Cancer Chemotherapy and Pharmacology最新文献

{"title":"Pharmacological inhibition of store-operated calcium entry enhances sorafenib-induced antitumor effects in Huh7 hepatocellular carcinoma cells.","authors":"Beste Yurdacan Yasar, Elmasnur Yilmaz, Yasemin Erac","doi":"10.1007/s00280-026-04934-5","DOIUrl":"10.1007/s00280-026-04934-5","url":null,"abstract":"<p><strong>Purpose: </strong>Sorafenib remains a systemic treatment option for advanced hepatocellular carcinoma (HCC), but its clinical efficacy is limited by rapid development of adaptive cellular responses that promote cell survival and phenotypic plasticity. Store-operated calcium entry (SOCE) is a key regulator of intracellular calcium signaling and has been implicated in proliferation, apoptosis, migration, and epithelial-mesenchymal plasticity in cancer. This study investigated the association between SOCE and early adaptive responses to sorafenib in Huh7 HCC cells.</p><p><strong>Methods: </strong>Huh7 cells were treated with sorafenib, the SOCE inhibitor SKF-96365, or their combination. Functional effects were evaluated using real-time proliferation assays, intracellular calcium measurements, apoptosis analysis, and wound-healing assays. Findings were complemented by integrated bioinformatic analyses of TCGA-LIHC and related HCC datasets.</p><p><strong>Results: </strong>Sorafenib treatment significantly enhanced calcium influx following endoplasmic reticulum calcium depletion, consistent with activation of SOCE as part of an adaptive response. Pharmacological inhibition of SOCE markedly attenuated this calcium influx and suppressed cell proliferation. Combined treatment enhanced sorafenib-induced apoptosis and reduced wound closure, accompanied by decreased expression of mesenchymal markers and increased E-cadherin levels, consistent with a shift toward a more epithelial phenotype. Integrated bioinformatic analyses revealed an association between TRPC6-related signaling and epithelial-mesenchymal plasticity, as well as subtype-specific expression patterns linked to aggressive tumour behavior in human HCC datasets.</p><p><strong>Conclusion: </strong>These findings suggest that SOCE is associated with early adaptive responses to sorafenib in Huh7 cells, and that its pharmacological inhibition may enhance sorafenib-induced antitumor effects. Given the reliance on a single cell line and a non-selective pharmacological inhibitor, these findings should be considered hypothesis-generating, and further validation using additional HCC models and genetic approaches is warranted.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis suppression by MYC confers oxaliplatin resistance in colorectal cancer via FTH1 and GPX4.","authors":"Yucheng Wang, Yulan Chen, Che Li, Jin Yang","doi":"10.1007/s00280-026-04936-3","DOIUrl":"https://doi.org/10.1007/s00280-026-04936-3","url":null,"abstract":"<p><strong>Purpose: </strong>Oxaliplatin resistance remains a major obstacle in the treatment of colorectal cancer (CRC). This study aimed to determine whether MYC contributes to oxaliplatin resistance by regulating ferroptosis and to clarify the downstream mechanisms involving FTH1 and GPX4.</p><p><strong>Methods: </strong>Parental CRC cell lines, including HCT116, HT-29 and SW480, together with oxaliplatin-resistant HCT116-R cells, were used. MYC expression was manipulated by knockdown or overexpression. Oxaliplatin sensitivity was evaluated using CCK-8 assays and IC50 analysis. Intracellular Fe²⁺ and reactive oxygen species (ROS) levels were measured to assess ferroptosis-associated changes. RT-qPCR and western blotting were performed to examine gene and protein expression. Chromatin immunoprecipitation-qPCR and dual-luciferase reporter assays were used to investigate the transcriptional regulation of FTH1 and GPX4 by MYC. Rescue experiments with FTH1 or GPX4 overexpression and sorafenib treatment were also conducted.</p><p><strong>Results: </strong>MYC knockdown significantly increased oxaliplatin sensitivity in both parental and resistant CRC cells and elevated intracellular Fe²⁺ and ROS levels. MYC directly bound to the promoter regions of FTH1 and GPX4 and enhanced their transcriptional activity. Downregulation of MYC reduced FTH1 and GPX4 expression, whereas re-expression of either FTH1 or GPX4 partially restored oxaliplatin resistance. Sorafenib further enhanced oxaliplatin sensitivity in resistant cells.</p><p><strong>Conclusion: </strong>MYC promotes oxaliplatin resistance in CRC cells, at least in part, by transcriptionally upregulating FTH1 and GPX4 and suppressing ferroptosis-associated cell death. The MYC-FTH1/GPX4-ferroptosis axis may represent a potential therapeutic target for overcoming oxaliplatin resistance in CRC.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dosing challenges for chemotherapy and immunotherapy in congenital achondroplasia: a case report and literature review.","authors":"Karolijn W M Groot Beumer, E M J Durlinger, S W J Zielhuis, R Ter Heine, A D R Huitema, J J M A Hendrikx","doi":"10.1007/s00280-026-04932-7","DOIUrl":"10.1007/s00280-026-04932-7","url":null,"abstract":"<p><strong>Introduction: </strong>Currently, no established guidelines exist for dosing chemotherapy or immunotherapy in patients with achondroplasia.</p><p><strong>Case: </strong>A 69-year old female with congenital achondroplasia was diagnosed with stage IV non-small cell lung carcinoma type adenocarcinoma, with high Tumor Mutational Burden and 20% programmed death-ligand 1 expression. The patient received carboplatin dose based on renal function utilizing measured creatinine clearance, pemetrexed based on body surface area and pembrolizumab at a fixed dose of 100mg for body weight <65 kg. The doses of carboplatin and pemetrexed were adjusted after the first cycle based on therapeutic drug monitoring (TDM). The treatment was generally well tolerated, with the exception of grade 2 neutropenia, which resolved after a one-week delay of the third treatment cycle. A favorable clinical response was achieved after four treatment cycles.</p><p><strong>Conclusion: </strong>Given the uncertainty regarding the accuracy of dosing algorithms in patients with congenital achondroplasia, TDM may support dose optimization and attainment of adequate drug exposure.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13433722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A rare variant in DPYD c.812delT causes severe adverse events of S-1 in a patient with tongue cancer.","authors":"Hiroki Ishimura, Atsushi Suehiro, Daiki Hira, Eiji Hishinuma, Midori Kato, Masamitsu Maekawa, Taishi Yasuda, Yurie Katsube, Yoshiki Katada, Natsuki Imayoshi, Yuki Shigetsura, Shunsaku Nakagawa, Masahiro Tsuda, Masahiro Hiratsuka, Tomohiro Terada","doi":"10.1007/s00280-026-04930-9","DOIUrl":"10.1007/s00280-026-04930-9","url":null,"abstract":"<p><p>Dihydropyrimidine dehydrogenase (DPD), which is encoded by the DPYD gene, plays an important role in the metabolism of fluoropyrimidine (FP) drugs, including tegafur, in S-1. A decrease in DPD activity can cause severe FP-related toxicity. The Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for FP and DPYD polymorphisms recommend FP dose adjustments based on the four major DPYD polymorphisms. However, multiple rare variants of DPYD have been reported. We present the case of a man in his 50s with cT3N0M0 tongue squamous cell carcinoma who developed severe myelosuppression and diarrhea after the initiation of S-1 (tegafur/gimeracil/oteracil) despite appropriate dosing. On day 20 of treatment, the patient developed grade 4 neutropenia and septic shock and required ICU admission. Genetic testing identified a rare heterozygous DPYD variant (c. 812delT) that causes a frameshift and a presumed loss of enzyme function, suggesting an underlying cause of the severe adverse events. Although severe toxicity occurred, marked tumor shrinkage allowed for less invasive surgery. This case highlights the need for expanded genetic screening beyond the guideline-listed variants, particularly in Asian populations, where common variants differ. Combining genotypic and phenotypic evaluations of DPD activity may improve the prediction and prevention of FP-related toxicities, supporting safer and more effective use of FP drugs.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13433389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a simplified population pharmacokinetic-pharmacodynamic framework for exposure-informed risk stratification of neutropenia during amrubicin treatment.","authors":"Yoshinori Makino, Takanori Ogawa, Reiko Makihara-Ando, Naomi Sakiyama, Masahito Yamazaki, Chizuru Naito, Hiroki Takayama, Genji Ueda, Shunsuke Kohyama, Maki Todo, Yasuhiro Kuwata, Masataka Hirasaki, Tetsuya Hamaguchi","doi":"10.1007/s00280-026-04931-8","DOIUrl":"10.1007/s00280-026-04931-8","url":null,"abstract":"<p><strong>Background: </strong>Amrubicin is an important chemotherapeutic agent for small cell lung cancer; however, severe neutropenia is a major dose-limiting toxicity. Exposure to its active metabolite, amrubicinol, has been associated with neutropenia severity, suggesting potential utility for exposure-informed risk stratification. Given the lack of a clearly defined therapeutic window for cytotoxic agents, alternative strategies to mitigate toxicity are needed.</p><p><strong>Methods: </strong>A previously published population pharmacokinetic-pharmacodynamic (PK-PD) model of amrubicin was simplified to enhance its practical applicability by removing the enterohepatic circulation component and associated genetic covariate. Model performance was evaluated using prediction-corrected visual predictive checks and nonparametric bootstrapping. A prototype interactive application was developed using R Shiny and RsNLME to enable Bayesian estimation and visualization of individual PK and neutrophil profiles based on sparse first-cycle data.</p><p><strong>Results: </strong>The simplified model adequately described the plasma concentration-time profiles of amrubicin and amrubicinol and the time course of neutrophil counts. Internal validation demonstrated consistency between observed and simulated data. The application enabled visualization of predicted neutrophil trajectories and associated uncertainty, facilitating exposure-informed assessment of neutropenia risk with visualization of predictive uncertainty.</p><p><strong>Conclusion: </strong>We developed a simplified PK-PD framework and implemented it in a prototype application to support risk stratification of neutropenia during amrubicin treatment. The framework does not provide dose recommendations but may support identification of patients who could benefit from prophylactic supportive care, such as pegylated G-CSF. Prospective studies are ongoing to evaluate its clinical utility.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13415490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drug repurposing as a promising therapeutic strategy against renal cell carcinoma.","authors":"Ali Nakhaei, Atefeh Taghavi, Mahdieh Aliyari, Amir R Afshari, Elaheh Gheybi, Mohammad Jalili-Nik","doi":"10.1007/s00280-026-04923-8","DOIUrl":"https://doi.org/10.1007/s00280-026-04923-8","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is a highly vascularized and metastatic malignancy of the kidney. The 5-year overall survival rate of RCC patients remains poor despite the development of therapeutic modalities. Therefore, identifying novel approaches to increase the sensitivity of RCC cells to drugs could help prolong patient survival. Recently, Drug repurposing, which leverages the established safety profiles and pharmacological properties of existing medications, has emerged as a promising alternative to traditional drug development. This approach can accelerate the translation of new therapies into clinical practice and is often associated with lower attrition rates in clinical trials. Recent evidence supports the therapeutic potential of various repurposed drugs against RCC. This review article summarizes and shows the effectiveness and potential of repurposed drugs including metabolic and cardiovascular modulators (metformin, simvastatin), antimicrobial and antiparasitic agents (artesunate, ivermectin, ketoconazole, chloroquine, hydroxychloroquine, niclosamide, doxycycline, pentamidine), mTOR inhibitors (temsirolimus, everolimus, rapamycin), anti-inflammatory and analgesic agents (aspirin, celecoxib), and agents with other mechanisms of action (acetazolamide, disulfiram). These agents exert their anticancer effects against RCC by modulating multiple signaling pathways, including PI3K/AKT/mTOR, AMPK, JAK2/STAT3, ERK1/2, Wnt/β-catenin, and RhoA/ROCK, as well as by inducing autophagy inhibition, ferroptosis, oxidative stress, and mitochondrial dysfunction, highlighting their utility in RCC therapy and emphasizing their clinical relevance.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Red blood cell partitioning and the interpretation of palbociclib plasma concentrations - a letter to the editor.","authors":"Julie Sowa, Sophia Chabane, Fanny Bret, Samuel Huguet, Manon Launay","doi":"10.1007/s00280-026-04928-3","DOIUrl":"10.1007/s00280-026-04928-3","url":null,"abstract":"","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zolbetuximab-induced gastric mucosal injury and hypoalbuminemia: a mechanism-informed clinical analysis.","authors":"Yoshitomo Yanagimoto, Kazuyoshi Yamamoto, Kei Yamamoto, Yasunori Masuike, Yuki Ushimaru, Takeshi Omori, Daisuke Sakai, Toshihiro Kudo, Norihiro Matsuura, Takahito Sugase, Takashi Kanemura, Ryota Mori, Masahiko Kubo, Yasunari Fukuda, Masatoshi Kitakaze, Hisateru Komatsu, Masaaki Miyo, Toshinori Sueda, Junichi Nishimura, Yoshinori Kagawa, Kunihito Goto, Shogo Kobayashi, Hiroshi Miyata","doi":"10.1007/s00280-026-04927-4","DOIUrl":"https://doi.org/10.1007/s00280-026-04927-4","url":null,"abstract":"<p><strong>Purpose: </strong>Zolbetuximab plus chemotherapy is standard first-line therapy for HER2-negative, CLDN18.2-positive advanced gastric or gastroesophageal junction cancer (GC/GEJC), but the incidence, course, and clinical correlations of zolbetuximab-related gastric mucosal injury and hypoalbuminemia remain unclear. We thus evaluated these relationships and the clinical course in real-world practice.</p><p><strong>Methods: </strong>We retrospectively analyzed 38 patients with HER2-negative, CLDN18.2-positive, advanced GC/GEJC treated with zolbetuximab plus chemotherapy at a single center. Associations between endoscopic findings and albumin changes from baseline were analyzed.</p><p><strong>Results: </strong>Median albumin decreased from 3.7 to 2.6 g/dL. The median albumin decline was greater in patients without gastrectomy (- 1.0 g/dL) or with partial gastrectomy (- 1.1 g/dL) than in those with total gastrectomy (- 0.3 g/dL; P = 0.009 and 0.007). Albumin levels fell rapidly at weeks 1-3 and recovered toward baseline by weeks 19-27. Upper gastrointestinal endoscopies were performed in patients with a remaining stomach, showing peak abnormalities within 7-12 weeks; no cases with grade ≥ 2 gastric mucosal injury were observed after week 25. White exudate was associated with albumin decline (- 0.9 vs. -0.4 g/dL, P = 0.023).</p><p><strong>Conclusions: </strong>The presence of white exudate demonstrated a significant association with a marked decrease in serum albumin levels. The risk of hypoalbuminemia appeared to be lower in patients after total gastrectomy. Serum albumin levels decreased after treatment initiation and subsequently showed a tendency to recover over time. Gastric mucosal abnormalities were most frequently observed during the early phase of treatment and were less common in examinations performed after week 25.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: The CetuxIMAX study: a population pharmacokinetic approach to modelling the pharmacokinetics and pharmacodynamics relationships of Cetuximab in patients with head and neck cancer.","authors":"Clémence Marin, Anthéa Deschamps, Quentin Gerbault, Clémence Toullec, Florian Clatot, Maureen Bernadach, Jérôme Fayette, Amaury Daste, Philippe Ceruse, Mickael Burgy, Cédric Champetier, Cyril Abdeddaim, Esma Saada-Bouzid, Xavier Tchiknavorian, Sylvie Zanetta, Pascal Auquier, Joseph Ciccolini, Sébastien Salas","doi":"10.1007/s00280-026-04917-6","DOIUrl":"https://doi.org/10.1007/s00280-026-04917-6","url":null,"abstract":"","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design characteristics of mass balance studies conducted for protein kinase inhibitors.","authors":"Benthe Riechelman, Ramon Bolks, Thijs H Oude Munnink, Jesse J Swen, Frank G A Jansman, Frank Klont","doi":"10.1007/s00280-026-04926-5","DOIUrl":"10.1007/s00280-026-04926-5","url":null,"abstract":"<p><strong>Purpose: </strong>Protein kinase inhibitor (PKI) therapy increasingly relies on personalized approaches such as therapeutic drug monitoring and pharmacogenetic testing. Understanding PKI metabolism is essential for these methods to be effective, notably for determining the substance to be quantified and the enzyme for which the genotypic metabolizer status needs to be predicted. For most drugs, however, human in vivo metabolite profiles are derived from the mass balance studies conducted by drug developers, typically in small and homogeneous populations.</p><p><strong>Methods: </strong>We studied mass balance study characteristics for PKIs, assessing number of participants, sex, and health state, as well as dosing regimen, study location, study duration, and consideration of genetic variation in metabolic enzymes and transporters. Data were primarily extracted from European Public Assessment Reports, supplemented with information from the Drugs@FDA database, ClinicalTrials.gov, and peer-reviewed mass balance study publications.</p><p><strong>Results: </strong>Mass balance studies were conducted for 68 out of the 69 PKIs listed as \"authorized\" human drugs in the European Medicines Agency database on July 7, 2025 (updated April 18, 2026; +3 PKIs). The studies included 2-12 participants (median = 6), with 90% enrolling only healthy volunteers, 88% enrolling only males, 97% administering a single dose, and four studies mentioning consideration of genetic variation in metabolic enzymes during participant inclusion.</p><p><strong>Conclusion: </strong>PKI mass balance studies exhibit similar, rather homogeneous design characteristics, potentially limiting the generalizability of their insights into drug metabolism across diverse patient populations. Still, most align with recent FDA guidelines on mass balance studies, despite being issued after study conduct.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"96 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13364880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}