Oncology Reviews最新文献

{"title":"Treatment of oligometastatic disease in colorectal cancer: from molecular biology to multimodal strategies.","authors":"G Arrichiello, A Piccolo, F Carlino, E Franzese, A Ventriglia, M Annunziata, V Patanè, M De Siero, M D Bisceglia, M Orditura","doi":"10.3389/or.2026.1932297","DOIUrl":"https://doi.org/10.3389/or.2026.1932297","url":null,"abstract":"<p><p>The management of oligometastatic colorectal cancer (OMD-CRC) has undergone a profound evolution, transforming what was once a uniformly fatal diagnosis into a clinical scenario in which long-term survival and even cure are attainable for a carefully selected subset of patients. This review provides a comprehensive synthesis of integrated, multidisciplinary strategies for OMD-CRC, with particular emphasis on hepatic and pulmonary metastases. We examine the biological foundations that differentiate oligometastatic from polymetastatic disease, including molecular subtypes that inform prognosis and therapeutic responsiveness. Local treatment modalities are critically evaluated, ranging from surgical metastasectomy-the standard of care in adequately selected patients-to minimally invasive approaches such as thermal ablation and Stereotactic Body Radiotherapy (SBRT). Recent randomized trials and prospective studies have suggested possible non-inferiority of these alternatives to surgery in selected contexts, thereby broadening the spectrum of curative-intent interventions. Equally pivotal is the integration of systemic therapy. We discuss optimal timing (neoadjuvant, adjuvant, perioperative) and regimen selection for both resectable and initially unresectable disease. The role of conversion therapy, combining intensive chemotherapy with targeted agents guided by molecular determinants such as RAS/BRAF mutational status and tumor sidedness, is highlighted as a cornerstone in expanding surgical eligibility. Looking ahead, emerging technologies-including radiomics and liquid biopsy approaches such as circulating tumor DNA (ctDNA)-hold promise for refining patient selection, detecting minimal residual disease, and further individualizing treatment pathways. The convergence of advanced local therapies, precision-guided systemic regimens, and novel biomarkers delineates the new frontier in optimizing outcomes for patients with OMD-CRC.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1932297"},"PeriodicalIF":4.0,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the immune enhancement effect of radiotherapy combined with NK cells on non-small cell lung cancer based on proteomics technology.","authors":"Cui Chang, Tang Youming, Lu Ying, Lei Ningning, Guo Chunhui, Wei Dekai, Liang Mei, Wu Qiyuan, Liu Gechen, Wu Fasheng, Chen Jibing","doi":"10.3389/or.2026.1853377","DOIUrl":"10.3389/or.2026.1853377","url":null,"abstract":"<p><strong>Background: </strong>Although radiotherapy (RT) and natural killer (NK) cell-based therapy have shown promising potential in the treatment of non-small cell lung cancer (NSCLC), the therapeutic efficacy and safety of their combination remain to be fully elucidated. In this study, we evaluated the efficacy and safety of combined RT and NK cell therapy and performed preliminary proteomic profiling to characterize its potential effects on the tumor immune microenvironment (TIME), providing new insights and a theoretical and clinical basis for the development of NK cell-based therapeutic strategies for NSCLC.</p><p><strong>Methods: </strong>C57BL/6-derived subcutaneous Lewis lung carcinoma models were established to determine the minimal effective dose of both radiotherapy and adoptively transferred natural killer cells. Based on the MED-derived findings, the mice were further randomized into five experimental groups for therapeutic efficacy evaluation: the Control group, the RT group, the NK group, the combination therapy group (RN group), and the repeated combination therapy group (RN2 group). Tumour volume and body weight were monitored longitudinally. Differentially abundant proteins were interrogated by Gene Ontology enrichment and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analyses to systematically describe the synergistic antitumor efficacy of differentially expressed proteins.</p><p><strong>Results: </strong>Compared with RT or NK cell-based immunotherapy as monotherapies, the RN group exhibited markedly enhanced tumor growth inhibition, with no overt treatment-related toxicities observed. Following the second cycle of combined therapy, mice in the RN2 group displayed a more pronounced reduction in tumor growth rate with those in the single-cycle combination cohort; notably, no significant adverse events associated with the combined regimen were detected throughout the entire experimental duration. Proteomic profiling unraveled that RT disrupted the core regulatory networks governing intracellular DNA replication and repair processes in tumor cells in a therapy-specific manner, whereas NK cell immunotherapy potently and selectively activated the classical pathway of the host complement system.</p><p><strong>Conclusion: </strong>Collectively, RT and NK cell therapy demonstrate superior synergistic efficacy and no overt toxicity was observed, with repeated treatments further delaying tumor progression. Mechanistically, proteomics shows that RT disrupts DNA replication/repair networks, whereas NK cell therapy was associated with upregulation of multiple complement components, including those belonging to the classical and lectin pathways, suggesting a potential involvement of these pathways.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1853377"},"PeriodicalIF":4.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary pulmonary NUT carcinoma: pathological features, clinical diagnosis, treatment, and prognosis - An extended review.","authors":"Shan Wu, Miao Zhang, Hui Wang","doi":"10.3389/or.2026.1967215","DOIUrl":"10.3389/or.2026.1967215","url":null,"abstract":"<p><p>NUT carcinoma is a rare and aggressive lung tumor driven by NUTM1 gene rearrangements. It accounts for less than 1% of all lung cancers, with fewer than 100 cases reported worldwide. The disease is often misdiagnosed due to non-specific symptoms and histological overlap with other tumors. This review provides an updated overview of its pathological features, clinical presentation, diagnosis, treatment, and prognosis, aiming to serve as a practical reference for clinicians and pathologists.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1967215"},"PeriodicalIF":4.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunosuppressive cell populations as potential drivers of extrinsic immune checkpoint inhibition resistance in clear cell renal cell carcinoma.","authors":"Usman Humayun Temuri","doi":"10.3389/or.2026.1953850","DOIUrl":"10.3389/or.2026.1953850","url":null,"abstract":"<p><p>Clear cell renal cell carcinoma (ccRCC) is an immunogenic cancer in which the use of Immune checkpoint inhibitors (ICIs) has provided clinical benefit. However, long-term therapeutic benefit is limited, as some do not respond initially while others develop resistance after treatment. Although extensive studies have been conducted on tumor intrinsic mechanisms, cells within the tumor microenvironment are also recognized as extrinsic factors in ICI resistance. A critical evaluation of the roles of tumor-associated macrophages, regulatory T cells, myeloid-derived suppressor cells, dysfunctional CD8⁺ T cells, natural killer cells, and dendritic cells in driving immune dysfunction in ccRCC has been provided in this narrative review. The evidence reviewed in this article suggests that these cell populations collectively impair antigen presentation, effector-cell activation, and cytotoxic function, while also promoting an immunosuppressive microenvironment. However, most of this evidence is collected from mechanistic or prognostic studies rather than from ICI-treated ccRCC cohorts. A single immune cell population cannot explain overall resistance to checkpoint blockade. Instead, resistance to ICIs due to extrinsic factors appears to result from multiple interactions among several immune cell populations. This emphasizes the need for studies that examine the function of immune cells in relation to ICIs to distinguish mechanisms that directly drive resistance to ICIs from general prognostic immune dysfunction.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1953850"},"PeriodicalIF":4.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adoptive T Cell therapy for cancer and autoimmune disease: current advances, challenges, and future directions.","authors":"Qiu-Hong Bao, Angel Wu, Jianming Pang, Junwei Wang, Qingqing Chen, SuWen Wu","doi":"10.3389/or.2026.1905358","DOIUrl":"https://doi.org/10.3389/or.2026.1905358","url":null,"abstract":"<p><p>Adoptive T Cell Therapy (ACT) is a kind of immunotherapy that eliminates target cells by autologous T cells. Since the mechanism of adoptive immune was elucidated, ACT has been developed for more than half a century. As one of ACTs, chimeric antigen receptor (CAR)-T cell therapy produced remarkable clinical responses in some hematological malignancies that is considered revolutionary strategy of immunotherapy. However, the effects of CAR-T cell therapy in solid tumors are hindered by immunosuppressive environment and limit of CAR to only recognize antigens on the cell surface. T cell receptor-engineered T cell (TCR-T) therapy is another type of ACT that the TCR is programmed to match crucial tumor antigens according to next-generation sequencing and bioinformatics analysis. The therapy overcomes the obstacles in solid tumor treatment by CAR-T, while there are also some problems dampening the response such as tumor immune escape, T cell exhaustion and toxicity. Beyond oncology, ACT is also applied in autoimmune diseases for it can specifically target and kill related immunocytes. In this review, we summarize the characteristics and clinical trials of CAR-T and TCR-T for cancer and autoimmune diseases. Differences, challenges and prospect of these ACTs are also described for reference to novel strategy of ACT.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1905358"},"PeriodicalIF":4.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the heterogeneity of the immune microenvironment of bone metastases and new strategies of nanotechnology intervention.","authors":"Chenyang Wu, Xueli Qiu, Chao Wang, Jinyu Bai, Xiaozhong Zhou","doi":"10.3389/or.2026.1820639","DOIUrl":"10.3389/or.2026.1820639","url":null,"abstract":"<p><p>Bone metastases constitute one of the most severe complications in patients with advanced malignancies. Conventional treatment approaches face significant limitations: surgical intervention carries a high risk of recurrence; radiotherapy and chemotherapy often cause myelosuppression; and anti-resorptive agents provide only limited control over tumor progression. Although immunotherapy has achieved remarkable success in various solid tumors in recent years, its therapeutic impact on bone metastases remains limited. This limitation is largely attributed to the distinct immunosuppressive microenvironment within bone lesions, which is marked by (1) a substantial decline in both the quantity and functional activity of effector immune cells, coupled with an abnormal accumulation of immunosuppressive cell populations, and (2) the formation of a vicious cycle of \"tumor growth-bone metabolic imbalance-immune suppression,\" driven by complex signaling interactions among osteoblasts, osteoclasts, and tumor cells. Recently, nanomaterials have emerged as promising therapeutic platforms due to their precise targeting and delivery capacity, inherent immune-stimulatory properties, and potential to restore bone homeostasis. Nonetheless, translating nanoplatforms into clinical practice for skeletal lesions remains a formidable challenge. This review highlights how specialized organic-inorganic hybrids and biomimetic nanoplatforms have achieved the most significant microenvironment remodeling and osteolytic inhibition within intraosseous murine models. Ultimately, we provide an actionable roadmap detailing how integrating multi-omics precision profiles and temporal programmable delivery can bridge the gap between preclinical nanomedicine and clinical oncological translation.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1820639"},"PeriodicalIF":4.0,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149063297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineering probiotic consortia to improve chemotherapy tolerance and reduce toxicity in breast cancer patients: a new frontier in supportive precision oncology.","authors":"Emmanuel Ifeanyi Obeagu","doi":"10.3389/or.2026.1909404","DOIUrl":"10.3389/or.2026.1909404","url":null,"abstract":"<p><p>Chemotherapy is a cornerstone of breast cancer treatment but is often limited by systemic toxicities, gastrointestinal mucositis, immunosuppression, and treatment interruptions, which compromise patient outcomes. Emerging evidence highlights the gut microbiome as a central mediator of chemotherapy tolerance and toxicity. Cytotoxic regimens induce dysbiosis, characterized by depletion of beneficial commensals, expansion of pathobionts, and impaired microbial metabolic function, exacerbating mucosal injury, inflammation, and systemic side effects. Engineered probiotic consortia-rationally designed multi-strain microbial communities-offer a novel strategy to restore microbial balance, reinforce epithelial barrier function, modulate immune responses, and enhance chemotherapy tolerance. Preclinical and emerging clinical studies demonstrate that multi-strain consortia can increase short-chain fatty acid production, reduce pro-inflammatory signaling, preserve mucosal integrity, and improve patient resilience during treatment. Advances in synthetic biology and microbiome engineering enable precise design of microbial consortia with complementary functions and ecological stability. This review provides a comprehensive overview of the mechanistic rationale, preclinical and clinical evidence, technological strategies, and translational implications of engineered probiotic consortia, highlighting their potential to transform supportive care in breast cancer therapy.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1909404"},"PeriodicalIF":4.0,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond tobacco: understanding the growing burden of lung adenocarcinoma in women.","authors":"Michael Christian A Virata, Rizal Michael Ramos Abello, Edroico Mari Beltran Brillante, Jasmine Soco Interior, Patrick Reyes Relacion, Ryan Gabriel C Molen, Eryll Paolo M Alea, John Cedric P Mojica","doi":"10.3389/or.2026.1813124","DOIUrl":"https://doi.org/10.3389/or.2026.1813124","url":null,"abstract":"<p><p>Primary lung adenocarcinoma is the most common histological subtype of lung cancer. It disproportionately affects female sex, especially never-smokers. The rising incidence among females without a smoking history suggests roles for hormonal, genetic, and environmental factors. We conducted a comprehensive literature review using several databases. We examined global epidemiology data, molecular mechanisms, hormone-related pathways, and new diagnostic and therapeutic approaches. The findings show that estrogen signaling, especially via estrogen receptor beta (ERβ), contributes to oncogenesis. The mechanism involves cross-talk with <i>EGFR</i> and downstream MAPK/PI3K pathways. <i>EGFR</i> mutations appear more frequently in females. The association between KRAS and other cell cycle drivers is mixed across studies. Non-tobacco exposures, including air pollution and secondhand smoke, further increase risk among females. Diagnostic disparities persist because current screening guidelines focus on smoking. This approach excludes many high-risk never-smoking females. This review aims to narrate and synthesize growing evidence highlighting how female sex is associated with a distinct epidemiological footprint, unique molecular and biological profiles, and tailored therapeutic strategies in lung adenocarcinoma, driven by mechanisms beyond traditional tobacco exposure. Incorporating sex-specific risk assessment, hormonal level modification, and targeted gene therapies into clinical practice may improve screening and outcomes for females with lung adenocarcinoma.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1813124"},"PeriodicalIF":4.0,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolic reprogramming in clear cell renal cell carcinoma: focus on high-density lipoprotein-related pathways.","authors":"Lize Wu, Huaying Xue, Yifei Wu, Ningning Shen, Zhiqing Yang, Lifang Gao, Wenxia Ma, Chen Wang","doi":"10.3389/or.2026.1887460","DOIUrl":"10.3389/or.2026.1887460","url":null,"abstract":"<p><p>Clear cell renal cell carcinoma (ccRCC) is one of the most prevalent solid tumors characterized by lipid metabolic reprogramming, with extensive lipid droplet accumulation in tumor cells as a hallmark feature. Traditionally, this phenotypic trait is attributed to enhanced fatty acid synthesis, increased triglyceride (TG) storage, and impaired β-oxidation. However, emerging transcriptomic and lipidomic evidence suggests that cholesterol metabolism is also profoundly reprogrammed in ccRCC, particularly via increased reliance on high-density lipoprotein (HDL)-derived cholesterol. The classical fatty acid-TG pathway and the HDL-cholesterol axis are metabolically linked through shared substrates, collectively shaping lipid homeostasis in ccRCC. In this review, we summarize recent advances in ccRCC lipid metabolic reprogramming, with a focus on HDL-related cholesterol metabolism. We discuss the mechanisms involving von Hippel-Lindau (VHL) loss and hypoxia-inducible factor (HIF) activation, including SCARB1-mediated cholesterol uptake, LXRα-ABCA1/ABCG1-dependent cholesterol efflux, and SOAT1-driven re-esterification of free cholesterol into cholesteryl esters (CE). Furthermore, we outline potential therapeutic targets within these pathways and highlight critical knowledge gaps that merit further investigation. This review provides a conceptual framework for understanding HDL-centered cholesterol metabolism in ccRCC and highlights potential metabolic vulnerabilities for therapeutic targeting.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1887460"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13575387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148977340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical value of combined <i>SHOX2</i> and <i>RASSF1A</i> methylation in lung cancer diagnosis across tissue and liquid biopsy samples: a systematic review and meta-analysis.","authors":"Ting Wang, Jianguo Zhang, Jiayang Wang, Xiaoqun Dong, Qiushi Lin, Leiming Guo, Bo Zhang, Yue Cao, Yining Zhai, Mathhew Hadfield, Khan Hina, Abbas E Abbas, Hong Ge, Liang Cheng, Hang Xing, Yifei Liu","doi":"10.3389/or.2026.1876563","DOIUrl":"10.3389/or.2026.1876563","url":null,"abstract":"<p><p>Lung cancer remains the leading cause of cancer-related mortality worldwide, with poor prognosis in advanced stage diseases. Although early diagnosis has the potential to improve patient outcomes, current diagnostic methods remain suboptimal, highlighting the need for accurate molecular biomarkers. We systematically reviewed 49 studies to evaluate the diagnostic performance of SHOX2 methylation, RASSF1A methylation, and their combined panel for lung cancer detection. The combined SHOX2/RASSF1A methylation panel demonstrated a pooled sensitivity of 77.8% (95% CI: 72.3%-82.5%) and specificity of 89.0% (95% CI: 86.6%-91.1%), with an HSROC area under the curve (AUC) of 0.916. SHOX2 methylation alone yielded a sensitivity of 69.4% and specificity of 91.7%, whereas RASSF1A methylation showed lower sensitivity (45.7%) but the highest specificity (93.8%). Pairwise comparisons demonstrated that the combined panel significantly improved sensitivity compared with either SHOX2 or RASSF1A alone while maintaining specificity comparable to SHOX2, although lower than that of RASSF1A. Subgroup analyses showed that assay method and pathological subtype contributed to differences in pooled sensitivity, whereas leave-one-out sensitivity analyses confirmed the robustness of the pooled estimates. In conclusion, the combined SHOX2/RASSF1A methylation panel provides a more balanced diagnostic performance than either biomarker alone and represents a promising adjunctive approach for lung cancer detection. Future studies should focus on standardizing detection methods, integrating these biomarkers with other diagnostic modalities, and evaluating their diagnostic performance in early-stage lung cancer to further enhance their clinical utility.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"20 ","pages":"1876563"},"PeriodicalIF":4.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148956404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}