Translational cancer research最新文献

{"title":"Global hotspots and trends of stereotactic radiotherapy for pancreatic cancer: a bibliometric analysis and visual analysis from 2015 to 2025.","authors":"Xiaoqin Huang, Ke Yuan, Yunfei Li, Wen-Qiong Ma","doi":"10.21037/tcr-2026-1050","DOIUrl":"10.21037/tcr-2026-1050","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer (PC) is a highly aggressive malignant tumor with extremely poor prognosis. Most patients are locally advanced or unresectable at the time of diagnosis. Stereotactic body radiotherapy (SBRT) has received extensive attention in this field in recent years due to its advantages of high precision, short course of treatment and low toxicity. However, there is a lack of summary of recent research trends and hotspots. This study aimed to characterize the current status, hotspots, and future directions of this field.</p><p><strong>Methods: </strong>Based on the core collection of Web of Science, we searched relevant publications on SBRT in PC treatment published from January 2015 to December 2025. CiteSpace and VOSviewer were used for bibliometric analysis and visual analysis of publications in this field, covering annual publication trends, countries/regions, institutions, highly cited literatures, authors, journals and keywords.</p><p><strong>Results: </strong>Web of Science Core Collection (WOSCC) included 296 articles from 28 countries. Since 2015, the number of publications on SBRT for PC has increased annually. The United States (USA) was the most productive country, Johns Hopkins University was the leading institution, <i>Cancers and Frontiers in Oncology</i> were tied as the most prolific journals, and Herman JM was the most productive author. Besides topic-relevant high frequency and high betweenness centrality (BC) keywords, other notable keywords included \"overall survival\", \"dose escalation\", \"MR image guided radiotherapy\", and \"adaptive radiotherapy\".</p><p><strong>Conclusions: </strong>SBRT has been increasingly studied in PC, focusing on dose and technical optimization. The future development direction will focus on the development and improvement of artificial intelligence (AI) applications, MR-guided adaptive radiotherapy, and combined immune strategy to further improve the survival and quality of life of PC patients.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"610"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of miR-188-5p enhancing radioresistance in nasopharyngeal carcinoma by targeting PTEN to activate the PI3K/Akt signaling pathway.","authors":"Fuming Zhou, Jia Wan, Haiyan Zhang, Feng Chen, Jin Wang, Yanli Yang, Huan Wang","doi":"10.21037/tcr-2026-0702","DOIUrl":"10.21037/tcr-2026-0702","url":null,"abstract":"<p><strong>Background: </strong>Radiotherapy resistance remains a critical obstacle in nasopharyngeal carcinoma (NPC) treatment, yet the underlying mechanisms are not fully understood. Although miR-188-5p has been implicated in the malignant progression of various tumors, its role in NPC radioresistance requires further investigation. This study aims to explore whether miR-188-5p mediates radioresistance by targeting PTEN to activate the PI3K/AKT signaling pathway and induce epithelial-mesenchymal transition (EMT).</p><p><strong>Methods: </strong>Radioresistant NPC cell lines C666-1R were established. Cell proliferation and radioresistance were evaluated using Cell Counting Kit-8 (CCK-8) and colony forming assays. C666-1R cells were transfected with miR-188-5p inhibitor/mimic and sh-PTEN, followed by 4 Gy irradiation. Quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Transwell assay, wound healing assay, flow cytometry, and dual-luciferase reporter assay were performed to assess the effects of miR-188-5p on cell proliferation, invasion, migration, apoptosis, and the PTEN/PI3K/AKT pathway.</p><p><strong>Results: </strong>Radioresistant NPC cell lines were successfully established and validated. miR-188-5p was highly expressed in NPC tissues and NPC cell lines, particularly in the radioresistant C666-1R cells. Inhibition of miR-188-5p enhanced radiosensitivity, as evidenced by reduced cell viability, invasion, migration, and increased apoptosis. Dual-luciferase reporter assay confirmed that miR-188-5p directly bound to the 3'-UTR of PTEN and suppressed its expression. Rescue experiments demonstrated that PTEN knockdown reversed the miR-188-5p inhibition-induced suppression of PI3K/AKT activity and EMT phenotype, restoring p-PI3K, p-AKT, N-cadherin, and Vimentin levels while downregulating E-cadherin. These findings indicate that miR-188-5p activates the PI3K/AKT pathway and promotes EMT by directly targeting PTEN, thereby mediating NPC radioresistance.</p><p><strong>Conclusions: </strong>miR-188-5p enhances radioresistance in NPC cells by suppressing PTEN expression, relieving its negative regulation of the PI3K/AKT signaling pathway, activating this pathway, and inducing EMT. Thus, inhibiting miR-188-5p may represent a promising strategy to overcome radioresistance in NPC.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"627"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Midkine restrains T-cell mediated anti-tumor immunity by suppressing macrophage M1 polarization in lung adenocarcinoma.","authors":"Ting Qian, Zijian Sun, Xin Wang, Yan Sun","doi":"10.21037/tcr-2026-1204","DOIUrl":"10.21037/tcr-2026-1204","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is characterized by a highly immunosuppressive tumor microenvironment (TME), which limits the efficacy of current anti programmed cell death protein 1 (anti-PD-1) immunotherapy. Midkine (MDK), a heparin-binding growth factor, is frequently overexpressed in various malignancies; however, its specific role in regulating anti-tumor immunity in LUAD remains unclear. This study aimed to investigate the immunomodulatory role of MDK in LUAD, and to evaluate the therapeutic potential of MDK neutralization.</p><p><strong>Methods: </strong>In this study, we analyzed single-cell sequencing datasets and validated MDK expression across multiple non-small cell lung cancer (NSCLC) cell lines. To explore the immunomodulatory functions of MDK, we established <i>ex vivo</i> co-culture models using human peripheral blood mononuclear cells (PBMCs) and LUAD cells. We assessed the impact of recombinant MDK and an MDK-neutralizing antibody (α-MDK) on T cell proliferation, differentiation, and cytotoxicity, as well as macrophage polarization, using flow cytometry, lactate dehydrogenase (LDH) release assays, and multiplex cytokine measurement.</p><p><strong>Results: </strong>We confirmed that MDK is significantly upregulated in malignant LUAD cells compared to normal lung epithelial cells. Functional analysis revealed that MDK signaling suppresses T cell-mediated anti-tumor immunity by inhibiting the expansion of cytotoxic CD8⁺ T cells and restricting T helper type 1 cell (T_H1) polarization. Furthermore, MDK impaired the polarization of macrophages towards the pro-inflammatory M1 phenotype, and dampened antigen-presenting cell function. Notably, blocking MDK signaling with a neutralizing antibody effectively reversed these immunosuppressive effects, restoring T cell cytotoxicity and enhancing the secretion of pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α).</p><p><strong>Conclusions: </strong>Our findings demonstrate that MDK acts as a key regulator in the LUAD TME by simultaneously restraining T cell activation and M1 macrophage polarization. These data suggest that targeting MDK offers a promising therapeutic strategy to overcome immune suppression and improve clinical outcomes in LUAD.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"591"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Measuring toxicity better: patient-reported outcome-informed calibration for CTCAE assessment.","authors":"Minji K Lee, Robert W Mutter, Sumithra J Mandrekar","doi":"10.21037/tcr-2026-1394","DOIUrl":"10.21037/tcr-2026-1394","url":null,"abstract":"","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"669"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria related gene signature serves as prognosis prediction and risk stratification of cholangiocarcinoma.","authors":"Shenji Li, Wei Xiang, Wei Wei, Hongrong Zhang, Qianyu Xie, Bo Yin, Hongsheng Lin, Shunchi Xu","doi":"10.21037/tcr-2026-0605","DOIUrl":"10.21037/tcr-2026-0605","url":null,"abstract":"<p><strong>Background: </strong>Cholangiocarcinoma (CHOL) is a highly aggressive biliary malignancy with poor clinical outcomes and limited effective prognostic biomarkers. Mitochondrial dysfunction participates in multiple oncological processes of CHOL, yet the prognostic roles of mitochondria‑related genes (MRGs) remain poorly understood. This study aimed to characterize MRGs expression in CHOL and develop a molecular prognostic model for predicting patient survival and guiding clinical management.</p><p><strong>Methods: </strong>RNA sequencing (RNA-seq) and clinical data of CHOL were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) (GSE89748) databases. Differentially expressed MRGs were identified, and 10 machine learning algorithms were used to construct prognostic models. The optimal model (highest average C-index) was selected to establish a mitochondria-related risk score (MRRS), which was validated internally and externally. A nomogram integrating clinical factors and MRRS was developed, and biological mechanisms were explored via functional and immune analyses.</p><p><strong>Results: </strong>A 3-MRG (MAP3K1, MRPL18, PYGB) prognostic signature was constructed, stratifying patients into high- and low-risk groups with significantly different overall survival. The model showed high predictive accuracy, with an area under the curve (AUC) up to 0.845, and MRRS was an independent prognostic factor. The signature was associated with mitochondrial pathways, and the high-risk group had distinct immune infiltration and mutation profiles.</p><p><strong>Conclusions: </strong>A validated MRG prognostic model effectively stratifies CHOL patients and has potential clinical value for prognosis prediction. Further validation in larger cohorts is needed to confirm its applicability.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"607"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A model of cellular proliferation and mitochondrial biogenesis predicts prognosis and immunotherapy response in lung adenocarcinoma.","authors":"Mi Zou, Guangda Zheng, Yanju Bao","doi":"10.21037/tcr-2025-1-2721","DOIUrl":"10.21037/tcr-2025-1-2721","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD), which is the leading subtype of non-small cell lung cancer (NSCLC), poses considerable difficulties in accurate prognostic assessment and targeted therapeutic options. Cell proliferation-related genes (CPGs) and mitochondrial biogenesis-related genes (MBGs) play critical roles in tumor metabolic reprogramming; however, their prognostic value and molecular mechanisms in LUAD are poorly understood. This study aims to construct a CPG/MBG-based prognostic risk model for LUAD, evaluate its clinical utility in predicting prognosis and immunotherapy response, and experimentally validate the functional role of key model genes in LUAD progression.</p><p><strong>Methods: </strong>By utilizing The Cancer Genome Atlas (TCGA)-LUAD and GSE72094 datasets, this investigation formulated a risk scoring model through differential expression screening combined with least absolute shrinkage and selection operator (LASSO)-Cox regression analysis. The molecular characteristics and clinical implications of the risk model were investigated via immune microenvironment evaluation, genomic alteration analysis, and drug sensitivity prediction. The functional contributions of key genes were further substantiated using quantitative reverse transcription polymerase chain reaction (qRT-PCR), commercial assay kits, the JC-1 fluorescent probe, the Cell Counting Kit-8 (CCK-8), Transwell invasion assays, and wound healing assays.</p><p><strong>Results: </strong>A risk model based on seven CPGs and MBGs (<i>PLK1</i>, <i>HMMR</i>, <i>CYP27A1</i>, <i>LDHA</i>, <i>NPAS2</i>, <i>KRT17</i>, <i>CIDEC</i>) showed reliable predictive performance in both GSE72094 and the TCGA-LUAD cohorts. Enhanced tumor heterogeneity and an immunosuppressive microenvironment were observed in the high-risk group. Drug sensitivity analysis indicated that the risk model could guide personalized treatment strategies; for instance, high-risk patients showed increased susceptibility to agents such as docetaxel and 5-fluorouracil. <i>In vitro</i> experiments demonstrated that the key gene <i>CIDEC</i> exhibited upregulated expression in LUAD tissues and cells. Knockdown of <i>CIDEC</i> led to enhanced cellular energy metabolism and increased mitochondrial membrane potential, while also effectively suppressing cell invasion, proliferation, and migration.</p><p><strong>Conclusions: </strong>The established MBGs/CPGs prognostic model provides a novel tool for stratified treatment planning in LUAD, underscoring the crucial roles of cellular proliferation and mitochondrial biogenesis in tumor progression. Functional validation of <i>CIDEC</i> offers experimental support for the development of potential therapeutic strategies.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"611"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between primary tumor surgery and survival in patients with <i>de novo</i> stage IV triple-negative breast cancer with visceral metastases: a SEER-based propensity score-matched study.","authors":"Ruizhe Yue, Zheng Wang, Hao Zhang","doi":"10.21037/tcr-2026-1163","DOIUrl":"10.21037/tcr-2026-1163","url":null,"abstract":"<p><strong>Background: </strong>The role of primary tumor surgery in patients with <i>de novo</i> stage IV triple-negative breast cancer (TNBC) with visceral metastases remains controversial. This study investigated the association between primary tumor surgery and survival outcomes in this high-risk population.</p><p><strong>Methods: </strong>Female patients diagnosed with <i>de novo</i> stage IV TNBC with liver, lung, and/or brain metastases between 2010 and 2020 were identified from the Surveillance, Epidemiology, and End Results (SEER) database. Overall survival (OS) and breast cancer-specific survival (BCSS) were compared between patients who underwent primary tumor surgery and those who did not. Propensity score matching (PSM), Kaplan-Meier analysis, Cox regression, subgroup analysis, robust sensitivity analysis, and restricted mean survival time (RMST) analysis were performed.</p><p><strong>Results: </strong>A total of 1,827 patients were included, of whom 543 underwent primary tumor surgery and 1,284 did not. After 1:1 PSM, 507 matched pairs were generated. After matching, the median OS was 15 months in the surgery group and 9 months in the non-surgery group, while the median BCSS was 15 months and 10 months, respectively. In multivariable Cox analysis, primary tumor surgery was independently associated with longer OS [hazard ratio (HR) =0.532, 95% confidence interval (CI): 0.462-0.612, P<0.001] and BCSS (HR =0.544, 95% CI: 0.470-0.629, P<0.001). These associations remained stable in robust Cox sensitivity analyses. RMST analyses at 24 and 36 months further supported the robustness of the observed survival association.</p><p><strong>Conclusions: </strong>Primary tumor surgery was associated with longer OS and BCSS in patients with <i>de novo</i> stage IV TNBC with visceral metastases. This observed association may partly reflect patient selection, underlying health status, metastatic burden, and response to systemic therapy. Therefore, these findings should be interpreted as hypothesis-generating real-world evidence rather than definitive evidence of a causal treatment benefit. Individualized surgical decision-making should be based on careful patient selection and multidisciplinary evaluation.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"619"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Construction and validation of a β-hydroxybutyrylation-related molecular model for predicting prognosis of papillary thyroid carcinoma.","authors":"Xiaoxiao An, Biao Li, Baowei Zhai","doi":"10.21037/tcr-2026-0917","DOIUrl":"10.21037/tcr-2026-0917","url":null,"abstract":"<p><strong>Background: </strong>Papillary thyroid carcinoma (PTC) usually has a favorable prognosis, yet a subset of patients develops persistent, recurrent, or biologically aggressive disease. The clinical relevance of lysine β-hydroxybutyrylation (Kbhb)-related transcriptional programs in PTC remains unclear. Accordingly, this study aimed to characterize Kbhb-related molecular heterogeneity in PTC, construct a prognostic signature, and explore its association with the tumor microenvironment (TME).</p><p><strong>Methods: </strong>Transcriptomic and clinical data from PTC samples within The Cancer Genome Atlas Thyroid Carcinoma (TCGA-THCA) cohort were analyzed to identify Kbhb-related differentially expressed genes (DEGs), define molecular subtypes, construct a prognostic signature, and characterize tumor microenvironmental features. Single-cell RNA-sequencing data from PTC were further used to explore the cellular distribution of representative genes.</p><p><strong>Results: </strong>We identified 51 Kbhb-related DEGs in PTC and defined two Kbhb molecular subtypes. The Kbhb_C2 subtype showed shorter progression-free interval (PFI) and a more immune- and stroma-enriched microenvironment. A six-gene prognostic signature comprising <i>TARID</i>, <i>CDSN</i>, <i>PIMREG</i>, <i>KLRC1</i>, <i>SYT13</i>, and <i>NPR3</i> was then established. High-risk patients had significantly worse PFI in the full, training, and testing cohorts, with 1-, 3-, and 5-year areas under the curve (AUCs) of 0.715, 0.793, and 0.771, respectively, in the full cohort. High-risk tumors also exhibited higher stromal, immune, and ESTIMATE scores, altered immune infiltration, and increased expression of multiple immune checkpoint molecules. Single-cell analysis confirmed distinct cell-type-specific expression patterns of representative genes.</p><p><strong>Conclusions: </strong>Kbhb-related transcriptional programs define clinically relevant molecular heterogeneity in PTC and are closely associated with prognosis and TME remodeling. The identified six-gene signature provides a biologically interpretable framework for risk stratification in PTC.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"643"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"lncRNA JPX promotes radioresistance in nasopharyngeal carcinoma via the miR-1301-3p/PIK3R2-mediated autophagy pathway.","authors":"Si Ouyang, Jingyao Lv, Yilong Wang, Yongjie Ying, Qiaozhi Jin","doi":"10.21037/tcr-2026-1270","DOIUrl":"10.21037/tcr-2026-1270","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC) represents an aggressive head and neck malignancy with high metastatic potential. Radioresistance remains a major therapeutic obstacle associated with poor prognosis. Although the long non-coding RNA (lncRNA) JPX has been implicated in various cancers, its specific role in NPC radioresistance requires further elucidation. This study aimed to investigate whether JPX modulates radiosensitivity through autophagy regulation and to delineate the underlying molecular mechanisms.</p><p><strong>Methods: </strong>JPX expression was analyzed in NPC cell lines and The Cancer Genome Atlas (TCGA) datasets, with subcellular localization determined through cellular fractionation. Functional characterization was performed using short hairpin RNA (shRNA)-mediated knockdown in CNE-2 and HONE-1 cell lines. Radiosensitivity was evaluated by clonogenic survival assays at a clinically relevant radiation dose, with cell viability assessed by MTT as a screening measure. while autophagy activity was assessed through Western blot analysis of LC3-II and p62. Molecular interactions were validated using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays.</p><p><strong>Results: </strong>JPX was significantly upregulated in head and neck squamous cell carcinoma (HNSCC) tissues and NPC cell lines, showing predominant cytoplasmic localization. Clinical association analysis in the TCGA-HNSCC cohort revealed that elevated JPX expression correlated with advanced tumor stage and poor overall survival, although NPC-specific clinical validation remains to be established. Genetic silencing of JPX attenuated autophagic flux and enhanced radiosensitivity. Mechanistic investigations revealed that JPX functions as a competitive endogenous RNA (ceRNA) functionally associating with miR-1301-3p, thereby alleviating miR-1301-3p-mediated repression of PIK3R2 and subsequently activating pro-survival autophagy pathways.</p><p><strong>Conclusions: </strong>The findings demonstrate that JPX promotes radioresistance in NPC through a ceRNA mechanism involving the miR-1301-3p/PIK3R2/autophagy regulatory axis. The JPX/miR-1301-3p/PIK3R2 axis thus emerges as a potential mechanistic candidate for radiosensitization; however, this notion remains strictly provisional and requires rigorous validation in authenticated NPC models, in vivo systems, and patient-derived samples before any translational consideration can be justified. Despite the cell line limitations acknowledged herein, our findings provide a mechanistic framework for understanding JPX-mediated radioresistance that warrants further investigation in more physiologically relevant models.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"573"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based prediction of survival in breast cancer patients with lung metastasis: a SEER-based study.","authors":"Cairong Wu, Guantong Liu, Haijie Xu, Hongguang Liu, Hansheng Wu","doi":"10.21037/tcr-2026-1211","DOIUrl":"10.21037/tcr-2026-1211","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer remains the most prevalent malignancy among women, and breast cancer with lung metastasis (BCLM) significantly increases morbidity and mortality. Accurate prognosis prediction for BCLM patients is critical for guiding personalized treatment strategies, yet effective predictive tools remain limited. This study aimed to develop a machine learning (ML)-based predictive framework for BCLM prognosis by leveraging data from the Surveillance, Epidemiology, and End Results (SEER) database (2011-2020).</p><p><strong>Methods: </strong>We analyzed data of 2,921 female BCLM patients from the SEER database (2011-2020). Advanced oversampling techniques (SMOTEENN, SMOTETomek) addressed class imbalance, and Bayesian optimization tuned model hyperparameters. Six ML classifiers-linear regression, elastic net, random forest, support vector machine (SVM), extreme gradient boosting (XGBoost), and gradient boosting machine (GBM)-were evaluated. SHapley Additive exPlanations (SHAP) provided model interpretability and identified key prognostic factors.</p><p><strong>Results: </strong>SVM achieved the highest performance in 1-year prediction [area under the curve (AUC): 0.770; 95% confidence interval (CI): 0.737-0.803], while XGBoost demonstrated slightly higher discrimination in 3-year (AUC: 0.770; 95% CI: 0.739-0.802) and 5-year (AUC: 0.746; 95% CI: 0.709-0.783) predictions. Key prognostic factors-marital status [specifically for the hormone receptor (HR)+/human epidermal growth factor receptor 2 (HER2)- subtype] and metastatic sites (bone/liver)-were consistently identified as critical determinants of survival across models. SHAP analysis revealed interactions between sociodemographic and molecular factors.</p><p><strong>Conclusions: </strong>The findings demonstrate that ML-based frameworks, particularly those integrating multimodal clinical data, can improve risk stratification for BCLM patients and provide actionable insights for personalized oncology. Limitations include reliance on retrospective registry data and unmeasured confounders; future research should incorporate longitudinal and imaging biomarkers to further refine predictive accuracy.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 8","pages":"623"},"PeriodicalIF":2.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}