Discover. Oncology最新文献

{"title":"Ubiquitin-specific protease 34 serves as a novel prognostic biomarker through correlating with immune responses and cell proliferation in acute myeloid leukemia.","authors":"Zhihui Li, Cuijuan Shi","doi":"10.1007/s12672-025-03662-1","DOIUrl":"10.1007/s12672-025-03662-1","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence showed that ubiquitin-specific proteases (USPs) are promising therapeutic targets for hematopoietic malignancies. The roles of USP34 on acute myeloid leukemia (AML) pathogenesis remain completely unknown.</p><p><strong>Methods: </strong>Gene expression and prognostic relevance were analyzed utilizing public AML datasets from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), and validated with the Gene Expression Profiling Interactive Analysis (GEPIA), BloodSpot and the human protein atlas (HPA) databases. Systematical analyses are performed to characterize the immune infiltration and biological function of USP34 in AML. MTS, colony formation and EdU assays were also employed to confirm the effect of USP34 on cell proliferation in AML cells.</p><p><strong>Results: </strong>USP34 expression was significantly higher in AML compared to its matched normal samples. Higher USP34 expression predicted worse prognosis in AML, and USP34 acted as an independent prognostic predictor for AML patients (HR:1.365, 95%CI:1.032-1.805, p = 0.029). Moreover, the expression of USP34 was associated with several immune cells, including Treg cells, indicating its potential role in modulating immune responses. Finally, functional experiments revealed that USP34 knockdown reduced cell proliferation in Molm-13 and Kasumi cells.</p><p><strong>Conclusions: </strong>USP34 is an independent prognostic predictor in AML and may contribute to leukemogenesis via intervening immune processes and promoting proliferation.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1914"},"PeriodicalIF":2.9,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307040","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":"Causal plasma metabolites for breast cancer risk: a two-sample Mendelian randomization study with colocalization evidence.","authors":"Hanghang Chen, Yueyuan Xu, Zepeng Wang, Xufeng Cheng","doi":"10.1007/s12672-025-03721-7","DOIUrl":"10.1007/s12672-025-03721-7","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer pathogenesis involves complex metabolic dysregulation, yet causal biomarkers remain elusive. This study aimed to assess causal effects of 1,400 human plasma metabolites on breast cancer (BC) risk using a two-sample Mendelian randomization (MR) framework.</p><p><strong>Methods: </strong>We employed a rigorous two-sample Mendelian randomization framework with tiered quality control (Bonferroni correction, sensitivity analyses, meta-analyses) to investigate causal metabolite-BC associations. Colocalization (PPH4 > 0.80) and phenome-wide MR (2,099 FinnGen phenotypes) validated mechanistic specificity and clinical safety profiles.</p><p><strong>Results: </strong>Five genetically determined plasma metabolites were identified as the potential causal biomarkers for BC risk: 3,5-dichloro-2,6-dihydroxybenzoic acid (odds ratio [OR]: 0.90; 95% confidence interval [CI] 0.87-0.94; p < 0.001), carnitine C14 (OR: 0.72; 95% CI 0.64-0.83; p < 0.001) and epiandrosterone sulfate (OR: 1.04; 95% CI 1.01-1.06; p < 0.001), Glyco-beta-muricholate (OR: 0.95; 95% CI 0.93-0.97; p < 0.001), N4-acetylcytidine (OR: 0.93; 95% CI 0.91-0.96; p < 0.001). Colocalization analysis showed strong evidence for Glyco - beta - muricholate and Epiandrosterone sulfate with BC risk (PPH4 = 1). PheWAS-MR revealed metabolite-specific safety profiles, with carnitine C14 showing broadest phenotypic associations (96 outcomes).</p><p><strong>Conclusions: </strong>This study establishes carnitine C14 as a novel protective biomarker and epiandrosterone sulfate as a risk biomarker for breast cancer, with colocalization evidence supporting their therapeutic targeting. The metabolic risk profile provides a foundation for precision prevention strategies.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1910"},"PeriodicalIF":2.9,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307178","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":"Integrative analysis of angiogenesis-related genes highlights prognostic indicators in colorectal cancer through single-cell sequencing and immune infiltration analysis.","authors":"Neelam Bhola, Sameer Bhardwaj, Chanchal Bareja, Daman Saluja","doi":"10.1007/s12672-025-03614-9","DOIUrl":"10.1007/s12672-025-03614-9","url":null,"abstract":"<p><p>Angiogenesis plays a pivotal role in colorectal cancer (CRC) progression and is closely intertwined with the tumor microenvironment (TME) and immune infiltration. This study aimed to identify key angiogenesis-related genes (ARGs) with prognostic significance in colorectal cancer using integrative bioinformatics and single-cell transcriptomic analysis. 526 common differentially expressed genes (DEGs) were extracted from three Gene Expression Omnibus (GEO) datasets and intersected with ARGs from MSigDB, resulting in identification of 18 candidate genes. A protein-protein interaction (PPI) network was constructed using the STRING database, followed by the extraction of 10 hub genes using the Cytoscape software. Five hub genes (MMP14, CXCL12, SPP1, TIMP1, and VCAN) showed significant association with poor overall survival. Expression analysis using UALCAN revealed significant upregulation of these genes, and their correlation with tumor-stage-specific expression. Utilizing the Tumor Immune Estimation Resource (TIMER) database immune infiltration analysis was carried out to explore the immune landscape. Tumor Immune Single-cell Hub2 (TISCH2), Tumor Immunotherapy Gene Expression Resource (TIGER), IMMUcan scDB and single-cell TIME (scTIME) databases revealed the expression of these hub genes in key TME components including fibroblasts, macrophages, and endothelial cells, and their link to immunosuppressive landscapes. Additionally, we discovered a substantial positive correlation between the expression of these hub genes and immune infiltration cells, such as macrophages, myofibroblasts and regulatory T cells (Treg). Notably, CXCL12 and SPP1 were implicated in immune cell recruitment, while TIMP1 and MMP14 were associated with ECM remodeling and myeloid cell differentiation. This study highlights the relevance of ARGs in tumor progression, prognosis and immune infiltration in CRC, offering potential targets for novel therapeutic interventions.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1905"},"PeriodicalIF":2.9,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307209","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":"Gut microbiota and risk of cervical cancer: a Mendelian multivariable randomization study.","authors":"Lihuan Lu, Zhengqi Li, Ping Qiang, Yang Shao","doi":"10.1007/s12672-025-03717-3","DOIUrl":"10.1007/s12672-025-03717-3","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>Epidemiological evidence demonstrates associations between gut microbial dysbiosis and cervical cancer, though causal inference remains limited by potential confounding.</p><p><strong>Study design: </strong>A meta-analysis of the largest available genome-wide association study (GWAS) meta-analysis using the MiBioGen consortium (n = 14,306 individuals; 8,107,040 SNPs analyzed) was conducted for the summary statistics of the gut microbiome. A two-sample Mendelian randomization study was performed using the statistics of cervical cancer from BioBank Japan (BBJ) and the European Bioinformatics Institute (EBI) GWAS Catalog. The causal relationship between the gut microbiome and cervical cancer was examined using inverse variance weighting, maximum likelihood, MR-Egger, weighted median, weighted model, and MR-PRESSO methods. The Cochran Q statistic was used to quantify the heterogeneity of the instrumental variables.</p><p><strong>Study results: </strong>The odds ratio (OR) values obtained by the IVW method indicate that the consistent microbial communities in the validation results from two different cervical cancer datasets are: Actinomyces (BBJ OR = 0.52, 95% CI: 0.29-0.92, P < 0.05), (EBI OR = 0.55, 95% CI: 0.29-0.87, P < 0.05) It has a protective effect on the occurrence of cervical cancer, Lachnospiraceae UCG001 (BBJ OR = 2.00, 95% CI: 1.11-3.58, P < 0.05), ( EBI OR = 1.91, 95% CI: 1.16-3.13, P < 0.05) It has a promoting risk effect on the occurrence of cervical cancer, and there is no significant heterogeneity or horizontal pleiotropy.</p><p><strong>Conclusions: </strong>Both datasets consistently showed that Actinomyces was protective against cervical cancer (BBJ OR = 0.52; EBI OR = 0.55), while Lachnospiraceae UCG001 increased risk (BBJ OR = 2.00; EBI OR = 1.91), with no evidence of heterogeneity or pleiotropy in these robust MR analyses.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1912"},"PeriodicalIF":2.9,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307181","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":"The expression of miR-381-3p in acute myeloid leukemia and its effect on corresponding cell proliferation and apoptosis.","authors":"Jiali Hu, Peixin Zhang, Hongxia Zhang","doi":"10.1007/s12672-025-03743-1","DOIUrl":"10.1007/s12672-025-03743-1","url":null,"abstract":"<p><strong>Background: </strong>To investigate the expression, clinical significance, progression, and prognosis of miR-381-3p in acute myeloid leukemia (AML), as well as its impact on AML cell proliferation and apoptosis, in order to provide theoretical basis for the treatment of AML.</p><p><strong>Method: </strong>Using bioinformatics analysis to identify differentially expressed miRNAs, clinical data and blood samples of AML patients were collected, and the expression levels of miRNAs in the bone marrow fluid of the included patients were measured to further elucidate the relationship between miRNAs and AML. The included patients were followed up to calculate overall survival (OS) and disease-free survival (DFS); In vitro cultivation of AML cells, construction of miR-381-3p plasmids, overexpression of miR-381-3p and knockdown of miR-381-3p in AML, divided into five groups: control, miR-381 mimics, mimics NC, miR-381 inhibitor, inhibitor NC. The proliferation and apoptosis of AML cells were detected using CCK-8 and flow cytometry.</p><p><strong>Results: </strong>Differentially expressed miRNAs were identified using bioinformatics analysis, and miR-381-3p was ultimately determined as the study molecule. A total of 90 AML patients were included. The expression level of miR-381 in AML patients was lower than that in the control group, and all FAB subtypes were lower than that in the normal group; The expression level of miR-381 is not related to the age, gender, peripheral blood leukocytes, lymphocytes, and FAB typing of AML patients, and the OS and PFS of miR-381 patients with high expression are significantly prolonged, with statistically significant differences; In vitro experiments have shown that knocking down miR-381 can inhibit apoptosis and promote proliferation of AML cells. Overexpression of miR-381 can promote apoptosis and inhibit proliferation of AML cells.</p><p><strong>Conclusion: </strong>miR-381-3p is low expressed in AML patients, and its overexpression can significantly prolong OS and PFS. miR-381-3p can promote apoptosis of AML cells, inhibit proliferation, and may become a targeted molecule for the treatment of AML.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1907"},"PeriodicalIF":2.9,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307065","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":"Integrated single-cell and Mendelian randomization analyses: dissecting underlying causes of varied efficacy in immune neoadjuvant therapy for esophageal carcinoma.","authors":"Jiaxin Li, Sibo Meng, Ying Zhou, Yufeng Cheng","doi":"10.1007/s12672-025-03751-1","DOIUrl":"10.1007/s12672-025-03751-1","url":null,"abstract":"<p><strong>Background: </strong>Esophageal cancer has a low 5-year survival rate despite treatments. scRNA-seq and MR offer insights into neoadjuvant treatment efficacy for precision medicine.</p><p><strong>Methods: </strong>Three post-neoadjuvant treatment datasets underwent QC for Seurat analysis. Marker genes identified cell subsets. MR analyzed eQTL data from GWAS cohorts for causal links. Single-cell and MR-derived genes intersected to reveal PLTP in CD4⁺T cells.</p><p><strong>Results: </strong>Single-cell analysis of 16 samples found 40,198 genes and 120,102 cells. CD4⁺T cell numbers differed significantly between groups after therapy. Differentially expressed genes were immune-related. Pseudotime and cell-cell communication varied. PLTP, linked to esophageal cancer, co-expressed with genes involved in cell cycle processes.</p><p><strong>Conclusion: </strong>The study highlights CD4⁺T cells' predictive role in therapy efficacy via scRNA-seq and MR. PLTP emerges as a key gene, offering new precision medicine strategies for esophageal cancer.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1904"},"PeriodicalIF":2.9,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12532960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298941","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":"Correction: Smoking and alcohol specific alterations in miRNA expression in head and neck squamous cell carcinoma.","authors":"Mohd Younis Bhat, Vishalakshi Nanjappa, Mariana Brait, David Sidransky, Aditi Chatterjee, Jayshree Advani","doi":"10.1007/s12672-025-03828-x","DOIUrl":"10.1007/s12672-025-03828-x","url":null,"abstract":"","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1903"},"PeriodicalIF":2.9,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12532950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298823","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 prognostic signature based on insulin-signaling-pathway genes for hepatocellular carcinoma.","authors":"Yanyan Zhang, Haoqian Song, Wenshuai Cui, Kunwei Peng","doi":"10.1007/s12672-025-03763-x","DOIUrl":"10.1007/s12672-025-03763-x","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is the most common subtype of liver cancer. HCC occurrence, metastasis and therapeutic effect are closely related to tumor metabolic microenvironment. However, the role of insulin-related glucose metabolism in HCC has also not been extensively studied.</p><p><strong>Method: </strong>Transcriptional profiles and clinical data of HCC samples were retrieved from The Cancer Genome Atlas (TCGA). The insulin signaling pathway related genes were derived from GeneCards and only the protein-coding genes with the top 100 relevance score were retained. Univariate Cox analysis, least absolute shrinkage and selection operator (LASSO) regression analysis and multivariate Cox analysis were conducted to develop the prognosis model. The predictive performance of our prognosis model was assessed by using receiver operating characteristic (ROC) curve, calibration curve and nomogram. Further studies, such as enrichment analysis, drug sensitivity and immunotherapy response were performed to assess the tumor microenvironment and treatment response. The clinical significance of SLC2A1 in HCC was validated with an independent cohort.</p><p><strong>Results: </strong>We constructed a prognostic signature based on 4 insulin pathway related genes: RHEB, PRKAA2, SLC2A1 and FOXO1. HCC patients divided into high-risk and low-risk group according to the median risk score. We evaluated the signature in training set, validation set and entire set. The Kaplan-Meier (K-M) survival curve revealed that patients in low-risk group had longer survival. Even in different clinicopathological subgroups, the prognostic signature had good prognostic performance. We also identified that commonly used chemotherapy agents such as 5-fluorouracil, gemcitabine, paclitaxel, sorafenib and sunitinib showed significant sensitivity in the high-risk group. The TIDE algorithm suggested that patients in high-risk group may be more sensitive to immunotherapy. SLC2A1 was selected as the core gene, and the Kaplan-Meier survival curve showed that SLC2A1 positive was significantly associated with prognosis in a HCC independent cohort. Univariate and multivariate Cox analysis demonstrated that SLC2A1 was an independent risk variable for poor prognosis.</p><p><strong>Conclusions: </strong>In summary, we constructed a prognostic signature based on insulin signaling pathway genes. The excellent performance and applicability of our model underscores its advantages and reliability as a clinical tool. Moreover, we validated SLC2A1 was an independent prognostic factor in a HCC independent cohort.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1901"},"PeriodicalIF":2.9,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12528513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291571","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":"Blood expression of CTLA-4, PD-1, and PD-L1 as potential prognostic and diagnostic markers for breast cancer: a systematic review.","authors":"Mina Niusha, Saba Hajazimian, Nayemeh Soltani, Pouya Goleij, Parisa Pagard, Farshid Oruji, Javad Behroozi, Shima Shabani, Alireza Isazadeh, Behzad Baradaran","doi":"10.1007/s12672-025-03744-0","DOIUrl":"10.1007/s12672-025-03744-0","url":null,"abstract":"<p><p>The risk of developing cancer is significantly higher for individuals with compromised immune function, as the immune system plays a crucial role in defending the body against tumor cells. In the present study, we aimed to evaluate the blood expression of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) as prognostic markers for patients with breast cancer. We searched the PubMed, EMBASE, Web of Science, and Medline (Ovid) databases to find relevant studies. The search strategy encompassed utilization of CTLA-4, PD-1, PD-L1, breast cancer, mRNA expression, blood, and prognostic markers as keywords. We chose seven studies published between July 2010 and July 2022, involving 1328 patients. Our study indicated that blood mRNA expression of CTLA-4, PD-1, and PD-L1 is higher in patients with breast cancer than in healthy individuals. Blood CTLA-4, PD-1, and PD-L1 high levels can be considered as poor prognosis in patients with breast cancer. However, it appears that simultaneously using several prognostic biomarkers at the same time can be more useful.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1897"},"PeriodicalIF":2.9,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12528640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291582","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":"Heparanase2 inhibits the growth of gallbladder cancer by regulating the VEGF/VEGFR pathway.","authors":"Dengyi Cao, Jiawei Chen, Shaobo Zhou, Jie Tang, Zixiang Liu, Zixiang Zhang","doi":"10.1007/s12672-025-03696-5","DOIUrl":"10.1007/s12672-025-03696-5","url":null,"abstract":"<p><p>Heparanase 2 (Hpa2), a homolog of heparinase, lacks the conventional heparinase activity associated with heparin degradation. However, it exhibits a greater affinity for heparin sulfate (HS) compared to heparinase. In our study, overexpression of Hpa2 significantly inhibited the viability, migration, and invasion of gallbladder cancer cells, both in vivo and in vitro. Moreover, this inhibitory effect of Hpa2 was reversed upon administration of agonists targeting the VEGF/VEGFR pathway. These findings suggest that Hpa2 overexpression may impede the growth of NOZ cells, potentially through modulation of the VEGF/VEGFR signaling pathway.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1889"},"PeriodicalIF":2.9,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12528560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291599","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}