Cancer gene therapy最新文献

{"title":"CircRNA-mediated regulation of ferroptosis in cancer: mechanistic networks and therapeutic implications.","authors":"Yuliang Zhang, Xingyu Du, Jin Liu, Yujia Guo, Xiaoxia Wang","doi":"10.1038/s41417-026-01092-x","DOIUrl":"https://doi.org/10.1038/s41417-026-01092-x","url":null,"abstract":"<p><p>Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation. In cancer, metabolic reprogramming is characterized by enhanced iron uptake, altered lipid metabolism, and sustained oxidative stress, creating a paradoxical state that increases vulnerability to ferroptosis while simultaneously activating antioxidant defense systems to sustain survival. Therefore, identifying and characterizing key regulators of pro-ferroptotic and anti-ferroptotic pathways is essential for precise modulation of ferroptosis sensitivity in cancer therapy. Circular RNAs (circRNAs) have emerged as important regulators of the ferroptosis network. Recent evidence indicates that circRNAs coordinate iron metabolism, lipid remodeling, redox balance, and stress-responsive signaling, thereby influencing tumor progression, stemness maintenance, immune adaptation, and therapy resistance. This review summarizes circRNA-mediated regulation of ferroptosis and highlights its mechanistic significance and translational potential in cancer.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoration of p53 function via hybrid strontium sulfite nanoparticles modified LNP improves the antitumor efficacy in breast cancers.","authors":"Md Emranul Karim, Mark M Banaszak Holl, Simon Corrie, Ezharul Hoque Chowdhury","doi":"10.1038/s41417-026-01085-w","DOIUrl":"https://doi.org/10.1038/s41417-026-01085-w","url":null,"abstract":"<p><p>The astounding success of mRNA empowers the diverse application of mRNA therapeutics in multiple genetic disorders. Besides the vaccines, the rational design of mRNA drugs has been explored widely to target the undruggable gene therapy for managing cancer. Restoration of the p53 tumor suppressor gene via introducing foreign p53-mRNA therapeutics may inhibit the growth and development of tumors. Since the development of mRNA transporting vehicles, liposome-based nanoparticles are the mainstay and are widely used in several ex vivo and clinical studies. But the delivery of mRNA outside the immune cells and hepatocytes for protein replacement therapy through systemic administartion is very limited and requires additional optimization. Here, we modified classical LNP (lipid nanoparticles) with SSNs (strontium sulfite nanoparticles) and complexed the LNP with p53 mRNA to improve the delivery efficiency of p53 mRNA. We assumed that restoration of p53 function in breast tumor cells might improve antitumor efficacy against breast cancer. We screened the SSNs-LNP to get the favorable physicochemical properties and to improve the delivery efficiency. The SSNs-LNP showed a threefold increase of luciferase gene expression in breast cancer cell lines compared to the classical LNP. In the animal model, the SSNs-LNP improved the biological stability and tumor targeting efficiency and restored the expression of p53, resulting in a significant reduction of tumor volume. Thus, we anticipate that the hybrid SSNs-LNP particles could be a translatable nanocarrier system in transporting mRNA drugs for the treatment of cancers.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LAMB3 orchestrates EGFR-MAPK-PKM cascade to promote glycolytic reprogramming and progression in laryngeal carcinoma.","authors":"Lu Zhang, Cheng Kang, Kai Wang","doi":"10.1038/s41417-026-01088-7","DOIUrl":"https://doi.org/10.1038/s41417-026-01088-7","url":null,"abstract":"<p><p>Laryngeal carcinoma (LC) remains a challenging malignancy with poor prognosis, necessitating the identification of novel therapeutic targets. This study investigates the functional role and underlying mechanism of the extracellular matrix protein Laminin Subunit Beta-3 (LAMB3) in LC progression. Bioinformatics analysis of multiple GEO datasets demonstrated that LAMB3 is significantly overexpressed in LC tissues and that high LAMB3 expression correlates with reduced overall survival in patients. Functional validation using two distinct LC cell lines revealed that knockdown of LAMB3 potently suppresses cellular proliferation, migration, clonogenic capacity, and glycolytic metabolism in vitro, and inhibits tumor growth in xenograft models. Mechanistically, we identified that LAMB3 activates the EGFR-MAPK signaling axis, increasing the phosphorylation of EGFR and ERK, leading to transcriptional upregulation of the key glycolytic enzyme PKM, resulting in enhanced glycolytic flux, as evidenced by increased glucose uptake and lactate production. Critically, the oncogenic effects of LAMB3 are entirely dependent on this axis; both genetic silencing of PKM and pharmacological inhibition of the EGFR or MAPK abrogate LAMB3-driven glycolytic reprogramming and tumor-promoting phenotypes in vitro and in vivo. Our findings establish LAMB3 as a novel prognostic biomarker and reveal the LAMB3-EGFR-MAPK-PKM signaling axis as a promising therapeutic target for intervention in laryngeal carcinoma.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Whole-genome DNA methylation analysis reveals distinct subtype characteristics in epithelial ovarian cancer.","authors":"Qiaoling Ren, Yingqing Deng, Caizhou Zhong, Dongmei Zhou, Renci Liu, Xiujie Sheng, Deqiang Sun","doi":"10.1038/s41417-026-01079-8","DOIUrl":"https://doi.org/10.1038/s41417-026-01079-8","url":null,"abstract":"<p><p>Epithelial ovarian cancer (EOC) is characterized by high mortality, insidious onset, and pronounced heterogeneity, underscoring the critical need for effective biomarkers for early detection and subtype-specific diagnosis. While DNA methylation represents a stable epigenetic marker, prior studies have largely relied on profiling techniques with limited genomic coverage and have often overlooked subtype-specific differences essential for guiding treatment decisions. To address this, we performed whole-genome bisulfite sequencing on 44 normal ovarian tissues and 89 EOC tissues encompassing all five histological subtypes, integrated with transcriptome sequencing, to comprehensively evaluate the diagnostic and prognostic utility of DNA methylation across EOC subtypes. Our analyses revealed that genome-wide methylation profiles effectively distinguished normal from tumor tissues and captured the substantial heterogeneity inherent to EOC. Differentially methylated regions (DMRs) and differentially expressed genes were enriched in immune-related processes and epithelial differentiation, aligning with the increased proportions of epithelial and immune cells identified through deconvolution analysis. Subtype-specific DMRs further implicated hormonal pathways in endometrioid (EC) and clear cell (CCOC) carcinomas, and linked mucinous ovarian cancer (MOC) to fluid regulation. Integrative analysis of DMRs and cellular composition indicated that epithelial cells in high-grade serous (HG), low-grade serous (LG), and EC tumors most closely resembled fallopian tube, ovarian, and endometrial epithelial cells, respectively, whereas MOC and CCOC epithelial cells showed similarity to gastrointestinal and renal epithelia. Moreover, weighted gene co-expression network analysis identified epithelia-associated DMRs that achieved up to 90% specificity for subtype classification in internal validation and demonstrated prognostic relevance in independent public datasets. In conclusion, the subtype-specific DNA methylation markers identified in this study accurately reflect the distinct histological features of each EOC subtype and hold promise for application in subtype classification and prognosis prediction, thereby providing a scientific foundation for future clinical interventions in EOC.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RSL24D1 links ribosome biogenesis to p53 activation in melanoma.","authors":"Leonie Stahl, Sebastian Staebler, Anja K Bosserhoff","doi":"10.1038/s41417-026-01089-6","DOIUrl":"https://doi.org/10.1038/s41417-026-01089-6","url":null,"abstract":"<p><p>Melanoma cells exhibit elevated translation activity and rely on intact ribosomes to sustain their high protein synthesis demand. To support this process, efficient ribosome biogenesis is essential. RSL24D1 is a ribosome biogenesis factor required for late-stage maturation of the 60S ribosomal subunit. By ensuring correct ribosomal assembly, RSL24D1 supports global protein translation and maintains cellular homeostasis. Transcript and protein analyses revealed that RSL24D1 is upregulated in melanoma cells compared to normal human epidermal melanocytes. This overexpression correlates with reduced patient survival, suggesting an oncogenic role. Reduction of RSL24D1 expression impaired protein synthesis, decreased cell growth and resulted in the accumulation of unincorporated ribosomal proteins RPL5 and RPL11, which form the 5S RNP complex and inhibit the binding of MDM2 to p53. This inhibition stabilised p53 and activated downstream targets, including CDKN1A, resulting in G1 phase arrest and a senescence-like phenotype. These findings identify RSL24D1 as a critical component linking ribosome biogenesis to the p53 stress response. Targeting RSL24D1 creates a translational bottleneck, suppressing cell growth in p53 wild-type and p53-mutant cancer cells, highlighting it as a potential therapeutic target.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-mediated m⁶A methylation of E2F2 targets MCU to promote the malignant phenotype of gastric cancer cells.","authors":"Huan Liu, ZhongCong Guo, Lan Li, YuXuan Dong, Nian Chen, ZhengTai Yuan","doi":"10.1038/s41417-026-01086-9","DOIUrl":"https://doi.org/10.1038/s41417-026-01086-9","url":null,"abstract":"<p><p>Gastric cancer (GC) is a highly prevalent malignancy worldwide, and its progression is closely linked to aberrant epigenetic regulation. E2F transcription factor 2 (E2F2), a member of the E2F transcription factor family, has been identified as an oncogene in various cancers. However, the regulatory effects of epigenetic modifications on E2F2 in GC remain incompletely clarified. To address this knowledge gap, the current study was designed to elucidate the impact of Methyltransferase-like 3 (METTL3)-mediated N⁶-methyladenosine (m⁶A) methylation of E2F2 on mitochondrial function in GC cells by regulating the mitochondrial calcium uniporter (MCU). Both in vitro and in vivo analyses revealed a critical oncogenic axis in GC driven by METTL3. This axis, mediated by m⁶A modification, post-transcriptionally stabilizes E2F2 mRNA, resulting in the upregulation of MCU expression and consequent aberrant mitochondrial calcium uptake. Functional assays revealed that activation of the METTL3/E2F2/MCU axis promotes GC cell proliferation and migration and inhibits apoptosis, whereas knockdown of METTL3 or E2F2 reverses these malignant phenotypes. Mechanistically, METTL3 binds to the 3' untranslated region of E2F2 mRNA to enhance its stability, and E2F2 in turn transcriptionally activates MCU expression. Clinical data analysis indicated positive correlations among METTL3, E2F2, and MCU expression, with high levels associated with poor patient prognosis. These findings suggest that targeting the m⁶A modification pathway holds promise for GC therapy, as the newly identified METTL3-E2F2-MCU axis plays a key role in regulating mitochondrial calcium homeostasis.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted degradation of protein in hematologic malignancies: mechanisms, therapeutic strategies, and clinical prospects","authors":"Sana Nafees,&nbsp;Glowi Alasiri,&nbsp;Mohammad Suhail Akhter,&nbsp;Nemat Ali","doi":"10.1038/s41417-026-01082-z","DOIUrl":"10.1038/s41417-026-01082-z","url":null,"abstract":"Hematological malignancies, including leukemia, lymphoma, and multiple myeloma, remain a major cause of illness and death worldwide. Although treatment options such as targeted therapies and immunotherapies have improved survival and clinical outcomes, many tumors still develop resistance due to persistent oncogenic signaling and the inability of most small-molecule therapies to effectively target these proteins. Recently, targeted protein degradation has emerged as a new therapeutic approach that selectively degrades pathogenic proteins instead of only blocking their function. This approach uses cellular degradation mechanisms, especially the ubiquitin–proteasome system, to induce ubiquitination and proteasomal degradation of target proteins. PROTACs and molecular glue degraders are emerging strategies for selectively removing cancer-promoting proteins in hematologic malignancies. These approaches make it possible to target key regulators such as BCR-ABL, BTK, and BRD4, which are involved in leukemogenesis, lymphoma progression, and treatment resistance. Moreover, emerging degradation strategies such as LYTACs and AUTACs further expand the range of proteins that can be targeted. This review discusses the molecular mechanisms of targeted protein degradation and its therapeutic potential in hematologic malignancies. We summarize recent advances in degradation technologies, highlight key targets in leukemia, lymphoma, and multiple myeloma, and discuss current clinical developments across both preclinical and clinical studies.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1177-1188"},"PeriodicalIF":6.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"POLE2 of tumor cells promotes OPN secretion based on PCLAF to drive M2 macrophage polarization in clear cell renal cell carcinoma.","authors":"An-Rui Li, Jing-Wen Xu, Zhi-Hang Wu, Zhi-Jian Kang, Run-Sheng Luo, Ya-Juan Su, Qi Yuan, Li-Chen Teng","doi":"10.1038/s41417-026-01083-y","DOIUrl":"https://doi.org/10.1038/s41417-026-01083-y","url":null,"abstract":"<p><p>The malignant progression of renal cell carcinoma (RCC) is closely associated with the establishment of an immunosuppressive tumor microenvironment (TME). This study aims to elucidate the oncogenic functions of DNA polymerase ε subunit POLE2 in RCC and its mechanism in modulating the tumor immune microenvironment. We found that POLE2 was significantly upregulated in clear cell RCC (ccRCC) tissues and cell lines. Gain-of-function and loss-of-function experiments demonstrated that POLE2 markedly enhanced tumor cell proliferation, migration, and tumorigenicity both in vitro and in vivo. Mechanistically, POLE2 binds to the PCNA-associated factor PCLAF and stabilizes the PCLAF protein by inhibiting its ubiquitin-proteasome-mediated degradation, thereby leading to increased expression and secretion of SPP1/osteopontin (OPN) in tumor cells. OPN acts as a key cytokine that drives macrophage M2 polarization by activating the CD44/integrin receptors on macrophages and their downstream STAT6 signaling pathway. Moreover, we identified the transcription factor NFATc2 as an upstream regulator of POLE2, which directly binds to the POLE2 promoter and activates its transcription. Our study unveils a comprehensive NFATc2/POLE2/PCLAF signaling axis that promotes ccRCC progression via OPN-mediated M2 macrophage polarization, providing a solid rationale and potential therapeutic targets for developing novel immunocombination therapies.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F3 amplification primes bladder cancer cells for premature mitosis.","authors":"Kathryn A Wierenga, Isabel S Nieland, Qingwu Liu, Pepijn R J Rakers, Anita van den Heuvel, Mara Pateli, Richard W Wubbolts, Frank M Riemers, Saskia C van Essen-Dorresteijn, Elsbeth A van Liere, Bart Westendorp","doi":"10.1038/s41417-026-01084-x","DOIUrl":"https://doi.org/10.1038/s41417-026-01084-x","url":null,"abstract":"<p><p>The E2F-RB pathway controls the G1/S checkpoint, and tumors often bypass it through RB1 or CDKN2A loss. Unlike these lesions, E2F3 amplification drives persistent excessive E2F-dependent transcription through S and G2 phases. This oncogene is frequently amplified in for example bladder cancer, but its impact on the cancer cell cycle remains unclear. Using isogenic bladder cancer models and patient data, we show that E2F3 amplification hyperactivates a mitotic gene expression program, including cyclin B1. This predisposes cells to unscheduled mitosis when the G2/M checkpoint is inhibited using the PKMYT1 inhibitor lunresertib, alone or in combination with low dosages of the WEE1 inhibitor zederosertib. E2F3-amplified cells acquired resistance to lunresertib by permanently reducing cyclin B1 expression, thereby preventing premature mitotic entry. Importantly, this resistance was reversed by co-treatment with a low dose of WEE1 inhibitor. These findings identify PKMYT1-dependent CDK1 inhibition as a critical safeguard against premature mitosis in E2F3-amplified bladder cancer. Thus, we uncover an opportunity for precision medicine strategies aimed at G2/M checkpoint inhibition to promote catastrophic mitosis in bladder cancer patients with E2F3 amplification and excessive cyclin B1 expression.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TWF1 inhibition overcomes cisplatin resistance in NSCLC by inducing ferroptosis via p53-dependent SLC7A11 repression and autophagy-mediated glutathione metabolism reprogramming","authors":"Mengwei Zhang,&nbsp;Yu Wang,&nbsp;Siyi Li,&nbsp;Gengwei Huo,&nbsp;Yuchao He,&nbsp;Xiaomeng Hu,&nbsp;Wenshuai Chen,&nbsp;Xinrui Wen,&nbsp;Liwei Chen,&nbsp;Yi Luo,&nbsp;Peng Chen,&nbsp;Hua Guo","doi":"10.1038/s41417-026-01081-0","DOIUrl":"10.1038/s41417-026-01081-0","url":null,"abstract":"Non-small-cell lung cancer (NSCLC) ranks among the most prevalent causes of cancer-related mortality worldwide, with cisplatin-based chemotherapy being a cornerstone of clinical treatment despite the inevitable emergence of drug resistance. This study systematically investigated the molecular mechanisms underlying cisplatin resistance in NSCLC, focusing on the role of TWF1 in regulating ferroptosis. Mechanistic analyses revealed that TWF1 acts as a dual-function suppressor of ferroptosis. Through direct interaction with p53, TWF1 inhibits p53 nuclear translocation, thereby upregulating SLC7A11 and promoting system Xc⁻-mediated cystine uptake, which supports GSH biosynthesis and redox homeostasis. TWF1 induces autophagy-related metabolic reprogramming, increasing intracellular glutamate levels to sustain system Xc⁻ activity and suppress lipid peroxidation. In cisplatin-resistant A549/cisplatin (DDP) cells, TWF1 knockdown significantly reduced SLC7A11 expression, depleted GSH reserves, and enhanced lipid reactive oxygen species (ROS) accumulation, sensitizing cells to cisplatin via ferroptosis induction. This study identifies TWF1 as a critical regulator of cisplatin resistance and ferroptosis, highlighting the therapeutic potential of TWF1 inhibition combined with cisplatin to overcome chemoresistance, possibly providing new strategies for improving NSCLC treatment outcomes.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1126-1140"},"PeriodicalIF":6.4,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}