Yingzi Yang, Ayizhati Tuerxun, Xinqi Cai, Xinyu Chen, Zhuoya Zhao, Yang Zhao, Zinuo Lin, Shengfeng Wang
{"title":"Prediction models for different types of leukemia: a systematic review and critical appraisal.","authors":"Yingzi Yang, Ayizhati Tuerxun, Xinqi Cai, Xinyu Chen, Zhuoya Zhao, Yang Zhao, Zinuo Lin, Shengfeng Wang","doi":"10.1007/s00432-025-06314-7","DOIUrl":"10.1007/s00432-025-06314-7","url":null,"abstract":"<p><strong>Objectives: </strong>To systematically review and evaluate the methodological quality and risk of bias (ROB) of leukemia prediction models essential for clinical decision-making.</p><p><strong>Methods: </strong>We reviewed 148 prediction models published before August 2023 from PubMed, Embase, Cochrane Library, and Web of science databases. Two reviewers independently screened articles and extracted data using CHARMS criteria. ROB was assessed using PROBAST. Models were categorized by leukemia subtype and analyzed for methodological characteristics.</p><p><strong>Results: </strong>A total of 61 acute myeloid leukemia (AML) models primarily predicted survival (82.0%), diagnosis (4.9%), or death (4.9%) using predictors including age, cytogenetic risk, and white blood cell count. Among the 22 chronic myeloid leukemia (CML) models, the focus was on survival (72.7%) and time to treatment (19.0%), utilizing blast percentage, age, and platelet count. A total of 21 chronic lymphocytic leukemia (CLL) models primarily predicted survival (71.4%) using IGHV status, Rai stage, and age. The methodological shortcomings including incomplete reporting, methodological limitations, and high ROB were consistent across different leukemia subtypes. Traditional statistical methods predominated (Cox regression 72.9%, logistic regression 12.2%), with only nine machine learning models. Critical methodological limitations included lack of internal validation (52.0%) and external validation (57.4%). Only 43.2% reported discrimination metrics (AUC 0.60-0.99), with 28.0% achieving AUC > 0.7. Calibration was reported in only 23.0% of models. High ROB affected 93.9% of studies, primarily due to inadequate data handling and validation.</p><p><strong>Conclusions: </strong>Existing leukemia prediction models have limited clinical utility due to methodological shortcomings and high ROB. Future research should prioritize transparent reporting, rigorous validation, and external validation to enhance clinical applicability and generalizability.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"268"},"PeriodicalIF":2.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145175379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Onur Erdoğan, Alaattin Fidan, Mustafa Sakar, Beste M Atasoy
{"title":"Effect of gamma knife dose rate and tumor-specific factors on treatment outcomes in brain metastases: insights from a cohort study.","authors":"Onur Erdoğan, Alaattin Fidan, Mustafa Sakar, Beste M Atasoy","doi":"10.1007/s00432-025-06322-7","DOIUrl":"10.1007/s00432-025-06322-7","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to investigate the influence of Gamma Knife dose rate on treatment outcomes, in conjunction with tumor-specific factors of composition, size, and primary tumor location.</p><p><strong>Methods: </strong>This retrospective cohort study analyzed 173 patients with 451 brain metastases treated between 2011 and 2015. Radiosurgery was performed using the Leksell Gamma Knife System, with dose rates categorized into four groups based on cobalt-60 decay: 2.9-2.7, 2.7-2.5, 2.5-2.3, and 2.3-2.1 Gy/min. Tumors were further classified according to dose rate into a simplified high/low classification (cutoff: 2.5 Gy/min) for clinical applicability. The Response Assessment in Neuro-Oncology Brain Metastases Group (RANO-BM) criteria were employed to evaluate treatment response. Statistical analyses were conducted to assess associations between dose rate, tumor characteristics, and outcomes.</p><p><strong>Results: </strong>No significant association was identified between dose rates and treatment response (p = 0.35), indicating effective tumor control even at lower dose rates. Tumor composition and size had a significant impact on outcomes; cystic tumors demonstrated poorer responses compared to solid tumors, and larger tumors exhibited reduced efficacy. Specific primary tumor sites, particularly renal cell carcinoma and malignant melanoma, were linked to less favorable responses, confirming their radioresistant characteristics.</p><p><strong>Conclusion: </strong>This study highlights that dose rate does not significantly impact treatment outcomes in Gamma Knife radiosurgery for brain metastases, indicating that effective tumor control can be achieved even at lower dose rates. These findings provide reassurance regarding the efficacy of treatments utilizing decaying cobalt-60 sources and highlight the importance of patient- and tumor-specific factors in predicting radiosurgical outcomes.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"266"},"PeriodicalIF":2.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12460865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bingqian Deng, Saipeng Chen, Dan Zhong, Guojing Song, Heting Liu, Langlang Xie, Youxin Liu, Rongrong Ni, Wenhao Shen, Gang Huang
{"title":"PDGFC facilitates enzalutamide resistance in prostate cancer through activation of the Rap1-MAPK pathway.","authors":"Bingqian Deng, Saipeng Chen, Dan Zhong, Guojing Song, Heting Liu, Langlang Xie, Youxin Liu, Rongrong Ni, Wenhao Shen, Gang Huang","doi":"10.1007/s00432-025-06276-w","DOIUrl":"10.1007/s00432-025-06276-w","url":null,"abstract":"<p><strong>Purpose: </strong>Prostate cancer (PCa) is a highly heterogeneous malignant tumor within the male genitourinary system, characterized by its invasive and metastatic potential. Although the second-generation androgen receptor (AR) antagonist enzalutamide has shown therapeutic efficacy in PCa patients, enzalutamide resistance (EnzaR) will inevitably develop and the underlying mechanisms are not fully understood.</p><p><strong>Methods: </strong>Platelet Derived Growth Factor C (PDGFC) expression in PCa cells was measured by qRT‒PCR and Western blot. The effect of PDGFC on PCa was examined both in vitro and in vivo. CCK8, Colony formation, and EdU assays were used to assess the phenotypes of PCa cells. A tumor xenograft model was used to evaluate the impact of PDGFC on PCa in vivo. Luciferase assays and chromatin immunoprecipitation (ChIP) assays were performed to demonstrate the mechanism of signal transducer and activator of transcription 4 (STAT4)-mediated transcriptional regulation of PDGFC.</p><p><strong>Results: </strong>The expression of PDGFC is significant elevated in EnzaR PCa and positively correlates with PCa proliferation in vitro and in vivo. Silencing PDGFC increases the sensitivity of EnzaR PCa cells to enzalutamide, thereby inhibiting PCa progression. Mechanistically, overexpression of PDGFC activates the PDGFR-Rap1-MAPK signaling in an autocrine manner in EnzaR cells. Notably, PDGFR inhibitors, alone or combined with enzalutamide, significantly inhibit xenograft progression in EnzaR PCa models. Additionally, the transcription factor STAT4 binds to a specific DNA sequence in the PDGFC promoter region, which is essential for PDGFC upregulation.</p><p><strong>Conclusion: </strong>Our results confirmed the pivotal role of PDGFC in the development of enzalutamide resistance in PCa. Targeting PDGFC or PDGFC mediate Rap1-MAPK pathway may serve as a promising therapeutic strategy for EnzaR PCa.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"267"},"PeriodicalIF":2.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12460851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advancements in the diagnosis and management of capecitabine-induced hand-foot syndrome.","authors":"Baohua Chen, Xingyu Wang, Lingjun Meng","doi":"10.1007/s00432-025-06319-2","DOIUrl":"10.1007/s00432-025-06319-2","url":null,"abstract":"<p><strong>Purpose: </strong>This narrative review aims to synthesize existing evidence on hand-foot syndrome (HFS) associated with capecitabine therapy. By examining HFS pathogenesis, clinical manifestations, severity classifications, influencing factors, and management strategies, the study seeks to provide clinically actionable insights to mitigate HFS-related quality-of-life deterioration and treatment discontinuation in patients receiving this widely used capecitabine.</p><p><strong>Methods: </strong>This narrative review summarizes recent literature on HFS caused by capecitabine, highlighting its relationship among different populations and the prevention and treatment of HFS.</p><p><strong>Results: </strong>The review establishes that HFS manifests through sensory abnormalities (tingling, numbness) and dermatological changes (erythema, desquamation), though its precise pathophysiology remains incompletely defined. Incidence is modulated by demographic variables (age, sex, ethnicity), therapeutic variables (drug combinations, capecitabine dosage), and possibly genetic factors. The study highlights that co-administration of diclofenac demonstrates significant potential in reducing both HFS occurrence and symptom severity based on current evidence.</p><p><strong>Conclusion: </strong>Based on critical assessment of available literature, the review concludes that the concomitant use of diclofenac with capecitabine represents an effective clinical strategy for alleviating HFS. In addition, topical urea cream, pyridoxal, lactic acid, etc. can also be used prophylactically to produce certain effects. This pharmacological approach is recommended to enhance treatment adherence and preserve patient quality of life during antineoplastic therapy.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"265"},"PeriodicalIF":2.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advancing our understanding of the influence of myeloid-derived suppressor cells in chronic myeloid leukemia.","authors":"Xing Meng, Yue Zhang, Hong Xu, Yanyan Zhang, Hao He, Jianmin Ma, Xiaoyan Zhang","doi":"10.1007/s00432-025-06315-6","DOIUrl":"10.1007/s00432-025-06315-6","url":null,"abstract":"<p><p>Chronic myeloid leukemia (CML) is a malignant clonal proliferative disease originating from hematopoietic stem cells. While treatment with tyrosine kinase inhibitors (TKIs) effectively eliminates the majority of leukemia cells in patients, residual leukemia cells can still be detected in those achieving deep molecular remission, ultimately leading to drug resistance or relapse. But the exact mechanism is unclear. In recent years, the immune microenvironment has been a hot research topic in hematologic malignancies. CML patients exhibit abnormalities in antitumor immunity. Myeloid-derived suppressor cells (MDSCs), which possess immune-suppressing functions, inhibit the proliferation and activation of CD4<sup>+</sup>/CD8<sup>+</sup> T cells, Tregs, B cells, and NK cells, and play a central role in the antitumor immune response in a wide range of cancers. Abnormalities in numbers and functions of MDSCs are exhibited in CML patients, which affect the immune status of CML patients through multiple mechanisms. This review summarizes the biological properties of MDSCs, their alterations in CML patients, their roles and specific mechanisms in the development of CML, and how these mechanisms can be leveraged to develop new therapeutic strategies, aiming to provide novel insights and approaches for the treatment of CML.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"263"},"PeriodicalIF":2.8,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12449292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Low expression of HSP27 and HSP70 predicts poor prognosis in laryngeal squamous cell carcinoma.","authors":"Jędrzej Borowczak, Dariusz Łaszczych, Adrianna Czyżnikiewicz, Andrzej Marszałek, Łukasz Szylberg, Magdalena Bodnar","doi":"10.1007/s00432-025-06309-4","DOIUrl":"10.1007/s00432-025-06309-4","url":null,"abstract":"<p><strong>Purpose: </strong>Molecular alterations drive the pathogenesis of laryngeal squamous cell carcinoma (LSCC), yet reliable prognostic biomarkers remain elusive. Heat shock proteins (HSPs), which mediate cellular stress responses, are implicated in cancer progression and treatment resistance. This study aimed to evaluate whether HSP27 and HSP70 expression correlate with clinicopathological features and survival outcomes in LSCC. Specifically, we assessed their potential as prognostic biomarkers in this malignancy.</p><p><strong>Methods: </strong>Immunohistochemistry was performed on 158 LSCC tissue samples from 40 patients and compared to 30 normal laryngeal tissue samples. Expression levels of HSP27 and HSP70 were correlated with clinicopathological variables. Validation was conducted using transcriptomic and survival data from 112 LSCC cases in The Cancer Genome Atlas (TCGA). Kaplan-Meier and Cox regression analyses were used to assess survival.</p><p><strong>Results: </strong>HSP27 was significantly overexpressed in LSCC tissues compared to controls and was associated with advanced tumor stage, nodal metastasis, alcohol abstinence, and older age. HSP70 expression correlated with higher tumor grade and female sex but did not differ significantly between cancerous and noncancerous tissues. In the TCGA cohort, low expression of HSP27 and HSP70 was significantly associated with worse overall survival. Low HSP27 expression emerged as an independent predictor of shorter survival (hazard ratio 2.28; 95% confidence interval, 1.11-4.67; p = 0.024).</p><p><strong>Conclusion: </strong>HSP27 and HSP70 show potential as prognostic biomarkers in LSCC, with high expression linked to favorable outcomes. These findings warrant further investigation into their mechanistic roles in tumor progression, therapy resistance, and their potential utility as therapeutic targets.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"264"},"PeriodicalIF":2.8,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12449290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ghazal Mehri-Kakavand, Sibusiso Mdletshe, Mehdi Amini, Alan Wang
{"title":"Multimodal radiomics fusion for predicting postoperative recurrence in NSCLC patients.","authors":"Ghazal Mehri-Kakavand, Sibusiso Mdletshe, Mehdi Amini, Alan Wang","doi":"10.1007/s00432-025-06311-w","DOIUrl":"10.1007/s00432-025-06311-w","url":null,"abstract":"","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"261"},"PeriodicalIF":2.8,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12446158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MiR-26b-5p mediates radioresistance and immunosuppression via targeting PRKCD in non-small cell lung cancer.","authors":"Xu Chen, Rui Kong, Yaxian Qi, Lingchen Li, Chenrui Yin, Lingyou Sun, Chunli Jian, Ping Cai, Qiao Yang, Jianguo Sun","doi":"10.1007/s00432-025-06310-x","DOIUrl":"10.1007/s00432-025-06310-x","url":null,"abstract":"<p><strong>Purpose: </strong>Overcoming miRNA-mediated radioresistance and enhancing its synergy with immunotherapy remained significant challenges.</p><p><strong>Methods: </strong>A total of 23 patients with locally advanced non-small cell lung cancer (NSCLC) undergoing thoracic radiotherapy from a single center were enrolled. Pre-radiotherapy blood samples were collected and analyzed using real time qPCR array to detect miRNA expression profiles, identifying differential miRNAs between responders and non-responders. In vitro experiments further assessed the impact of radiotherapy on significant differential miRNAs. Targeted immune genes of miRNAs were predicted through bioinformatics websites and validated by cellular experiments. Using TCGA and GEO datasets, the association between immune gene of interest and survival outcomes and immune infiltration were investigated. In vivo experiment was further performed to investigate the relationship between dendritic cell (DC) expression and miR-26b-5p following radiotherapy.</p><p><strong>Results: </strong>Using pre-radiotherapy blood samples from 23 NSCLC patients, 22 differentially expressed miRNAs were identified between responders and non-responders. Among them, miR-26b-5p exhibited significant differential expression, suggesting its role as a potential radioresistant molecule. The dual-luciferase assay confirmed miR-26b-5p targeted PRKCD, an immune-related gene. After continuous three days of 2-Gy irradiation, the expression of miR-26b-5p decreased significantly, while the expression of PRKCD increased. The effect of radiotherapy on PRCKD expression were further validated in clinical samples, which demonstrated elevated PRCKD expression after thoracic radiotherapy. Bioinformatic analysis using TCGA and GEO datasets revealed that a higher PRKCD expression was correlated with better survival outcomes, increased immune cell infiltration, and better outcomes. Further in vivo experiments showed that, after radiotherapy, the inhibition of miR-26b-5p showed a significantly higher proportion of DCs than the controls, along with increased expression of CD80, CD86, and TNFSF4.</p><p><strong>Conclusion: </strong>miR-26b-5p and PRKCD modulates dual resistance of both radiotherapy and immunotherapy in NSCLC. These insights demonstrate that downregulating miR-26b-5p could offer a promising therapeutic strategy to enhance radiosensitivity and immune responses.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"262"},"PeriodicalIF":2.8,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12446157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Wang, Jing Liang, Shiyu Zhang, Yingxin Zhang, Fangbu Cheng, Ning Ji, Jing Li, Qianming Chen, Xin Zeng
{"title":"PPARγ accelerates OSCC progression via Th17 polarization and CEBPA/IL-17C signaling.","authors":"Ying Wang, Jing Liang, Shiyu Zhang, Yingxin Zhang, Fangbu Cheng, Ning Ji, Jing Li, Qianming Chen, Xin Zeng","doi":"10.1007/s00432-025-06296-6","DOIUrl":"10.1007/s00432-025-06296-6","url":null,"abstract":"<p><strong>Background: </strong>Oral squamous cell carcinoma (OSCC) is a marked invasive epithelial tumor with limited treatment efficacy, especially in advanced stages. The immunosuppressive nature of the tumor microenvironment (TME) is a major contributor to OSCC development and therapeutic resistance. Peroxisome proliferator-activated receptor gamma (PPARγ) is known to influence tumor biology in a multifaceted and context-specific manner. The objective of this research was to explore the role of PPARγ in modulating the TME and its impact on OSCC progression.</p><p><strong>Methods: </strong>A 4NQO-induced OSCC model was used to verify PPARγ overexpression by Immunohistochemistry (IHC). Bulk RNA-seq and single-cell RNA-seq analyses were employed to dissect PPARγ-driven tumor-promoting mechanisms. Co-cultivation of OSCC cells and CD4 + T cells in vitro, combined with subcutaneous tumor model in vivo, was employed to investigate the influence of PPARγ on Th17 cells differentiation.</p><p><strong>Results: </strong>Inhibition of PPARγ significantly suppressed OSCC cell growth and downregulated IL-17 pathway-related genes, including IL-17C. PPARγ promoted Th17 cells differentiation via transcriptional upregulation of CEBPA/IL-17C/IL-17A signaling pathway. Evidence from cell-based and animal experiments confirmed that GW9662 treatment impaired Th17 cells polarization and reduced expression of CEBPA, IL-17C, and IL-17A.</p><p><strong>Conclusion: </strong>This study identifies a novel PPARγ/CEBPA/IL-17C/IL-17A signaling axis that promotes Th17 differentiation and contributes to tumor-associated inflammation in OSCC. Targeting PPARγ represents a promising strategy to inhibit tumor progression and modulate the immune microenvironment, providing new insight into immunotherapeutic approaches for OSCC.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"259"},"PeriodicalIF":2.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12436265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chenglong Liu, Long Han, Xiang Ding, Junshan Hao, Peng Yang, Ying Wang, Weifu Zhang, Zhe Yang
{"title":"Development of a predictive model for distant metastasis in HCC patients post-TACE using clinical data, radiomics, and deep learning.","authors":"Chenglong Liu, Long Han, Xiang Ding, Junshan Hao, Peng Yang, Ying Wang, Weifu Zhang, Zhe Yang","doi":"10.1007/s00432-025-06308-5","DOIUrl":"10.1007/s00432-025-06308-5","url":null,"abstract":"<p><strong>Purpose: </strong>Hepatocellular carcinoma (HCC) is a perilous malignant tumor, and transcatheter arterial chemoembolization (TACE) is a widely adopted treatment technique for advanced HCC. Nevertheless, TACE may not effectively reduce the risk of distant metastases. As emerging and rapidly evolving technologies, radiomics (RAD) and deep learning (DL) have potential for predicting the outcomes post-TACE for HCC patients. This study aimed to develop a predictive model that integrates clinical data, Rad and DL to assess the risk of distant metastasis in HCC patients following TACE, and to evaluate its efficacy for these patients.</p><p><strong>Methods: </strong>475 cases were included in our study and were divided into training, testing, and external validation cohorts. Rad, DL, DLR (Deep learning and radiomics) models were developed and compared. The combined model was constructed by combining DLR with clinical data using logistic regression analysis. The calibration and decision curves were generated to assess model performance.</p><p><strong>Results: </strong>Clinical features, including tumor size, node numbers and alpha-fetoprotein (AFP) levels, were associated with the risk of metastasis (p < 0.05). The combined model achieved area under the Receiver Operating Characteristic curve (AUC) values of 0.931, 0.861, and 0.854 in the training, testing, and external validation cohorts. Decision curve analysis (DCA) curves demonstrated the superior clinical utility of these models.</p><p><strong>Conclusion: </strong>The combined model can accurately predict distant metastases in HCC patients after TACE. This nomogram model improves personalized clinical decision-making by stratifying TACE-treated HCC patients into distinct risk cohorts, enabling tailored surveillance protocols and adjuvant therapy allocation for high-risk metastasis subgroups.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 10","pages":"258"},"PeriodicalIF":2.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12436248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}