BMC Cancer最新文献

{"title":"Innovative inhalable dry powder: nanoparticles loaded with Crizotinib for targeted lung cancer therapy.","authors":"Faiza Naureen, Yasar Shah, Maqsood Ur Rehman, Fazli Nasir Fazli Nasir, Abdul Saboor Pirzada, Jamelah Saleh Al-Otaibi, Maria Daglia, Haroon Khan","doi":"10.1186/s12885-025-15015-w","DOIUrl":"https://doi.org/10.1186/s12885-025-15015-w","url":null,"abstract":"<p><p>Crizotinib is a targeted therapy for metastatic non-small cell lung cancer (NSCLC) that is ALK- or ROS1-positive, as well as for conditions such as ALK-positive anaplastic large cell lymphoma and inflammatory myofibroblastic tumor. However, the associated toxicity poses a significant challenge to its use. To mitigate this issue, a novel dry powder inhalation formulation was developed using Crizotinib-loaded polyethylene glycol-based polymeric nanoparticles (NPs). These nanoparticles were created through a nanoprecipitation approach and improved employing central composite design. The capabilities of the formulation were assessed with Anderson Cascade Impactor, revealing a fine particle fraction of 56.2% and a mass median aerodynamic diameter of around 1.5 μm, indicating appropriate aerodynamic characteristics for inhalation. Key properties of the optimized nanoparticles included Encapsulation efficiency (82.3%, Zeta potential (-31.9 mV), Particle size (167 nm), Polydispersity index (0.462) and Release efficiency (60.6%) In vitro studies indicated that the polymeric nanoparticles exhibited greater anticancer activity compared to free Crizotinib. Additional characterization using techniques like XRD, DSC, FTIR, and SEM confirmed that the polymeric nanoparticle formulation has promising physicochemical properties, suggesting it could enhance local drug delivery and efficacy in lung cancer treatment while potentially reducing systemic toxicity.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1526"},"PeriodicalIF":3.4,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Male-origin microchimerism and risk of cancer: a systematic review and meta‑analysis.","authors":"Jun Li, Tingting Shao, Junyan Kou, Liwei Ni","doi":"10.1186/s12885-025-14860-z","DOIUrl":"https://doi.org/10.1186/s12885-025-14860-z","url":null,"abstract":"<p><strong>Background: </strong>Many women carry male cells of presumed fetal origin-so-called male-origin microchimerism (MOM) in their circulation and tissues. The association between MOM and cancer risk remains unclear. We aim to evaluate the effect of MOM on cancer risk among postpartum women.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted to identify relevant articles in databases of PubMed, EMBASE, and Web of Science. The data were extracted from eligible studies on the relationship between MOM and cancer risk. A random-effects model was applied to obtain the pooled relative risks (RRs) with 95% confidence intervals (95%CIs). Subgroup analysis, sensitivity analysis and publication bias and were also conducted.</p><p><strong>Results: </strong>Twelve studies involving 3078 participants were enrolled in the pooled analysis. Data on the risk of breast, colon, ovarian, endometrial, thyroid, and brain cancer were collected for quantitative analysis. Pooled analysis showed a significantly reduced rate of cancer (pooled RR = 0.51, 95%CI 0.32-0.82) among MOM-positive women.</p><p><strong>Conclusions: </strong>Individuals harboring MOM exhibits a significantly low risk of cancer.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1528"},"PeriodicalIF":3.4,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-related differences in adjuvant chemotherapy use and outcomes in stage II colon cancer: a retrospective cohort study.","authors":"Qiyang Zhou, Chunxian Zhou, Gang Zhang, Xinyang Xia, Xiaojun Zhou, Jianhua Lang","doi":"10.1186/s12885-025-14848-9","DOIUrl":"https://doi.org/10.1186/s12885-025-14848-9","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1527"},"PeriodicalIF":3.4,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel anticancer effect of substituted imidazole derivatives against urothelial carcinoma: integrating In vitro screening and molecular docking for target kinases.","authors":"Basma Emad Aboulhoda, Abdelsattar M Omar, Sara Elfarrash, Mansour Abdullah Alghamdi, Ahmed A Emam, Randa El-Gamal, Soad E Abo-Elhoda, Mohamed F Zayed","doi":"10.1186/s12885-025-15012-z","DOIUrl":"https://doi.org/10.1186/s12885-025-15012-z","url":null,"abstract":"<p><p>Four novel substituted imidazole derivatives-5a (Kim-161), 5b (Kim-111), 5c (Kim-261), and 5d (Kim-231) were evaluated for their antiproliferative activity against urothelial carcinoma. Among these, the two derivatives Kim-161 (5a) and Kim-111 (5b) demonstrated potent cytotoxicity against the T24 transitional carcinoma cell line, with IC₅₀ values of 56.11 µM and 67.29 µM, respectively, as determined by MTT assay. Further mechanistic investigations revealed that these compounds modulate key pathways involved in cancer progression including cell cycle regulation; (p53), oncogenic signaling (Kras), cell apoptosis; (BAX and caspase 3), inflammatory response (Interleukin 6 (IL6), Tumor Necrosis Factor alpha (TNFα), and Nuclear Factor kappa B (NF-κB), autophagy regulation (phosphoinositide 3-kinase signaling (PIK3CA) and its targets protein kinase Akt and mammalian target of rapamycin (mTOR) and metastasis (Matrix metalloproteinase-9 (MMP-9)). Molecular docking and dynamic simulations against key cancer targets PTK6, FLT3, and BCL-2 revealed exceptional binding affinity and stable protein-ligand complexes. Furthermore, these compounds exhibited favorable drug-like properties, including optimal physicochemical and pharmacokinetic profiles. This integrated approach, combining the in vitro validation and computational modeling, places Kim-161 and Kim-111 as promising lead compounds for targeted urothelial carcinoma therapy. The findings underscore the therapeutic potential of dual kinase/tubulin inhibition in combating aggressive malignancies, offering a robust foundation for further preclinical development.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1524"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Habitat-based transformer model in pretreatment ¹⁸F-FDG PET imaging for predicting prognosis in cervical cancer: a two-center retrospective study.","authors":"Ruihe Lai, Qianqian Tan, Chongyang Ding, Yiduo Xu, Tingting Tang, Zhengyang Zhou","doi":"10.1186/s12885-025-14977-1","DOIUrl":"https://doi.org/10.1186/s12885-025-14977-1","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1515"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AI-driven chemotoxicity prediction in colorectal cancer: impact of race, SDOH, and biological aging.","authors":"Claire Han, Christin Burd, Jesse Plascak, Fode Tounkara, Ashley Rosko, Anne Noonan, Alai Tan, Diane Von Ah, Xia Ning","doi":"10.1186/s12885-025-14831-4","DOIUrl":"https://doi.org/10.1186/s12885-025-14831-4","url":null,"abstract":"<p><strong>Background: </strong>Patients with colorectal cancer (CRC) often experience chemotoxicity that impacts treatment adherence, survival, and quality of life. Early screening for chemotoxicity risk is vital, yet comprehensive predictive models are lacking. The objective of this study was to develop effective artificial intelligence (AI)/machine learning (ML) models, integrating racialized group, social determinants of health (SDOH) (Area Deprivation Index [ADI], employment status), and biological aging (Levine Phenotypic Age) to predict overall, gastrointestinal (GI), and hematological chemotoxicity.</p><p><strong>Methods: </strong>We used electronic health records data from 1,735 adult patients with CRC. Sociodemographic/clinical variables, Levine Phenotypic Age (biological aging), and SDOH (including geospatial variations measured by ADI) were analyzed using descriptive statistics. Associations with chemotoxicity (overall, GI, hematological) were evaluated via univariate tests. Significant predictors from univariate tests were selected for AI/ML modeling. Six supervised ML models were trained on 80% of cases (n = 1,388), with 20% (n = 347) reserved for testing. Performance was assessed via accuracy, area under the curve (AUC), and F1-score. Permutation feature importance ranked predictors to define the most significant predictors of chemotoxicity.</p><p><strong>Results: </strong>Support Vector Machine and XGBoost models demonstrated high accuracy in both the training and test datasets. Notably, the AUC (0.988) was highest for the Support Vector Machine model in predicting overall chemotoxicity within the training dataset. Key predictors of overall and GI toxicities included higher Levine Phenotypic Age, elevated inflammatory markers (e.g., C-reactive protein), and poor SDOH (e.g., higher ADI, unemployment). Hematological toxicity was linked to lower inflammatory markers, higher Levine Phenotypic Age, and younger chronological age. Race (non-Hispanic Black), body mass index, and lifestyle also influenced overall and GI toxicities.</p><p><strong>Conclusions: </strong>ML-based chemotoxicity prediction models incorporating racialized group, SDOH, and biological aging had high accuracy. Greater biological aging, poor SDOH including ADI, and higher inflammation markers were common risk factors for overall and GI chemotoxicity. In contrast, chronological and biological ages and immune/inflammation markers were only linked to hematological chemotoxicity. Integrating these factors into predictive models can help clinicians identify at-risk patients and tailor interventions (e.g., anti-inflammatory, anti-aging strategies) to reduce chemotoxicity and improve survivorship outcomes.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1513"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral blood multimodal integration via cross-attention for cancer immune profiling.","authors":"Xiong Li, Yi Hua, Hongwei Liu, Juan Zhou, Yuejin Zhang, Haowen Chen","doi":"10.1186/s12885-025-14969-1","DOIUrl":"https://doi.org/10.1186/s12885-025-14969-1","url":null,"abstract":"<p><strong>Objective: </strong>Accurate cancer risk prediction is hindered by complex, multi-layered immune interactions, and traditional tissue biopsies are invasive and lack scalability for large-scale or repeated assessments. Peripheral blood offers a minimally invasive and accessible alternative for immune profiling. This study aims to develop CAMFormer, a deep learning framework that integrates multimodal peripheral blood-derived immune features for precise, non-invasive early cancer risk prediction.</p><p><strong>Methods: </strong>CAMFormer combines mRNA expression, immune cell frequencies, and TCR diversity index, leveraging a cross-attention-based multimodal Transformer to capture cross-scale immune interactions.</p><p><strong>Results: </strong>In five-fold cross-validation, CAMFormer achieved an AUC of 0.92 and an F1-score of 0.85 on the validation set, outperforming unimodal and baseline methods.</p><p><strong>Conclusion: </strong>These results highlight the potential benefits of integrating multimodal immune features with cross-attention mechanisms for early cancer detection and for guiding future personalized immunotherapy studies.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1523"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NFKBIE as a prognostic biomarker and therapeutic target for GBM: role in Hedgehog signaling activation.","authors":"Feng Mo, Yang Li, Ce Dong, Lijun Yang, Xiaoli Ma, Baogen Pan, Zhenzeng Fan","doi":"10.1186/s12885-025-14775-9","DOIUrl":"https://doi.org/10.1186/s12885-025-14775-9","url":null,"abstract":"<p><p>Glioblastoma (GBM), as one of the most common and aggressive primary brain tumors, pose significant challenges in diagnosis and treatment, highlighting the urgent need for the identification of novel biomarkers, NFKBIE, which may play a critical role in tumor progression, immune modulation, and therapeutic response. We investigated the role of NFKBIE in GBM through both bioinformatics analysis and experimental validation. Initially, bioinformatics analysis based on public databases revealed significant differential expression of NFKBIE across various cancer types, particularly in GBM, where elevated expression was correlated with poor patient prognosis, including overall survival, disease-specific survival, and progression-free survival. Furthermore, genetic alterations in NFKBIE, such as copy number variations (CNVs) and tumor mutational burden (TMB), were significantly associated with tumor progression. In the experimental validation phase, we utilized small interfering RNA (siRNA) technology to silence NFKBIE expression in GBM cell lines, including U87 and T98G. Functional assays were then performed to assess the impact of NFKBIE knockdown. Cell proliferation assays, including CCK-8 and clonogenic assays, demonstrated that silencing NFKBIE significantly inhibited the proliferation of GBM cells. Migration and invasion assays, including wound healing and Transwell assays, further confirmed that NFKBIE knockdown markedly suppressed the migratory and invasive abilities of GBM cells. Additionally, apoptosis assays, such as TUNEL staining, revealed that NFKBIE silencing significantly promoted apoptosis in GBM cells. Western blot analysis confirmed the changes in the expression of key markers associated with proliferation, stemness, migration, invasion, and apoptosis. Furthermore, in a mouse xenograft model, NFKBIE knockdown significantly slowed tumor growth. Histological analysis of the excised tumors confirmed that reduced NFKBIE expression was closely associated with the inhibition of tumor growth. Notably, NFKBIE silencing also led to the downregulation of components of the Hedgehog signaling pathway, suggesting that NFKBIE may regulate tumor progression through modulation of this critical pathway. In conclusion, high NFKBIE expression is strongly associated with GBM progression and poor prognosis, and targeting its expression may offer a promising therapeutic strategy for GBM treatment.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1512"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AI-Driven predictive modeling of cervical intraepithelial neoplasia severity: a comprehensive analysis with clinical adoption frameworks.","authors":"Farah Farzaneh, Amir Soltani, Fatemeh Dastyar, Marzieh Mohammadi, Maryam Sadat Hosseini","doi":"10.1186/s12885-025-14974-4","DOIUrl":"https://doi.org/10.1186/s12885-025-14974-4","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1521"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine: a promising strategy to combat cetuximab-resistance in colorectal cancer.","authors":"Jianmin Ye, Bingchan Sun, Fengmei Xia, Guoxin Wang, Huimin Liu, Jianghua Ding, Mingfu Tong","doi":"10.1186/s12885-025-15013-y","DOIUrl":"https://doi.org/10.1186/s12885-025-15013-y","url":null,"abstract":"<p><p>Cetuximab, a monoclonal antibody against epidermal growth factor receptor (EGFR), is approved as a front-line treatment for metastatic colorectal cancers, but limited efficacy is obtained. Combinatory therapy is a potentially promising strategy to enhance anticancer effects, overcome drug resistance and improve overall clinical survival. Here, we show that berberine combined with cetuximab created a synergistic inhibitory effect on cetuximab-resistant CRC cells in vitro and in vivo. Human phospho-kinase assay explored that the phosphorylation of Src and Chk-2 was inhibited by berberine and decreased greatly when combined with cetuximab. Adding KX2-391 (Src inhibitor) rather than BML-277 (Chk-2 inhibitor) with cetuximab resulted in more cell death and apoptosis. Conversely, activation of Src with MLR-1023 mitigated the inhibitory effect of berberine alone or in combination with cetuximab. Additionally, the activities of downstream kinases of Src such as mTOR, STAT3 and the production of ROS were inhibited greatly by berberine plus cetuximab. Taken together, we concluded that the synergistic effects of BBR and cetuximab may be mediated by decreasing the activities of Src/mTOR/STAT3 and the production of ROS, thus inducing greater extent of apoptosis in cancer cells.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1520"},"PeriodicalIF":3.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}