Discover. Oncology最新文献

{"title":"NTRK expression and its clinical significance in pancreatic neuroendocrine tumors.","authors":"Pingping Yan, Xiaoqin Dai, Fenfen Zhang, Yu Dong, Huijuan Shi, Anjia Han","doi":"10.1007/s12672-025-03506-y","DOIUrl":"https://doi.org/10.1007/s12672-025-03506-y","url":null,"abstract":"<p><strong>Background: </strong>The neurotrophic TRK family, which includes NTRK1, 2, and 3, could be the oncogenic driving force in various cancers, when they undergo fusion mutations with other genes and form a chimeric oncoprotein. In our study, we aimed to explore the expression and gene alterations of NTRK in pancreatic neuroendocrine tumors (pNETs).</p><p><strong>Methods: </strong>Immunohistochemistry (IHC) staining was utilized to assess NTRK expression in pNETs, using pan-TRK cocktail (clone LBP2-NTRK). Any intensity of staining in ≥ 1% of tumor cells was classified as positive. IHC-positive specimens then underwent Fluorescence In Situ Hybridization (FISH) analysis, using the NTRK1-3 gene fragmentation probe. Clinical data were obtained through retrospective chart review.</p><p><strong>Results: </strong>NTRK expression was observed in 16.7% (7/42) of pNETs: 4 patients were females and 3 were males; 6 were over 50 years old, with only one patient aged 29 years; 3 tumors were WHO G1, 3 were G2 and 1 was G3. Lymphovascular invasion was identified in 3 cases. No NTRK expression was detected in any of the 8 cases with liver-metastatic pNETs. No statistically significant difference was identified between the NTRK-expression and the clinicopathological parameters, such as the age, tumor location, tumor size, tumor grade, lymphovascular invasion, metastatic disease, and the expression of MGMT and SSTR2. Furthermore, no NTRK fusions were identified in any of the 7 cases by FISH analysis.</p><p><strong>Conclusions: </strong>Our data suggest that NTRK expression could be present in some pNETs, but not associated with its gene translocation. The pathophysiology of this phenotype is discussed.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1647"},"PeriodicalIF":2.9,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946310","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":"HADHB mediates 5-fluorouracil sensitivity in colorectal cancer.","authors":"Xue Zhang, Hui Jin, Dan Li, Jiayin Liu, Jing Han","doi":"10.1007/s12672-025-03503-1","DOIUrl":"https://doi.org/10.1007/s12672-025-03503-1","url":null,"abstract":"<p><strong>Purpose: </strong>5-Fluorouracil (5FU) is a primary chemotherapy for colorectal cancer (CRC), but resistance reduces its effectiveness. HADHB, important in mitochondrial fatty acid β-oxidation, is linked to tumor metabolism changes in various cancers. Its potential influence on 5FU sensitivity in CRC remains unclear. This study aims to elucidate the role of HADHB in modulating 5FU sensitivity in CRC.</p><p><strong>Methods: </strong>Collect CRC tissue samples treated with 5FU and perform immunohistochemical staining to evaluate the relationship between HADHB expression and 5FU efficacy. We assessed the impact of HADHB on 5FU IC₅₀ in CRC cells via CCK-8, confirmed HADHB-DUOX2 interaction through co-IP, and used fluorescence staining and flow cytometry to measure ROS levels. Metabolomics and transcriptomics were employed to investigate DUOX2-related metabolic pathways.</p><p><strong>Results: </strong>HADHB was significantly upregulated in 5FU-resistant CRC tissues compared to sensitive ones. HADHB knockdown in CRC cell lines improved 5FU sensitivity, increased apoptosis, and caused cell cycle arrest. We identified DUOX2 as a novel HADHB-interacting protein, with their protein levels showing strong positive correlation. Silencing either HADHB or DUOX2 can result in a decrease in ROS production, while DUOX2 overexpression reversed the ROS reduction caused by HADHB knockdown, thereby establishing a functional connection between these two elements in the regulation of ROS. This mechanism may play a crucial role in modulating the sensitivity to 5FU mediated by HADHB.</p><p><strong>Conclusion: </strong>HADHB overexpression is linked to 5FU resistance in CRC, indicating it as a potential therapeutic target, likely via the HADHB-DUOX2-ROS pathway.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1648"},"PeriodicalIF":2.9,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946374","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 of a prognostic risk-scoring model based on SASP-related genes in patients with skin cutaneous melanoma.","authors":"Ming-Feng Li, Jing Du, Gang Wang, Wei Feng, Ju-Gao Chen, Chao Zhang","doi":"10.1007/s12672-025-02935-z","DOIUrl":"https://doi.org/10.1007/s12672-025-02935-z","url":null,"abstract":"<p><strong>Background: </strong>Skin cutaneous melanoma (SKCM) is a highly aggressive and deadly subtype of skin cancer. Lack of efficient biomarkers for prognosis has limited the improvement of survival outcome for patients with SKCM.</p><p><strong>Methods: </strong>In this study, we obtained RNA-seq data from TCGA and GTEx databases, followed by identification of differential expressed genes, univariate Cox regression, and LASSO regression to identify prognostic SASP-related genes in the TCGA datasets and constructed a prognostic risk-scoring model.</p><p><strong>Results: </strong>The establishment of prognostic model was based on the expression levels of 14 SASP-related genes, including ASPRV1, ICAM1, IL2RA, ABCC2, HLA-B, TPMT, ATM, CD59, KIR2DL4, CTLA4, ITGB3, FOXM1, NOX4, and TRIM21. Patients with melanoma who were in the high-risk group had a shorter overall survival (OS), indicating that the model served as an independent prognostic index. Furthermore, we found that the risk score was potentially linked to immune scores, estimate score, immune cell infiltration level, and immunotherapy efficacy.</p><p><strong>Conclusions: </strong>This study presented a new prognostic model for assessing therapy in melanoma patients, providing a fresh perspective for combating melanoma.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1636"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945827","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":"Potential role of DKK3 and WIF1 in prostate cancer: bioinformatics and clinical analysis.","authors":"Zhiliang Xia, Zhonggui Hu, Dan Du, Zhi Zhang, Zonglai Liu, Xinyu Li, Xiong Guo, Ziqiu He","doi":"10.1007/s12672-025-03488-x","DOIUrl":"https://doi.org/10.1007/s12672-025-03488-x","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Prostate Cancer (PCa) is one of the most common malignant tumors in men. Some patients may progress to metastatic and Castration-Resistant Prostate Cancer (CRPC), leading to increased treatment difficulty and poor prognosis. With advancements in bioinformatics and machine learning technologies, the integration of multiple databases can efficiently identify core genes associated with the occurrence of PCa. Additionally, the Tumor Microenvironment (TME) and immune cell infiltration play crucial roles in the development and therapeutic response of PCa. Investigating the interactions between core genes and the immune microenvironment will enhance the understanding of the molecular mechanisms underlying PCa and provide new avenues for precision treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study obtained gene expression data of prostate cancer and normal tissues from the GEO (GSE69223, GSE46602) and TCGA (TCGA-PRAD) databases. Initially, each dataset was standardized, batch effects were corrected, and differentially expressed genes (DEGs) were identified, followed by GO and KEGG enrichment analyses. Subsequently, the STRING database was utilized to construct a protein-protein interaction (PPI) network, and core modules were selected using Cytoscape software. Lasso regression and Random Forest (RF) algorithms were employed to further pinpoint core genes from the key genes. In the external validation dataset (GSE46602), the diagnostic value and expression level differences of these core genes were assessed. Combining data from TCGA-PRAD, their correlations with immune cell infiltration were analyzed. The application value in molecular pathways and potential therapeutic interventions was explored through GSEA and CTRP drug sensitivity data. Finally, immunohistochemistry and Western blot experiments were conducted to confirm the expression changes of core genes in Benign Prostatic Hyperplasia (BPH) and prostate cancer tissues, alongside correlation analyses with clinical pathological parameters.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Multi-omics integrative analysis identified a total of 339 common DEGs. The PPI network and machine learning algorithms further identified four potential core genes: DKK3, SNAI2, WIF1, and FOXA1. External validation and diagnostic value assessments revealed that DKK3 and WIF1 were significantly downregulated in PCa tissues and positively correlated with higher PSA levels and Gleason scores. Immune cell infiltration analysis indicated that the downregulation of these genes was closely associated with impaired adaptive immune function and matrix remodeling, and synergistically interacted with abnormalities in the Wnt/TGF-β pathways. Further analysis using the CTRP database showed that high expression of DKK3 increased cellular sensitivity to various anti-tumor drugs, whereas high expression of WIF1 might reduce the efficacy of certain small molecule inhibitors. Immunohistochemistry and protein level d","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1637"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946348","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":"CAF-derived exosomal LncRNA ANRIL promotes glycolytic metabolism and proliferation in non-small cell lung cancer via the miR-186-5p/HIF-1α axis.","authors":"Baofan Zhang, Ruiyan Huang, Zhongjie Tang, Yufeng Hu","doi":"10.1007/s12672-025-03109-7","DOIUrl":"https://doi.org/10.1007/s12672-025-03109-7","url":null,"abstract":"<p><strong>Background: </strong>Cancer-associated fibroblasts (CAFs) critically regulate tumor microenvironment remodeling, with exosomes (Exos) derived from CAFs serving as key mediators of intercellular communication. However, the functional significance of CAF-derived exosomal long non-coding RNA ANRIL (lncRNA ANRIL) in modulating non-small cell lung cancer (NSCLC) glycolytic metabolism and proliferation remains incompletely characterized. This study systematically investigated the lncRNA ANRIL/miR-186-5p/HIF-1α regulatory axis in NSCLC progression.</p><p><strong>Methods: </strong>CAFs were isolated from fresh NSCLC surgical specimens, followed by Exo isolation through differential ultracentrifugation. The functional impacts of CAF-derived Exos on NSCLC cellular proliferation and glycolytic activity were comprehensively evaluated using CCK-8 assays, EdU incorporation tests, glucose consumption measurements, lactate production quantification, and extracellular acidification rate (ECAR) assessments. Molecular interactions within the ANRIL/miR-186-5p/HIF-1α axis were mechanistically validated through dual-luciferase reporter systems, RNA pull-down assays, and RT-qPCR profiling. Functional validation was achieved via targeted overexpression and siRNA-mediated knockdown approaches.</p><p><strong>Results: </strong>CAF-derived Exos significantly enhanced NSCLC cell proliferation indices and glycolytic parameters. CRISPR-mediated ANRIL silencing in CAFs substantially attenuated these pro-tumorigenic effects, establishing exosomal ANRIL as a critical molecular effector. Integrated bioinformatics prediction and experimental validation confirmed direct binding between lncRNA ANRIL and miR-186-5p, with subsequent identification of HIF-1α as the downstream target of miR-186-5p. Functional perturbation experiments demonstrated that miR-186-5p overexpression or HIF-1α knockdown effectively suppressed NSCLC proliferation and glycolysis, while rescue assays confirmed HIF-1α as the terminal mediator of miR-186-5p regulatory effects.</p><p><strong>Conclusions: </strong>This mechanistic study demonstrates that CAF-secreted exosomal lncRNA ANRIL drives NSCLC progression by enhancing glycolytic metabolism through competitive sponging of miR-186-5p, thereby derepressing HIF-1α expression. Our findings provide novel insights into exosome-mediated metabolic reprogramming in NSCLC and propose therapeutic targeting of the ANRIL/miR-186-5p/HIF-1α signaling axis as a potential precision medicine strategy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1638"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946358","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":"Microsurgical resection of a giant thoracolumbosacral Schwannoma in an adolescent with intraoperative neuromonitoring and anatomical laminoplasty reconstruction.","authors":"Wenhua Zhang, Yaxiong Li, Honglei Liu, Jianfeng Liu","doi":"10.1007/s12672-025-03469-0","DOIUrl":"https://doi.org/10.1007/s12672-025-03469-0","url":null,"abstract":"","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1640"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946196","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 : Glutathiones' life in multi-cancers: especially their potential micropetides in liver hepatocellular carcinoma.","authors":"Didi Ma, Zhenguo Wu, Mengying Zhang, Jian Mao, Wenqin Xu, Lan Jiang, Zuzhen Wang","doi":"10.1007/s12672-025-03464-5","DOIUrl":"https://doi.org/10.1007/s12672-025-03464-5","url":null,"abstract":"","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1644"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945821","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":"Metabolic genes interaction perturbation network identified and validated CD24 as a novel prognostic gene in hepatocellular carcinoma.","authors":"Hao Liu, Hongyi Yan, Ying Huang, Xiangkun Meng, Long Liu, Yuyuan Zhang, Hui Xu, Yanchao Hu","doi":"10.1007/s12672-025-03232-5","DOIUrl":"https://doi.org/10.1007/s12672-025-03232-5","url":null,"abstract":"<p><strong>Purpose: </strong>Molecular subtype of hepatocellular carcinoma (HCC) is primarily identified via high throughput expression profiles, largely ignoring the dynamic changes of gene expressions. Yet, biological networks remain steadily characterize disease state irrespective of time and conditions. We aim to utilize a metabolic genes interaction perturbation network-based approach to facilitate the subtyping and precision treatment of HCC patients.</p><p><strong>Methods: </strong>We employed the metabolic genes interaction perturbation network-based approach to identify metabolic reprogramming (MR) subtypes in 922 HCC samples from four independent public datasets and further investigated their clinical and biofunctional implications, immune landscape, multi-omics features and biomarker.</p><p><strong>Results: </strong>We stratified patients into three unique MR subtypes: (i) MR1 (\"immune-deficiency\"), frequent CTNNB1 mutation, and moderate prognosis; (ii) MR2 (\"immune-activated\"), advanced pathological staging and histological grading, frequent TP53 mutation, response to anti-PD-1 therapy, and the worst prognosis; (iii) MR3 (high metabolic activity), low-grade pathological staging and histological grading, fewer mutations and copy number variations, and the best prognosis. Besides, CD24 was identified and validated as a biomarker for MR2 which indicated a poor prognosis with higher expression.</p><p><strong>Conclusion: </strong>Taken together, the interactome taxonomy could effectively facilitate the stratified management and precise treatment of heterogeneous HCC patients.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1643"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12391576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946251","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 40-year bibliometric analysis of global research on neoadjuvant chemotherapy for oral cancer (1985-2024).","authors":"Xu Xiang, Ping Shi, Li Yang, Shumin Ma, Jian Kang","doi":"10.1007/s12672-025-03411-4","DOIUrl":"https://doi.org/10.1007/s12672-025-03411-4","url":null,"abstract":"<p><strong>Background: </strong>Neoadjuvant chemotherapy (NAC) has become a critical component in the treatment of oral cancer, enhancing tumor resectability and improving patient survival. This study aimed to perform a bibliometric analysis to systematically explore global research trends, key contributors, and emerging hotspots in NAC for oral cancer.</p><p><strong>Methods: </strong>Publications from 1985 to 2024 were retrieved from the Web of Science Core Collection. Bibliometric data were analyzed using R (version 4.3.3), VOSviewer (version 1.6.20), and CiteSpace (version 6.3.R1). These tools were employed to examine publication trends, co-authorship networks, institutional collaborations, and keyword co-occurrence and burst analysis.</p><p><strong>Results: </strong>A total of 235 publications were identified, showing an annual growth rate of 7%. Japan led in publication output (47 publications), followed by China (38) and Germany (33), while the United States exhibited the strongest international collaboration. Chang Gung Memorial Hospital was the leading contributor, with 51 publications. The leading journals included Oral Oncology, Head and Neck, and the Journal of Cranio-Maxillofacial Surgery. Kreppel Matthias ranked first with an H-index of 9, 10 publications, and 234 total citations. Emerging research hotspots focused on \"induction chemotherapy\", \"biomarker expression\", and \"multidisciplinary management\".</p><p><strong>Conclusion: </strong>This study provides a bibliometric analysis of global research trends and hotspots in NAC for oral cancer, offering valuable insights into key contributors, emerging themes, and collaborative networks. The findings have significant implications for guiding future research directions and integrating evidence-based strategies into clinical practice to improve patient outcomes.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1642"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946258","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":"Tissue-specific profiling of human protein phosphatases identifies G6PC1 as a liver cancer-selective biomarker.","authors":"Adil R Sarhan","doi":"10.1007/s12672-025-03454-7","DOIUrl":"https://doi.org/10.1007/s12672-025-03454-7","url":null,"abstract":"<p><p>Protein phosphatases are essential regulators of cellular signalling, yet their tissue-specific expression profiles and functional roles in cancer remain underexplored. This study aimed to systematically profile protein phosphatases expression across human tissues and malignancies to identify potential biomarkers. The transcriptomic data from GTEx, FANTOM, and HPA, were analysed assessing 265 protein phosphatases across 60 human tissues. Tissue specificity was quantified using the Tau index and coefficient of variation. Top candidates were further evaluated in TCGA and PCAWG cancer cohorts. Protein-level validation was performed using immunohistochemistry (IHC) data from HPA. Functional relevance was investigated through protein-protein interaction (PPI) network analysis and KEGG pathway annotations. G6PC1 emerged as the most liver-specific phosphatase (Tau > 0.99) with high inter-tissue expression variability. Its expression was sharply confined to liver tissue and retained in hepatocellular carcinoma (LIHC), with very low expression across other tumour types. IHC confirmed G6PC1 protein presence in liver cancer samples. PPI analysis positioned G6PC1 as a central metabolic regulator, interacting with key enzymes involved in gluconeogenesis and glucose homeostasis. Notably, G6PC1 expression remained stable across sex, age, tumour stage, ploidy, tumour purity, and tumour mutational burden (TMB) in PCAWG liver cancer patients. This integrative multi-omic analysis identifies G6PC1 as a highly liver-specific, biologically relevant, and potential diagnostic candidate for hepatocellular carcinoma. Its selective expression, protein-level detectability, and network centrality support its potential utility as a diagnostic candidate for liver cancer, warranting further experimental validation in independent clinical cohorts.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1635"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946279","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}