Molecular Cancer最新文献

{"title":"Evidence of endothelial anergy and T-cell exclusion in microsatellite stable colorectal liver metastases revealed through human hemi-liver perfusion and spatial transcriptomics.","authors":"Peter Kok-Ting Wan,Ranchu Cheng,David Johnson,Carl Lee,Shihong Wu,Areeb Mian,Ahmet Hazini,Sorayya Moradi,Kate Friesen,Flurin Caviezel,Syed Hussain Abbas,Brannon Nicholls,Hatem Sadik,Adil Lakha,Keaton Jones,Girishkumar Kumaran,Matthew J Bottomley,Rob Jones,Mark Coles,Rachael Bashford-Rogers,Constantin Coussios,Len Seymour,Robert Carlisle,Kerry Fisher,Alex Gordon-Weeks","doi":"10.1186/s12943-026-02732-4","DOIUrl":"https://doi.org/10.1186/s12943-026-02732-4","url":null,"abstract":"BACKGROUNDColorectal liver metastasis (CRLM) is the terminal stage of colorectal cancer and remains largely resistant to immunotherapeutics, yet the underlying immune escape mechanisms remain poorly understood. Through novel observational methods focused on human living and fixed tissue, we profiled the spatial and molecular features of microsatellite stable (MSS) CRLM and the surrounding liver microenvironment.METHODSFirst, we re-purposed normothermic hepatic machine perfusion as a preclinical model of MSS CRLM, enabling delivery of labelled T-cells through physiological vascular routes into living, tumour-bearing human livers. Second, to dissect the liver microenvironment, we spatially map the transcriptomes of MSS CRLM and adjacent liver at single-cell resolution across ~ 1.9 million cells, and perform multiplexed immunofluorescence applying a19-marker panel to a validation cohort.RESULTSWhilst T-cells readily extravasated within the peri-tumoural liver, they failed to extravasate into MSS CRLM. Spatial analyses revealed a progressive shift in endothelial phenotypes across regions: from a non-inflamed state in normal liver, to a highly inflamed, peri-tumoural endothelium, and finally to an anergic, angiogenic endothelial population within CRLM characterised by reduced expression of adhesion molecules required for T-cell extravasation. CD4 T-cells that extravasate in the peri-tumoural liver are TCR-reactive yet exhausted, whereas CD4 T-cells within CRLM show stress responses, impaired cytokine gene expression and reduced TCR reactivity, residing within hypoxic niches. These divergent CD4 phenotypes are associated with distinct fibroblast-myeloid niches across peri-tumoural and tumour regions.CONCLUSIONBased on these observations, MSS CRLM impair T-cell extravasation and simultaneously drive intra-tumoural endothelial anergy, peri-tumoural T-cell exhaustion and an intra-tumoural T-cell stress response. Further mechanistic work is needed to validate these findings and guide the development of novel immunotherapeutics.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"37 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148522055","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":"ADSL drives fumarate mediated scrib-rictor complex formation to promote metastasis dissemination in triple-negative breast cancer.","authors":"Yidan Fan,Xiaofang He,Wei Deng,Jianxiang Sun,Jinkun Qin,Yutian Zou,Xudong Zhu,Xiaoming Xie,Hailin Tang,Ping Yu,Weiyu Bao,Feng Ye","doi":"10.1186/s12943-026-02742-2","DOIUrl":"https://doi.org/10.1186/s12943-026-02742-2","url":null,"abstract":"BACKGROUNDTriple-negative breast cancer (TNBC) is characterized by aggressive metastatic behavior and limited therapeutic options. Although metabolic reprogramming is increasingly recognized as a hallmark of TNBC, the mechanisms by which specific metabolic enzymes and intermediates drive metastasis remain poorly defined.METHODSWe performed untargeted metabolomic profiling on TNBC tumors and matched normal tissues to identify dysregulated metabolic pathways. Functional assays, chemoproteomic succination profiling, molecular interaction analyses, and in vivo cancer metastasis models were used to define the mechanistic and biological consequences of altered metabolism. In vitro experiments validated the effects of N-acetylcysteine (NAC) in TNBC cell lines.RESULTSMetabolomic analyses revealed aberrant activation of the alanine-aspartate-glutamate axis and upregulation of adenylosuccinate lyase (ADSL) in TNBC. ADSL promoted tumor cell proliferation and metastasis by generating fumarate, which accumulated primarily through covalent protein succination. Chemoproteomic profiling identified the cell polarity regulator SCRIB as a critical fumarate target. Fumarate-mediated succination of SCRIB impaired its membrane localization, promoted epithelial-mesenchymal transition, and facilitated aberrant interaction with the mTORC2 component RICTOR, leading to activation of AKT/mTOR signaling. Genetic disruption of SCRIB succination abrogated these effects. Importantly, pharmacological perturbation of fumarate using NAC reduced SCRIB succination and attenuated the malignant phenotypes of TNBC cells in vitro.CONCLUSIONSThese findings identify an ADSL-fumarate-SCRIB signaling axis that links metabolic reprogramming to the loss of cell polarity and activation of pro-metastatic signaling in TNBC. Targeting fumarate-mediated protein succination represents a previously unrecognized and experimental vulnerability in TNBC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"40 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148498753","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":"RNA modifications in cancer: regulators of tumor evolution and therapeutic response.","authors":"Xinyu Gu,Yuting He,Ziyi Xu,Shujun Zhang,Yafeng Liu,Zihan Yang,Hongyan Liu,Wenjuan Chen,Lifan Zhang,Yingda Xie,Jiaxiang Hu,Huiwu Xing,Jing Yan,Qingmiao Shi","doi":"10.1186/s12943-026-02745-z","DOIUrl":"https://doi.org/10.1186/s12943-026-02745-z","url":null,"abstract":"RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I) editing, constitute a dynamic epitranscriptomic network that profoundly regulates RNA metabolism and gene expression. Their dysregulation is increasingly recognized as a hallmark of cancer. This review critically synthesizes the multifaceted roles of RNA modifications to bridge the gap between descriptive epitranscriptomic mapping and functional tumor biology. We systematically evaluate how writers, readers, and erasers dictate transcript stability and translation efficiency, driving tissue-specific tumor evolution across diverse malignancies. Crucially, we explore the intersection of RNA modifications and the tumor immune microenvironment, detailing their mechanisms in orchestrating immune evasion, altering antigen presentation, and regulating immune checkpoints. Furthermore, we examine how epitranscriptomic reprogramming dictates cellular responses to chemotherapy, radiotherapy, targeted treatments, and immunotherapy. By comprehensively analyzing these mechanisms, this review aims to facilitate the translation of epitranscriptomic findings into clinical applications, laying a theoretical foundation for targeted anti-tumor strategies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"37 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148498746","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":"Protein lactylation in cancer: principles, programmes and therapeutic opportunities.","authors":"Xiaoyun Bu,Xinyue Yu,Jie Wang,Mingjing Peng,Min Su,Yanyan Tang,Jie Jiang,Xia Luo,Mingzhi Xia,Yong Yi,Xianjie Jiang","doi":"10.1186/s12943-026-02743-1","DOIUrl":"https://doi.org/10.1186/s12943-026-02743-1","url":null,"abstract":"Lactylation is a recently identified metabolism-associated post-translational modification that provides a mechanistic link between tumor metabolic reprogramming and epigenetic regulation. Although aberrant lactate accumulation in tumor tissues has long been recognized, a comprehensive and unified understanding of how lactate-derived modifications contribute to tumor initiation and progression remains lacking. Here, we use lactate metabolism as a conceptual framework to systematically review the biogenesis and regulatory networks of lactylation, with a particular focus on its functions and underlying molecular mechanisms in key malignant processes, including tumor proliferation, invasion and metastasis, angiogenesis, immune evasion, radiotherapy resistance and systemic therapy resistance. Furthermore, we review emerging anti-tumor therapeutic strategies targeting lactate metabolism and tumor lactylation, highlighting that glucose metabolism-driven lactate accumulation and lactylation play a pivotal role in sustaining tumor cell survival and immunosuppressive phenotypes. Inhibition of lactate metabolism markedly attenuates tumor-associated lactylation and exhibits substantial synergistic efficacy when combined with other anti-tumor therapies. Overall, this work advances a systematic understanding of the roles of lactylation in tumor malignant progression and provides an important conceptual and theoretical foundation for the development of novel cancer therapeutic strategies targeting protein lactylation.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"2 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148476086","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":"Breaking barriers: nano-boosted drug delivery systems in overcoming the defenses of pancreatic cancer.","authors":"Yujia Wang,Yuxin Zhang,Xueyan Wang,Wei Zhao,Qiuyi Li,Minglu Zhou,Ying Liu,Xiaoli Yi,Jinhan He,Yanping Li,Jie Zhou","doi":"10.1186/s12943-026-02712-8","DOIUrl":"https://doi.org/10.1186/s12943-026-02712-8","url":null,"abstract":"Pancreatic cancer (PC) remains a highly lethal malignancy presenting formidable therapeutic challenges, primarily attributable to the substantial barriers posed by its dense desmoplastic stroma, profoundly immunosuppressive microenvironment, and poor drug bioavailability. Nanotechnology offers an effective strategy to enhance therapeutic efficacy through improved targeting, optimized pharmacokinetics, enhanced tissue penetration, increased biosafety, and high clinical translational potential. Consequently, this nanotechnology-based platform has been extensively investigated over the past decade for treating PC. This review examines a comprehensive overview of nanoparticle-mediated delivery systems for targeted PC therapy, critically evaluating recent developments and ongoing hurdles along the bench-to-bedside pathway. We discuss applications across chemotherapy, immunotherapy, gene therapy, and other modalities employed as monotherapies or combination regimens.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"40 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148462656","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":"Correction: CHEK1 and circCHEK1_246aa evoke chromosomal instability and induce bone lesion formation in multiple myeloma.","authors":"Chunyan Gu, Wang Wang, Xiaozhu Tang, Tingting Xu, Yanxin Zhang, Mengjie Guo, Rongfang Wei, Yajun Wang, Artur Jurczyszyn, Siegfried Janz, Meral Beksac, Fenghuang Zhan, Anja Seckinger, Dirk Hose, Jingxuan Pan, Ye Yang","doi":"10.1186/s12943-026-02734-2","DOIUrl":"10.1186/s12943-026-02734-2","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"25 1","pages":""},"PeriodicalIF":42.2,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13378329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148471861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remodeling of the tumor microenvironment in muscle-invasive bladder cancer: insights from single-cell and spatial transcriptomics after neoadjuvant immunochemotherapy.","authors":"Guozhi Zhao,Yuanyuan Bai,Xin Chen,Junwu Li,Hai Chang,Yongtang Zhu,Haoyu Xu,Yiqing You,Gautam Sethi,Deyu Zuo,Wei Tang,Lei Yang,Weiyang He","doi":"10.1186/s12943-026-02738-y","DOIUrl":"https://doi.org/10.1186/s12943-026-02738-y","url":null,"abstract":"BACKGROUNDNeoadjuvant immunochemotherapy (nICT), defined in this study as PD-L1 blockade combined with cisplatin-based chemotherapy, provides substantial clinical benefits in muscle-invasive bladder cancer (MIBC). However, the tumor immune microenvironment (TIME) is highly heterogeneous, resulting in variable patient responses and persistent therapy resistance. This study investigates key immune cell subsets, intercellular communication networks, and spatial distributions within the TIME of MIBC, with a focus on cellular and spatial features associated with nICT response.METHODSPatients were classified into responder and non-responder groups according to RECIST 1.1-based radiological evaluation. Responders were defined as patients achieving complete or partial response, whereas non-responders were defined as patients with stable or progressive disease after adequate nICT exposure and evaluable imaging. Representative computed tomography images and fresh tissue samples were collected from four no-treatment controls (NT), three nICT responders (R), and three nICT non-responders (NR). Samples underwent single-cell RNA sequencing and spatial transcriptomics sequencing. Cell populations were annotated to assess infiltration abundance, cell-cell communication networks, and pseudotime trajectories. Resistance-associated cell subsets and their spatial niches were identified.RESULTSFollowing quality control, the tumor microenvironment (TME) was classified into ten major cell subsets based on canonical markers. Cross-sectional group comparative analyses showed significant remodeling of the TME in the NR and R groups. B-cell infiltration was elevated in the NR group, whereas macrophages, fibroblasts, and mast cells were enriched in the R group. Functional alterations in activated CD4 + T cells and impaired differentiation of naive CD8 + T cells were identified as key drivers of acquired therapy resistance. Accumulation of macrophage-derived CXCL8 was also observed as a resistance driver. Cancer-associated fibroblasts (CAFs) served as a physical barrier, contributing to the establishment of an immunosuppressive TME. Notably, strong spatial co-localization between macrophage-derived CXCL8 and CAFs was observed in NR tumors, suggesting a cooperative role in mediating resistance to nICT. Further cell-cell communication analysis using spatial transcriptomics indicated that SPP1 signaling from macrophages (CXCL8) to CAFs contributes to TME reprogramming and resistance to nICT.CONCLUSIONThe integrated analysis identifies distinct immunological features that underlie differential nICT responses in MIBC. These findings provide a theoretical basis for optimizing personalized neoadjuvant therapy strategies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"348 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148462445","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":"Mutation-specific dynamics of dedifferentiation trajectories and tumor-stromal interactions in thyroid cancer.","authors":"Eun Hye Joo,Young Shin Song,Han Sai Lee,Gyeongseo Jung,Eun-Jae Chung,Su-Jin Kim,Yoo Hyung Kim,Sun Wook Cho,Hongyoon Choi,Jae-Kyung Won,Woong-Yang Park,Young Joo Park","doi":"10.1186/s12943-026-02699-2","DOIUrl":"https://doi.org/10.1186/s12943-026-02699-2","url":null,"abstract":"Progression from differentiated thyroid cancer to anaplastic thyroid cancer (ATC) involves profound epithelial plasticity and remodeling of the tumor microenvironment (TME), but how BRAFV600E and RAS driver mutations shape these processes remains unclear. Here, we integrated single-nucleus RNA-seq, spatial transcriptomics, and bulk RNA-seq across BRAFV600E- and RAS-driven thyroid tumors to delineate mutation-specific progression trajectories. BRAFV600E-driven tumors exhibited a gradual dedifferentiation trajectory with immune pathway activation, whereas RAS-driven tumors displayed abrupt transitions characterized by aneuploidy, epithelial-mesenchymal transition, hypoxia, and extracellular matrix remodeling. Cancer-associated fibroblasts (CAFs) emerged as key regulators, with mutation-specific ligand-receptor interactions: integrin-based signaling predominated in BRAFV600E-mutant ATCs, while PLAU-PLAUR, TNFSF10-TNFRSF10B, and AREG-EGFR were additionally enriched in RAS-driven ATCs. These CAF-epithelial circuits were spatially validated and associated with poor prognosis. Together, our findings reveal mutation-dependent epithelial and TME dynamics associated with thyroid cancer dedifferentiation and highlight the potential importance of molecular-tailored approaches in the management of advanced thyroid cancer.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"76 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148451452","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":"Plasma proteomic and metabolomic profiling reveals molecular features relevant to neoadjuvant therapy response in locally advanced esophageal squamous cell carcinoma.","authors":"Chu Xiao,Ziqin Deng,Guochao Zhang,Zhenlin Yang,Long Zhang,Hongfei Yin,Tao Fan,Di Wang,Yixiao Liu,Wenpeng Cai,Yu Ji,Jia Li,Tianle Liao,Chunxiang Li,Jie He","doi":"10.1186/s12943-026-02733-3","DOIUrl":"https://doi.org/10.1186/s12943-026-02733-3","url":null,"abstract":"BACKGROUNDNeoadjuvant therapy (NAT) followed by radical surgery is the standard treatment for locally advanced esophageal squamous cell carcinoma (LA-ESCC), yet many patients fail to achieve pathologic complete response (pCR). Predictive biomarkers and biological mechanisms underlying NAT resistance remain elusive. We aimed to address this challenge through longitudinal multi-omics profiling of patient plasma during NAT.METHODSWe performed longitudinal plasma proteomic and metabolomic analyses in a discovery cohort of patients with LA-ESCC (n = 40) receiving neoadjuvant chemotherapy (nCT) or neoadjuvant immunochemotherapy (nICT) to reveal molecular features relevant to treatment response. Predictive biomarkers for pCR were assessed in plasma samples from an independent validation cohort (n = 93) by ELISA. Mechanistic studies were conducted through in vitro cell co-culture, in vivo mouse experiments, and analysis of ESCC tissue samples from another validation cohort (n = 33).RESULTSMulti-omics analysis revealed distinct molecular profiles between treatment responders and non-responders. Metabolomic profiling revealed dynamic treatment-associated changes in amino acid and lipid metabolism during NAT, and proteomic profiling highlighted baseline differences related to neutrophil activity and inflammatory responses. DEFA1 was validated as an unfavorable predictive biomarker for achieving pCR after nICT. Mechanistic studies demonstrated that DEFA1 fosters an immunosuppressive microenvironment by promoting myeloid-derived suppressor cell (MDSC) differentiation and impairing CD8+ T cell cytotoxicity.CONCLUSIONSThis study delineates the longitudinal plasma multi-omic landscape associated with NAT response in LA-ESCC and identifies DEFA1 as a predictive biomarker and potential therapeutic target for overcoming immunotherapy resistance.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"22 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148451448","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":"Correction: Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m⁶A reader YTHDF3.","authors":"Wen Ni, Su Yao, Yunxia Zhou, Yuanyuan Liu, Piao Huang, Aijun Zhou, Jingwen Liu, Liheng Che, Jianming Li","doi":"10.1186/s12943-026-02719-1","DOIUrl":"10.1186/s12943-026-02719-1","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"25 1","pages":""},"PeriodicalIF":42.2,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}