American journal of cancer research最新文献

{"title":"Association between ultrasound radiomics features and central lymph node metastasis in patients with papillary thyroid carcinoma.","authors":"Zexiang Zhang, Zequn Wang, Wenjie Li, Zhaolin Yin","doi":"10.62347/SRFQ9286","DOIUrl":"https://doi.org/10.62347/SRFQ9286","url":null,"abstract":"<p><strong>Objective: </strong>To develop and validate a predictive model combining ultrasound radiomics score (Rad-score) with clinical and conventional ultrasound features for preoperative assessment of central lymph node metastasis (CLNM) risk in papillary thyroid carcinoma (PTC).</p><p><strong>Methods: </strong>This retrospective study included 500 PTC patients, randomly assigned (7:3) to training (n = 350) and validation (n = 150) sets. Radiomics features underwent repeatability validation, standardization, variance filtering, correlation-based redundancy removal, and LASSO logistic regression to construct the Rad-score. Four models were established: clinical/laboratory (Model A), conventional ultrasound (Model B), radiomics (Model C), and combined (Model D). Model performance was assessed using ROC curves, calibration curves, and decision curve analysis (DCA).</p><p><strong>Results: </strong>Baseline analysis revealed that the CLNM group had a higher proportion of males (29.14% vs. 18.59%, P = 0.0286) and a significantly younger mean age (44.15±12.03 years vs. 49.25±11.80 years, P<0.001). Conventional ultrasonographic features demonstrated that the CLNM group presented higher rates of maximum tumor diameter >10 mm (57.62% vs. 31.66%, P<0.001), calcification (74.83% vs. 54.77%, P<0.001) and multifocality (51.66% vs. 35.68%, P = 0.0039). A total of 10 radiomic features were selected via the LASSO algorithm to establish the Rad-score. Univariate logistic regression analysis indicated that male gender, age ≥55 years, maximum tumor diameter >10 mm, calcification, multifocality and Rad-score were correlated with CLNM. Multivariate logistic regression analysis showed that age ≥55 years was associated with a reduced risk of CLNM (OR = 0.531, 95% CI: 0.311-0.907, P = 0.020). Tumor maximum diameter >10 mm (OR = 1.949, 95% CI: 1.192-3.187, P = 0.008) and Rad-score (OR = 35.074, 95% CI: 10.385-118.458, P<0.001) were correlated with an elevated risk of CLNM. Model performance evaluation showed that the areas under the curve (AUCs) of Model A, B, C and D were 0.632, 0.687, 0.757 and 0.764 in the training set, and 0.643, 0.702, 0.788 and 0.798 in the validation set, respectively.</p><p><strong>Conclusion: </strong>The combined model incorporating Rad-score, age stratification, maximum tumor diameter, and conventional ultrasound features effectively predicts CLNM risk in PTC patients, demonstrating good discrimination, calibration, and clinical net benefit. It has potential value for preoperative risk stratification and individualized decision support.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2814-2826"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148763117","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":"Exploration of the mechanism by which H3K27ac activates APOC1 to promote PTC proliferation.","authors":"Jiayin Song, Suwei Zuo, Yuanyuan Wang, Sinuo Sun, Yanmeng Zhou, Shibo Liu, Yanping Li, Yachao Liu, Gang Xue, Xu Lin, Jingfang Wu","doi":"10.62347/QHYG5969","DOIUrl":"https://doi.org/10.62347/QHYG5969","url":null,"abstract":"<p><p>Early studies have suggested that apolipoprotein C1 (APOC1) functions as an oncogenic factor in papillary thyroid carcinoma (PTC), where it promotes tumor cell proliferation. Here, we focus on the regulatory mechanisms underlying APOC1-mediated PTC cell growth, with particular attention to histone modification-driven changes in APOC1 expression and disease progression. Our bioinformatics analysis revealed that APOC1 was differentially expressed in PTC and might be involved in tumor-related biological processes. The influence of APOC1 on PTC cell growth and glycolysis was studied. The impact of APOC1-induced glycolytic reprogramming on PTC cell proliferation was assessed. Cells were treated with the a selective p300/CBP histone acetyltransferase inhibitor (C646) and the histone deacetylase inhibitor sodium butyrate (NaB) to modulate histone acetylation levels. Subsequently, chromatin immunoprecipitation (ChIP) assays were carried out to assess the role of histone modifications in APOC1 expression regulation. Finally, nude mouse xenograft models were used to confirm the oncogenic role of APOC1 in PTC development. Bioinformatics and experimental analyses confirmed that APOC1 expression showed a strong correlation with glycolysis-related genes and PTC cell proliferation was influenced by changes in glycolysis. Meanwhile, APOC1 expression was activated by H3K27ac. Xenograft models were subsequently used to further validate these findings in vivo. H3K27ac-mediated activation of APOC1 may promote glycolytic reprogramming in PTC cells, thereby driving their proliferation.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3049-3065"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757523","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":"An interpretable machine learning model for diagnostic classification of liver cancer using multivariable clinical data.","authors":"Dianyu Wang, Xiao Li, Zuheng Wang, Chunmeng Wei, Wenhao Lu, Rongbin Zhou, Leifeng Liang, Fubo Wang, Junyi Chen","doi":"10.62347/FTNM6925","DOIUrl":"https://doi.org/10.62347/FTNM6925","url":null,"abstract":"<p><p>In this retrospective analysis, we used routinely collected clinical variables to develop a machine learning model for liver cancer diagnosis and examined the variables that contributed to model performance. We studied 3,629 people who were assessed because they were suspected to have liver cancer or other liver diseases. Patients who had pathologically confirmed liver cancer, and controls comprised of healthy subjects, patients with chronic hepatitis B, chronic hepatitis C, or cirrhosis. From 87 clinical parameters, least absolute shrinkage and selection operator regression was applied to identify candidate predictors. Nine machine learning algorithms were then trained and tested through 10-fold cross-validation and external validation in an independent cohort. Performance of the models was measured based on area under the receiver operating characteristic curve, sensitivity, specificity, calibration and decision curve analysis. The variables that contributed most to discrimination included carbohydrate antigen 19-9, alpha-fetoprotein-related indicators, liver function parameters, and inflammatory markers. Among the nine algorithms, Extreme Gradient Boosting achieved the highest discriminative performance, with an AUC of 1.000 in the training cohort and 0.937 in the validation cohort. In the SHapley Additive exPlanations analysis, carbohydrate antigen 19-9 made the largest contribution to the final model. These findings suggest that machine learning algorithms, particularly Extreme Gradient Boosting, may integrate heterogeneous clinical indicators and provide a useful auxiliary tool for distinguishing liver cancer from non-liver cancer conditions in individuals undergoing clinical assessment. Further prospective validation in high-risk surveillance cohorts is required before the model can be applied to early risk prediction or population-level screening.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3119-3135"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757465","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":"Timing of multiple primary malignancies does not affect overall survival in lymphoma patients: a comparative study of 167 synchronous vs. metachronous cases.","authors":"Zheng Li, Jiajie Shi, Xiaolin Wu, Cuiying He, Haisheng Liu, Beichen Liu","doi":"10.62347/OWCP3340","DOIUrl":"https://doi.org/10.62347/OWCP3340","url":null,"abstract":"<p><p>In recent years, growing attention has been paid to the clinical management and prognosis of lymphoma patients with multiple primary malignancies (MPMs). This study aimed to determine whether the timing of MPM diagnosis affects the clinical characteristics and prognosis of these patients. A total of 167 patients with lymphoma complicated by MPMs were retrospectively analyzed. Patients were divided into a synchronous cancer group (SC, interval ≤6 months between diagnoses) and a metachronous cancer group (MC, interval >6 months) based on the interval between the diagnoses of lymphoma and the second malignancy. Clinical characteristics were recorded and compared between the two groups. Overall survival (OS) was estimated using the Kaplan-Meier method, and independent prognostic factors were identified through a multivariate Cox proportional hazards regression analysis. No significant differences were observed in baseline clinical characteristics between the SC and MC groups. The 1-, 3-, and 5-year OS rates for the entire cohort were 94.01%, 74.25%, and 72.46%, respectively. Multivariate analysis revealed that aggressive lymphoma (hazard ratio [HR]=2.618; 95% confidence interval [CI], 1.169-5.863; P=0.026) and Ann Arbor stages III-IV (HR=5.793; 95% CI, 2.658-12.625; P<0.005) were independent predictors of poor prognosis. The temporal sequence of MPMs was not identified as a significant factor influencing OS. Overall, prognosis in patients with lymphoma with MPMs is determined primarily based on the biological behavior and treatment response of lymphoma, whereas the diagnostic interval and sequence of MPM occurrence do not appear to significantly affect long-term survival. These results highlight the importance of focusing on lymphoma-specific features and treatment response in prognostic evaluation of patients with lymphoma with MPMs.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3162-3172"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757693","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":"Retrospective study on maintenance therapy with PD-1 inhibitor combined with S-1 or capecitabine after first-line treatment for recurrent or metastatic nasopharyngeal carcinoma.","authors":"Hao Yuan, Yudan Wang, Junyin Tan, Xiaomei Lin, Yan Wei","doi":"10.62347/EWRN6009","DOIUrl":"https://doi.org/10.62347/EWRN6009","url":null,"abstract":"<p><p>This study aimed to investigate the clinical efficacy and safety of programmed death-1 (PD-1) inhibitor combined with S-1 or capecitabine as maintenance therapy in patients with recurrent or metastatic nasopharyngeal carcinoma (R/M NPC) following first-line systemic treatment. Clinical data of 95 patients diagnosed with R/M NPC were retrospectively analyzed. All patients were pathologically confirmed as having non-keratinizing undifferentiated NPC with metastatic lesions verified by imaging or pathological examination. After receiving at least 4 cycles of first-line treatment with PD-1 inhibitor combined with gemcitabine plus cisplatin chemotherapy regimen, patients entered the maintenance stage and were divided into two groups: the combination maintenance group (PD-1 inhibitor plus S-1 or capecitabine) and the PD-1 inhibitor monotherapy maintenance group. Baseline characteristics, objective response rate (ORR), disease control rate (DCR), changes of Epstein-Barr virus DNA (EBV-DNA) load, inflammatory indicators, nutritional status indicators, quality of life scores, adverse events, and survival outcomes were compared between the two groups. A logistic regression model was adopted to analyze the influencing factors of poor prognosis. After maintenance treatment, the secondary ORR and DCR were slightly higher in the combination maintenance group without statistical significance (both P > 0.05). The EBV-DNA negative conversion rate was significantly elevated in the combination group (P < 0.05). Inflammatory indicators of both groups were remarkably improved after treatment (P < 0.05). No significant inter-group differences were observed in nutritional status indicators, SF-36 quality of life scores, incidence and severity distribution of grade ≥ 3 adverse events, or immune-related adverse events (all P > 0.05). Progression-free survival (PFS) was significantly longer in the combination maintenance group (P < 0.05). Univariate logistic regression analysis showed that treatment regimen, EBV-DNA negative conversion rate and ECOG score were correlated with poor prognosis. Multivariate logistic regression analysis revealed that an ECOG score of 0-1 and EBV-DNA negative conversion rate were independent protective factors against poor prognosis. In conclusion, maintenance therapy with PD-1 inhibitor combined with S-1 or capecitabine after first-line treatment for R/M NPC yields definite therapeutic efficacy. The ORR and DCR showed an upward trend in the combination group, though the difference was not statistically significant. Meanwhile, this regimen can significantly elevate the EBV-DNA negative conversion rate, ameliorate systemic inflammatory responses and prolong PFS without increasing the risk of severe adverse reactions. Combined maintenance therapy did not trigger remarkable declines in most dimension scores of SF-36, and patients' overall quality of life remained relatively stable.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2997-3009"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759060","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":"Erratum: Macrophage polarization involved the inflammation of chronic obstructive pulmonary disease by S1P/HDAC1 signaling.","authors":"Min Zhang, Ruoxuan Hei, Zhou Zhou, Wendi Xiao, Xi Liu, Yanwei Chen","doi":"10.62347/GZTT6600","DOIUrl":"https://doi.org/10.62347/GZTT6600","url":null,"abstract":"<p><p>[This corrects the article on p. 4478 in vol. 13, PMID: 37818082.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3198-3200"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148756926","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":"Erratum: Profiling the epigenetic interplay of lncRNA RUNXOR and oncogenic RUNX1 in breast cancer cells by gene in situ cis-activation.","authors":"Yuanyuan Nie, Lei Zhou, Hong Wang, Naifei Chen, Lin Jia, Cong Wang, Yichen Wang, Jingcheng Chen, Xue Wen, Chao Niu, Hui Li, Rui Guo, Songling Zhang, Jiuwei Cui, Andrew R Hoffman, Jifan Hu, Wei Li","doi":"10.62347/KRMR3020","DOIUrl":"https://doi.org/10.62347/KRMR3020","url":null,"abstract":"<p><p>[This corrects the article on p. 1635 in vol. 9, PMID: 31497347.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3183-3184"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757319","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":"Actin-related protein 2/3 complex subunit 1B promotes cervical cancer cell tumorigenesis in vitro and in vivo.","authors":"Xin Jin, Qiyue Zhang, Xinru Ling, Yanbo Liu, Tiantian Wu, Guannan Feng","doi":"10.62347/XCGE7946","DOIUrl":"https://doi.org/10.62347/XCGE7946","url":null,"abstract":"<p><p>Cervical cancer (CC) is a major cause of cancer-related mortality in women, with limited therapeutic options for advanced-stage disease. Although Actin-related protein 2/3 complex subunit 1B (ARPC1B) has been shown to play a role in multiple tumours, it is not yet well understood in cervical cancer. Our study has demonstrated that ARPC1B is an important contributor in CC progression. Bioinformatic analysis and tissue microarray (TMA) results revealed that ARPC1B is much more expressed in human cervical carcinoma tissues and positively correlates with poor prognosis. Through a series of in vitro and in vivo functional assays, we showed that ARPC1B plays a decisive role in the proliferation, migration and invasion of cervical cancer cells. Specifically, ARPC1B knockout suppresses the aforementioned malignant phenotypes, whereas its overexpression enhances them. We also proved that ARPC1B promotes tumorigenesis in xenograft models. These findings collectively establish ARPC1B as a novel oncogene in cervical cancer, indicating its potential role as both a biological prognostic marker and a therapeutic target for patients with cervical cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2955-2970"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758256","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":"MCPB-21 targets glycogenin-2 to regulate fatty acid oxidation and promote ferroptosis of breast cancer.","authors":"Mengjie Mao, Chunyu Wang, Yingchun Lu, Qingxiu Tao, Long Zeng, Jing Li, Bin Liu","doi":"10.62347/DIDU5607","DOIUrl":"https://doi.org/10.62347/DIDU5607","url":null,"abstract":"&lt;p&gt;&lt;p&gt;This study systematically evaluated the anti-breast cancer potential and mechanisms of the cannabidiol (CBD) derivative MCPB-21. The structure of MCPB-21 was confirmed by nuclear magnetic resonance (NMR). The study analyzed differentially expressed genes associated with breast cancer using public databases and verified the binding affinity of MCPB-21 to glycogenin-2 (GYG2) through molecular docking. Additionally, the effects of MCPB-21 on apoptosis, invasion capacity, and lipid metabolism were evaluated in MDA-MB-231 and MCF-7 breast cancer cells using flow cytometry, Transwell invasion assays, cell proliferation assays, and Oil Red O staining. Western blot was employed to examine expression changes in proteins related to fatty acid β-oxidation and ferroptosis, including Acyl-CoA Oxidase 1 (ACOX1), ATP Binding Cassette Subfamily D Member 3 (ABCD3), ATP Binding Cassette Subfamily D Member 4 (ABCD4), Peroxisomal l-bifunctional enzyme (EHHADH), Carnitine palmitoyltransferase 1α (CPT1α), Glutathione Peroxidase 4 (GPX4), Solute Carrier Family 7 Member 11 (SLC7A11), and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4). The role of fatty acid oxidation in ferroptosis was further analyzed using the ACOX1 inhibitor 10,12-Tricosadiynoic acid (500 nM). Additionally, the effects of MCPB-21 on fatty acid oxidation and ferroptosis were evaluated by interfering with GYG2 expression. Ferrostatin-1 (Fer-1) rescue experiments were conducted to verify the dependence of MCPB-21-induced cell death. Finally, the anti-tumor efficacy of various doses of MCPB-21 was compared to the control drug CBD. &lt;i&gt;In vitro&lt;/i&gt; experimental results showed that MCPB-21 can affect the behavior of breast cancer cells by inducing cancer cell apoptosis, increasing reactive oxygen species (ROS) levels, and promoting lipid accumulation. At the same time, Western blot detection showed that MCPB-21 could downregulate key enzymes of fatty acid β-oxidation (ACOX1, ABCD3, ABCD4, EHHADH, CPT1α) and antioxidant factors (GPX4, SLC7A11), and upregulate the enzyme ACSL4 that promotes lipid peroxidation. Mechanistic studies further showed that MCPB-21 affects the expression of ACOX1 by regulating GYG2, inhibits fatty acid β-oxidation, and induces ferroptosis. At the same time, the combined use of ACOX1 inhibitors enhanced lipid accumulation and ROS levels, verifying its role in regulating fatty acid oxidation. In animal experiments, MCPB-21 (10 and 40 mg/kg) significantly inhibited the growth of nude mouse transplanted tumors, caused tumor tissue necrosis, inhibited the proliferation marker Ki67, and regulated the expression of ferroptosis-related proteins (GPX4 and SLC7A11 decreased, and ACSL4 increased). Immunohistochemical analysis showed that MCPB-21 had a stronger anti-tumor effect than CBD, mainly by regulating the fatty acid β-oxidation pathway to promote ferroptosis. In summary, MCPB-21 exhibits excellent anti-breast cancer potential. Its mechanism of action is mainly to achieve an","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2763-2782"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757208","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":"Temporal trends in the incidence and prognosis of lung metastasis in gallbladder cancer: risk stratification and survival analysis.","authors":"Yang Yu, Xuan Li, Jia-Jun Hui, Dong Li","doi":"10.62347/MVDD7837","DOIUrl":"https://doi.org/10.62347/MVDD7837","url":null,"abstract":"<p><p>Lung metastases are the second most common visceral metastatic site in gallbladder cancer (GBC); however, population-based evidence regarding this metastatic pattern remains limited. In this study, we sought to define the incidence trend of lung metastasis in GBC, identify risk factors associated with its occurrence, and comprehensively assess survival outcomes in this patient population. Data on GBC patients diagnosed 2010-2022 were retrieved from the Surveillance, Epidemiology, and End Results (SEER) database. Joinpoint regression was used to evaluate temporal trends. Multivariate logistic regression was performed to identify independent risk factors. Overall survival (OS) was analyzed via Kaplan-Meier, multivariate Cox regression, and propensity score matching (PSM). The incidence of lung metastasis in GBC patients showed a modest but statistically significant increasing trend from 2010 to 2022, with an average annual percent change of 3.6% (95% CI 1.4%-5.8%, P<0.05). Independent risk factors for lung metastasis included advanced N stage (N1 and N2) and synchronous bone, liver, or brain metastases. GBC patients with lung metastasis exhibited poor prognosis, with a median OS of 5.0 months (95% CI 4.0-6.0). The 1-, 2-, and 3-year OS rates were 18.1%, 4.3%, and 1.0%, respectively. Isolated lung metastasis conferred better survival than concurrent other distant metastases (median OS: 7.0 vs. 4.0 months, P<0.001). Chemotherapy significantly improved survival (HR=0.39, 95% CI 0.32-0.49), whereas primary tumor resection showed no benefit after PSM. Survival rates in this population did not change significantly between 2010 and 2022. In conclusion, this comprehensive, population-based analysis provides contemporary insights into the epidemiology and management of this challenging patient population.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2838-2847"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757310","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}