Translational Oncology最新文献

{"title":"In vivo inhibition of angiogenesis by htsFLT01/MiRGD nano complex","authors":"Mohadeseh Khoshandam ,&nbsp;Zahra-Soheila Soheili ,&nbsp;Saman Hosseinkhani ,&nbsp;Shahram Samiee ,&nbsp;Hamid Latifi-Navid ,&nbsp;Hamid Ahmadieh ,&nbsp;Hossein Soltaninejad ,&nbsp;Babak Jahangiri","doi":"10.1016/j.tranon.2025.102400","DOIUrl":"10.1016/j.tranon.2025.102400","url":null,"abstract":"<div><div>The inhibition of angiogenesis is a crucial therapeutic strategy in cancer treatment, as it limits tumor growth and metastasis. In this study, we investigate the anti-angiogenic potential of a novel htsFLT01/MiRGD nanocomplex, designed to target key angiogenesis markers in cancer. This nanocomplex integrates the anti-angiogenic fusion protein htsFLT01 with the MiRGD peptide to enhance its efficacy. Our findings demonstrate that htsFLT01/MiRGD effectively suppresses angiogenesis both in vitro and in vivo, particularly in breast cancer models. Histological and molecular analyses reveal a significant reduction in blood vessel formation, accompanied by structural changes in tumor tissue. Furthermore, the expression levels of key angiogenesis-related genes, including VEGF, VEGFR, and CD31, are markedly downregulated, highlighting the therapeutic potential of this nanocomplex. Beyond its anti-angiogenic effects, the treatment also induces apoptosis and inhibits tumor cell proliferation, reinforcing its role as a promising targeted therapy for angiogenesis-dependent malignancies. These results underscore the potential of htsFLT01/MiRGD in cancer treatment and pave the way for future clinical applications in anti-angiogenic therapies.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102400"},"PeriodicalIF":5.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant overexpression of m6A writer and reader genes in pediatric B-Cell Acute Lymphoblastic Leukemia (B-ALL)","authors":"Sumedha Saluja ,&nbsp;Shuvadeep Ganguly ,&nbsp;Jay Singh ,&nbsp;Ayushi Jain ,&nbsp;Gunjan Sharma ,&nbsp;Shilpi Chaudhary ,&nbsp;Karthikeyan Pethusamy ,&nbsp;Parthaprasad Chattopadhyay ,&nbsp;Anita Chopra ,&nbsp;Archna Singh ,&nbsp;Subhradip Karmakar ,&nbsp;Sameer Bakhshi ,&nbsp;Jayanth Kumar Palanichamy","doi":"10.1016/j.tranon.2025.102403","DOIUrl":"10.1016/j.tranon.2025.102403","url":null,"abstract":"<div><h3>Background</h3><div>m6A modification, regulated by writers (METTL3, METTL14), erasers (ALKBH5, FTO), and readers (IGF2BPs), is implicated in various cancers, including leukemias.</div></div><div><h3>Methods</h3><div>In our study, we examined a cohort of 227 pediatric B-ALL patients (152 primary and 75 relapsed) and assessed the expression profiles of m6A machinery genes, including both writers and erasers, as well as the IGF2BP RNA-binding proteins, which are known as m6A readers. We also quantified the absolute percentage of m6A (m6A%). The correlation between m6A machinery gene expression and patient prognosis was studied using univariate and multivariate analyses.</div></div><div><h3>Results</h3><div>Our analysis revealed a significant upregulation of m6A writers (METTL3 and METTL14), erasers (FTO), and m6A readers (IGF2BPs 1 and 3) in B-ALL patients, both in the primary and relapsed groups. m6A% levels were markedly higher in B-ALL samples than in controls. Multivariate analysis revealed that the expression of IGF2BP3, METTL3, and FTO genes, independently predicted lower overall survival and event-free survival in primary B-ALL patients.</div></div><div><h3>Conclusions</h3><div>Despite the collective dysregulation of the m6A machinery, the writers and readers appear to have a more dominant phenotype, as evidenced by the significantly elevated m6A% levels. This is the first study to analyze and establish the role of m6A machinery gene expression and its correlation with survival outcomes in a large group of B-ALL patients. These findings could aid in the development of new therapeutics targeting the m6A machinery and help predict relapse in pediatric B-ALL patients.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102403"},"PeriodicalIF":5.0,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143876527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine inhibits metastasis of ovarian cancer by blocking lipid metabolism, alleviating aging of adipose tissue and increasing tumor infiltrating immune cells","authors":"Xiaojie Zhang ,&nbsp;Bing Xiong ,&nbsp;Yujie Cheng ,&nbsp;Jimei Huang ,&nbsp;Jiaying Xue ,&nbsp;Xiao Li ,&nbsp;Wei Lu ,&nbsp;Jihui Zhu ,&nbsp;Lian Wang ,&nbsp;Weihong Yang ,&nbsp;Zhongping Cheng","doi":"10.1016/j.tranon.2025.102380","DOIUrl":"10.1016/j.tranon.2025.102380","url":null,"abstract":"<div><div>Extensive peritoneal metastasis and malignant ascites continue to pose substantial challenges in achieving favorable treatment outcomes for ovarian cancer. Berberine (BBR), an active component of numerous traditional Chinese herbs, has demonstrated potent anti - tumor effects across various malignancies, including ovarian cancer. In this study, we comprehensively evaluated the impact of BBR on the growth and metastasis of ovarian cancer both <em>in vitro</em> and <em>in vivo</em>. RNA - sequencing was employed to elucidate the underlying mechanisms. Specifically, we investigated lipid metabolism and mitochondrial function in ovarian cancer cells and mice, comparing BBR - treated and untreated groups. Additionally, CIBERSORT analysis and immunohistochemical (IHC) staining were utilized to confirm BBR's ability to enhance the infiltration of tumor-infiltrating immune cells into adipose tissue and improve the inflammatory tumor microenvironment. Our findings indicate that BBR significantly inhibits the growth and metastasis of ovarian cancer <em>in vitro</em> and <em>in vivo</em>. The effects can be attributed to two key processes. Firstly, BBR suppresses the lipid metabolism by downregulating lipid uptake related receptor CD36, lipid metabolic enzyme and mitochondrial function. Secondly, BBR alleviates the aging of adipose tissue and adipose derived stem cells (ADSCs), thereby decreasing the secretion of senescence-associated secretory phenotype (SASP). These ultimately lead to the increasing the improvement of tumor infiltrating immune cells, such as CD4⁺ helper T cells (CD3⁺CD4⁺) and cytotoxic T lymphocytes (CD3⁺CD8⁺), and inflammation in ovarian cancer tissue. Collectively, these findings suggested a potential therapeutic effect of BBR in the treatment of advanced ovarian cancer, particularly cases complicated by peritoneal metastasis and malignant ascites.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102380"},"PeriodicalIF":5.0,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM25 facilitates ferroptosis in ovarian cancer through promoting PIEZO1 K63-linked ubiquitination and degradation","authors":"Ya Li,&nbsp;Fei Zhou,&nbsp;Zhengmei Xu","doi":"10.1016/j.tranon.2025.102386","DOIUrl":"10.1016/j.tranon.2025.102386","url":null,"abstract":"<div><h3>Background</h3><div>Ovarian cancer represents a significant threat to women's health. and ferroptosis is recognized as a potential natural inhibitor in cancer therapy, the regulatory mechanism of TRIM25 in ovarian cancer and its potential for regulating ferroptosis as a treatment remain unclear.</div></div><div><h3>Methods</h3><div>The role of TRIM25 in ovarian cancer was examined through functional gain- and loss-of-function assays both in vitro and in vivo, while its target genes were identified. The stability and ubiquitination sites of PIEZO1 were analyzed using protein docking and ubiquitination experiments.</div></div><div><h3>Results</h3><div>TRIM25 is highly expressed in ovarian cancer and promotes the growth and metastasis of ovarian cancer cells both in vivo and in vitro. Mechanistically, it facilitates PIEZO1 degradation through ubiquitination-dependent proteasome activity, inhibits ferroptosis, and stimulates ovarian cancer cell growth.</div></div><div><h3>Conclusion</h3><div>Our study clearly shows that TRIM25 stimulates ovarian cancer by inducing K63-linked ubiquitination of PIEZO1, which suppresses ferroptosis and promotes excessive proliferation of ovarian cancer cells. Further research identified the ubiquitination modification site on PIEZO1, providing insights for ovarian cancer treatment.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102386"},"PeriodicalIF":5.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic predictive power of TP53 signatures in breast cancer prognosis: Pre- and post-neoadjuvant chemotherapy insights","authors":"Keiju Sasaki ,&nbsp;Shin Takahashi ,&nbsp;Kota Ouchi ,&nbsp;Hidekazu Shirota ,&nbsp;Nobuaki Sato ,&nbsp;Kouji Kaneko ,&nbsp;Norikazu Masuda ,&nbsp;Fumiyoshi Fujishima ,&nbsp;Satoko Sato ,&nbsp;Chikashi Ishioka","doi":"10.1016/j.tranon.2025.102398","DOIUrl":"10.1016/j.tranon.2025.102398","url":null,"abstract":"<div><h3>Background</h3><div>The <em>TP53</em> signature determined using a biopsy specimen before neoadjuvant chemotherapy (pre-NAC biopsy specimens) predicts NAC response and prognosis in breast cancer. We aimed to compare the clinical utility of the <em>TP53</em> signature determined using pre-NAC biopsy specimens and surgical specimens after NAC (post-NAC surgical specimens).</div></div><div><h3>Methods</h3><div>This observational cohort study included patients with paired pre-NAC biopsy and post-NAC surgical specimens, analyzing the association between the <em>TP53</em> signature from each specimen and prognosis (UMIN000042055).</div></div><div><h3>Results</h3><div>Pre-NAC biopsy specimens classified 71 patients into those having a <em>TP53</em> mutant signature (pre-mt, <em>n</em> = 47) and wild-type signature (pre-wt, <em>n</em> = 24), with the same for post-NAC surgical specimens (post-mt, <em>n</em> = 16 and post-wt, <em>n</em> = 55). Among the 47 pre-mt patients, 31 became post-wt (pre-mt/post-wt), whereas 16 remained post-mt (pre-mt/post-mt). All pre-wt patients remained post-wt (pre-wt/post-wt). Recurrence-free survival (RFS) was significantly shorter in the pre-mt group than in the pre-wt group, although no significant difference was observed between the post-mt and post-wt groups. Change in the <em>TP53</em> signature following NAC did not affect predictive ability of the <em>TP53</em> signature determined using pre-NAC biopsy specimens.</div></div><div><h3>Conclusions</h3><div>The <em>TP53</em> signature status should be determined using pre-NAC biopsy specimens.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102398"},"PeriodicalIF":5.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown TNF family prognosis index crucial gene PDE4B promoted PANoptosis of ovarian carcinoma cell:Based in vitro and in vivo experiments","authors":"Qianqian Yu ,&nbsp;Yunxiao Wang ,&nbsp;Ting Fu ,&nbsp;Dongyu Han ,&nbsp;Linlin Wang ,&nbsp;Lin Zhao ,&nbsp;Yongle Xu","doi":"10.1016/j.tranon.2025.102333","DOIUrl":"10.1016/j.tranon.2025.102333","url":null,"abstract":"<div><div>Ovarian cancer represents a malignancy characterized by high incidence and mortality rates, necessitating further elucidation of its underlying mechanisms. We conducted an analysis using bulk transcriptomic data of ovarian cancer and normal ovarian tissues, as well as single-cell sequencing data according to publicly available databases. Through calculation of Gene Set Variation Analysis (GSVA) scores for TNF family genes, weighted gene co-expression network analysis (WGCNA) for hub genes identification, and subsequent Gene Ontology (GO) enrichment analysis, we delineated pathways crucial in ovarian cancer pathogenesis. Furthermore, differential expression gene analysis facilitated the identification of genes with pronounced expression levels in tumor tissues and their intersection with hub genes, followed by GO analyses across molecular functions (MF), cellular components (CC), and biological processes (BP). Utilizing multivariable Cox regression and LASSO analyses, we constructed a prognostic model comprising 14 genes (GFPT2, PDE4B, PODNL1, TGFBI, CSF1R, PTGIS, SFRP2, COL5A2, TRAC, SLAMF7, VCAN, GBP1P1, C2, TRBV28). Both training and validation sets demonstrated robust diagnostic and prognostic capabilities. Clinical information and immune cell infiltration analyses were further conducted based on the model. In the single-cell sequencing analysis, reducing dimensional complexity and classifying cell types were performed, followed by exploration of gene expression patterns within each subtype and investigation of temporal expression variations across cell subtypes. Biological functional exploration and drug sensitivity analyses were also conducted. Our study contributes novel insights and theoretical foundations for prognosis, treatment, and development of drugs in patients.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102333"},"PeriodicalIF":5.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LUNAR: Full Moon or Eclipse? An exploration into tumor treating fields in lung cancer","authors":"Timothée Olivier ,&nbsp;Vinay Prasad","doi":"10.1016/j.tranon.2025.102397","DOIUrl":"10.1016/j.tranon.2025.102397","url":null,"abstract":"<div><div>The LUNAR trial investigated the addition of Tumor Treating Fields (TTFs) to “standard therapy” in patients with metastatic lung cancer after at least one line of platinum-based chemotherapy. The “standard therapy” was either an anti-PD(L)1 therapy (immunotherapy) or docetaxel. The addition of TTFs provided a 3.3 months median survival gain. We raised concerns about LUNAR results internal and external validity.</div><div>First, patient selection and the control arm do not mirror current practice. Two-thirds of patients did not receive prior immunotherapy, which is standard in first-line treatment. Also, the “choice” of the “standard therapy” was restricted by drug availability, resulting in 41 % of patients not receiving immunotherapy during the trial – those allocated to receive docetaxel – had no prior exposure to immunotherapy. Some patients may have harbored actionable mutations, and did not receive targeted therapy.</div><div>Second, we raised statistical questions. The sample size was shrunk after an unplanned analysis, with unshared and unclear justifications. The decision may have been influenced by a chance deviation in data favoring the intervention. Also, as significantly more patients were censored after withdrawals in the TTFs group, informative censoring could have amplified the survival gain.</div><div>Third and last, without a sham-control design (the equivalent of placebo for devices), it's hard to isolate the impact of TTFs from the extra-attention associated with its administration (continuous 24/7 support, frequent home-based interactions).</div><div>Overall, LUNAR do not apply to clinical settings where immunotherapy and molecular testing is offered, and many factors may have artificially boosted the reported survival gain. A sham-controlled trial is needed to answer whether TTFs are beneficial.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102397"},"PeriodicalIF":5.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bidirectional roles of neutrophil extracellular traps in oral microbiota carcinogenesis: A systematic review","authors":"Jie Shen ,&nbsp;Haitao Lin ,&nbsp;Kangnan Mo ,&nbsp;Zhong Liang ,&nbsp;Yan Zhang ,&nbsp;Huatao Quan ,&nbsp;Xing Wang ,&nbsp;Chenping Zhang ,&nbsp;Chao Chen","doi":"10.1016/j.tranon.2025.102361","DOIUrl":"10.1016/j.tranon.2025.102361","url":null,"abstract":"<div><h3>Background</h3><div>Neutrophil extracellular traps (NETs) are network structures composed of DNA, histones, and antimicrobial proteins,released by activated neutrophils to trap and eliminate extracellular pathogens. Recent research has demonstrated a strong correlation between NETs and various diseases, including immune dysregulation, thrombosis, and malignancies. This review synthesizes current research on NETs, focusing on its biological role in oral squamous cell carcinoma (OSCC) and explores its potential in treating.</div></div><div><h3>Methods</h3><div>A literature review in the PubMed database was conducted to examine the impact of NETs on the homeostasis of oral microbiota and the involvement in the development of oral microbiota-related carcinogenesis.</div></div><div><h3>Results</h3><div>Various microorganisms, including <em>Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus</em> spp., along with <em>Candida albicans</em>, as well as certain viruses such as Human papillomavirus (HPV), Human herpes virus 8 (HHV-8), and Herpes simplex virus-1 (HSV-1)are regulated by NETs during oral colonization and proliferation and have been identified as contributors to the pathogenesis of oral squamous cell carcinoma. NETs have been shown to play a dual role in the carcinogenic process of oral microbiota in humans. At the initial stage of tumor formation, NETs inhibit tumorigenesis by eliminating tumorigenic bacteria that infiltrated the tumor; however, following tumor establishment, various cytokines and chemokines that promote tumor progression are released by neutrophils during the NETs formation.</div></div><div><h3>Conclusion</h3><div>This article reviews the oncogenic mechanisms of NETs in the oral microbiota, with potential implications for early tumor detection and the development of microbe-targeted therapies.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102361"},"PeriodicalIF":5.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting FASN enhances cisplatin sensitivity via SLC7A11-mediated ferroptosis in cervical cancer","authors":"Xiaojun Wang ,&nbsp;Qiqiao Du ,&nbsp;Qiuwen Mai ,&nbsp;Qiaojian Zou ,&nbsp;Shuyi Wang ,&nbsp;Xiaoying Lin ,&nbsp;Qianrun Chen ,&nbsp;Mengxun Wei ,&nbsp;Chudan Chi ,&nbsp;Zhangqing Peng ,&nbsp;Karima Abdugheni ,&nbsp;Liu Du ,&nbsp;Yili Chen ,&nbsp;Shuzhong Yao ,&nbsp;Junxiu Liu","doi":"10.1016/j.tranon.2025.102396","DOIUrl":"10.1016/j.tranon.2025.102396","url":null,"abstract":"<div><h3>Objective</h3><div>The cisplatin resistance significantly hinders the prospects for curing patients with advanced, recurrent, and metastatic cervical cancer (CC). Our study aims to clarify the mechanisms underlying cisplatin resistance in CC and provide a novel treatment strategy to overcome the cisplatin resistance of CC patients.</div></div><div><h3>Methods</h3><div>Intracellular levels of reactive oxygen species, glutathione, malondialdehyde and Fe²⁺ were measured as indicators of ferroptosis. Biological information analyses, IC₅₀, immunofluorescence assays, qPCR and western blot analyses were conducted to elucidate the functions of FASN in CC. In vivo studies were conducted to examine the antitumor effects of the combination of TVB-2640 and cisplatin.</div></div><div><h3>Results</h3><div>Fatty acid synthase (FASN) was identified as a key driver of cisplatin resistance in CC through transcriptome sequencing and Gene Expression Omnibus (GEO) data analysis. The clinically safe FASN inhibitor TVB-2640 was found to restore cisplatin sensitivity, resulting in synergistic tumor growth attenuation in xenograft models. Mechanistically, FASN downregulation promoted ferroptosis and reduced solute carrier family 7 member 11 (SLC7A11) expression, both in vitro and in vivo models.</div></div><div><h3>Conclusion</h3><div>Targeting FASN enhances cisplatin sensitivity in CC by promoting SLC7A11-mediated ferroptosis. TVB-2640 combined with cisplatin had superior synergistic antitumor effects in cisplatin-resistant CC models.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102396"},"PeriodicalIF":5.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenteric benign lymph node enlargement in colorectal cancer: Friend or foe?","authors":"Wang Junwei ,&nbsp;Chen Xin ,&nbsp;Guo Limei ,&nbsp;Li Fei ,&nbsp;Lu Siyi ,&nbsp;Ma Yao ,&nbsp;Hsinyi Lin ,&nbsp;Shi Xiangchao ,&nbsp;Fu Wei ,&nbsp;Zhou Xin","doi":"10.1016/j.tranon.2025.102368","DOIUrl":"10.1016/j.tranon.2025.102368","url":null,"abstract":"<div><h3>Introduction</h3><div>Benign lymph node enlargement (BLNE) is common in colorectal cancer; however, few studies have investigated its influence on prognosis, clinicopathological features, and pathogenesis.</div></div><div><h3>Methods</h3><div>A cohort study was conducted to analyze the clinicopathologic features and prognosis of colorectal cancer patients, categorized based on the presence or absence of BLNE. Given the correlation between lymph nodes and immune response, immunohistochemistry, transcriptome analysis, and exon sequencing were employed to further investigate the differences in the immune microenvironment of primary tumors.</div></div><div><h3>Results</h3><div>Overall, 630 AJCC stage I/II patients were included in the study, with 131 in the BLNE group and 499 in the Non-BLNE (NBLNE) group. Patients in the BLNE group were found to have a significantly better disease-free survival (DFS) (hazard ratio [HR] 0.44, <em>P</em> = 0.016) and overall survival (OS) (HR 0.46, <em>P</em> = 0.011) than those in the NBLNE group. Pathologically, compared with the NBLNE group, the BLNE group had more mature tertiary lymphoid structures (66.7 % vs. 36.5 %, <em>P</em> = 0.002) and higher immunoscores (18.8 % vs. 2.1 %, <em>P</em> = 0.004) in primary tumor tissue. Also, transcriptome analysis showed that, compared with NBLNE, the genes upregulated in BLNE were enriched in immune-related pathways, such as adaptive immune response and immuno-regulatory interactions. Whole-exon sequencing analysis revealed a higher tumor mutation burden (TMB) in the BLNE group [6.03 (5.59, 7.59) vs. 5.33 (4.62, 6.34), <em>P</em> = 0.025].</div></div><div><h3>Conclusion</h3><div>BLNE is positively associated with the prognosis of colorectal cancer, possibly because patients with BLNE have a stronger anti-tumor immune response.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"56 ","pages":"Article 102368"},"PeriodicalIF":5.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}