Cancer metastasis reviews最新文献_第5页

The Hippo signaling pathway in pediatric brain tumors: molecular mechanisms and therapeutic opportunities. 儿童脑肿瘤中的Hippo信号通路：分子机制和治疗机会。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-06-13 DOI: 10.1007/s10555-026-10349-8

Maria A Papanikolaou, Antonios N Gargalionis, Christos Adamopoulos, Christina Piperi

{"title":"The Hippo signaling pathway in pediatric brain tumors: molecular mechanisms and therapeutic opportunities.","authors":"Maria A Papanikolaou, Antonios N Gargalionis, Christos Adamopoulos, Christina Piperi","doi":"10.1007/s10555-026-10349-8","DOIUrl":"10.1007/s10555-026-10349-8","url":null,"abstract":"Pediatric brain tumors are the second most prevalent malignancy in children with therapeutic options remaining challenging due to vulnerability of the developing brain and the significant side effects of current treatment with targeted therapies offering a promising alternative strategy. The Hippo signaling pathway has emerged as a promising molecular approach since it effectively integrates biochemical and mechanical cues to regulate cell growth and survival, tissue integrity and stem cell behaviour through interaction with major signalling pathways such as Wnt-β-catenin, TGF-β/SMAD, PI3K/Akt/mTOR, GPCR, Notch, Hedgehog and MAPK/ERK. Dysregulation of Hippo signaling has been associated with a broad range of human diseases, including cardiovascular disease, skeletal and neurodegenerative disorders, as well as multiple pediatric malignancies. Activation of the transcriptional co-activators YAP/TAZ-TEAD has proved essential for tumor growth and progression of high-grade pediatric tumors harbouring RTK or histone H3 mutations. Recent data show that YAP activation can distinguish glioblastomas from low-grade tumors in the context of MAPK and PI3K activation while YAP suppression inhibits cell proliferation and tumor growth in vivo. Herein, we describe the molecular mechanisms underlying Hippo pathway dysregulation in pediatric gliomas and propose potential therapeutic strategies for effective targeting in different subsets of pediatric brain tumors.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13264582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148255492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antibody-drug conjugates in breast cancer brain and leptomeningeal metastases: mechanistic insights and therapeutic progress. 抗体-药物偶联物在乳腺癌脑和脑膜转移中的作用：机制见解和治疗进展。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-06-09 DOI: 10.1007/s10555-026-10346-x

Hanqi Zhang, Yaqing Qin, Hanzhi Chu, Yidan Fan, Jiayi Tang, Wei Deng, Xinhao Zheng, Ze Yuan, Yutian Zou, Yanan Kong

{"title":"Antibody-drug conjugates in breast cancer brain and leptomeningeal metastases: mechanistic insights and therapeutic progress.","authors":"Hanqi Zhang, Yaqing Qin, Hanzhi Chu, Yidan Fan, Jiayi Tang, Wei Deng, Xinhao Zheng, Ze Yuan, Yutian Zou, Yanan Kong","doi":"10.1007/s10555-026-10346-x","DOIUrl":"10.1007/s10555-026-10346-x","url":null,"abstract":"Antibody-drug conjugates (ADCs) are targeted therapies that employ monoclonal antibodies to deliver potent cytotoxic agents to cancer cells. The treatment of breast cancer with brain and leptomeningeal metastases has long been limited by the assumption that the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) restrict the penetration of large molecules into the central nervous system (CNS). However, recent evidence from several trails (DESTINY-Breast12, DEBBRAH, TUXEDO-3, etc.) challenges this paradigm. In these studies, trastuzumab deruxtecan, a HER2-targeted ADC, demonstrated notable intracranial responses in patients with active CNS disease, suggesting that CNS barriers are dynamically remodeled within the tumor microenvironment to permit drug access. These findings have renewed interest in understanding how macromolecular ADCs penetrate the CNS and exert anti-tumor effects. By integrating emerging clinical evidence with key pharmacological determinants and tumor-associated microenvironmental changes, this review delineates the mechanisms governing ADC activity in brain metastases and identifies critical factors underlying intracranial response. Collectively, these insights provide a mechanistic framework to guide the rational design of next-generation ADCs and optimize therapeutic strategies for patients with advanced CNS involvement.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148207554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prognostic, diagnostic and therapeutic value of the cancer tubulin code. 肿瘤微管蛋白代码的预后、诊断和治疗价值。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-06-08 DOI: 10.1007/s10555-026-10347-w

Carolina Vilela, Daniela Gomes-Andrade, Sónia Silva, Helder Maiato

{"title":"Prognostic, diagnostic and therapeutic value of the cancer tubulin code.","authors":"Carolina Vilela, Daniela Gomes-Andrade, Sónia Silva, Helder Maiato","doi":"10.1007/s10555-026-10347-w","DOIUrl":"10.1007/s10555-026-10347-w","url":null,"abstract":"Microtubules are essential cytoskeleton polymers composed of α/β-tubulin heterodimers that play a central role in the regulation of various cellular processes, including cell division, cell shape, cell polarity, motility and intracellular trafficking. The expression of different tubulin genes results in a variety of isotypes that, combined with post-translational modifications (PTMs), define a \"tubulin code\" that generates microtubule diversity. Growing evidence has shown promising links between tubulin isotypes and PTMs with several cancer properties, leading to the emergence of the concept of a \"cancer tubulin code\". In this review, we focus on dissecting the impact of tubulin acetylation, detyrosination and polyglutamylation on microtubule properties and functions, and how these PTMs, together with specific tubulin isotypes, affect cancer cell division, invasion and metastasis. Because conventional chemotherapy with microtubule-targeting drugs often leads to resistance and accounts for a high mortality rate among cancer patients, we discuss possible directions that explore the potential of the cancer tubulin code and respective microtubule diversity in improving drug response, while overcoming resistance. Lastly, we address the therapeutic value of small-molecule inhibitors of tubulin-modifying enzymes in cancer treatment. Overall, this review showcases the potential of exploring the cancer tubulin code to open new avenues in diagnostic, prognostic and therapeutic applications for precision oncology.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148202016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanobiology of solid tumor vasculature: implications for tumor progression. 实体肿瘤血管系统的机械生物学：对肿瘤进展的影响。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-06-02 DOI: 10.1007/s10555-026-10345-y

Raghu Vamsi Kondapaneni, Sarah Libring, Sid Dsa, Cynthia A Reinhart-King

{"title":"Mechanobiology of solid tumor vasculature: implications for tumor progression.","authors":"Raghu Vamsi Kondapaneni, Sarah Libring, Sid Dsa, Cynthia A Reinhart-King","doi":"10.1007/s10555-026-10345-y","DOIUrl":"10.1007/s10555-026-10345-y","url":null,"abstract":"Under normal physiological conditions, the vasculature forms a selective barrier that regulates molecular and cellular transport, largely maintained through vascular endothelial cadherin (VE-cadherin)-mediated junctions formed by endothelial cells. However, in the tumor microenvironment (TME) of solid tumors, the vasculature is disrupted due to biochemical and mechanical signals. In this review, we discuss the latest studies that describe how various mechanical forces in the TME, including matrix stiffening, fluid shear stress, compressive forces, and interstitial fluid pressures, influence the mechanical phenotype of endothelial cells, including vascular integrity and angiogenesis. Additionally, we emphasize how these forces activate key mechanotransduction pathways, notably actin cytoskeletal reorganization through RhoA activation, downstream of FAK/Src and YAP/TAZ signaling, and remodel the tumor vasculature by increasing vascular permeability and neovascularization. Overall, we summarize the pivotal role of mechanotransduction in vascular barrier disruption and angiogenesis, providing new avenues for therapeutic strategies targeting tumor vasculature.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148152852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antibody-drug conjugates in cancer therapy: do we need biomarkers? A comprehensive review. 癌症治疗中的抗体-药物结合物：我们需要生物标志物吗？全面审查。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-26 DOI: 10.1007/s10555-026-10344-z

Lei Lei, Ya-Bing Zheng, Shou-Ching Tang

{"title":"Antibody-drug conjugates in cancer therapy: do we need biomarkers? A comprehensive review.","authors":"Lei Lei, Ya-Bing Zheng, Shou-Ching Tang","doi":"10.1007/s10555-026-10344-z","DOIUrl":"10.1007/s10555-026-10344-z","url":null,"abstract":"Antibody-drug conjugates (ADCs) have revolutionized targeted cancer therapy, yet a fundamental clinical contradiction remains: while some ADCs require strict companion diagnostic testing, others demonstrate robust efficacy in biomarker-negative tumors. This review investigates the underlying mechanisms of this discrepancy, proposing that ADC linker cleavability is the primary determinant of both biomarker dependence and systemic toxicity profiles. By analyzing data from 40 clinical trials encompassing 7879 patients, we observed a distinct dichotomy based on linker design. ADCs utilizing noncleavable linkers function in a strictly biomarker-dependent manner, correlating with a targeted safety profile (34% severe toxicity rate) but relying entirely on antigen-mediated internalization. Conversely, ADCs with cleavable linkers facilitate premature payload release in the systemic circulation and tumor microenvironment. This enables a potent, biomarker-independent bystander effect-achieving a 29.7% tumor response rate even without target expression-but at the cost of significantly increased off-target systemic toxicities (47% severe toxicity rate). Recognizing this inherent trade-off between antitumor potency and safety, we further explore the development of next-generation, conditionally cleavable linkers. These advanced platforms are engineered for selective activation exclusively within the tumor microenvironment. We conclude that transitioning towards conditionally released linkers is essential to balance efficacy and systemic toxicity, optimizing the therapeutic index and fully realizing the potential of the \"magic bullet.\"","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13201299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148020456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Humoral immunity in pancreatic cancer: B-cell heterogeneity, regulatory networks, and therapeutic opportunities. 胰腺癌的体液免疫：b细胞异质性、调节网络和治疗机会。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-22 DOI: 10.1007/s10555-026-10342-1

Joshua Kalapala, Andrew M Turunen, Kyle A Burton, Daniel R Principe

{"title":"Humoral immunity in pancreatic cancer: B-cell heterogeneity, regulatory networks, and therapeutic opportunities.","authors":"Joshua Kalapala, Andrew M Turunen, Kyle A Burton, Daniel R Principe","doi":"10.1007/s10555-026-10342-1","DOIUrl":"10.1007/s10555-026-10342-1","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is characterized by a profoundly immunosuppressive tumor microenvironment and remains largely refractory to immunotherapy. Though T-cell-directed strategies have dominated the immunotherapy landscape, there is emerging data to suggest that B-cells and humoral immune products also have a critical role in PDAC pathobiology. However, therapies broadly targeting B-cells have failed in clinical trial, raising important questions regarding the complex, often contradictory roles for humoral immunity in PDAC development. Studies exploring humoral immunity in PDAC generally favor an immunosuppressive role. This occurs through several mechanisms including the accumulation of suppressive regulatory B-cells, paradoxical complement activation favoring immunosuppression and broad class switching skewed toward inhibitory immunoglobulin subclasses. However, in select contexts, secreted antibodies neutralize tumor antigens, facilitate antibody-dependent cytotoxicity, and coordinate anti-tumor responses within tertiary lymphoid structures. Here, we discuss the often-contradictory roles of humoral immunity in PDAC pathobiology, highlighting mechanisms contributing to T-cell exclusion, chemoresistance, and metastasis. We further discuss the role of humoral immunity in bolstering anti-tumor immune responses and need for biomarker guidance in future trials. These opposing roles in tumor development may explain the clinical failure of broad B-cell depletion strategies and offer opportunities for selective targeting of immunosuppressive populations while preserving anti-tumor humoral responses.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147990782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Astrocyte-associated immunosuppressive programs in brain tumors: a STAT3-centered perspective. 星形胶质细胞相关的免疫抑制程序在脑肿瘤：以stat3为中心的观点。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-13 DOI: 10.1007/s10555-026-10343-0

Wei Sun, Jia-Qi Zhang, Wei-Lin Jin

{"title":"Astrocyte-associated immunosuppressive programs in brain tumors: a STAT3-centered perspective.","authors":"Wei Sun, Jia-Qi Zhang, Wei-Lin Jin","doi":"10.1007/s10555-026-10343-0","DOIUrl":"10.1007/s10555-026-10343-0","url":null,"abstract":"Astrocytes are increasingly recognized as important contributors to the immunosuppressive tumor microenvironment in glioblastoma and brain metastases. Rather than acting in isolation, tumor-associated astrocytes interact with tumor cells, myeloid populations, and vascular components to shape local immune dysfunction. Here, we propose modular immunosuppressive hubs (MISH) as an astrocyte-centered conceptual framework to describe how distinct suppressive programs may be organized within established tumor niches, with particular emphasis on STAT3-centered signaling. This review systematically deconstructs the composition, spatial regulation, and signaling output of these modules, highlighting how they mediate critical cell-cell communication within the TME. We further emphasize emerging pharmacological strategies aimed at dismantling MISH by targeting these specific signaling pathways, thereby reprogramming TAAs from immunosuppressive barriers into potential allies for immunotherapy. Targeting MISH signaling networks represents a promising avenue to overcome resistance to current immunotherapies and improve outcomes for patients with brain tumors.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147937070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of iron in driving sex-biased differences in cancer. 铁元素在癌症性别差异中的作用。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-12 DOI: 10.1007/s10555-026-10340-3

Aurosman Pappus Sahu, James R Connor

引用次数: 0

Risk of cancer incidence and mortality in patients with chronic pain: A systematic review and meta-analysis. 慢性疼痛患者癌症发病率和死亡率的风险：一项系统回顾和荟萃分析。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-11 DOI: 10.1007/s10555-026-10341-2

Chun Hei Lai, Natalia Hefteh, Sophie Kingsford, Adam La Caze, Mahdi Sheikh, Shakti Shrestha, Marie-Odile Parat

{"title":"Risk of cancer incidence and mortality in patients with chronic pain: A systematic review and meta-analysis.","authors":"Chun Hei Lai, Natalia Hefteh, Sophie Kingsford, Adam La Caze, Mahdi Sheikh, Shakti Shrestha, Marie-Odile Parat","doi":"10.1007/s10555-026-10341-2","DOIUrl":"10.1007/s10555-026-10341-2","url":null,"abstract":"Evidence from experimental studies suggests that pain may influence cancer development. We conducted a systematic review (registration osf.io/ms437) of the epidemiological studies assessing whether chronic pain, with minimal or non-inflammatory features, increases the risk of cancer incidence or mortality. The search used Scopus and Web of Science up to 11/03/2025. Quality assessment used the Newcastle-Ottawa Scale. Study characteristics and outcomes were analysed using narrative synthesis, with random-effects meta-analysis and meta-regression conducted where appropriate. A total of 23 studies (12 prospective, 11 retrospective) met the inclusion criteria, of which six were rated as high quality. The outcome data synthesis indicates a small increase in cancer mortality rate ratios, and a potential increase in a subset of organs. A total of three body site-specific analyses suggest that chronic pain may be associated with higher incidence for breast (SIR 2.12-4.8) and prostate (SIR 1.49-5.59) cancers, and with increased mortality for lung cancer (MRR 3.09, 95% CI 1.45-6.62). Ten studies were included for meta-analysis, including four studies rated as high quality. Meta-analysis of hazard ratios showed no association between cancer-related mortality and pain (HR 1.00, 95% CI 0.97-1.04), with consistent estimates across pain subtypes in meta-regression. Our review and meta-analysis do not support an overall association between chronic pain and increased risk of cancer mortality or incidence and highlight multiple methodological and conceptual obstacles to exploring this relationship, including reverse causation and confounding factors such as pain and opioid use association. High-quality studies that rigorously address reverse causation and confounding are warranted.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13160951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circadian clock control of breast cancer hallmarks: molecular mechanisms and therapeutic implications. 乳腺癌特征的生物钟控制：分子机制和治疗意义。

IF 8.7

Cancer metastasis reviews Pub Date : 2026-05-08 DOI: 10.1007/s10555-026-10337-y

Luis Ricardo Hernández-Barrientos, Lorena Aguilar-Arnal

{"title":"Circadian clock control of breast cancer hallmarks: molecular mechanisms and therapeutic implications.","authors":"Luis Ricardo Hernández-Barrientos, Lorena Aguilar-Arnal","doi":"10.1007/s10555-026-10337-y","DOIUrl":"10.1007/s10555-026-10337-y","url":null,"abstract":"Circadian rhythms regulate physiological functions and critical biological processes in almost all living forms. The circadian system enables organisms to anticipate and adapt to environmental fluctuations, thereby optimizing physiological responses. Proper synchronization between the master pacemaker in the brain and peripheral clocks throughout the organism is essential for maintaining homeostasis and promoting health. Conversely, circadian misalignment is increasingly recognized as a contributing factor in the pathogenesis of various diseases. Emerging evidence implicates circadian disruption as a driver of carcinogenesis. Indeed, epidemiological studies have associated night-shift work and chronic jet lag with an increased risk of cancer. At the molecular level, the biological clock comprises a complex network of transcriptional-translational feedback loops that generates approximately 24-h cycles in gene expression across all tissues. Notably, many clock-regulated genes participate in key pathways relevant to tumorigenesis, including cell cycle regulation, DNA damage repair, angiogenesis, and metabolism. Moreover, the circadian clock represents a promising therapeutic target in oncology. Numerous clinical trials have demonstrated that chronomodulation of chemotherapeutic agents can enhance treatment efficacy while mitigating adverse effects, thereby improving the quality of life for cancer patients. Hence, advancing our understanding of the molecular interplay between circadian regulation and cancer development may elucidate the role of circadian rhythms in tumorigenesis, facilitate the identification of novel prognostic markers and therapeutic targets, and ultimately improve outcomes in breast cancer patients.","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0