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Predictive value of nasopharyngeal microbiota for necrosis after re-irradiation in recurrent nasopharyngeal carcinoma. 鼻咽癌复发后再照射后鼻咽微生物群对坏死的预测价值。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-29 DOI: 10.1186/s12885-025-14842-1
Kai Wen, Ze-Rong Huang, Yong-Long Liu, Wen-Bin Wu, Zi-Han Qin, Yan-Feng Ouyang, Xiong Zou, Rui You, You-Ping Liu, Ming-Yuan Chen, Yi-Jun Hua
{"title":"Predictive value of nasopharyngeal microbiota for necrosis after re-irradiation in recurrent nasopharyngeal carcinoma.","authors":"Kai Wen, Ze-Rong Huang, Yong-Long Liu, Wen-Bin Wu, Zi-Han Qin, Yan-Feng Ouyang, Xiong Zou, Rui You, You-Ping Liu, Ming-Yuan Chen, Yi-Jun Hua","doi":"10.1186/s12885-025-14842-1","DOIUrl":"10.1186/s12885-025-14842-1","url":null,"abstract":"<p><strong>Background: </strong>Post-radiation nasopharyngeal necrosis (PRNN) is a severe complication following re-irradiation in patients with recurrent nasopharyngeal carcinoma (NPC). This study aimed to explore the association between nasopharyngeal microbiota and PRNN in patients with recurrent NPC undergoing re-irradiation and to evaluate the predictive value of the microbiota for PRNN.</p><p><strong>Methods: </strong>This retrospective study collected data from 113 patients with recurrent NPC who underwent re-irradiation at the Sun Yat-sen University Cancer Center (SYSUCC) between January 2020 and November 2022. Patients were divided into necrosis and non-necrosis groups based on the development of necrosis after re-irradiation. 5R 16S rRNA sequencing of nasopharyngeal biopsy tissues conducted before re-irradiation was used to assess microbiota composition, diversity, and functional predictions. Clinical features and selected microbial markers were used in a random forest model to predict the occurrence of PRNN.</p><p><strong>Results: </strong>Of the 113 patients with recurrent NPC who underwent re-irradiation, 60 developed PRNN, while 53 did not. Proteobacteria and Firmicutes were the dominant phyla in the nasopharyngeal microbiota of all the patients with recurrent NPC. The necrosis group exhibited significantly higher alpha diversity and distinct beta diversity than the non-necrosis group did. A predictive model that combined clinical features (gross tumor volume [GTV]) with microbiome characteristics achieved an AUC of 87.9% in the training set and 86.9% in the test set, demonstrating robust predictive performance.</p><p><strong>Conclusions: </strong>Nasopharyngeal microbial diversity prior to re-irradiation was significantly higher in the necrosis group. Our predictive model, integrating clinical and microbial features, demonstrated strong performance in predicting PRNN and offers a promising tool for early intervention and prevention strategies.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1436"},"PeriodicalIF":3.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191212","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}
引用次数: 0
Shared and non-overlapping functions of RECQL4 and BLM helicases in chemotherapeutics-induced glioma cell responses. RECQL4和BLM解旋酶在化疗诱导的胶质瘤细胞反应中的共享和非重叠功能
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-29 DOI: 10.1186/s12885-025-14932-0
Kamil Wojnicki, Bartosz Wojtas, Iwona A Ciechomska, Beata Kaza, Matthew Guille, Waldemar Priebe, Bozena Kaminska
{"title":"Shared and non-overlapping functions of RECQL4 and BLM helicases in chemotherapeutics-induced glioma cell responses.","authors":"Kamil Wojnicki, Bartosz Wojtas, Iwona A Ciechomska, Beata Kaza, Matthew Guille, Waldemar Priebe, Bozena Kaminska","doi":"10.1186/s12885-025-14932-0","DOIUrl":"10.1186/s12885-025-14932-0","url":null,"abstract":"<p><strong>Objectives: </strong>Human RECQL4 and BLM helicases participate in all DNA dependent processes, including replication stress, DNA damage repair. Both helicases are overexpressed in glioblastoma (GBM), a lethal primary brain tumour, characterised by resistance to radio- and chemotherapy. BLM-depleted glioma cells exhibit senescence-associated or polypoid phenotype when exposed to temozolomide (TMZ) and olaparib (OLA), a PARP inhibitor. This study aims to investigate how RECQL4 depletion influences the response of malignant gliomas to chemotherapeutics.</p><p><strong>Methods: </strong>We investigated the effect of RECQL4 depletion in glioma cells on cell growth, apoptosis, senescence and polyploidy in the response to combined TMZ and OLA treatment. We compared transcriptomes of RECQL4- and BLM-depleted LN18 and LN229 glioma cells. Drug-induced cytotoxicity, senescence-associated phenotypes, cell cycle alterations, and polyploidy were assessed using the MTT metabolic assay, β-galactosidase activity assay, and propidium iodide staining.</p><p><strong>Results: </strong>RECQL4 depletion modestly affected basal glioma cell viability and proliferation, similarly to knock out of the BLM protein. Deletion of RECQL4 in glioma cells (RQ4 KO) induced profound transcriptomic alterations, dissimilar to BLM depletion. RECQL4-depleted glioma cells treated with TMZ and OLA exhibited reduced viability and increased levels of apoptosis markers. The treatment induced cell cycle arrest, however, RQ4 KO cells did not show signs of senescence phenotype or polyploidisation, when compared to BLM KO glioma cells. Interestingly, both RQ4 KO and BLM KO cells were more resistant to WP744, a doxorubicin derivative, when compared to WT LN229 glioma cells.</p><p><strong>Conclusion: </strong>Our results highlight the distinct roles of RecQ helicases in a response to chemotherapeutics and support a rationale for targeting RECQL4 as a therapeutic strategy in glioblastoma.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1434"},"PeriodicalIF":3.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191233","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}
引用次数: 0
Pan-cancer analysis of the oncogenic role of ZNF703 in regulating tumor immunity. ZNF703在调节肿瘤免疫中的致瘤作用的泛癌分析。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-29 DOI: 10.1186/s12885-025-14636-5
Xianli Shi, Jingyu Lie, Rui Li, Haoming Chen, Rongxin Zhang
{"title":"Pan-cancer analysis of the oncogenic role of ZNF703 in regulating tumor immunity.","authors":"Xianli Shi, Jingyu Lie, Rui Li, Haoming Chen, Rongxin Zhang","doi":"10.1186/s12885-025-14636-5","DOIUrl":"10.1186/s12885-025-14636-5","url":null,"abstract":"<p><p>ZNF703, a member of the NET/NLZ family, plays a critical role in individual development and cancer progression. Despite its significance, a comprehensive pan-cancer analysis of ZNF703 remains underexplored. In this study, we performed a systematic pan-cancer analysis to elucidate the mechanistic and functional roles of ZNF703 in tumorigenesis. Our findings reveal that elevated ZNF703 expression is significantly correlated with cancer progression, adverse clinical outcomes, and the enrichment of immune cells within the tumor microenvironment (TME), particularly cancer-associated fibroblasts (CAFs), CD8<sup>+</sup> T cells, and M2 macrophages, suggesting its pivotal role in modulating tumor immunity. Mechanistically, ZNF703 regulates tumor immunity by binding to promoter sequences, thereby suppressing the expression of CD274, ICAM1, and CXCL3, which may facilitate tumor immune escape. Additionally, we identified functional hub genes associated with ZNF703, including DDHD2, LSM1, and BAG4. Notably, ZNF703, DDHD2, LSM1, and BAG4 are co-localized within the amplicons at the chromosome 8p11-p12 region, indicating a potential cooperative role in driving cancer initiation and progression. Collectively, these findings underscore the essential roles of ZNF703 in cancer development, patient prognosis, and the regulation of anti-tumor immunity, highlighting its potential as a biomarker for cancer detection and as a novel immunotherapeutic target.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1437"},"PeriodicalIF":3.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191188","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}
引用次数: 0
Combined effects of slow movement training with tonic force generation and aerobic exercise prior to cancer therapy in patients with lung cancer (START-lung): a pilot feasibility trial. 肺癌患者癌症治疗前慢速运动训练与强直力生成和有氧运动的联合作用(START-lung):一项试点可行性试验。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-29 DOI: 10.1186/s12885-025-14728-2
Utae Katsushima, Takuya Fukushima, Jiro Nakano, Kazuki Fujii, Yutaro Nagata, Keisuke Kamisako, Yukiko Okuno, Kiyori Yoshida, Tatsuki Ikoma, Yuki Takeyasu, Yuta Yamanaka, Hiroshige Yoshioka, Takayasu Kurata, Eisuke Ochi
{"title":"Combined effects of slow movement training with tonic force generation and aerobic exercise prior to cancer therapy in patients with lung cancer (START-lung): a pilot feasibility trial.","authors":"Utae Katsushima, Takuya Fukushima, Jiro Nakano, Kazuki Fujii, Yutaro Nagata, Keisuke Kamisako, Yukiko Okuno, Kiyori Yoshida, Tatsuki Ikoma, Yuki Takeyasu, Yuta Yamanaka, Hiroshige Yoshioka, Takayasu Kurata, Eisuke Ochi","doi":"10.1186/s12885-025-14728-2","DOIUrl":"10.1186/s12885-025-14728-2","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1438"},"PeriodicalIF":3.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191258","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}
引用次数: 0
Non-truncating BMPR1A variants associated with familial colorectal cancer and adenomatous polyps. 与家族性结直肠癌和腺瘤性息肉相关的非截断BMPR1A变异。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-29 DOI: 10.1186/s12885-025-14865-8
Taina T Nieminen, Outi Kuismin, Riitta Laine, Anna Lepistö, Laura Koskenvuo, Laura Renkonen-Sinisalo, Markus J Mäkinen, Ari Ristimäki, Jukka-Pekka Mecklin, Päivi Peltomäki
{"title":"Non-truncating BMPR1A variants associated with familial colorectal cancer and adenomatous polyps.","authors":"Taina T Nieminen, Outi Kuismin, Riitta Laine, Anna Lepistö, Laura Koskenvuo, Laura Renkonen-Sinisalo, Markus J Mäkinen, Ari Ristimäki, Jukka-Pekka Mecklin, Päivi Peltomäki","doi":"10.1186/s12885-025-14865-8","DOIUrl":"10.1186/s12885-025-14865-8","url":null,"abstract":"<p><strong>Background: </strong>Pathogenic variants of the bone morphogenetic protein receptor type 1 A (BMPR1A) gene underlie juvenile polyposis syndrome (JPS), a rare autosomal dominant condition characterized by multiple gastrointestinal hamartomatous polyps. Recent findings indicate that constitutional BMPR1A variants can also be associated with various non-JPS phenotypes without hamartomatous polyps. The basis of varying genotype - phenotype relationships is poorly understood.</p><p><strong>Methods: </strong>We investigated four families with non-truncating variants of BMPR1A affecting different functional domains. Clinical presentation resembled familial colorectal cancer type X-like syndrome with dominantly inherited microsatellite-stable gastrointestinal adenomas and carcinomas. To gain insights into genotype-phenotype associations, exome sequencing was conducted on normal and tumor tissue DNAs. Constitutional BMPR1A variants underwent a thorough evaluation for clinical significance, by, e.g., co-segregation analyses and in silico modeling, supplemented by haplotyping and genealogical studies. All available tumors were examined for histology and molecularly for BMPR1A \"second hits\" and mutational signatures.</p><p><strong>Results: </strong>Targeted sequencing of blood DNA revealed a three-nucleotide deletion (BMPR1A c.264_266 del) in one family, a three-nucleotide insertion (BMPR1A c.506_507insTCC) in two families, and a missense change (BMPR1A c.766G > A) in a fourth family. The two families with BMPR1A c.506_507insTCC had a shared ancestral origin. Co-segregation of the variants with colorectal cancer and/or polyps, in-silico modeling, and two hit inactivation by loss of heterozygosity or somatic point mutations in tumors, together with the absence of other possible predisposing variants by exome sequencing, supported the idea of tumor predisposition being attributable to the BMPR1A variants. Polyps examined from variant carriers had adenomatous histology, except for three polyps with hamartomatous features, originating from two BMPR1A carriers from two families. While no hamartoma samples were available for molecular investigation, somatic mutational profiles of colorectal adenomas and carcinomas resembled those of mismatch repair-proficient colorectal tumors in general.</p><p><strong>Conclusions: </strong>Our findings support the notion that the clinical phenotype of BMPR1A variants may extend beyond classical JPS. Genotype-phenotype correlations are complex, since molecular comparison of constitutional and tumor features of our families to those published from JPS families in the literature show a significant overlap. The variety of clinical phenotypes warrants recognition in the clinical management of BMPR1A carriers and their family members.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1435"},"PeriodicalIF":3.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191206","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}
引用次数: 0
Multi-omics analysis reveals disrupted gut microbiota and metabolism in gastric cancer patients with high SIRI. 多组学分析揭示了高SIRI胃癌患者的肠道微生物群和代谢紊乱。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-25 DOI: 10.1186/s12885-025-14852-z
Falong Zou, Shenghe Deng, Bo Liu, Mian Chen, Denglong Chen, Jun Wang, Junnan Gu, Fuwei Mao, Yinghao Cao, Kailin Cai
{"title":"Multi-omics analysis reveals disrupted gut microbiota and metabolism in gastric cancer patients with high SIRI.","authors":"Falong Zou, Shenghe Deng, Bo Liu, Mian Chen, Denglong Chen, Jun Wang, Junnan Gu, Fuwei Mao, Yinghao Cao, Kailin Cai","doi":"10.1186/s12885-025-14852-z","DOIUrl":"10.1186/s12885-025-14852-z","url":null,"abstract":"<p><strong>Background: </strong>Inflammation significantly affects the progression of gastric cancer (GC). The Systemic Inflammation Response Index (SIRI) is an emerging prognostic marker for various malignant tumors, including GC. However, the mechanisms by which SIRI influences patient outcomes remain unclear. This study employed a multi-omics approach to analyze GC patients with different SIRI levels, aiming to identify factors underlying differences in prognosis.</p><p><strong>Methods: </strong>A cohort of 495 GC patients was classified into high SIRI (n = 276) and low SIRI (n = 219) groups using a threshold of 2.6. Kaplan-Meier analysis and Receiver operating characteristic (ROC) curves were used to assess survival outcomes and the predictive accuracy of SIRI compared to other inflammatory markers. Gut microbiota and untargeted metabolomics analyses were conducted on stool samples from 45 GC patients, including 21 with high SIRI and 24 with low SIRI.</p><p><strong>Results: </strong>Elevated SIRI levels were significantly associated with worse OS (P = 0.004, HR = 1.845, 95% CI: 1.231-2.766) and DFS (P < 0.0001, HR = 3.102, 95% CI: 2.016-4.772) in GC patients. Multi-omics analysis revealed distinct gut microbial and metabolic profiles between high- and low-SIRI subgroups. High SIRI was linked to increased Escherichia-Shigella and decreased levels of Blautia and Klebsiella. Metabolomic differences included elevated N-Acetylcadaverine and Epsilon-caprolactam, and decreased S-(PGA2)-glutathione. Integrative analysis identified significant microbe-metabolite correlations, such as Escherichia-Shigella with N-Acetylcadaverine and Epsilon-caprolactam. These findings suggest that SIRI-associated microbial and metabolic features may serve as non-invasive markers for inflammatory risk stratification in GC.</p><p><strong>Conclusion: </strong>High SIRI levels are associated with poorer prognosis in GC patients. Significant differences in gut microbiota and metabolites were observed across different SIRI levels in GC patients, showing their potential as non-invasive markers for GC risk stratification based on SIRI levels.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1433"},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147920","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}
引用次数: 0
Syntaxin-7 promotes EMT and tumor progression via NF-κB signaling and is associated with macrophage infiltration: pan-cancer analysis and experimental validation in hepatocellular carcinoma. Syntaxin-7通过NF-κB信号传导促进EMT和肿瘤进展,并与巨噬细胞浸润相关:肝细胞癌泛癌分析和实验验证。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-25 DOI: 10.1186/s12885-025-14819-0
Langhuan Lei, Wei Shi, Xing Yang, Jiali Lin, Qiuyu Liang, Xiaozhi Huang, Liuxian Pan, Wei Li
{"title":"Syntaxin-7 promotes EMT and tumor progression via NF-κB signaling and is associated with macrophage infiltration: pan-cancer analysis and experimental validation in hepatocellular carcinoma.","authors":"Langhuan Lei, Wei Shi, Xing Yang, Jiali Lin, Qiuyu Liang, Xiaozhi Huang, Liuxian Pan, Wei Li","doi":"10.1186/s12885-025-14819-0","DOIUrl":"10.1186/s12885-025-14819-0","url":null,"abstract":"","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1430"},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147841","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}
引用次数: 0
Clinicopathological and molecular correlates of clinical benefit from disitamab vedotin (RC48), a HER-2-targeting antibody-drug conjugate, in metastatic urothelial carcinoma: a multi-center, real-world study. diitamab vedotin (RC48)是一种her -2靶向抗体-药物偶联物,用于转移性尿路上皮癌的临床获益的临床病理和分子相关:一项多中心、真实世界的研究。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-25 DOI: 10.1186/s12885-025-14870-x
Zhaopei Liu, Kaifeng Jin, Ziyue Xu, Han Zeng, Xiaohe Su, Jingtong Xu, Yawei Ding, Hailong Liu, Yu Zhu, Le Xu, Jiejie Xu, Zewei Wang, Yuan Chang
{"title":"Clinicopathological and molecular correlates of clinical benefit from disitamab vedotin (RC48), a HER-2-targeting antibody-drug conjugate, in metastatic urothelial carcinoma: a multi-center, real-world study.","authors":"Zhaopei Liu, Kaifeng Jin, Ziyue Xu, Han Zeng, Xiaohe Su, Jingtong Xu, Yawei Ding, Hailong Liu, Yu Zhu, Le Xu, Jiejie Xu, Zewei Wang, Yuan Chang","doi":"10.1186/s12885-025-14870-x","DOIUrl":"10.1186/s12885-025-14870-x","url":null,"abstract":"<p><strong>Introduction: </strong>Disitamab Vedotin (DV), a HER-2-targeting antibody-drug conjugate, has exhibited substantial clinical advantages in individuals with metastatic urothelial carcinoma (mUC). Nonetheless, the extent of therapeutic efficacy in real-world scenarios for mUC patients and the specific patient profiles with the most benefit from DV remain unclear.</p><p><strong>Methods: </strong>In this multi-center, retrospective, observational study, a total of 30 patients with mUC were included between April 2021 and March 2024 from three distinct hospitals, along with clinicopathological features and targeted sequencing data. Our analysis encompassed the assessment of the objective response rate (ORR), progression-free survival (PFS), overall survival (OS), and the incidence of treatment-related adverse events (TrAEs).</p><p><strong>Results: </strong>In the general population, the median follow-up time was 12.1 months, and the median OS was not reached with a 12-month OS rate of 86.7%. The median PFS was 12.2 months (95% confidence interval [CI]: 6.6-17.7 months), with an ORR of 42.3% (95% CI: 23.4%-63.1%) and a DCR of 73.1% (95% CI: 55.2%-88.4%). Higher HER-2 expression is correlated with prolonged clinical benefit from DV (Log-rank P = 0.082. HER-2 IHC 2+ & 3 + vs. IHC 1+: Median PFS: 13.1 vs. 4.6 months; Response rate: 60.0% vs. 0.0%). History of durable response to platinum-based chemotherapy can also imply longer PFS and better response rate (Log-rank P = 0.086. Median PFS: 14.2 vs. 3.6 months. Response rate: 50.0% vs. 10.0%). Moreover, higher mutation burden (TMB) is closely related to better outcomes from DV therapy (Log-rank P = 0.011. Median PFS: 12.8 vs. 4.6 months. Response rate: 71.4% vs. 11.1%. Firth's penalized multivariable Cox regression: P = 0.015. Hazard Ratio: 0.165. 95% CI: 0.026-0.717).</p><p><strong>Conclusion: </strong>In conclusion, patients with higher HER-2 expression, positive responses to chemotherapy, or elevated TMB are more likely to benefit from DV. These discoveries support the rationale for employing HER-2 antibody-drug conjugates (ADCs) for mUC patients.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1432"},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147848","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}
引用次数: 0
The concurrent silencing of Tim-3 and STAT-3 promotes tumor regression both in vitro and in ovo. Tim-3和STAT-3同时沉默可促进体外和卵内肿瘤的消退。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-25 DOI: 10.1186/s12885-025-14830-5
Reza Karami, Shahla Khodayari, Farzaneh Eshaghi, Farbod Ebrahimi, Atefeh KhodaKarami, Bentolhoda Rashidi, Mahsa Nikdel, Hasti Moshtagh Mehr, Tohid Kazemi, Farhad Jadidi
{"title":"The concurrent silencing of Tim-3 and STAT-3 promotes tumor regression both in vitro and in ovo.","authors":"Reza Karami, Shahla Khodayari, Farzaneh Eshaghi, Farbod Ebrahimi, Atefeh KhodaKarami, Bentolhoda Rashidi, Mahsa Nikdel, Hasti Moshtagh Mehr, Tohid Kazemi, Farhad Jadidi","doi":"10.1186/s12885-025-14830-5","DOIUrl":"10.1186/s12885-025-14830-5","url":null,"abstract":"<p><strong>Background: </strong>Due to the intricate nature of the tumor microenvironment and the impairment of the anti-tumor responses of the immune system, finding a novel approach in the field of immunology-based therapy might influence the prognosis and survival of patients suffering from cancer. T-cell immunoglobulin and mucin-domain containing-3 (Tim-3) is a regulatory element of immune surveillance that exerts a pivotal function in the microenvironment of tumors. Although the precise functions of the Tim-3 remain incompletely understood, it has been established that it not only contributes to T cell exhaustion but also participates in the STAT-3/NF-κB (signal transducer and activator of transcription 3 / nuclear factor-κB) pathway, which plays a major role in the progression of tumors.</p><p><strong>Methods: </strong>In this research, we assessed the efficacy of co-blocking the Tim-3 and STAT-3 factors in inhibiting cancer cell growth. Therefore, we suppressed the expression of these factors in murine-derived malignant cell lines (4T1 and CT26), using siRNA (small interfering RNA) molecules encapsulated in chitosan lactate-based nano carriers we previously developed.</p><p><strong>Results: </strong>Transfecting the siRNAs into cancer cells with nanocarriers significantly downregulated the expression of Tim-3 and STAT-3 in both 4T1 and CT26 cells. Downregulation of Tim-3 and STAT-3 was correlated with diminished viability, proliferation, angiogenesis, and metastatic characteristics of cancerous cells, in vitro. Furthermore, co-silencing of Tim-3 and STAT-3 led to tumor regression, in ovo.</p><p><strong>Conclusion: </strong>These results revealed that the concurrent silencing of Tim-3 and STAT-3 can significantly suppresses the tumor growth by reducing cell proliferation, angiogenesis and metastasis in vitro and in ovo. However, future investigations-particularly in vivo models-are necessary to validate the current strategy as a potential anti-tumor therapeutic approach.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1431"},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147909","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}
引用次数: 0
Assessment of the reliability and quality of pancreatic cancer related short videos on mainstream platforms: cross-sectional study. 主流平台胰腺癌相关短视频的可靠性和质量评估:横断面研究。
IF 3.4 2区 医学
BMC Cancer Pub Date : 2025-09-24 DOI: 10.1186/s12885-025-14825-2
Jialun Peng, Muyang Tu, Shengwei Li, Xiong Ding, Qilong Zhai, Hongyu Wu, Jinzheng Li
{"title":"Assessment of the reliability and quality of pancreatic cancer related short videos on mainstream platforms: cross-sectional study.","authors":"Jialun Peng, Muyang Tu, Shengwei Li, Xiong Ding, Qilong Zhai, Hongyu Wu, Jinzheng Li","doi":"10.1186/s12885-025-14825-2","DOIUrl":"10.1186/s12885-025-14825-2","url":null,"abstract":"<p><strong>Background: </strong>Despite its high fatality rate, pancreatic cancer remains largely overlooked by the public. The rise of short-form video platforms has made them hubs for health-related content, yet the quality and reliability of this information are often in doubt.</p><p><strong>Objective: </strong>This study is poised to scrutinize the quality and trustworthiness of videos pertaining to pancreatic cancer across these digital landscapes.</p><p><strong>Methods: </strong>We analyzed the content and publishers of such videos on TikTok, Bilibili, and Kwai using the Global Quality Scale (GQS), modified DISCERN (mDISCERN), and Medical Quality Video Evaluation Tool (MQ-VET). We also correlated the findings with video rankings and compared the quality between the Chinese and USA platforms in 2023 and 2024.</p><p><strong>Results: </strong>In 2023, 300 videos were analyzed with median scores indicating medium quality but low reliability, the median GQS, mDISCERN and MQ-VET scores were 2, 2 and 45, respectively. The short videos created by medical practitioners demonstrated significantly higher median scores compared to those by non-medical practitioners in GQS scores (3 [IQR, 2-4] vs. 2 [IQR, 2-3]; P < 0.001), mDISCERN scores (2 [IQR, 2-3] vs. 2 [IQR, 1-2]; P < 0.001), and MQ-VET scores (46 [IQR, 40-52] vs. 37 [IQR, 30-45.5]; P < 0.001). mDISCERN scores showed superiority in treatment-related (3 [IQR, 2-3]), prevention-related (3 [IQR, 2.75-3]), and disease-related videos (including anatomical, pathologic, epidemiologic, and basic research related to pancreatic cancer)(2 [IQR, 2-3]) compared to News and Reports (2 [IQR, 1-2]) and invalid information content (1 [IQR, 1-1]; P < 0.001). TikTok had significantly higher mDISCERN scores (2 [IQR, 2-3] vs Bilibili: 2 [IQR, 1.75-3]; P = 0.024) and MQ-VET scores (47 [IQR, 43-53.5] vs Kwai: 44.5 [IQR, 38.25-49.75]; P = 0.033) for medical professional videos. Video quality showed a weak correlation with rankings. And the GQS scores of short videos in China in 2024 decreased compared with that in 2023 (2 [IQR, 2-3] vs 3 [IQR, 2-4]; P = 0.009). Additionally, in 2024, both medical and non-medical practitioners' videos on the Chinese TikTok platform exhibited lower quality and reliability compared to their counterparts in the USA.</p><p><strong>Conclusion: </strong>Pancreatic cancer-related short videos are of medium quality and low reliability, particularly on Chinese platforms. Videos from medical professionals are more trustworthy. There is a need for better curation and algorithms to ensure accurate health information dissemination and to enhance public understanding and management of pancreatic cancer.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"1428"},"PeriodicalIF":3.4,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136453","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}
引用次数: 0
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