Biochimica et biophysica acta. Reviews on cancer最新文献

{"title":"Targeting palmitoylation: A novel frontier in cancer biology and immunotherapy","authors":"Ye Yang ,&nbsp;Enqi Zhang ,&nbsp;Xuanli Mao ,&nbsp;Guohong Liu ,&nbsp;Yunbao Pan","doi":"10.1016/j.bbcan.2025.189509","DOIUrl":"10.1016/j.bbcan.2025.189509","url":null,"abstract":"<div><div>Protein palmitoylation, a dynamic post-translational modification involving the reversible attachment of palmitic acid to cysteine residues, has emerged as a pivotal regulator of tumor biology. This review synthesizes the latest insights into palmitoylation's contributions to cancer, emphasizing its roles in metabolic reprogramming, oncogenic signaling, immune modulation, and therapeutic responsiveness. The ZDHHC family of palmitoyltransferases, in concert with depalmitoylases, coordinates intricate regulatory networks that govern protein localization, stability, and interactions essential for tumor proliferation, invasion, and immune evasion. Driven by dysregulated lipid metabolism, aberrant palmitoylation modulates key pathways such as AKT-mTOR and Wnt/β-catenin, while also stabilizing immune checkpoints like PD-L1 and TIM-3 to sculpt an immunosuppressive tumor microenvironment. Advances in multi-omics integration and detection technologies, including high-resolution mass spectrometry and imaging modalities, have deepened our mechanistic understanding of these processes. Preclinical evidence underscores the promise of small-molecule inhibitors like 2-bromopalmitate and TVB-3166, which disrupt palmitoylation to inhibit tumor growth and potentiate immunotherapy. Nonetheless, hurdles in selectivity, toxicity, and resistance demand further optimization for clinical translation. Future research should focus on unraveling palmitoylation's interplay with immune dynamics and advancing biomarker-guided, personalized therapies to elevate cancer outcomes.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189509"},"PeriodicalIF":9.7,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of N7-methylguanosine in gastrointestinal tumors: Molecular mechanisms and therapeutic targets","authors":"Jingyuan Li ,&nbsp;Yangxian Xu ,&nbsp;Lisheng Wang ,&nbsp;Guang Ji ,&nbsp;Yanqi Dang","doi":"10.1016/j.bbcan.2025.189511","DOIUrl":"10.1016/j.bbcan.2025.189511","url":null,"abstract":"<div><div>N7-methylguanosine (m⁷G), a widely prevalent post-transcriptional modification of RNA, exhibits significant regulatory changes across diverse RNA molecules, thereby affecting essential RNA metabolic processes. Aberrant levels of m⁷G modification have been increasingly linked to a broad spectrum of diseases, influencing oncogene expression and contributing to pathological mechanisms. The relationship between m⁷G modification and the initiation and progression of various tumor types is intricate and multifaceted. Moreover, current evidence suggests that m⁷G may play a role in regulating processes within immune cells, thereby implicating it in immune-related pathologies, including cancer. The targeted manipulation of m⁷G and its regulatory pathways holds significant promise for advancements in immunotherapy, potentially enhancing the modulation of immune responses and overcoming drug resistance. In gastrointestinal (GI) tumors, where immune evasion and therapy resistance are prominent challenges, understanding the role of m⁷G becomes particularly critical. This comprehensive review systematically examines the current body of research on m⁷G within the context of GI tumors, offering a detailed analysis of its dysregulated patterns in both malignant and immune cells. The molecular mechanisms underlying tumorigenesis mediated by m⁷G epigenetics are summarized, and therapeutic strategies aiming at targeting m⁷G modifications are discussed. Additionally, this review provides insights into potential future directions in the fields of diagnosis and prognosis.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189511"},"PeriodicalIF":9.7,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated mitochondrial dynamics in cancer: Unlocking new strategies to combat drug resistance","authors":"Teresa Rossi ,&nbsp;Roberta Torcasio ,&nbsp;Ludovica Ganino ,&nbsp;Ilenia Valentino ,&nbsp;Christian Boni ,&nbsp;Massimo Gentile ,&nbsp;Antonino Neri ,&nbsp;Nicola Amodio ,&nbsp;Mariaelena Pistoni","doi":"10.1016/j.bbcan.2025.189510","DOIUrl":"10.1016/j.bbcan.2025.189510","url":null,"abstract":"<div><div>Mitochondria continuously alternate between fragmented and fused states, a process known as mitochondrial dynamics, which plays a pivotal role in essential cellular functions, including metabolism, apoptosis, reactive oxygen species production, and signal transduction. Disruptions in this dynamic equilibrium, frequently observed in aggressive cancers, can promote malignant transformation and tumor progression. A growing body of evidence indicates that dysregulated mitochondrial dynamics contribute to resistance against both conventional and targeted anticancer therapies. In this review, we explore the regulatory mechanisms governing mitochondrial dynamics, with a focus on the genetic and epigenetic modulation of key drivers such as DRP1, MFN1/2 and OPA1. We also discuss how altered mitochondrial dynamics converge into diverse mechanisms of drug resistance in cancer. Overall, these insights underscore aberrant mitochondrial dynamics as a potential biomarker of therapeutic resistance, and position mitochondrial dynamics–related GTPases, particularly DRP1 and Mitofusins, as exploitable targets for novel treatments in advanced solid and hematologic malignancies.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189510"},"PeriodicalIF":9.7,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YY1: Master regulator of metabolic reprogramming in cancer","authors":"Rimsha Akram ,&nbsp;Rendy Hosea ,&nbsp;Fuqiang Zhao ,&nbsp;Andrzej Górecki ,&nbsp;Małgorzata Figiel ,&nbsp;Shourong Wu ,&nbsp;Vivi Kasim","doi":"10.1016/j.bbcan.2025.189505","DOIUrl":"10.1016/j.bbcan.2025.189505","url":null,"abstract":"<div><div>Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to fulfill increased bioenergetic and biosynthetic demands for survival and proliferation. These adaptations arise directly from oncogenic mutations or indirectly via adaptive responses to nutrient scarcity. In addition to supporting survival and biomass production, these metabolic shifts are closely associated with changes in gene expression, cellular differentiation, and the tumor microenvironment, thereby contributing to tumorigenesis and progression. Importantly, the recognition of metabolic dysregulation as a hallmark of malignancy revealed novel avenues for therapeutic intervention, as disrupting these pathways may impair energy generation and biosynthetic processes essential for tumor proliferation. In this review, we integrate data indicating that the transcription factor Yin yang 1 (YY1) is a central regulator of oncogenic metabolic reprogramming. Yin yang 2 (YY2) is a paralog of YY1 and performs distinct role in metabolism and redox regulation. Mechanistically, YY1 enhances aerobic glycolysis by diverting glycolytic flux toward lactate production. Furthermore, it modulates hepatic lipid homeostasis via direct transcriptional control of lipogenic enzymes and crosstalk with nutrient-sensing signaling cascades. Additionally, YY1 rewires amino acid metabolism to fuel tumorigenesis by supplying macromolecules and enabling epigenetic remodeling. Collectively, these findings highlight the equilibrium between YY1 and its paralog YY2 in sustaining redox homeostasis and tumor progression while positioning YY1 as a metabolic checkpoint that dynamically regulates these processes. Understanding these pathways will support development of YY1-directed inhibitors and combinatorial therapies to modulate metabolic reprogramming in cancer.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189505"},"PeriodicalIF":9.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145703261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel insights in the diagnosis and treatment of non-small cell lung cancer: Post-translational modification of proteins","authors":"Yuting Sun ,&nbsp;Weijia Kong ,&nbsp;Xiaoyu Zhu ,&nbsp;Xuelei Chu,&nbsp;Xinmiao Wang,&nbsp;Guanghui Zhu,&nbsp;Xue He,&nbsp;Jie Li","doi":"10.1016/j.bbcan.2025.189507","DOIUrl":"10.1016/j.bbcan.2025.189507","url":null,"abstract":"<div><div>Non-small cell lung cancer (NSCLC) is associated with a high incidence and mortality rate, imposing a significant economic burden worldwide. The development of standardized diagnostic and targeted therapeutic approaches is essential. Protein post-translational modifications (PTMs) play a critical role in regulating biological functions during both physiological and pathological states, as they reversibly and dynamically adjust protein activity in response to changes in internal and external conditions. Various types of PTMs, including ubiquitination, phosphorylation, glycosylation, Small Ubiquitin-like Modifier (SUMO)ylation, acetylation, palmitoylation, and lactylation, have been shown to correlate significantly with the onset, progression, metastasis, treatment, and drug resistance of NSCLC. These modifications are involved in the initiation and progression of NSCLC and are linked to patient survival outcomes. Additionally, different therapeutic modalities, such as chemotherapy, radiation therapy, and immunotherapy, can influence treatment efficacy by altering PTMs. However, the challenge of drug resistance significantly undermines therapeutic effectiveness and patient outcomes. This review emphasizes the importance of PTMs in drug resistance and highlights their potential to inform more precise treatment strategies for NSCLC, ultimately contributing to a reduction in disability-adjusted life years, which is of considerable practical importance.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189507"},"PeriodicalIF":9.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145703231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting MAO offers a novel immunotherapeutic strategy for prostate cancer by modulating the “tumor-stroma-immune” interaction network","authors":"Yaohua Hu ,&nbsp;Zhite Zhao ,&nbsp;Yifan Ma ,&nbsp;Xinglin He ,&nbsp;Changhong Shi","doi":"10.1016/j.bbcan.2025.189506","DOIUrl":"10.1016/j.bbcan.2025.189506","url":null,"abstract":"<div><div>Prostate cancer (PCa) is a highly prevalent malignant tumor in men, often progressing to castration-resistant prostate cancer (CRPC) and metastasis or neuroendocrine differentiation, leading to treatment failure. Its high heterogeneity and immunosuppressive tumor microenvironment (TME) are major challenges in treatment, characterized by low immunogenicity and a complex “tumor-stroma-immune” interaction network. Monoamine oxidase (MAO), a mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines via MAOA and MAOB isoforms. Studies have shown that MAOA and MAOB exhibit differential expression patterns in cancer cells, stromal cells, and immune cells, and may function cooperatively to promote PCa progression. This review clarifies how MAO influence PCa progression by regulating the “tumor-stroma-immune” interaction network, elucidate the impact of MAO on CD8⁺ T-cell infiltration and tumor-associated macrophages (TAMs) polarization in the TME, and proposes that precision targeting of MAO offers a stage- and cell-type-spanning strategy to surmount immunotherapy resistance in PCa. It provides a theoretical basis for developing intervention strategies based on MAO inhibitor to achieve effective immunotherapy for PCa.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189506"},"PeriodicalIF":9.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Same mutation, different fates: The Yin-Yang of BRAF-driven therapeutic responses in melanoma and colorectal cancer","authors":"Carme Solé-Blanch ,&nbsp;Sofia España ,&nbsp;Alba de la Puente-Noel ,&nbsp;Oskar Marin-Béjar ,&nbsp;José Luis Manzano ,&nbsp;Anna Martinez-Cardús","doi":"10.1016/j.bbcan.2025.189503","DOIUrl":"10.1016/j.bbcan.2025.189503","url":null,"abstract":"<div><div>BRAF mutations are key oncogenic drivers across multiple cancers, yet their therapeutic exploitation varies markedly by tumor type. In melanoma, the combination of BRAF and MEK inhibitors has revolutionized treatment, yielding unprecedented clinical benefits. However, both intrinsic and acquired resistance mechanisms continue to limit long-term efficacy. In contrast, BRAF-targeted therapies in colorectal cancer (CRC) have shown limited success, even when combined with EGFR inhibitors to counteract compensatory survival pathways. Despite these differences, resistance ultimately emerges in both malignancies, driven by partially overlapping mechanisms that remain incompletely understood in CRC. This review dissects the “yin-yang” of BRAF as a therapeutic vulnerability in these two malignancies, we underscore the critical importance of tumor-specific context in precision oncology. Understanding the divergent responses to BRAF inhibition across cancer types is essential to refine current approaches and guide the development of more effective, personalized treatment strategies.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189503"},"PeriodicalIF":9.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145679505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of in vitro and in vivo cancer models to study the impact of the tumor immune microenvironment on anticancer therapy","authors":"Rajat Gupta ,&nbsp;Raghu Radhakrishnan ,&nbsp;Shama Prasada Kabekkodu ,&nbsp;Sanjiban Chakrabarty","doi":"10.1016/j.bbcan.2025.189504","DOIUrl":"10.1016/j.bbcan.2025.189504","url":null,"abstract":"<div><div>The tumor microenvironment is a dynamic, heterogeneous cellular ecosystem that includes cancer cells, cancer-associated fibroblasts (CAFs), endothelial cells, and immune cells. Immortalized cancer cell lines specific to a particular cancer type have been extensively used to investigate the anticancer effects and functional aspects of novel drugs. However, cancer cell lines do not accurately mimic the complex multicellular nature of organs. Since species-specific differences in mouse models of human cancer impact the interpretation of therapeutic efficacy, efforts have been made to reduce and replace the use of animals in the drug development process. It is now acknowledged that existing tumor models may not adequately simulate the tumor microenvironment. This has led to an increasing need for complex tumor models that can accurately represent the tumor immune microenvironment (TIME). The Organ-on-Chip (OoC) device has features that enable high-throughput screening and repeatable drug testing procedures by accurately simulating the tumor microenvironment (TME). Furthermore, although animal models remain vital for systemic analysis, the interpretation of therapeutic efficacy is often hindered by species-specific differences in immune and physiological responses. This limitation has created a critical conceptual gap in preclinical research. We acknowledge the pressing need for complex tumor models that can accurately simulate the tumor immune microenvironment (TIME).</div><div>The immune system plays two key roles in cancer: fighting tumors and promoting the development of carcinogenesis. Recent advances have been made in understanding how the immune system contributes to cancer progression and the development of immune cell treatments for improved prognosis. In vivo and in vitro models have been created to investigate therapy resistance and the function of the tumor immune microenvironment (TIME) in anticancer therapy. This review provides a critical and balanced evaluation of the various in vitro (organoids, organ-on-chip, bioprinting) and in vivo (PDX, Humanized Mice) models utilized to study the TIME. We move beyond descriptive summaries to offer a functional comparison of these platforms, specifically delineating their utility in overcoming the clinical challenges of therapy resistance mechanisms and translational immunotherapy evaluations. This comparative approach demonstrates how advanced models, such as organ-on-chip (OoC), which enable dynamic control of the microenvironment and integration of multiple organs, can complement and refine the drug development process.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189504"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M6A methylation in tumor immune microenvironment: Multidimensional mechanism and targeted therapy strategies","authors":"Senxu Lu ,&nbsp;Junxiu Liu ,&nbsp;Shixin Chen ,&nbsp;Binghao Li ,&nbsp;Zhaoming Ye","doi":"10.1016/j.bbcan.2025.189489","DOIUrl":"10.1016/j.bbcan.2025.189489","url":null,"abstract":"<div><div>N6-methyladenosine (m⁶A) modification, a dynamic and reversible post-transcriptional RNA alteration, plays a critical role in the precise regulation of gene expression and is fundamentally implicated in the interplay between tumor cells and the immune system. This review focuses on the regulatory mechanisms of m⁶A methylation in tumor immunology. We examine how m⁶A modifications within tumor cells reprogram the tumor immune microenvironment by modulating immune checkpoints, canonical signaling pathways, and cytokine secretion, as well as directly regulating immune-related genes. Crucially, we also dissect how m⁶A modification within immune cells shapes the immune microenvironment. Furthermore, we propose novel therapeutic strategies combining m⁶A targeting with immunotherapy. Collectively, this review provides novel insights into the role of m⁶A methylation in tumor immunology and paves the way for future research directions.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 6","pages":"Article 189489"},"PeriodicalIF":9.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperthermia-induced apoptosis: The role of magnetic nanoparticles in targeted delivery for breast cancer treatment","authors":"Pankaj Garg ,&nbsp;Madhu Krishna ,&nbsp;David Horne ,&nbsp;Ravi Salgia ,&nbsp;Sharad S. Singhal","doi":"10.1016/j.bbcan.2025.189490","DOIUrl":"10.1016/j.bbcan.2025.189490","url":null,"abstract":"<div><div>Magnetochemistry is opening new frontiers in the targeted treatment of breast cancer (BC), offering a precise and innovative way to deliver therapies exactly where they're needed. Beyond drug delivery, magnetic nanoparticles (MNPs) can generate localized heat under alternating magnetic fields, initiating controlled hyperthermia that induces apoptotic cell death in tumor tissues. MNPs, particularly iron-oxide-based magnetite (Fe₃O₄) and maghemite (γ-Fe₂O₃), can be magnetically guided toward tumor sites and subsequently activated under alternating magnetic field (AMFs) (typically 100–500 kHz and 10–40 kA m⁻¹) to generate therapeutic heat through Néel and Brownian relaxation losses. At the tumor, drugs can be released in a controlled manner in response to environmental cues such as pH changes, enzymes, or magnetic stimuli. By harnessing this dual role of MNPs, as targeted carriers and thermal effectors, researchers achieve spatially selective, minimally invasive treatment. Mechanistically, magnetically induced hyperthermia elevates local temperature to 42–46 °C, which triggers reactive oxygen species (ROS) generation, mitochondrial membrane depolarization, and caspase-3/9 activation—hallmarks of apoptosis in BC cells. This integrated approach not only concentrates drugs at the tumor but also sensitizes cancer cells to chemo- and radiotherapy, while minimizing systemic toxicity. Static or dynamic magnetic fields can be used to steer these particles, while their surfaces can be engineered through chemical bonding, physical encapsulation, or adsorption techniques. Moreover, combining magnetic targeting with antibody-based recognition improves specificity and therapeutic impact. While the promise of magnetochemistry in BC treatment is clear, ongoing research is essential to optimize these technologies and bring them fully into clinical practice.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 6","pages":"Article 189490"},"PeriodicalIF":9.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}