations, and potential medical uses of aptamer–antidote combinations. Its academic value lies in bridging the gap between theoretical design and practical applications, providing researchers and clinicians with a comprehensive resource to advance aptamer-based solutions in medicine and biotechnology.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 5","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70180","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085047","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":"Carotid Plaque-Derived Small Extracellular Vesicles Mediate Atherosclerosis and Correlate With Plaque Vulnerability","authors":"Xin Xu,&nbsp;Taoyuan Lu,&nbsp;Yao Feng,&nbsp;Wenbo Cao,&nbsp;Dianwei Liu,&nbsp;Peng Gao,&nbsp;Yan Ma,&nbsp;Yabing Wang,&nbsp;Bin Yang,&nbsp;Yanfei Chen,&nbsp;Jian Chen,&nbsp;Ran Xu,&nbsp;Xinyu Wang,&nbsp;Lebin Chen,&nbsp;Yuanyuan Ji,&nbsp;Liqun Jiao","doi":"10.1002/mco2.70220","DOIUrl":"https://doi.org/10.1002/mco2.70220","url":null,"abstract":"<p>Carotid plaque-derived small extracellular vesicles (psEVs) offer insights into tissue- and disease-specific pathobiology, but their roles in plaque vulnerability and their diagnostic potential remain unclear. Herein, we isolated psEVs from stable and vulnerable (intraplaque hemorrhage [IPH] or fibrous cap rupture [FCR]) plaques in patients with asymptomatic carotid artery stenosis (aCAS). Our findings demonstrated that psEVs alone were sufficient to induce inflammatory endothelial dysfunction in vitro and exacerbate atherogenesis in ApoE-deficient mice. MicroRNA sequencing of psEVs (sequencing cohort, <i>n</i> = 18) identified 21 differentially expressed microRNAs (DEmiRNAs) distinguishing stable and vulnerable plaques, and 41 DEmiRNAs differentiating IPH from FCR subtypes. Subsequent validation using qRT-PCR and the High-throughput nano-bio chip integrated system for liquid biopsy system revealed that plasma-derived sEV miR-497-5p, miR-152-3p, and miR-204-5p effectively differentiated stable plaques from vulnerable plaques, while miR-23a-3p and miR-143-5p further distinguished IPH from FCR subtypes, in <i>both</i> the discovery cohort (n = 178) and an independent external cohort (n = 82). Mechanistic investigations identified miR-497-5p as a key mediator of vulnerable psEVs' proinflammatory and proatherogenic effects through directly targeting atheroprotective uncoupling protein 2 (UCP2). These findings highlight the roles of psEVs in atherogenesis and plaque vulnerability, providing valuable insights for risk stratification and therapeutic decision-making in aCAS patients.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085376","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":"A Combined-Mode Machine Learning Model for Predicting Stroke Recurrence During Hospitalization in Patients with Acute Minor Ischemic Stroke","authors":"Wanxing Ye,&nbsp;Jin Gan,&nbsp;Meng Wang,&nbsp;Ziyang Liu,&nbsp;Hongqiu Gu,&nbsp;Xin Yang,&nbsp;Chunjuan Wang,&nbsp;Xia Meng,&nbsp;Yong Jiang,&nbsp;Hao Li,&nbsp;Liping Liu,&nbsp;Yongjun Wang,&nbsp;Zixiao Li","doi":"10.1002/mco2.70234","DOIUrl":"https://doi.org/10.1002/mco2.70234","url":null,"abstract":"<p>Acute minor ischemic stroke patients often experience recurrence shortly after symptom onset, highlighting the importance of predicting stroke recurrence for guiding treatment decisions. This study evaluated the effectiveness of machine learning models in predicting in-hospital recurrence. The study cohort comprised 322,135 patients with acute minor ischemic stroke from 1439 centers, as established by Chinese Stroke Center Alliance. Patients were randomly allocated into training and test sets by different centers. Models including extreme gradient boosting (XGB), light gradient boosting (LGB), and adaptive boosting (ADA) were developed using fivefold cross-validation on the training set. Optimization was performed for all models based on the most important variable, history of ischemic stroke. Compared with the traditional generalized linear model (GLM), the XGB, LGB, ADA models yielded area under the curve (AUC) values ranging from 0.788 to 0.803 after optimization. All models showed significant improvements in AUC compared with GLM, with LGB exhibiting the most substantial enhancement after optimization. For the first time, this study developed models specifically designed to predict in-hospital stroke recurrence in acute minor ischemic stroke patients. This finding aids in identifying high-risk patients and prompts physicians to provide targeted treatment. However, further external validation is warranted to confirm the model's generalizability.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70234","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085042","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":"Immune Reconstitution after Haploidentical Hematopoietic Stem Cell Transplantation with Different Non-T-Cell Depletion Protocols","authors":"Xiao-Di Ma,&nbsp;Zheng-Li Xu,&nbsp;Xiao-Jun Huang","doi":"10.1002/mco2.70206","DOIUrl":"https://doi.org/10.1002/mco2.70206","url":null,"abstract":"<p>Haploidentical hematopoietic stem cell transplantation (haplo-HSCT) has emerged as a critical treatment for hematological diseases. However, challenges, such as graft rejection and graft-versus-host disease (GVHD), have historically been faced with this procedure. Immune reconstitution (IR) has been shown to have profound effects on posttransplantation complications, such as relapse, infections, and GVHD. Recent advances in non-T-cell depletion protocols including the Beijing protocol and Baltimore protocol have significantly influenced the outcomes of haplo-HSCT by improving IR. Clinical studies and multiomic analyses have revealed that different protocols offer distinct mechanisms for IR patterns and further influence clinical outcomes. However, there is a lack of comprehensive reviews that systematically link the differences in IR between two protocols to their clinical outcomes, which leaves a critical gap in understanding the optimal strategies for IR in haplo-HSCT. This review provides an analysis of IR following haplo-HSCT with different protocols; it compares the clinical outcomes of various protocols, addresses the role of each immune cell subset in influencing outcomes and discusses emerging strategies aimed at improving IR. This review highlights the importance of ongoing research for improving immune reconstitution strategies, ultimately reducing posttransplant complications and offering targeted treatments to improve patient outcomes.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70206","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085467","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":"Platelet-to-Neutrophil Ratio: A Novel Prognostic Indicator for Anti-PD-1-Based Therapy in Relapsed/Refractory Hodgkin Lymphoma and Solid Tumors","authors":"Yuting Pan,&nbsp;Xin Zhang,&nbsp;Chunmeng Wang,&nbsp;Nannan Lu,&nbsp;Yang Liu,&nbsp;Yixin Chang,&nbsp;Xueting Qin,&nbsp;Weidong Han,&nbsp;Jing Nie","doi":"10.1002/mco2.70199","DOIUrl":"https://doi.org/10.1002/mco2.70199","url":null,"abstract":"<p>Program cell death-1 (PD-1) blockade treatment has been shown effective in cases with relapsed/refractory classical Hodgkin Lymphoma (R/R cHL), while prognostic biomarkers remain unclear. Seventy-seven cases with R/R cHL who received immunotherapy for the first time were included. Receiver operator characteristic analysis displayed platelet-to-neutrophil ratio (PNR) as the most probable indicator among distinct inflammatory-cell ratios. Patients with high pretreatment PNR (≥ 51.6) achieved significantly higher complete response (CR) rate as compared with patients with low PNR (&lt; 51.6), and PNR^high patients displayed significantly longer progression-free survival (PFS) versus PNR^low patients (<i>p</i> = 0.001). Cox analysis indicated PNR as an independent factor for prognosis (hazard ratio, 0.34, 95% CI, 0.18–0.65, <i>p</i> = 0.001). Among patients acquiring CR, higher PNR was associated with improved PFS and relapse-free survival. Moreover, PNR correlations with CR rate and PFS were validated in external cohort of cHL. Notably, PNR was also a strong prognostic biomarker for PFS and overall survival after anti-PD-1 combination therapy in patients with solid tumors, such as biliary tract carcinoma, gastric carcinoma, or colon cancer. In conclusion, this study for the first time reveals a correlation between pretreatment peripheral PNR and prognosis of anti-PD-1-based therapy in patients with relapsed/refractory cHL and advanced solid tumor.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70199","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074280","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":"Application of 68Ga- and 177Lu-Labeled FAP Inhibitor in Evaluation and Treatment of Cardiac Fibrosis After Myocardial Infarction","authors":"Yiheng Zhao,&nbsp;Xiangyu Su,&nbsp;Boyang Xiang,&nbsp;Shuchen Zhang,&nbsp;Xiang Zhou","doi":"10.1002/mco2.70198","DOIUrl":"https://doi.org/10.1002/mco2.70198","url":null,"abstract":"<p>⁶⁸Ga and ¹⁷⁷Lu-labeled fibroblast activation protein inhibitor (FAPI) have been introduced for the diagnosis and treatment of multiple malignant and non-malignant diseases. While several studies have examined the application of ⁶⁸Ga-FAPI in myocardial infarction (MI), research on the use of ¹⁷⁷Lu-FAPI for the treatment of MI is still scarce. In this study, we evaluated the effects of ⁶⁸Ga-FAPI and ¹⁷⁷Lu-FAPI in cardiac fibrosis after MI using permanent coronary artery ligation rat models. ⁶⁸Ga-FAPI-04 effectively targeted fibroblasts within the MI area. Rats treated with ¹⁷⁷Lu-FAPI-04 had a significant increase in left ventricular ejection fraction at 28 days post-MI, with no obvious kidney or liver toxicity. Magnetic resonance imaging and histological analysis revealed a reduced fibrotic area in the ¹⁷⁷Lu-FAPI group. ¹⁷⁷Lu-FAPI-04 exerted its therapeutic effect by suppressing activation and inducing apoptosis of fibroblasts. In summary, we demonstrated that ¹⁷⁷Lu-FAPI-04 could effectively target FAP and eliminate activated fibroblasts after MI, thereby contributing to the development of new strategies for the treatment of MI.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70198","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074279","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}