Discover. Oncology最新文献

{"title":"Bioinformatic characterization of SLC25A39 across cancers with validation in hepatocellular carcinoma.","authors":"Liufeng Qin, Yuanqian Yao, Jianlin Lv","doi":"10.1007/s12672-026-05621-w","DOIUrl":"10.1007/s12672-026-05621-w","url":null,"abstract":"<p><strong>Introduction: </strong>Solute carrier family 25 member 39 (SLC25A39) is crucial for regulating mitochondrial oxidative metabolism and homeostasis, linking to various physiological and pathological processes. Its expression landscape and mechanistic roles across cancer types remain largely unexplored. This study systematically profiled SLC25A39 in pan-cancer and assessed its prognostic relevance, molecular associations, and therapeutic potential.</p><p><strong>Methods: </strong>Multi-omics database resources were utilized to perform an integrated analysis of SLC25A39, including its expression profiles, prognostic value, molecular mechanisms, and associations with the immune microenvironment across diverse tumors. The oncogenic role of SLC25A39 was confirmed through in vitro gene knockdown in hepatocellular carcinoma.</p><p><strong>Results: </strong>SLC25A39 was predominantly over expressed in nearly all types of cancer. SLC25A39 serves as an unfavorable prognosis marker. Its expression was primarily linked to immune cell infiltration, the cancer immunity cycle, major histocompatibility complex, immune checkpoints, tumor mutation burden, microsatellite instability, and RNA modifications like m1A, m5C, m6A, as well as DNA methylation sites. Functional enrichment analysis reveals that SLC25A39 is commonly associated with immune-related pathways and cell cycle-related pathways in the pan-cancer dataset. Knockdown of SLC25A39 in Huh-7 and HepG2 cells significantly inhibited hepatocellular carcinoma cell proliferation.</p><p><strong>Conclusions: </strong>SLC25A39 induces pro-tumorigenic effects across various cancer types. It serves as a potential biomarker.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"17 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13447621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677452","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: The effect of delays in cancer surgery due to the COVID-19 pandemic on cancer resectability and postoperative mortality in different tumor entities.","authors":"Antonia L Stengler, Jörg Kleeff, Lisa Rieder, James C Glasbey, Aneel A Bhangu, Ewen M Harrison, Ulrich Ronellenfitsch","doi":"10.1007/s12672-026-05484-1","DOIUrl":"10.1007/s12672-026-05484-1","url":null,"abstract":"","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"17 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577479","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":"Comprehensive pan-cancer analysis of MEX3A in human tumors.","authors":"Xuezhong Zhang, Yongxin Pan, Ning Li, Meilin Gao, Tingting Chu, Xuebin Zhang","doi":"10.1007/s12672-026-05459-2","DOIUrl":"10.1007/s12672-026-05459-2","url":null,"abstract":"<p><p>MEX3A is an evolutionarily conserved RNA-binding protein characterized by two KH RNA-binding domains and a C-terminal RING domain, suggesting potential roles in both post-transcriptional regulation and protein modification. Although MEX3A has been implicated in several individual cancer types, its shared and cancer-specific roles across human cancers remain incompletely understood. In this study, we performed a comprehensive pan-cancer analysis of MEX3A by integrating publicly available datasets, including TCGA, GTEx, CPTAC, and other external resources. We systematically evaluated MEX3A expression, genetic alterations, phosphorylation status, clinical relevance, RNA modification-related associations, immune-related features, and functional enrichment profiles across multiple tumor types. MEX3A was significantly upregulated in most cancers and showed associations with advanced pathological stage in several tumor types. Survival analyses indicated that elevated MEX3A expression was correlated with poor overall survival and disease-specific survival in cancers such as ACC, LIHC, MESO, and SARC, supporting its potential value as a prognostic biomarker. Genetic alteration analysis revealed frequent copy number amplification of MEX3A in several cancers, whereas these alterations were not consistently associated with survival outcomes. Proteomic analyses further identified altered phosphorylation levels at S338 and S462 in tumor tissues, suggesting that post-translational modification may contribute to the regulation of MEX3A activity in a cancer-type-specific manner. Correlation analyses showed that MEX3A expression was associated with RNA modification-related genes, immune modulators, immune checkpoint genes, tumor-infiltrating immune cells, tumor mutational burden, and microsatellite instability across different cancers. These findings suggest that MEX3A may participate in RNA regulatory networks and tumor-immune microenvironment interactions. Functional enrichment analysis revealed that MEX3A-associated proteins are involved in pathways related to transcriptional dysregulation, mRNA stability, and translational regulation. However, as these findings are primarily based on bioinformatic and correlation-based analyses, they should not be interpreted as evidence that MEX3A is a validated therapeutic or immunotherapy target. Overall, this study provides a systematic pan-cancer characterization of MEX3A and supports its potential role as a prognostic biomarker and a hypothesis-generating candidate for future mechanistic and clinical validation.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"17 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825165","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":"Immune-related gene signature for predicting biochemical recurrence after RP in prostate cancer subtypes.","authors":"Yiwei Lin, Jiatong Zhou","doi":"10.1007/s12672-026-05623-8","DOIUrl":"10.1007/s12672-026-05623-8","url":null,"abstract":"<p><strong>Background: </strong>The prognostic role of molecular subtypes of prostate cancer (PCa) patients is still unclear. And we speculated whether the change of immunologic and hallmark gene sets of adjacent notumor tissues could promote the BCR of PCa patients.</p><p><strong>Methods: </strong>We intended to identify PCa subtypes and find significant gene sets based on the activity changes of immunologic and hallmark gene sets in tumor and nontumor tissues to predict biochemical recurrence (BCR)-free survival. In addition, cell-based assays were utilized to validate the function of the gene in PCa.</p><p><strong>Results: </strong>We calculated and analyzed these gene sets related to BCR in tumor and notumor tissues through gene set variation analysis (GSVA) and then found three clinically relevant subtypes of PCa by nonnegative matrix factorization method (NMF) in immunologic and hallmark gene sets. Patients with subtype 2 had better BCR-free survival than other subtypes. Using the least absolute shrinkage and selection operator method (LASSO), two prognostic gene sets in tumor but not in notumor tissue were identified frequently. Functional enrichment analysis revealed that genes from these two significant gene sets closely correlated with cell cycle in tumor tissue. Then, we applied random forest (RF) and artificial neural network (ANN), to identify gene In review biomarkers in predicting BCR and we found 36 genes related to the high risk of BCR. CENPE is the only common gene and can be used as a prognostic gene of BCR. Cell-based assays validated that CENPF promoted tumor proliferation in PCa.</p><p><strong>Conclusion: </strong>Three clinically relevant subtypes of PCa were identified. Two significant genes sets were related to the cell cycle and ATPase activity. And CENPF promotes tumor proliferation as an oncogene.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"17 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812114","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":"Anethole suppresses proliferation and migration of lung adenocarcinoma cells and modulates ESRβ/SRC/EGFR-related signaling","authors":"Yinghuan Sun, Jiacheng Zhu, Pengcheng Qiu, Zhenjie Sun, Kemu Zhang, Hongli Zhou, Bo Huang","doi":"10.1007/s12672-026-05607-8","DOIUrl":"https://doi.org/10.1007/s12672-026-05607-8","url":null,"abstract":"Despite advances in lung adenocarcinoma (LUAD) treatment, therapeutic efficacy remains limited and recurrence remains common, highlighting the need for additional therapeutic strategies. This study integrated network pharmacology, molecular docking, and in vitro assays to explore the potential anti-LUAD activity of anethole and its associated signaling changes. Potential targets of anethole were predicted using PharmMapper and intersected with LUAD-related targets obtained from GeneCards, yielding 44 overlapping targets. A protein–protein interaction network and GO/KEGG enrichment analyses suggested that estrogen receptor-related and SRC-associated signaling may be relevant to the response to anethole. Molecular docking provided computational evidence of possible interactions between anethole and selected candidate proteins, including ESRβ and SRC. In vitro assays showed that anethole reduced the viability and EdU incorporation of H1975 and PC-9 cells, impaired the survival or growth of pre-formed colonies, induced G0/G1-phase cell-cycle arrest, and reduced wound closure and transwell migration under the tested conditions. Western blot analysis showed decreased ESRβ expression and reduced phosphorylation of SRC and EGFR, accompanied by reduced activation of PI3K/AKT and MEK/ERK signaling. These findings suggest that anethole suppresses malignant phenotypes of LUAD cells and may modulate ESRβ/SRC/EGFR-related signaling.","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672132","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":"Temporal trends, risk factors, and future projections of gastric cancer burden in China, India, and the United States: a GBD 2023 analysis.","authors":"Fen Lin, Xueying Wei, Lihuan Song, Liyan Liu, Jing Li","doi":"10.1007/s12672-026-05633-6","DOIUrl":"10.1007/s12672-026-05633-6","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of gastric cancer (GC) in China, India, and the USA has different epidemiology, but comparative analyses with regard to their time trends and causes are underdeveloped.</p><p><strong>Methods: </strong>Using the 2023 Global Burden of Disease (GBD) database (1990-2023), we evaluated GC trends via Joinpoint regression. Das Gupta decomposition and comparative risk assessment quantified demographic/epidemiological drivers and behavioral risks. ARIMA models projected the burden through 2040.</p><p><strong>Results: </strong>Globally, gastric cancer age-standardized incidence rates (ASIR) declined from 26.31 to 14.00 per 100,000 between 1990 and 2023, whereas absolute incident cases increased from 1.05 to 1.28 million. China maintained the highest disease burden in 2023 (ASIR: 25.04/100,000) despite achieving the steepest reductions in age-standardized incidence, mortality, and DALY rates. India demonstrated the slowest decline in age-standardized rates, while incident cases nearly doubled from 42,800 to 85,400 during the study period. Joinpoint analysis identified significant upward ASIR trends after 2020 in China (APC = 3.62) and globally (APC = 1.61). Smoking remained the leading attributable risk factor, particularly in China. Decomposition analysis showed that population aging and growth were the principal drivers of increasing absolute burden. ARIMA projections suggested that China will continue to carry the highest gastric cancer burden through 2040.</p><p><strong>Conclusion: </strong>Despite declining standardized rates, population aging and growth continue to drive absolute case numbers upward. To mitigate this evolving burden, China requires optimized early screening and stringent behavioral risk control; India needs expanded cancer registry coverage and equitable rural healthcare access; while the USA should prioritize targeted strategies to mitigate internal disparities among subpopulations.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"17 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891144","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":"Trend dynamics of non-Hodgkin lymphoma and primary ocular adnexal lymphoma incidence in the United States from 1992 to 2021 using age-period-cohort and joinpoint analysis.","authors":"Jing Zeng, Xianfen Cao, Xi Yin, Zhiping Liu, Xida Liang, Lun He, Jun Lyu, Qing Zhou","doi":"10.1007/s12672-026-05615-8","DOIUrl":"https://doi.org/10.1007/s12672-026-05615-8","url":null,"abstract":"<p><strong>Background: </strong>This U.S. population-based study analyzed incidence trends of non-Hodgkin lymphoma (NHL) and its subtype, primary ocular adnexal lymphoma (POAL), from 1992 to 2021, and explored their underlying drivers.</p><p><strong>Methods: </strong>Data were extracted from the SEER-12 registries. Joinpoint regression identified significant changes in age-standardized incidence rates (ASIR). Age-period-cohort (APC) modeling estimated net drifts, local drifts, age curves, and period/cohort relative risks. Sex-stratified analyses were performed.</p><p><strong>Results: </strong>Both NHL and POAL exhibited a biphasic incidence pattern: an initial increase followed by a decline. NHL incidence peaked in 2009 (ASIR: 28.4 per 100,000, annual percent change: 0.41%, P < 0.001) and subsequently declined to 24.94 per 100,000 by 2021 (annual percent change: -1.04%, P < 0.001). POAL incidence rose until 2003 (ASIR: 0.46 per 100,000, annual percent change: 3.19%, P = 0.01) and then decreased to 0.30 per 100,000 (annual percent change: -2.41%, P < 0.001). APC analysis revealed similar age effects (increased risk with age) for both cancers, but significant divergences in period and cohort effects. Period effects strongly influenced POAL risk, while NHL risk was additionally shaped by birth cohort exposures. Notably, sex disparities were evident in NHL, with higher incidence and distinct cohort effects in males, whereas no significant sex difference was observed in POAL.</p><p><strong>Conclusions: </strong>Despite similar biphasic incidence trends, NHL and POAL differed in their underlying temporal dynamics: age effects were similar for both diseases, whereas period and cohort effects differed substantially. Sex disparities were present in NHL but not in POAL. These findings highlight the need for subtype-specific approaches in lymphoma epidemiology.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric analysis of programmed cell death and immunotherapy research in glioma.","authors":"Muyuan Jia, Gaoyuan Cui, Zhixiong Liu, Chengke Luo","doi":"10.1007/s12672-026-05535-7","DOIUrl":"https://doi.org/10.1007/s12672-026-05535-7","url":null,"abstract":"<p><p>Glioblastoma is the most lethal primary central nervous system malignancy, with limited therapeutic options and poor prognosis. This PubMed-based bibliometric study systematically analyzed publication trends, collaboration patterns, journal and author distributions, and thematic evolution at the intersection of programmed cell death (PCD) and glioma immunotherapy over the period 2006-2026. A total of 799 eligible records, including 644 original research articles and 155 narrative reviews, were included. Annual publications increased steadily, peaking at 131 in 2025. China and the United States dominated global output, while international collaboration varied across countries and regions. Keyword co-occurrence analysis identified core themes: apoptosis, necroptosis, pyroptosis, ferroptosis, tumor microenvironment (TME), immunotherapy-related strategies, and prognosis, reflecting a gradual shift from basic PCD mechanisms toward TME-targeted immunotherapy and prognostic stratification. This field is widely distributed across immunology, oncology, molecular biology, nanoscience, and multidisciplinary journals. Author and institutional analyses revealed key contributors within the dataset. In summary, this bibliometric landscape provides a structured overview of research hotspots, collaboration networks, and emerging directions in glioma PCD and immunotherapy. The findings offer descriptive insights for identifying research priorities, knowledge gaps, and collaborative opportunities, while they should be interpreted as observational patterns rather than direct evidence of clinical efficacy or translational priority.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A bibliometric analysis of arachidonic acid metabolism in colorectal cancer with a focus on COX inhibitors-related clinical trials landscape.","authors":"Xingcan Fan, Tao Yu, Yulin Song, Qiuyu Liao, Gang Liu","doi":"10.1007/s12672-026-05516-w","DOIUrl":"https://doi.org/10.1007/s12672-026-05516-w","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) remains a global malignancy with high morbidity and mortality. Long-term uncontrolled intestinal inflammation drives CRC initiation and development. As a vital essential fatty acid and prostaglandin precursor, arachidonic acid (AA) participates in inflammatory and immune regulation, and its metabolic disorder is tightly linked to multiple inflammatory diseases and CRC. This study clarified the progress of research on AA metabolism and CRC through bibliometric analysis, and analyzed the clinical application prospects of COX inhibitors in CRC by integrating clinical trial data.</p><p><strong>Methods: </strong>For bibliometric analysis, data were retrieved from WOSCC (1990-2025) using specific search terms, preprocessed, and analyzed via R Studio and LDA topic model to clarify publication trends and research hotspots. Meanwhile, relevant clinical trials of COX inhibitors for CRC and its precancerous lesions were collected from the Trialtrove database for multidimensional analysis.</p><p><strong>Results: </strong>This bibliometric analysis highlights the significant growth in research on AA metabolism in colorectal cancer, identifying key authors, countries, and research hotspots. The field has transitioned from a focus on COX-2 and PGE2 to a more integrated understanding that includes gut microbiota and immune modulation. For clinical trial analysis, among the 61 included trials, aspirin and celecoxib monotherapies were dominant, and combination regimens have drawn rising attention. Regarding trial status, less than one-third of trials were completed, while plenty remained active or terminated early.</p><p><strong>Conclusion: </strong>By synthesizing the results of bibliometric and clinical trial landscape studies, we summarized drugs targeting the AA pathway that inhibit inflammatory cancer transformation.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SH3BGRL3 is a pancancer prognostic and immunological biomarker.","authors":"Yuntao Yao, Zihui Zhao, Bingnan Lu, Haoyu Zhang, Donghao Lyu, Keqing Dong, Bolin Zhu, Maodong Wei, Runzhi Huang, Yifan Liu, Xiuwu Pan","doi":"10.1007/s12672-026-05572-2","DOIUrl":"https://doi.org/10.1007/s12672-026-05572-2","url":null,"abstract":"<p><strong>Background: </strong>SH3 Domain Binding Glutamate Rich Protein Like 3 (SH3BGRL3) plays a crucial part in regulating tumor necrosis factor (TNF)-induced effects and was involved in the onset and progression of various cancers. However, its role at pan-cancer level remains unclear.</p><p><strong>Methods: </strong>Firstly, SH3BGRL3 expression and its correlation with patients' survival, and other clinical variables were explored in our clinical cohort of 370 kidney neoplasm patients. Subsequently, differential expression analysis, competing endogenous RNA and protein-protein interaction network analysis, correlation analysis with clinical characteristics, tumor purity, gene alteration, immune landscape and signaling pathways were performed to evaluate the role of SH3BGRL3 in pan-cancer. Drug sensitivity analysis, molecular docking and in vitro experiments were also conducted to explore its possible pharmaceutical significance.</p><p><strong>Results: </strong>In our clinical cohort of kidney neoplasms, SH3BGRL3 was downregulated in tumor tissues (p < 0.001). Higher tumor SH3BGRL3 was linked to decreased overall survival (p = 0.022), advanced stages and was an independent risk factor for progression-free survival (hazard ratio = 2.11, 95%confidence interval = 1.05-4.2, p = 0.037). Further pan-cancer analysis revealed that SH3BGRL3 expression was upregulated in most tumors, and correlated with unfavorable outcomes and advanced tumor stages of various cancers. It was also associated with tumor purity, tumor genomics, tumor immunity, pathway enrichment, and drug sensitivity at pan-cancer level. Dasatinib was found to effectively suppress SH3BGRL3.</p><p><strong>Conclusions: </strong>SH3BGRL3 was an independent prognostic factor in our kidney neoplasm cohort. At the pan-cancer level, it served as a promising prognostic and immunological biomarker exhibiting cancer-type-specific variations.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}