Molecular Cancer最新文献

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Tumour-infiltrating microplastics disrupt the JAK-STAT-microbiota axis to promote immunotherapy resistance in colorectal cancer. 肿瘤浸润性微塑料破坏jak - stat -微生物群轴,促进结直肠癌免疫治疗耐药性。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-10 DOI: 10.1186/s12943-026-02588-8
Zhaohui Jiang, Yongting Liu, Peng Zhang, Jiang Fei, Kailing Wang, Yin Li, Xiangyang Zhang, Changjing Cai, Yihong Chen, Yinghui Peng, Hong Shen, Shan Zeng, Ying Han
{"title":"Tumour-infiltrating microplastics disrupt the JAK-STAT-microbiota axis to promote immunotherapy resistance in colorectal cancer.","authors":"Zhaohui Jiang, Yongting Liu, Peng Zhang, Jiang Fei, Kailing Wang, Yin Li, Xiangyang Zhang, Changjing Cai, Yihong Chen, Yinghui Peng, Hong Shen, Shan Zeng, Ying Han","doi":"10.1186/s12943-026-02588-8","DOIUrl":"10.1186/s12943-026-02588-8","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150435","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}
引用次数: 0
miRNA-driven cancer cell plasticity, tolerance and therapy resistance: lessons from melanoma. mirna驱动的癌细胞可塑性、耐受性和治疗耐药性:来自黑色素瘤的经验教训。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-10 DOI: 10.1186/s12943-026-02603-y
Arianna Ortolano, Rachele Frigerio, Gennaro Ciliberto, Luigi Fattore, Rita Mancini
{"title":"miRNA-driven cancer cell plasticity, tolerance and therapy resistance: lessons from melanoma.","authors":"Arianna Ortolano, Rachele Frigerio, Gennaro Ciliberto, Luigi Fattore, Rita Mancini","doi":"10.1186/s12943-026-02603-y","DOIUrl":"10.1186/s12943-026-02603-y","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150449","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}
引用次数: 0
Exploiting synthetic lethality in epithelial ovarian cancer: multi-dimensional approaches beyond DNA damage repair. 利用上皮性卵巢癌的合成致死性:DNA损伤修复以外的多维途径。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-10 DOI: 10.1186/s12943-025-02562-w
Mandana Bigdeli, Elizabeth Tremblay, Diane Provencher, Anne-Marie Mes-Masson, Francis Rodier
{"title":"Exploiting synthetic lethality in epithelial ovarian cancer: multi-dimensional approaches beyond DNA damage repair.","authors":"Mandana Bigdeli, Elizabeth Tremblay, Diane Provencher, Anne-Marie Mes-Masson, Francis Rodier","doi":"10.1186/s12943-025-02562-w","DOIUrl":"10.1186/s12943-025-02562-w","url":null,"abstract":"<p><p>Synthetic lethality (SL) is a therapeutic approach that selectively target cancer cells via the disruption of two interdependent molecular targets, which together become essential in the cancer context to ensure cancer cell survival. Among anticancer SL strategies, poly ADP-ribose polymerase (PARP) inhibitors have revolutionized the treatment of homologous recombination repair deficient breast and ovarian cancers by targeting the remaining DNA repair mechanisms. However, resistance emergence is nearly universal providing the rationale to expand beyond classical DNA repair targets. Severe DNA lesions like double-strand breaks or extended single-strand stretches trigger the complex DNA damage response signaling cascade (DDR), which provides many SL targets in addition to direct DNA repair mechanisms. Epithelial ovarian cancer is the deadliest gynecologic malignancy, in part because of late detection and treatment resistance, which provides a rich environment to explore the concept of combining multiple targets to produce SL synergies that kill cancer cells. In this context we discuss the interplay among varied components of the DDR including DNA damage signalers, cell cycle regulation, metabolism, epigenetics, and subsequent cell fate decisions like apoptosis or senescence. Based on this knowledge we further explore innovative SL approaches that may elicit or restore drug sensitivity in resistant tumors. Overall, we provide the rationale for multidimensional strategies linking classic DNA repair mechanisms to various molecular vulnerabilities sometimes apparently unrelated or downstream from DNA damage to improve cancer treatment outcomes via more effective and durable therapeutic responses, offering additional options for the personalized treatment of this highly heterogeneous disease.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146157884","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}
引用次数: 0
Correction: The chromosome 11q13.3 amplification associated lymph node metastasis is driven by miR-548k through modulating tumor microenvironment. 更正:染色体11q13.3扩增相关淋巴结转移是由miR-548k通过调节肿瘤微环境驱动的。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-09 DOI: 10.1186/s12943-026-02586-w
Weimin Zhang, Ruoxi Hong, Lin Li, Yan Wang, Peina Du, Yunwei Ou, Zitong Zhao, Xuefeng Liu, Wenchang Xiao, Dezuo Dong, Qingnan Wu, Jie Chen, Yongmei Song, Qimin Zhan
{"title":"Correction: The chromosome 11q13.3 amplification associated lymph node metastasis is driven by miR-548k through modulating tumor microenvironment.","authors":"Weimin Zhang, Ruoxi Hong, Lin Li, Yan Wang, Peina Du, Yunwei Ou, Zitong Zhao, Xuefeng Liu, Wenchang Xiao, Dezuo Dong, Qingnan Wu, Jie Chen, Yongmei Song, Qimin Zhan","doi":"10.1186/s12943-026-02586-w","DOIUrl":"10.1186/s12943-026-02586-w","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"25 1","pages":"27"},"PeriodicalIF":33.9,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12884628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143048","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}
引用次数: 0
Correction: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling. 纠正:组蛋白去甲基化酶KDM4D通过HIF1β/VEGFA信号传导促进胃肠道间质瘤进展。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-09 DOI: 10.1186/s12943-026-02579-9
Fuqing Hu, Haijie Li, Lu Liu, Feng Xu, Senyan Lai, Xuelai Luo, Junbo Hu, Xi Yang
{"title":"Correction: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling.","authors":"Fuqing Hu, Haijie Li, Lu Liu, Feng Xu, Senyan Lai, Xuelai Luo, Junbo Hu, Xi Yang","doi":"10.1186/s12943-026-02579-9","DOIUrl":"10.1186/s12943-026-02579-9","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"25 1","pages":"26"},"PeriodicalIF":33.9,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12884625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143051","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}
引用次数: 0
STING-Activating nanoplatforms for image-guided sonodynamic cancer therapy. 用于图像引导声动力癌症治疗的sting激活纳米平台。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-09 DOI: 10.1186/s12943-026-02591-z
Lingpu Zhang, Delong Huang, Jia Li, Linzhen Mo, Tian Qin, Bowen Xing, Bing Xiao, Chun Xu, Haihua Xiao, Leli Zeng, Kun Shang
{"title":"STING-Activating nanoplatforms for image-guided sonodynamic cancer therapy.","authors":"Lingpu Zhang, Delong Huang, Jia Li, Linzhen Mo, Tian Qin, Bowen Xing, Bing Xiao, Chun Xu, Haihua Xiao, Leli Zeng, Kun Shang","doi":"10.1186/s12943-026-02591-z","DOIUrl":"10.1186/s12943-026-02591-z","url":null,"abstract":"<p><p>Tumor precision treatment still faces the challenge of being unable to achieve real-time monitoring. The rapid advancements in nanomedicine within the biomedical sector have highlighted the potential of integrated nano-platforms for tumor diagnosis and treatment. Herein, we create a multimodal diagnostic nanodrug, ⁹⁹<sup>m</sup>Tc-NP<sup>AIE</sup>-MSA, which combines sonosensitizers, STING agonists, and radionuclides for immuno-sonodynamic therapy targeting breast cancer. This platform utilizes polymers with aggregation-induced luminescence properties that, when activated by US, generate cytotoxic reactive oxygen species, causing DNA and mitochondrial damage, activating the cGAS-STING pathway, and releasing the STING agonist MSA-2 to enhance the immune response. Additionally, ⁹⁹<sup>m</sup>Tc incorporation facilitates SPECT/CT and near-infrared fluorescence imaging, thereby improving tumor targeting and therapeutic monitoring precision. Both in vitro and in vivo studies confirm the significant anti-tumor effects and immunomodulation achieved by this nano-platform under US, presenting a novel strategy for precise tumor diagnosis and treatment.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12983522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150461","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}
引用次数: 0
HnRPD/AUF1 facilitates human ovarian cancer progression through activating FLI1 and maintaining cisplatin resistance. HnRPD/AUF1通过激活FLI1和维持顺铂耐药性来促进人类卵巢癌的进展。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-09 DOI: 10.1186/s12943-026-02599-5
Chao Tang, Chongying Zhu, Zihao An, Bin Cao, Qiang Xu, Lin Li, Yiyao Bao, Jiayong Li
{"title":"HnRPD/AUF1 facilitates human ovarian cancer progression through activating FLI1 and maintaining cisplatin resistance.","authors":"Chao Tang, Chongying Zhu, Zihao An, Bin Cao, Qiang Xu, Lin Li, Yiyao Bao, Jiayong Li","doi":"10.1186/s12943-026-02599-5","DOIUrl":"10.1186/s12943-026-02599-5","url":null,"abstract":"<p><p>Ovarian cancer (OC) is the predominant gynecological cancer and is associated with severe morbidity and high mortality worldwide. Therefore, clarifying the molecular mechanisms underlying OC progression and exploring novel therapeutic targets are important. Here, using human OC samples, different OC cell lines, and xenograft nude mouse models in combination with multiple sequencings, we report that hnRPD, an RNA binding protein that modulates RNA stability, is highly expressed in OC tissues, and contributes to OC cell malignancy in human OC cells cultured in vitro and in OC cell-derived xenograft nude mouse models in vivo. Mechanistically, ectopically expressed GPR137 binds to hnRPD and enhances hnRPD protein stability, which reciprocally transactivates GPR137 through the transcription factor FLI1. On the other hand, elevated hnRPD upregulates RAB8A expression by interacting with RAB8A mRNA and promoting its stability, leading to activation of downstream cell signaling and thereby enhanced OC cell malignant behaviors including cell proliferation, cell invasion, cell migration, and colony formation ability as well as OC xenograft growth in nude mice. Moreover, cisplatin in combination with silencing of hnRPD expression, significantly induces apoptosis in cisplatin-resistant OC cells through regulation of OC cell metabolism. Therefore, our data provide evidence that hnRPD could represent an innovative prognostic indicator for OC and may be an attractive therapeutic target for improving clinical outcomes in OC treatment.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12983857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150476","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}
引用次数: 0
Therapeutic reprogramming of tumour-associated macrophages in pancreatic cancer using a cytotoxic CCR2-targeted nanotheranostic. 使用细胞毒性ccr2靶向纳米疗法治疗胰腺癌中肿瘤相关巨噬细胞的重编程。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-07 DOI: 10.1186/s12943-026-02597-7
Vikas Kumar Somani, Xiaohui Zhang, Timothy Hung-Po Chen, Ashenafi Bulle, Sapana Bansod, Lin Li, Yutong Geng, Liang-I Kang, Gyu Seong Heo, Hannah Luehmann, Yuena Zhang, Muhammad A Saeed, Kory J Lavine, David G DeNardo, Russell K Pachynski, Yongjian Liu, Kian-Huat Lim
{"title":"Therapeutic reprogramming of tumour-associated macrophages in pancreatic cancer using a cytotoxic CCR2-targeted nanotheranostic.","authors":"Vikas Kumar Somani, Xiaohui Zhang, Timothy Hung-Po Chen, Ashenafi Bulle, Sapana Bansod, Lin Li, Yutong Geng, Liang-I Kang, Gyu Seong Heo, Hannah Luehmann, Yuena Zhang, Muhammad A Saeed, Kory J Lavine, David G DeNardo, Russell K Pachynski, Yongjian Liu, Kian-Huat Lim","doi":"10.1186/s12943-026-02597-7","DOIUrl":"10.1186/s12943-026-02597-7","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137772","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}
引用次数: 0
Identification of HSPE1 as a new actionable cancer vulnerability leads to an innovative and effective combination therapy for pancreatic ductal adenocarcinoma. 发现HSPE1是一种新的可操作的癌症易感性,为胰腺导管腺癌提供了一种创新有效的联合治疗方法。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-05 DOI: 10.1186/s12943-026-02587-9
Julien Boudreault, Shima Rahimirad, Ni Wang, Gang Yan, Leslie Chaltel Lima, Sophie Poulet, Meiou Dai, Suhad Ali, Jean-Jacques Lebrun
{"title":"Identification of HSPE1 as a new actionable cancer vulnerability leads to an innovative and effective combination therapy for pancreatic ductal adenocarcinoma.","authors":"Julien Boudreault, Shima Rahimirad, Ni Wang, Gang Yan, Leslie Chaltel Lima, Sophie Poulet, Meiou Dai, Suhad Ali, Jean-Jacques Lebrun","doi":"10.1186/s12943-026-02587-9","DOIUrl":"10.1186/s12943-026-02587-9","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146125755","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}
引用次数: 0
Fusobacterium nucleatum manipulates host autophagy to promote its intracellular survival and treatment resistance in nasopharyngeal carcinoma. 核梭杆菌操纵宿主自噬促进鼻咽癌细胞内存活和治疗耐药。
IF 33.9 1区 医学
Molecular Cancer Pub Date : 2026-02-04 DOI: 10.1186/s12943-026-02581-1
Jing-Yun Wang, Ying-Qi Lu, Xi-Rong Tan, Sheng-Suo Ma, Jia-Hao Dai, Sen-Yu Feng, Yu-Fei Duan, Jie-Wen Bai, Ying-Qing Li, Sha Gong, Ye-Lin Liang, Sai-Wei Huang, Jun Ma, Cheng Xu, Jun-Yan Li, Na Liu
{"title":"Fusobacterium nucleatum manipulates host autophagy to promote its intracellular survival and treatment resistance in nasopharyngeal carcinoma.","authors":"Jing-Yun Wang, Ying-Qi Lu, Xi-Rong Tan, Sheng-Suo Ma, Jia-Hao Dai, Sen-Yu Feng, Yu-Fei Duan, Jie-Wen Bai, Ying-Qing Li, Sha Gong, Ye-Lin Liang, Sai-Wei Huang, Jun Ma, Cheng Xu, Jun-Yan Li, Na Liu","doi":"10.1186/s12943-026-02581-1","DOIUrl":"10.1186/s12943-026-02581-1","url":null,"abstract":"<p><strong>Background: </strong>Growing evidence highlights the existence and tumor-promoting role of intratumoral bacteria in various types of cancers. However, the mechanisms enabling the intracellular survival of these microorganisms remain poorly understood, impeding the development of microbiota-targeting anticancer strategies.</p><p><strong>Methods: </strong>A transcriptomics analysis was used to identify the disease-related bacteria in nasopharyngeal carcinoma (NPC). Cell-bacteria coculture assay, cell viability assay, and mouse xenograft tumor model were used for functional investigation. Immunofluorescence, quantitative PCR analysis, RNA sequencing, immunoblot analysis, co-immunoprecipitation and mass spectrometry were utilized in mechanistic research. Fluorescent in situ hybridization in NPC specimens and clinical data were used for prognosis analysis.</p><p><strong>Results: </strong>We discovered that the Fusobacterium nucleatum (F. nucleatum), especially the C2 clade of F. nucleatum subsp. animalis (Fna C2), acts as an intracellular pathogen and exhibits distinct colonization advantages in NPC by inhibiting autophagy flux in host cells. Mechanistically, the virulence protein FadA of Fna C2 increases the ubiquitination and promotes the degradation of Ras-related protein RAB7A by enhancing the interaction between RAB7A and the E3 ligase TRIM28, which thus impairs the autophagosome-lysosome fusion and the autophagy machinery. The dysfunctional autophagy not only enables the persistent intracellular survival of F. nucleatum but also contributes to the treatment resistance of NPC. Clinically, a high intratumoral F. nucleatum colonization is associated with tumor relapse and poor outcome in NPC patients.</p><p><strong>Conclusion: </strong>Our findings elucidate a key mechanism by which F. nucleatum survives and promotes treatment resistance in NPC, providing a microbiological prognosis indicator for NPC patients.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":" ","pages":""},"PeriodicalIF":33.9,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113798","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}
引用次数: 0
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