BMC Cancer最新文献

{"title":"The effect of adding ovarian function suppression to adjuvant endocrine therapy in premenopausal patients with hormone receptor-positive, HER2-positive breast cancer who have undergone neoadjuvant therapy: a single-center experience.","authors":"Okan Aydin, Hale Gulcin Yildirim Dogan, Sermin Dinc Sonusen, Mert Erciyestepe, Ahmet Emin Ozturk, Asli Buyukkuscu, Zehra Sucuoglu Isleyen, Kayhan Erturk","doi":"10.1186/s12885-026-17017-8","DOIUrl":"10.1186/s12885-026-17017-8","url":null,"abstract":"<p><strong>Purpose: </strong>The role of ovarian function suppression (OFS) in premenopausal patients with hormone receptor (HR)-positive, HER2-positive breast cancer remains unclear in the era of anti-HER2 therapy. This study evaluated the effect of adding OFS to adjuvant endocrine therapy on outcomes in premenopausal patients receiving neoadjuvant anti-HER2 therapy.</p><p><strong>Methods: </strong>We retrospectively reviewed 138 premenopausal patients with HR-positive/HER2-positive non-metastatic breast cancer treated with anti-HER2-based neoadjuvant therapy and surgery between 2015 and 2024. Patients were grouped by receipt of OFS during the adjuvant period. The primary endpoints were disease-free survival (DFS), distant disease-free survival (DDFS), and overall survival (OS); pathological complete response (pCR; ypT0/is ypN0) was evaluated as a secondary endpoint.</p><p><strong>Results: </strong>Among 138 patients, 60 (43.5%) received OFS. Overall, 42% achieved pCR. After a median follow-up of 56 months, 20 patients (14.5%) recurred or developed metastasis, and 11 (8%) died. Five-year OS rates were 93.9% with OFS and 85.8% without (p = 0.4); DFS rates were 80.7% and 81.3% (p = 0.9). Patients with pCR had excellent survival (5-year OS 100%) irrespective of OFS. In those with residual disease, OFS was associated with numerically higher OS (89.9% vs. 77.6%) but no DFS benefit. Multivariate analysis showed no independent association between OFS and survival outcomes.</p><p><strong>Conclusion: </strong>In this retrospective real-world study, no independent association between OFS and survival outcomes was observed in premenopausal patients with HR-positive/HER2-positive breast cancer treated with anti-HER2-based neoadjuvant therapy. Patients achieving pCR had excellent prognoses regardless of OFS use. Given the limited statistical power and the predominantly tamoxifen-treated cohort, these findings should be interpreted with caution. Prospective studies are warranted to better define the role of OFS in this patient population.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics profiling reveals sphingolipid metabolism reprogramming of tumor-conditioned MDSCs in cervical cancer.","authors":"Qiuwen Mai, Chudan Chi, Xiaojun Wang, Yili Chen, Qiaojian Zou, Qianrun Chen, Feitianzhi Zeng, Mengxun Wei, Yanfei Chen, Aiting Wang, Yan Liao, Yuzhou Xiao, Xinjie Li, Qing Yan, Liping Zhan, Hongsuo Wei, Xu Jing, Qiqiao Du, Junxiu Liu","doi":"10.1186/s12885-026-16914-2","DOIUrl":"10.1186/s12885-026-16914-2","url":null,"abstract":"<p><strong>Background: </strong>Myeloid-derived suppressor cells (MDSCs) play a crucial role in the tumor microenvironment (TME) of cervical cancer (CC), yet the mechanisms underlying their reprogramming remain poorly understood.</p><p><strong>Methods: </strong>To explore the immune microenvironment change in CC, we applied TCGA-CC immune microenvironment infiltration estimation analysis via Timer 2.0 online datasets. To generate tumor-conditioned MDSCs, the culture medium of MDSCs was supplemented with supernatants from the murine CC cell lines U14 and TC1, respectively. CCK8 assays, transwell migration experiments and qPCR were executed to test the proliferation, migration and iNOS expression. We then conducted proteomics and metabolomics analyses of tumor-conditioned MDSCs.</p><p><strong>Results: </strong>The tumor immune microenvironment analysis identified MDSCs as key components, predicting poor prognosis in CC. Tumor-conditioned MDSCs presented higher proliferation, migration and iNOS expression. Proteomics and metabolomics analyses showed significant changes in lipid metabolism, especially sphingolipid metabolism. Specifically, the Kng1-sphingosine 1-phosphate axis was identified as a central protein-metabolite regulatory node. Gain- and loss-of-function experiments confirmed that KNG1 modulates multiple cellular processes including proliferation, migration, iNOS expression, and sphingosine 1-phosphate production.</p><p><strong>Conclusion: </strong>Our findings uncover sphingolipid metabolic reprogramming as a key mechanism in MDSCs-mediated immune suppression, and propose the Kng1-sphingosine 1-phosphate network as a potential therapeutic target for CC treatment.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: HLA Class II molecule HLA-DRA identifies immuno-hot tumors and predicts the therapeutic response to anti-PD-1 immunotherapy in NSCLC.","authors":"Jie Mei, Guanyu Jiang, Yundi Chen, Yongrui Xu, Yuan Wan, Ruo Chen, Feng Liu, Wenjun Mao, Mingfeng Zheng, Junying Xu","doi":"10.1186/s12885-026-16779-5","DOIUrl":"10.1186/s12885-026-16779-5","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13584547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Profiling proteomic responses in small intestinal neuroendocrine tumor GOT1 after [¹⁷⁷Lu]Lu-DOTATATE therapy.","authors":"Johan K E Spetz, Mikael E Montelius, Evelin Berger, Julia A M Johansson, Nishte Rassol, Maria Ljungberg, Eva B Forssell-Aronsson","doi":"10.1186/s12885-026-16975-3","DOIUrl":"10.1186/s12885-026-16975-3","url":null,"abstract":"<p><strong>Background: </strong>Peptide receptor radionuclide therapy with [¹⁷⁷Lu]Lu-DOTATATE is an established treatment for somatostatin receptor-expressing neuroendocrine tumors. Although strong anti-tumor effects have been demonstrated in experimental models, curative responses in patients remain limited. Improved understanding of the molecular responses induced by [¹⁷⁷Lu]Lu-DOTATATE may help identify strategies for treatment optimization. This study aimed to characterize proteomic alterations in GOT1 small intestinal neuroendocrine tumor xenografts following [¹⁷⁷Lu]Lu-DOTATATE therapy.</p><p><strong>Methods: </strong>GOT1 tumor-bearing BALB/c nude mice received a non-curative intravenous administration of 15 MBq [¹⁷⁷Lu]Lu-DOTATATE or saline control. Tumors were collected 1 or 13 days after treatment to represent early response and regrowth phases. Tumor volumes were monitored using magnetic resonance imaging. Proteomic profiling was performed using liquid chromatography tandem mass spectrometry with tandem mass tag labeling. Differential protein expression was analyzed using Welch's t-test with significance defined as fold change ≥ 1.5 and p < 0.01. Functional enrichment and pathway analyses were conducted using Gene Ontology annotation and Ingenuity Pathway Analysis.</p><p><strong>Results: </strong>Treatment induced a transient reduction in tumor volume followed by regrowth. In total, 3861 proteins were quantified, of which 155 showed significantly altered expression after treatment. Affected proteins were associated with cytoskeletal organization, oxidative stress response, protein metabolism, and systemic regulation. Pathway analyses identified inhibition of several signaling pathways linked to cell migration and invasiveness, including RhoA, Rac, integrin, and CXCR4 signaling. Upstream regulator analysis suggested activation of RABL6 and inhibition of p53 signaling during tumor regrowth. Proteins related to endoplasmic reticulum stress and ubiquitin-proteasome activity were also altered. Selected findings were validated by ELISA.</p><p><strong>Conclusions: </strong>[¹⁷⁷Lu]Lu-DOTATATE therapy induced extensive proteomic changes in GOT1 tumors, including suppression of pathways associated with invasiveness and modulation of p53- and stress-related signaling. These findings suggest potential therapeutic benefits of combining [¹⁷⁷Lu]Lu-DOTATATE with agents targeting p53 regulation or endoplasmic reticulum stress pathways to improve treatment efficacy in neuroendocrine tumors.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13584284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148987950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Belantamab mafodotin plus venetoclax in t(11;14)-positive relapsed or refractory multiple myeloma - the BELI(E)VE trial.","authors":"Christoph Schaefers, Cyrus Khandanpour, Mathias Hänel, Miriam Kull, Winfried Alsdorf, Abdulaziz Kamili, Ricardo Kosch, William Krüger, Stephan Bohl, Elias Karl Mai, Christof Scheid, Hermann Einsele, Monika Brüggemann, Anna Suling, Antonia Zapf, Carsten Bokemeyer, Katja Weisel, Lisa Leypoldt","doi":"10.1186/s12885-026-16905-3","DOIUrl":"10.1186/s12885-026-16905-3","url":null,"abstract":"<p><strong>Background: </strong>Multiple myeloma (MM) is a widely incurable B-cell malignancy that predominantly affects older adults, representing 10% of hematologic cancers. Despite advancements in therapy that have significantly extended median overall survival (OS), MM remains a clinical challenge with poor prognosis for patients refractory to multiple drug classes. There is a critical need for innovative and personalized treatments, including for patients with translocation (11;14), a subgroup characterized by specific therapeutic vulnerabilities. Combined targeting of B-cell maturation antigen (BCMA) and BCL-2 presents a promising personalized treatment strategy for inducing deep remissions and improving outcomes in this specific subgroup.</p><p><strong>Methods: </strong>The BELI(E)VE trial (NCT05853965) is a German investigator-initiated, prospective, multicenter, open-label phase I/IIa study designed to evaluate the combination of belantamab mafodotin and venetoclax, with or without dexamethasone, in patients with relapsed or refractory multiple myeloma (RRMM) with ≥1 prior treatment line and t(11;14) translocation. The study consists of a dose escalation phase (phase I) to determine the recommended phase 2 dose (RP2D), followed by a dose expansion phase (phase IIa) to assess clinical activity at the RP2D. The phase I portion employs a traditional 3+3 design across four dose levels, while the phase IIa expansion will include 25 additional patients treated at the RP2D. Safety, tolerability, and preliminary efficacy will be evaluated through comprehensive assessments, including assessment for minimal residual disease negativity and ocular exams.</p><p><strong>Discussion: </strong>The BELI(E)VE trial aims to establish a novel personalized therapeutic approach for a specific subset of MM patients by combining belantamab mafodotin and venetoclax. This combination targets BCMA and BCL-2, potentially inducing deep and durable remissions. The study will provide critical data on the safety and efficacy of this combination, aiming to improve outcomes in t(11;14)-positive RRMM patients. The translational component, examining circulating tumor cells and mitochondrial activity, may identify mechanisms of resistance and response, guiding future personalized therapeutic strategies.</p><p><strong>Trial registration: </strong>NCT05853965 (2023-04-22).</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: LINC00852 promotes the proliferation and invasion of ovarian cancer cells by competitively binding with miR-140-3p to regulate AGTR1 expression.","authors":"Zhi-Wei Qiao, Ying Jiang, Ling Wang, Lei Wang, Jing Jiang, Jing-Ru Zhang, Peng Mu","doi":"10.1186/s12885-026-16963-7","DOIUrl":"10.1186/s12885-026-16963-7","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13573324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: TWIST1 activates cancer stem cell marker genes to promote epithelial‑mesenchymal transition and tumorigenesis in esophageal squamous cell carcinoma.","authors":"Sima Ardalan Khales, Sina Mozaffari-Jovin, Dirk Geerts, Mohammad Reza Abbaszadegan","doi":"10.1186/s12885-026-16871-w","DOIUrl":"10.1186/s12885-026-16871-w","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and molecular prognostic factors associated with outcomes of first-line osimertinib in EGFR-Mutated advanced NSCLC: a systematic review and meta-analysis.","authors":"Yingding Ruan, Hongsheng Xue, Chuan Long, Wenjun Cao, Jianwei Han, Ting Zhang","doi":"10.1186/s12885-026-16852-z","DOIUrl":"https://doi.org/10.1186/s12885-026-16852-z","url":null,"abstract":"<p><strong>Background: </strong>Osimertinib is the standard first-line therapy for epidermal growth factor receptor (EGFR)-mutated advanced non-small cell lung cancer (NSCLC), but outcomes remain heterogeneous. This meta-analysis evaluated baseline clinical and molecular prognostic factors associated with poorer outcomes in this setting.</p><p><strong>Methods: </strong>PubMed, Embase, Web of Science, Scopus, and the Cochrane Library were searched through 20 May 2026. Eligible studies included patients with EGFR-mutated advanced, recurrent, or metastatic NSCLC receiving first-line osimertinib with extractable prognostic data. The primary outcome was progression-free survival or real-world progression-free survival (PFS/rwPFS); overall survival or real-world overall survival (OS/rwOS) was secondary. Hazard ratios (HRs) were pooled using random-effects models.</p><p><strong>Results: </strong>Eighteen studies involving 4,070 first-line osimertinib-treated patients were included. TP53 mutation was associated with shorter PFS/rwPFS (HR 1.65, 95% confidence interval [CI] 1.15-2.37) and worse OS/rwOS (HR 1.55, 95% CI 1.14-2.12). EGFR L858R, versus exon 19 deletion, was associated with shorter PFS/rwPFS (HR 1.62, 95% CI 1.39-1.90) and worse OS/rwOS (HR 1.63, 95% CI 1.40-1.88), with consistent estimates across sensitivity analyses. Eastern Cooperative Oncology Group performance status ≥ 2, central nervous system/brain metastasis, and liver metastasis were associated with poorer outcomes. The OS/rwOS association for liver metastasis was sensitive to alternative estimate selection. Evidence for bone metastasis and programmed death-ligand 1 expression was less robust.</p><p><strong>Conclusions: </strong>Evidence-tier assessment identified EGFR L858R, ECOG PS ≥ 2, and CNS/brain metastasis as high-certainty adverse prognostic factors. Liver metastasis was supported by moderate certainty for PFS/rwPFS but lower certainty for OS/rwOS. TP53 mutation, PD-L1 expression, and bone metastasis were lower-certainty or exploratory findings. These findings support future integrated prognostic models, but do not establish criteria for selecting intensified first-line therapy over osimertinib monotherapy.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13695278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149262738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Lycorine inhibits angiogenesis by docking to PDGFRα.","authors":"Fei Lv, XiaoQi Li, Ying Wang","doi":"10.1186/s12885-026-16962-8","DOIUrl":"10.1186/s12885-026-16962-8","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NNMT-associated metabolic-thromboinflammatory-immune co-activation in heterogeneous CTC clusters: a hypothesis-generating computational framework\".","authors":"Jiayang Gong, Zhe Wang, Yun Shi, Minlan Ren, Tingting Li, Gang Li, Rui Peng","doi":"10.1186/s12885-026-16692-x","DOIUrl":"10.1186/s12885-026-16692-x","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Heterogeneous circulating tumor cell (CTC) clusters interact with platelets, neutrophils, stromal cells, and immune cells, forming a protective state that may facilitate survival in the circulation and metastatic dissemination. Nicotinamide N-methyltransferase (NNMT) is associated with metabolic reprogramming, stromal activation, epithelial-mesenchymal plasticity, and immune suppression. However, its coordinated relationship with platelet/coagulation, neutrophil/ neutrophil extracellular trap (NET), and immune exhaustion programs in CTC-associated states has not been systematically evaluated. Therefore, we constructed a hypothesis-generating framework integrating mechanistic evidence, pan-cancer computational analyses, and single-cell transcriptomic analyses.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We performed a mechanistic evidence synthesis combined with TCGA PanCancer bulk RNA-seq analysis and cross-dataset evaluation of eight publicly available multi-cancer single-cell RNA-seq cohorts. Module scores were constructed for metabolic/EMT, platelet/coagulation, neutrophil/NET, immune checkpoint/exhaustion, and cytotoxic/NK cell programs. Correlation analyses across cancer types, feature-level pseudotime analysis, ligand- receptor mapping, and in silico perturbation simulations were applied to evaluate associations between NNMT and the composite tri-axial state. In addition, exploratory supervised machine learning models were used to determine whether axis-related features and ligand-receptor features could discriminate single CTCs from clustered or leukocyte-associated CTC states. Leave-one-cancer-out cross-validation was further used to assess the reproducibility of axis- associated survival risk across cancer types. No new experimental, animal, or clinical intervention data were generated.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Across 483,590 cells from eight publicly available single-cell datasets, NNMT expression was positively correlated with the composite tri-axial score across multiple cancer contexts. Feature-level pseudotime analysis indicated convergence of NNMT-associated metabolic, platelet/coagulation, neutrophil/NET, and immune exhaustion programs toward a common trajectory endpoint, although this analysis does not establish temporal causality. In silico NNMT perturbation preferentially implicated stromal and fibroblast-like populations as candidate responsive compartments. Ligand-receptor analyses further suggested an interconnected communication network involving CTC/epithelial and CAF/endothelial compartments, platelet/coagulation bridging, myeloid/NET recruitment, and downstream T/NK cell exhaustion.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;These integrated findings support NNMT-associated metabolic-thromboinflammatory-immune co-activation as a candidate feature of heterogeneous CTC-associated states and provide mechanistic rationale for a \"disaggregation-exposure-clearance\" strategy combining αIIbβ3 inhibition, NNMT ","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"26 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}