American journal of cancer research最新文献

{"title":"Procyanidin C1 combined with olaparib induces senescence in BRCA1-proficient breast cancer cells.","authors":"Chengsi Ren, Chengshi Fu, Xingtong Chen, Renfei Yang, Jinyong He, Anran Gao, Qunshan Su, Xiangyun Teng, Jianhua Xu","doi":"10.62347/LYCQ1366","DOIUrl":"10.62347/LYCQ1366","url":null,"abstract":"<p><p>PARP inhibitors (PARPi) are effective only in BRCA1-mutated tumors, with BRCA1-proficient patients deriving minimal benefit. Here, we demonstrate that PCC1 persistently induces double-strand DNA breaks (DSBs) in BRCA1-proficient breast cancer cells. Critically, PARP inhibition blocks base excision repair (BER), leading to accumulation of DNA damage and direct activation of senescence programs. Compared to monotherapy, the combination of olaparib and PCC1 significantly enhanced cellular senescence and suppressed tumor growth. In sum, we developed a novel therapeutic regimen that extends the utility of PARP inhibitors to BRCA1-proficient breast cancer patients through synergistic co-targeting of DNA damage responses.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3394-3407"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928682","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":"AI-assisted design and virtual profiling of targeted degraders for pancreatic cancer therapy via PROTAC technology.","authors":"Bing Du, Kunjie Wang, Zhu Wu, Shaofan Qiu, Filippiadis Dimitrios Konstantinos, Shuo Yu","doi":"10.62347/EKCM7279","DOIUrl":"10.62347/EKCM7279","url":null,"abstract":"<p><p>Pancreatic cancer remains one of the most lethal malignancies because of late diagnosis, aggressive progression, therapy resistance, and limited effective treatment options. Bromodomain-containing protein 4 (BRD4) is an important epigenetic regulator implicated in pancreatic cancer progression through its role in transcriptional control, cell proliferation, and survival signaling. Targeted protein degradation using proteolysis-targeting chimeras (PROTACs) offers a potential strategy for eliminating disease-associated proteins through ubiquitin-proteasome-mediated degradation rather than transient pharmacological inhibition. In this study, an AI-assisted and structure-guided computational workflow was used to design and virtually prioritize BRD4-targeting PROTAC candidates recruiting DCAF15 as the E3 ligase component. The workflow integrated protein-structure evaluation, pharmacophore-based ligand screening, ADMET and Lipinski filtering, binary protein-ligand docking, molecular-interaction analysis, rational linker selection, BRD4-DCAF15 protein-protein docking, PROTAC-mediated ternary-complex docking, and molecular dynamics simulation. The results identified CLTTMPBA-linker-E7820 as a computationally prioritized PROTAC architecture with favorable predicted binding behavior, residue-level interaction patterns, and simulated ternary-complex stability. Importantly, this study is entirely computational and should be interpreted as an early-stage in silico prioritization framework rather than experimental evidence of BRD4 degradation or anticancer efficacy. The proposed BRD4-DCAF15 PROTAC candidates represent lead hypotheses that require biochemical, cellular, pharmacological, and in vivo validation, including confirmation of target engagement, ternary-complex formation, proteasome-dependent BRD4 degradation, downstream transcriptional modulation, pancreatic cancer cell inhibition, selectivity, pharmacokinetics, toxicity, and antitumor efficacy.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3620-3643"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928782","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":"Efficacy of multimodal symptom management strategies for chemotherapy-induced nausea and vomiting in gynecologic cancer: a meta-analysis.","authors":"Weina Zhou, Minfen Chen, Tingting Wang, Liying Zhang","doi":"10.62347/MTIL8832","DOIUrl":"10.62347/MTIL8832","url":null,"abstract":"<p><p>This meta-analysis aimed to evaluate whether multimodal symptom management improves chemotherapy-induced nausea and vomiting (CINV) among patients with gynecologic cancer across acute, delayed, and overall treatment phases. We systematically searched major electronic databases and trial registries for eligible English-language studies from database inception to the final search date. Included studies enrolled female patients with gynecologic malignancies receiving chemotherapy and evaluated multimodal symptom management strategies for CINV control. Two independent researchers screened literature records and extracted data using a standardized form. Risk of bias of included studies were evaluated based on standard evaluation domains. All quantitative analyses were performed with a random-effects model. Dichotomous outcome data were pooled to calculate risk ratios (RRs) and 95% confidence intervals (CIs). Predefined subgroup analyses were conducted for acute, delayed, and overall phases. We assessed statistical heterogeneity via Cochran's Q test and I² statistics, and evaluated publication bias through visual inspection of funnel plots. Multimodal symptom management strategies yielded no significant improvements in overall complete CINV control (RR 1.02, 95% CI: 0.86-1.21), acute complete CINV control (RR 0.96, 95% CI: 0.80-1.15), or delayed complete CINV control (RR 0.94, 95% CI: 0.77-1.14), with low to no statistical heterogeneity across these analyses. Likewise, no significant benefit was observed for overall no-vomiting events (RR 1.46, 95% CI: 0.75-2.83) or overall no-significant-nausea events (RR 1.59, 95% CI: 0.71-3.54), with substantial heterogeneity detected for both outcomes. Notably, multimodal interventions significantly increased the rates of acute no-vomiting events (RR 1.99, 95% CI: 1.42-2.80) and acute no-significant-nausea events (RR 2.05, 95% CI: 1.43-2.94), with no detectable heterogeneity. Conclusion: Multimodal symptom management strategies offer tangible clinical benefits for acute CINV control in gynecologic cancer patients, especially in the prevention of vomiting and clinically significant nausea. These strategies show no obvious superiority for delayed and overall CINV comprehensive control.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3202-3221"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928873","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":"Development and validation of a novel disulfidptosis-associated LncRNA model for risk stratification and targeted therapy guidance in gastric adenocarcinoma.","authors":"Bingtuan Lu, Lili Tao, Xindan Zhang, Qiaoying Chen, Qian Hong, Xiaoming Yin","doi":"10.62347/GPBG3667","DOIUrl":"https://doi.org/10.62347/GPBG3667","url":null,"abstract":"<p><p>Disulfidptosis, as a newly discovered form of cell programmed cell death in recent years, is driving the in-depth understanding of the tumor occurrence mechanism and the exploration of innovative therapeutic approaches. Although the regulatory role of long non-coding RNAs (lncRNAs) in cancer development is well-known, whether they are involved in the disulfidptosis process and their significance in the prognosis of gastric adenocarcinoma remain unclear. This study, using sequencing and clinical data from The Cancer Genome Atlas (TCGA) database, through least absolute shrinkage and selection operator (LASSO) and Cox regression analysis, has for the first time constructed a prognostic evaluation model containing eight disulfidptosis-related lncRNAs (DRlncRNAs). This model covers molecules such as LIMS1-AS1, LINC00460, and AL590681.1, and can clearly distinguish gastric adenocarcinoma patients into high-risk and low-risk groups based on the median risk score. The analysis showed that there were significant differences between the two groups of patients in terms of total survival, relevant signal pathway activity, tumor immune microenvironment characteristics, gene mutation load, drug sensitivity, etc. The prognosis of patients in the low-risk group is obviously better. Moreover, the study further verified through cell experiments, animal models and clinical samples that these 8 types of lncRNA are abnormally expressed in gastric adenocarcinoma, which directly affects the survival of cancer cells. This series of work not only provides a new independent biomarker combination for the prognosis of gastric adenocarcinoma, but also lays an important foundation for an in-depth understanding of the disulfidptosis regulation network and the development of targeted treatment strategies for this pathway.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2680-2706"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148763133","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":"Methylation of DPP9 regulates immune surveillance in non-small cell lung cancer by promoting macrophage ferroptosis via WWP2 ubiquitination.","authors":"Haiyan Lin, Ying Chen, Nana Wang, Shan Zhang","doi":"10.62347/XZWR5194","DOIUrl":"https://doi.org/10.62347/XZWR5194","url":null,"abstract":"<p><p>Lung cancer is one of the most common malignancies worldwide, with approximately 2.2 million new cases diagnosed annually. About 75% of patients die within five years of diagnosis. Non-small cell lung cancer (NSCLC) is the predominant histological subtype. In the present study, we aimed to comprehensively elucidate the effects of dipeptidyl peptidase 9 (DPP9) in model of NSCLC. DPP9 mRNA expression and protein expression were up-regulation in patients with NSCLC. Then, Sh-DPP9 reduced cancer growth in mice model of NSCLC. N6-methyladenosine (m6A) increased DPP9 RNA stability of macrophage in NSCLC. DPP9 reduced immune surveillance and promoted Macrophage ferroptosis in vitro model. Meanwhile, si-DPP9 increased immune surveillance and reduced Macrophage ferroptosis in vitro model. DPP9 increased reactive oxygen species (ROS) ROS-mitochondrial oxidation and mitochondrial damage in Macrophage of vitro model. DPP9 reduced activating transcription factor 4 (ATF4) protein expression to promote WW domain-containing E3 ubiquitin protein ligase 2 (WWP2) ubiquitination in Macrophage. ATF4 inhibitor or WWP2 inhibitor reduced the effects of si-DPP9 in ferroptosis of macrophage in model of NSCLC. In conclusion, DPP9 up-regulation promotes WWP2 ubiquitination, thereby inhibiting the WWP2/ATF4 signaling pathway and enhancing macrophage ferroptosis, which leads to reduced immune surveillance and promotes tumor progression in NSCLC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3025-3048"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757294","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":"Mitochondrial calcium uniporter as a biomarker in lung adenocarcinoma: regulation of the immune microenvironment, apoptosis, cell cycle and mitophagy.","authors":"Yihao Liu, Zexia Zhao, Hua Huang, Chenxuan Zhao, Zhixuan Duan, Min Wang, Chen Ding, Wenhao Zhao, Yanzhan Liu, Hongbing Zhang, Yongwen Li, Wenjun Meng, Yin Li, Xiaobin Shang, Jun Chen, Haoling Zhang, Honglin Zhao","doi":"10.62347/PGQK3358","DOIUrl":"https://doi.org/10.62347/PGQK3358","url":null,"abstract":"<p><p>The mitochondrial calcium uniporter (MCU) complex is essential for maintaining mitochondrial calcium homeostasis and regulating cellular metabolism, apoptosis, proliferation, and mitochondrial quality control. Although MCU has been implicated in multiple malignancies, its biological role and regulatory mechanisms in lung adenocarcinoma (LUAD), a major subtype of non-small cell lung cancer (NSCLC), remain insufficiently defined. In this study, MCU expression was analyzed using pan-cancer and LUAD datasets from TCGA, GEO, UALCAN, and tissue microarray cohorts. GO, KEGG, and GSEA were performed to explore MCU-associated biological pathways, while ssGSEA, CIBERSORT, and TIDE algorithms were used to evaluate immune infiltration and predicted immunotherapy response. In vitro assays, including CCK-8, EdU, colony formation, Transwell assays, flow cytometry, qRT-PCR, Western blotting, immunofluorescence staining, JC-1 staining, and reactive oxygen species (ROS) detection, were conducted to assess the effects of MCU on LUAD cell behavior, mitophagy, and mitochondrial function. MCU was significantly upregulated in LUAD tissues and cell lines compared with normal controls. High MCU expression was associated with reduced immune cell infiltration, decreased immune checkpoint and HLA gene expression, and lower predicted sensitivity to immunotherapy. Functionally, MCU knockdown markedly inhibited LUAD cell proliferation, migration, and invasion, promoted apoptosis, and induced G1-phase cell cycle arrest, accompanied by increased p21 and cleaved caspase-3 expression and decreased CDK4 and Cyclin D1 expression. Conversely, MCU overexpression enhanced malignant phenotypes and suppressed apoptosis. Mechanistically, GSEA indicated that MCU was closely associated with mitophagy-related pathways. Further validation showed that MCU knockdown reduced PINK1 and PRKN expression, decreased mitochondrial LC3B accumulation, and weakened LC3B-mitochondria co-localization, indicating impaired mitophagy. MCU depletion also caused mitochondrial membrane potential dissipation and increased intracellular ROS accumulation. Collectively, these findings suggest that MCU promotes LUAD progression by remodeling the tumor immune microenvironment, enhancing malignant cellular behaviors, inhibiting apoptosis, and maintaining mitophagy-dependent mitochondrial homeostasis, highlighting MCU as a potential prognostic biomarker and therapeutic target in LUAD.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2783-2800"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757320","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":"Risk factors for cardiac dysfunction caused by anthracycline drugs in the treatment of lymphoma and the early monitoring value of three-dimensional echocardiography.","authors":"Jing Jiang, Xiaolei Mu, Xiaomei Chen, Qianqian Li","doi":"10.62347/GOZT5673","DOIUrl":"https://doi.org/10.62347/GOZT5673","url":null,"abstract":"<p><p>Anthracyclines (ANTs) are important chemotherapeutic drugs for the treatment of lymphoma. However, its cardiotoxicity poses a challenge to its continued use. The development of ARCD is influenced by multiple factors, making early detection challenging. Three-dimensional speckle tracking imaging (3D-STI) can quantitatively analyze myocardial strain by tracking the movement of myocardial spots. This study compared the parameters derived from conventional echocardiography, 3D-STI, and three-dimensional echocardiography at baseline (T0), 2 cycles of chemotherapy (T2) and 4 cycles of chemotherapy (T4), and analyzed the risk factors for ARCD. From January 2020 to December 2024, a total of 189 patients with non-Hodgkin lymphoma were recruited, all of whom received at least 4 cycles of ANT treatment. During chemotherapy and follow-up, 28 patients developed ARCD. Firth-penalized logistic regression demonstrated that age ≥65 years (aOR = 3.416, 95% CI: 1.241-9.913), hypertension (aOR = 3.051, 95% CI: 1.095-8.675), and cumulative ANT dose (aOR = 1.028, 95% CI: 1.017-1.040) were independently associated with an increased risk of ARCD. Conventional echocardiographic parameters, including LVEF, showed no significant changes. Compared with T0, right ventricular end-diastolic volume (RVEDV) and right ventricular end-systolic volume (RVESV) were significantly increased at T4 (P<0.05), left ventricular global longitudinal strain (LVGLS) was significantly decreased at T2 (P<0.05), and left ventricular global circumferential strain (LVGCS) was significantly decreased at T4 (P<0.05). The absolute change in LVGLS from T0 to T2 (ΔLVGLS) was significantly and positively correlated with the cumulative ANT dose (R = 0.336, P<0.001). The cut-off value for predicting ARCD using ΔLVGLS was 3.5%. The area under the curve (AUC) was 0.852 and the respective sensitivity and specificity were 0.929 and 0.739. 3D-STI, particularly LVGLS, demonstrated significant value in the early identification of cardiac dysfunction in patients with lymphoma undergoing ANT treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2725-2739"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757461","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: HSP105 suppresses the progression of cutaneous squamous cell carcinoma by activating the P53 signaling pathway.","authors":"Meng Jia, Kai-Yi Zhou, Li-Jia Deng, Sheng Fang","doi":"10.62347/YEXZ3177","DOIUrl":"https://doi.org/10.62347/YEXZ3177","url":null,"abstract":"<p><p>[This corrects the article on p. 3013 in vol. 13, PMID: 37559974.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3193-3197"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757150","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":"Ozone exposure promotes melanogenesis through MAPK-dependent oxidative stress signaling: attenuation by resveratrol in zebrafish and melanoma cells.","authors":"Che-Hsin Lee, Chi-Jie Chang, Wang-Ta Liu, Pei-Hsuan Chen, Chia C Wang","doi":"10.62347/JSCQ2095","DOIUrl":"https://doi.org/10.62347/JSCQ2095","url":null,"abstract":"<p><p>Ground-level ozone, a major air pollutant, primarily forms through photochemical reactions between nitrogen oxides (NOx) and volatile organic compounds (VOCs) in sunlight. Ozone is known to harm human health and skin, making it a significant environmental concern. In this study, we examined the effects of ozone exposure on melanogenesis and whether resveratrol could influence this process. Using zebrafish models and B16F10 melanoma cells, we assessed changes in melanin production. In B16F10 cells, we investigated the impact of 1 ppm ozone exposure on reactive oxygen species (ROS) production and its subsequent effect on mitogen-activated protein kinase (MAPK) signaling pathways, including the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Our findings showed that ozone exposure significantly increased melanin levels in both zebrafish and B16F10 cells. Ozone exposure enhanced p38 and JNK phosphorylation, reduced ERK phosphorylation, and upregulated microphthalmia-associated transcription factor (MITF) and tyrosinase expression. Resveratrol was selected as a candidate agent for its ability to inhibit MAPK signaling. Resveratrol treatment effectively reduced ozone-induced melanin production by decreasing MITF and its downstream enzyme, tyrosinase. These results highlight the role of MAPK signaling in ozone-induced pigmentation and suggest that resveratrol could be a promising agent for protecting against ozone-related skin damage.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2827-2837"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757291","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: tRF-20-M0NK5Y93-induced MALAT1 promotes colon cancer metastasis through alternative splicing of SMC1A.","authors":"Na Luan, Jiaojiao Wang, Biao Sheng, Qin Zhou, Xun Ye, Xiaoling Zhu, Jianguo Sun, Zhe Tang, Jianwei Wang","doi":"10.62347/NXUV8339","DOIUrl":"https://doi.org/10.62347/NXUV8339","url":null,"abstract":"<p><p>[This corrects the article on p. 852 in vol. 13, PMID: 37034215.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3185-3192"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762875","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}