Biomolecules & biomedicine最新文献

{"title":"Comprehensive analysis of angiogenesis and stemness-related genes in chemotherapy and immunotherapy of bladder cancer.","authors":"Zhi-Xiang Yin, Yifan Qiu, Chenfei Xu, Changsong Pei","doi":"10.17305/bb.2025.12046","DOIUrl":"https://doi.org/10.17305/bb.2025.12046","url":null,"abstract":"<p><p>Tumor angiogenesis and cancer stem cells (CSCs) are critical features of malignancies. Research has shown that CSCs promote blood vessel formation, while increased vasculature, in turn, supports CSC proliferation-creating a detrimental feedback loop that drives disease progression. However, studies investigating vascularization and stem-like properties in bladder cancer (BLCA) remain limited. In our investigation, we applied clustering techniques and LASSO methodology to assess the significance of vascularization- and stemness-related genes in predicting responses to chemotherapy and immunotherapy in BLCA. Using multivariate Cox regression analysis, we identified Von Hippel-Lindau (VHL) as the primary prognostic marker associated with both vascularization and stem-like traits. Tissue array analysis of 40 BLCA specimens, combined with molecular docking simulations, revealed interactions between HDAC6 and VHL that influence stem-like behavior and angiogenesis in BLCA. Additionally, VHL showed strong correlations with treatment responses to both chemotherapy and immunotherapy in BLCA. In conclusion, our findings highlight the critical role of vascularization- and stemness-related genes in determining therapeutic outcomes in BLCA and underscore the regulatory relationship between VHL and HDAC6 in modulating treatment response.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>TBRG4</i> as a prognostic biomarker and key regulator of cell cycle and EMT in lung cancer.","authors":"Ansheng Wang, Qiao Ge, Zhenkai Fan, Bing Xia, Zhao Jin, Haitao Liu, Haiwei Sang, Qicai Li, Congli Zhang, Haonan Zhu","doi":"10.17305/bb.2025.11353","DOIUrl":"https://doi.org/10.17305/bb.2025.11353","url":null,"abstract":"<p><p>Transforming growth factor β regulator 4 (TBRG4) is upregulated in lung cancer, but its biological role and underlying mechanisms remain poorly understood. In this study, we analyzed pancancer gene expression profiles and clinical data from University of California, Santa Cruz Xena (UCSC Xena) to evaluate the prognostic significance of TBRG4 using univariate and multivariate Cox regression analyses. Genes with a Pearson correlation coefficient above 0.4 with TBRG4 in lung cancer were identified via UALCAN, followed by pathway enrichment analyses to explore their functional associations. To investigate TBRG4's role in lung cancer progression, we assessed cell proliferation, colony formation, and cell cycle alterations in lung cancer cells following TBRG4 knockdown. Western blot analysis was performed to examine the effects of TBRG4 depletion on key cell cycle regulators and epithelial-mesenchymal transition (EMT) markers. Additionally, the biological significance of TBRG4 was evaluated in vivo using a mouse xenograft model. TBRG4 knockdown significantly inhibited cell proliferation and colony formation while inducing cell cycle arrest and apoptosis in lung cancer cells. Analysis of co-expressed genes in the The Cancer Genome Atlas - Lung Adenocarcinoma (TCGA-LUAD) cohort revealed enrichment in cell cycle-related pathways, aligning with our experimental findings. Furthermore, TBRG4 depletion reduced EMT marker expression and suppressed tumor growth in vivo. Collectively, these findings suggest that TBRG4 may serve as a promising prognostic biomarker and therapeutic target in lung cancer.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>DPP4</i> rs17574 polymorphism and elevated DPP4 levels linked to fatty liver in subclinical atherosclerosis: GEA study findings.","authors":"Gilberto Vargas-Alarcón, Juan Reyes-Barrera, Guillermo Cardoso-Saldaña, Neftali Antonio-Villa, Giovanny Fuentevilla-Álvarez, José Manuel Fragoso, Rosalinda Posadas-Sánchez","doi":"10.17305/bb.2025.11950","DOIUrl":"https://doi.org/10.17305/bb.2025.11950","url":null,"abstract":"<p><p>Dipeptidyl peptidase-4 (DPP4) concentrations are known to correlate with nonalcoholic fatty liver (FL), which is also associated with subclinical atherosclerosis (SA). This study aimed to determine whether DPP4 concentrations and the DPP4 rs17574 polymorphism are associated with FL in individuals with SA. The study included 378 participants with SA, of whom 143 had FL and 235 did not. DPP4 serum concentrations were measured using a Bioplex system, and DPP4 rs17574 genotypes were determined using TaqMan assays. Logistic regression was used to assess the relationships between FL, DPP4 concentrations, and rs17574 genotypes. Overall, DPP4 concentrations did not differ significantly between individuals with and without FL. No significant differences in DPP4 levels were observed among DPP4 genotypes in the total sample. However, within the FL group, significant differences in DPP4 concentration were observed across genotypes: AA genotype (134 [106-175] ng/mL), AG genotype (128 [114-149] ng/mL), and GG genotype (80 [71-117] ng/mL); P = 0.019. The DPP4 rs17574 polymorphism was associated with FL under a recessive model (P = 0.037). DPP4 concentration was also significantly associated with FL: the likelihood of presenting with FL increased by 6.2% for every 10 ng/mL increase in DPP4 levels (P = 0.009). These findings suggest that DPP4 concentration may serve as a biochemical risk marker for FL in individuals with SA. Moreover, the rs17574 polymorphism may influence DPP4 protein levels, particularly in those with FL. To our knowledge, this is the first study to describe an association between DPP4 concentration, the rs17574 polymorphism, and FL. Assessing DPP4 levels may offer a novel and effective strategy for risk stratification of FL in SA populations.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunogenic cell death-related risk signature for tumor microenvironment profiling and prognostic prediction in colorectal cancer.","authors":"Pengcheng Wang, Wei Zhao, Linghong Guo, Hailei Cao","doi":"10.17305/bb.2025.12028","DOIUrl":"https://doi.org/10.17305/bb.2025.12028","url":null,"abstract":"<p><p>Immunogenic cell death (ICD) reshapes the tumor immune microenvironment and activates the adaptive immune response. However, the clinical significance of ICD-associated genes in colorectal cancer (CRC) remains unclear. In this study, we used weighted gene co-expression network analysis (WGCNA) to identify ICD-related gene modules. An ICD-related risk score (ICDRS) was then constructed using Cox regression modeling and LASSO analysis. Immune cell infiltration in patients with different risk levels was assessed using the ESTIMATE and single-sample Gene Set Enrichment Analysis algorithms (GSEA). The oncoPredict package was employed to explore the association between the ICDRS and chemotherapy drug sensitivity. Finally, the expression levels of ICD-related genes were validated through in vitro cellular experiments. Three CRC prognostic genes-CLMP, Neuropilin-1 (NRP1), and PLEKHO1-were identified from a set of 34 ICD-associated genes based on WGCNA and LASSO analyses. These genes were used to construct the ICDRS model. Notably, a high ICDRS was found to be an independent predictor of poorer overall survival (OS) in CRC patients. High-risk patients also exhibited increased immune cell infiltration. Moreover, the ICDRS was significantly correlated with sensitivity to conventional chemotherapeutic drugs, suggesting its potential utility in guiding personalized chemotherapy. Cellular assays confirmed that CLMP, NRP1, and PLEKHO1 were differentially expressed between normal and cancerous cells, and that NRP1 specifically promoted the proliferation, migration, and invasion of CRC cells. In conclusion, the ICDRS may serve as a reliable predictor of CRC prognosis and offers a promising direction for the clinical management of CRC patients.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Müllerian hormone in PCOS: Molecular regulation and emerging therapeutic strategies.","authors":"Yunmei Ke, Dan Tang, Qin Yang, Han Zhao, Jinyan Zheng, Caifen Zhu","doi":"10.17305/bb.2025.12070","DOIUrl":"https://doi.org/10.17305/bb.2025.12070","url":null,"abstract":"<p><p>Anti-Müllerian hormone (AMH), a glycoprotein belonging to the transforming growth factor-beta (TGF-β) superfamily, is a key regulator of ovarian folliculogenesis. Dysregulated AMH expression is a hallmark of polycystic ovary syndrome (PCOS), a common endocrine and metabolic disorder characterized by hyperandrogenism, anovulation, and polycystic ovarian morphology. Elevated AMH levels in PCOS impair follicle-stimulating hormone (FSH) sensitivity, disrupt follicular maturation, and contribute to androgen excess-creating a feedback loop that exacerbates ovarian dysfunction. This review explores the complex regulatory mechanisms governing AMH expression, including transcriptional, post-transcriptional, and post-translational processes. It highlights the interplay between AMH, FSH, and androgen signaling pathways, emphasizing their roles in the pathophysiology of PCOS. Particular attention is given to the downstream SMAD-dependent signaling cascade, which mediates many of AMH's biological effects. Additionally, we summarize emerging therapeutic strategies targeting AMH signaling, such as AMHR2 (anti-Müllerian hormone receptor type 2) antagonists, GnRH (gonadotropin-releasing hormone) antagonists, and aromatase inhibitors. A deeper understanding of AMH regulation and signaling provides critical insights into its role in PCOS progression and supports the development of novel, targeted treatments aimed at alleviating both reproductive and metabolic symptoms.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of gut microbiota and immune response in breast cancer progression.","authors":"Xiaofang Zhang, Na Ma, Conghui Jin, Xiaoli Cao","doi":"10.17305/bb.2025.12003","DOIUrl":"https://doi.org/10.17305/bb.2025.12003","url":null,"abstract":"<p><p>Breast cancer is one of the most prevalent cancers among women and is associated with high mortality rates. Emerging evidence suggests a link between gut microbiota and the development of various tumors, particularly those involving immune-mediated mechanisms. However, the potential relationship between gut microbiota and breast cancer-and whether this relationship is mediated by immune cells-remains unclear. This Mendelian randomization (MR) study utilized summary statistics from genome-wide association studies of 412 gut microbiota, 731 immune cell traits, and breast cancer (including its subtypes). Two-sample MR analyses were conducted to assess potential causal relationships between gut microbiota and breast cancer. To further validate the findings, Bayesian weighted MR was applied. Robustness was ensured through sensitivity, specificity, and pleiotropy analyses. A reverse MR analysis was also performed to assess the potential for reverse causality. Finally, mediation analysis was employed to investigate whether immune cells mediate the pathway from gut microbiota to breast cancer. The MR analysis identified 15 gut microbiota and related metabolic pathways significantly associated with breast cancer, with nine showing positive associations and six showing negative associations. The reverse MR analysis did not support a causal effect of breast cancer on gut microbiota. Mediation analysis revealed that DP (CD4⁺CD8⁺) % leukocyte mediated the pathway between gut microbiota (PWY-6263: superpathway of menaquinol-8 biosynthesis II) and breast cancer. These findings suggest a causal relationship between gut microbiota and breast cancer, with a small portion of this effect mediated by immune cells. This study underscores the potential role of gut microbiota and immune modulation in the pathogenesis of breast cancer.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormonal predictors of the insulin sensitive phenotype in humans.","authors":"Mohamed Badie Ahmed, Abdella M Habib, Saif Badran, Abeer Alsherawi, Sherouk Essam Elnefaily, Mansour Binfayed, Atalla Hammouda, Graeme E Glass, Ibrahem Abdalhakam, Humam Emad Rajha, Abdul-Badi Abou-Samra, Suhail A Doi","doi":"10.17305/bb.2025.12210","DOIUrl":"https://doi.org/10.17305/bb.2025.12210","url":null,"abstract":"<p><p>Clinical obesity, a chronic condition marked by excessive fat accumulation, often leads to insulin resistance and a heightened risk of comorbidities. This study aimed to identify hormonal predictors of an insulin-sensitive phenotype (ISP) in patients undergoing body contouring surgeries, focusing on the relationship between gut hormones, adipokines, and fat mass. ISP was defined as the highest tertile of HOMA insulin sensitivity. We prospectively followed patients undergoing abdominoplasty, lower body lift, or thigh lift at Hamad General Hospital from January 2021 to December 2023. Body composition, glycemic indices, and hormonal levels were assessed, with data analyzed using descriptive statistics and regression models. The study included 34, 22, and 27 subjects at visits 1, 2, and 3, respectively. Fat percentage decreased slightly at visits 2 and 3 compared to baseline, though not significantly. Median levels of glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), liver-expressed antimicrobial peptide 2 (LEAP2), and amylin varied significantly across visits, initially rising at visit 2 before declining at visit 3. Logistic regression revealed that ISP was negatively associated with serum GIP, LEAP2, and leptin levels while positively associated with PP. History of bariatric surgery was only weakly associated with the ISP after hormonal associations were accounted for. Notably, total body fat percentage did not predict ISP after accounting for hormonal factors. This study highlights GIP, PP, leptin, and LEAP2 as key predictors of ISP, with GIP being the primary negative regulator. These findings underscore the importance of hormonal interplay in insulin sensitivity, emphasizing the role of gut hormones and adipokines in predicting ISP in humans.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic correlation, shared loci, and causal link between obesity and diabetic microvascular complications: A genome-wide pleiotropic analysis.","authors":"Wei Zhang, Qinghua Zhang, Yan Luo, Leilei Ma, Xuejun Wang, Qiao Zheng, Xiaotian Zhang, Shentao Wu, Zhan Li, Yingfei Bi","doi":"10.17305/bb.2025.11897","DOIUrl":"https://doi.org/10.17305/bb.2025.11897","url":null,"abstract":"<p><p>Observational studies have identified a connection between obesity and microvascular complications in diabetes, yet the genetic contributions to their co-occurrence remain incompletely understood. Our research aims to explore the shared genetic architecture underlying both conditions. We employed linkage disequilibrium score regression (LDSC) and Local Analysis of [co]Variant Association (LAVA) to assess genetic correlations between obesity and diabetic microvascular complications. To validate shared genetic regions, we conducted pleiotropic analysis under the composite null hypothesis (PLACO), functional mapping and annotation (FUMA), and colocalization analysis. Additionally, we applied Multimarker Analysis of GenoMic Annotation (MAGMA), Summary-based Mendelian Randomization (MR), multi-trait colocalization, and enrichment analysis to identify potential functional genes and pathways. Finally, MR and latent causal variable (LCV) analysis were used to clarify causal and pleiotropic relationships across trait pairs. Among 21 trait pairs analyzed, 15 exhibited significant global genetic correlations, and 97 regions showed significant local correlations. PLACO identified 3659-20,489 potentially pleiotropic single nucleotide polymorphisms (SNPs) across 15 trait pairs, with 828 lead SNPs detected via FUMA. Colocalization analysis confirmed 52 shared loci. Gene-based analysis identified seven unique candidate pleiotropic genes, with ribosomal protein S26 (RPS26) emerging as the strongest shared gene. MR and LCV analyses supported a causal relationship between BMI and diabetic kidney disease (DKD). Our findings highlight a shared genetic basis linking obesity with diabetic microvascular complications. These insights offer potential pathways for understanding the mechanisms driving their comorbidity and may inform more integrated therapeutic approaches.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144047326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCF12 enhances angiogenesis and affects sorafenib response in liver cancer via HIF-1α interaction.","authors":"Yuanbin Chen, Xiaolong Wang, Jin Chen, Min Dai, Xinyue Zhang, Jie Yin, Xiao He","doi":"10.17305/bb.2025.12022","DOIUrl":"https://doi.org/10.17305/bb.2025.12022","url":null,"abstract":"<p><p>Transcription factor 12 (TCF12), a member of the basic Helix-Loop-Helix (bHLH) protein family, plays a crucial role in regulating cell growth and differentiation. It has been implicated in the development and progression of malignant tumors; however, its specific mechanisms in vascularization and drug resistance in liver cancer remain poorly understood. This study aims to explore how the interaction between TCF12 and Hypoxia-Inducible Factor 1-alpha (HIF-1α) affects vascularization and drug sensitivity in liver cancer. Using bioinformatics analysis (n = 374 TCGA samples and n = 50 clinical specimens), we assessed TCF12 expression levels in liver cancer and evaluated their association with patient prognosis. Gene Set Enrichment Analysis (GSEA) was employed to identify related signaling pathways. The expression of TCF12 in liver cancer tissues was examined via Western blotting and immunohistochemistry, while Kaplan-Meier survival analysis was used to analyze the relationship between TCF12 expression and overall survival. Functional assays-including scratch wound repair, tube formation, and endothelial cell permeability tests-were conducted to assess TCF12's role in angiogenesis. Cell viability assays were performed to evaluate the impact of TCF12 on sorafenib sensitivity, and co-immunoprecipitation experiments were carried out to investigate the interaction between TCF12 and HIF-1α. Our bioinformatics analysis revealed that both TCF12 and HIF-1α are significantly overexpressed in liver cancer and are associated with poor prognosis. Immunohistochemical staining showed a positive correlation between TCF12 expression and the vascularization marker CD31. Furthermore, survival analysis demonstrated that patients with elevated TCF12 expression had significantly shorter overall survival. Functional assays indicated that TCF12 knockdown suppressed blood vessel formation and reduced endothelial cell permeability. Moreover, reducing TCF12 expression increased the sensitivity of liver cancer cells to sorafenib. Notably, overexpression of HIF-1α reversed these effects, and co-immunoprecipitation experiments confirmed a direct interaction between TCF12 and HIF-1α. In summary, this study demonstrates that TCF12 is highly expressed in liver cancer and is associated with poor prognosis. TCF12 promotes angiogenesis by stabilizing HIF-1α and modulates tumor sensitivity to sorafenib, highlighting its potential as a therapeutic target in liver cancer.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemiology, prognostic factors, and survival analysis in small cell esophageal carcinoma: A population-based study with external validation.","authors":"Jiahao Zhu, Benjie Xu, Yuanyuan Li, Xiangyi Pang, Shengjun Ji, Jie Lian, Haibo Lu","doi":"10.17305/bb.2024.11090","DOIUrl":"10.17305/bb.2024.11090","url":null,"abstract":"<p><p>Small cell esophageal carcinoma (SCEC) is a poorly differentiated esophageal neuroendocrine neoplasm with a poor prognosis. This study aimed to explore the factors and treatment approaches influencing the prognosis of SCEC. In this retrospective study, we collected data from the 18 Surveillance, Epidemiology, and End Results (SEER) registries cohort between 2004 and 2019, as well as from a Chinese institutional registry covering the period from 2012 to 2022. We assessed the annual percentage change (APC) in incidence of SCEC. Kaplan-Meier and Cox regression analyses were conducted to evaluate survival outcomes. Additionally, nomograms were developed for overall survival (OS) and cancer-specific survival (CSS) in the SEER cohort for SCEC and validated in an independent Chinese cohort. This analysis included 299 SCEC patients from the SEER cohort and 66 cases from the Chinese cohort. During the period of 2004-2019, the incidence of SCEC reached a plateau, with an APC of -1.40 (95% confidence interval [CI]: -4.3 to 1.40, P > 0.05). Multivariable Cox regression analysis revealed that age, distant metastasis, and chemotherapy were independent factors for OS, while distant metastasis and chemotherapy were independent factors for CSS. The nomograms developed for OS and CSS in SCEC exhibited remarkable accuracy and reliable predictive capacity in estimating 1-year, 3-year, and 5-year OS and CSS. SCEC is a rare malignancy with aggressive behavior. Distant metastasis is significantly associated with worse OS and CSS in patients with SCEC. Currently, chemotherapy remains the primary treatment approach for SCEC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1009-1022"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142127527","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}