IF 3.4

NAR cancer Pub Date : 2024-12-18 eCollection Date: 2024-12-01 DOI: 10.1093/narcan/zcae046

María José Jiménez-Santos, Santiago García-Martín, Marcos Rubio-Fernández, Gonzalo Gómez-López, Fátima Al-Shahrour

{"title":"Spatial transcriptomics in breast cancer reveals tumour microenvironment-driven drug responses and clonal therapeutic heterogeneity.","authors":"María José Jiménez-Santos, Santiago García-Martín, Marcos Rubio-Fernández, Gonzalo Gómez-López, Fátima Al-Shahrour","doi":"10.1093/narcan/zcae046","DOIUrl":"10.1093/narcan/zcae046","url":null,"abstract":"Breast cancer patients are categorized into three subtypes with distinct treatment approaches. Precision oncology has increased patient outcomes by targeting the specific molecular alterations of tumours, yet challenges remain. Treatment failure persists due to the coexistence of several malignant subpopulations with different drug sensitivities within the same tumour, a phenomenon known as intratumour heterogeneity (ITH). This heterogeneity has been extensively studied from a tumour-centric view, but recent insights underscore the role of the tumour microenvironment in treatment response. Our research utilizes spatial transcriptomics data from breast cancer patients to predict drug sensitivity. We observe diverse response patterns across tumour, interphase and microenvironment regions, unveiling a sensitivity and functional gradient from the tumour core to the periphery. Moreover, we find tumour therapeutic clusters with different drug responses associated with distinct biological functions driven by unique ligand-receptor interactions. Importantly, we identify genetically identical subclones with different responses depending on their location within the tumour ducts. This research underscores the significance of considering the distance from the tumour core and microenvironment composition when identifying suitable treatments to target ITH. Our findings provide critical insights into optimizing therapeutic strategies, highlighting the necessity of a comprehensive understanding of tumour biology for effective cancer treatment.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 4","pages":"zcae046"},"PeriodicalIF":3.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RAD51 recruitment but not replication fork stability associates with PARP inhibitor response in ovarian cancer patient-derived xenograft models. 在卵巢癌患者来源的异种移植模型中，RAD51募集而非复制叉稳定性与PARP抑制剂反应相关。

IF 3.4

NAR cancer Pub Date : 2024-11-28 eCollection Date: 2024-12-01 DOI: 10.1093/narcan/zcae044

Francien Talens, Vivian Oliviera Nunes Teixeira, Yannick P Kok, Mengting Chen, Efraim H Rosenberg, Rashmie Debipersad, Evelien W Duiker, Nathalie van den Tempel, Marketa Janatova, Petra Zemankova, Petra M Nederlof, G Bea A Wisman, Zdenek Kleibl, Steven de Jong, Marcel A T M van Vugt

{"title":"RAD51 recruitment but not replication fork stability associates with PARP inhibitor response in ovarian cancer patient-derived xenograft models.","authors":"Francien Talens, Vivian Oliviera Nunes Teixeira, Yannick P Kok, Mengting Chen, Efraim H Rosenberg, Rashmie Debipersad, Evelien W Duiker, Nathalie van den Tempel, Marketa Janatova, Petra Zemankova, Petra M Nederlof, G Bea A Wisman, Zdenek Kleibl, Steven de Jong, Marcel A T M van Vugt","doi":"10.1093/narcan/zcae044","DOIUrl":"10.1093/narcan/zcae044","url":null,"abstract":"Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPis) are currently used to treat BRCA1/2 mutant cancers. Although PARPi sensitivity has been attributed to homologous recombination (HR) defects, other roles of HR factors have also been linked to response to PARPi, including replication fork protection. In this study, we investigated PARPi sensitivity in ovarian cancer patient-derived xenograft (PDX) models in relation to HR proficiency and replication fork protection. Analysis of BRCA1/2 status showed that in our cohort of 31 ovarian cancer PDX models 22.6% harbored a BRCA1/2 alteration (7/31), and 48.3% (15/31) were genomically unstable as measured by copy number alteration analysis. In vivo, PARPi olaparib response was measured in 15 selected PDX models. Functional assessment of HR using ex vivo irradiation-induced RAD51 foci formation identified all olaparib-sensitive PDX models, including four models without BRCA1/2 alterations. In contrast, replication fork protection or replication speed in ex vivo tumor tissue did not correlate with olaparib response. Targeted panel sequencing in olaparib-sensitive models lacking BRCA1/2 alterations revealed a MUS81 variant as a possible mechanism underlying PARPi sensitivity. Combined, we show that ex vivo RAD51 analysis effectively predicts in vivo olaparib response and revealed a subset of PARPi-sensitive, HR-deficient ovarian cancer PDX models, lacking a BRCA1/2 alteration.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 4","pages":"zcae044"},"PeriodicalIF":3.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11604054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Massively parallel reporter assays identify enhancer elements in oesophageal Adenocarcinoma. 大规模并行报告实验确定食管腺癌中的增强子元素

IF 3.4

NAR cancer Pub Date : 2024-10-16 eCollection Date: 2024-12-01 DOI: 10.1093/narcan/zcae041

Shen-Hsi Yang, Ibrahim Ahmed, Yaoyong Li, Christopher W Bleaney, Andrew D Sharrocks

{"title":"Massively parallel reporter assays identify enhancer elements in oesophageal Adenocarcinoma.","authors":"Shen-Hsi Yang, Ibrahim Ahmed, Yaoyong Li, Christopher W Bleaney, Andrew D Sharrocks","doi":"10.1093/narcan/zcae041","DOIUrl":"10.1093/narcan/zcae041","url":null,"abstract":"Cancer is a disease underpinned by aberrant gene expression. Enhancers are regulatory elements that play a major role in transcriptional control and changes in active enhancer function are likely critical in the pathogenesis of oesophageal adenocarcinoma (OAC). Here, we utilise STARR-seq to profile the genome-wide enhancer landscape in OAC and identify hundreds of high-confidence enhancer elements. These regions are enriched in enhancer-associated chromatin marks, are actively transcribed and exhibit high levels of associated gene activity in OAC cells. These characteristics are maintained in human patient samples, demonstrating their disease relevance. This relevance is further underlined by their responsiveness to oncogenic ERBB2 inhibition and increased activity compared to the pre-cancerous Barrett's state. Mechanistically, these enhancers are linked to the core OAC transcriptional network and in particular KLF5 binding is associated with high level activity, providing further support for a role of this transcription factor in defining the OAC transcriptome. Our results therefore uncover a set of enhancer elements with physiological significance, that widen our understanding of the molecular alterations in OAC and point to mechanisms through which response to targeted therapy may occur.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 4","pages":"zcae041"},"PeriodicalIF":3.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11482635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoding the molecular symphony: interactions between the m⁶A and p53 signaling pathways in cancer. 解码分子交响乐：癌症中 m6A 和 p53 信号通路之间的相互作用。

IF 3.4

NAR cancer Pub Date : 2024-09-26 eCollection Date: 2024-09-01 DOI: 10.1093/narcan/zcae037

Rachel Shoemaker, Mo-Fan Huang, Ying-Si Wu, Cheng-Shuo Huang, Dung-Fang Lee

{"title":"Decoding the molecular symphony: interactions between the m6A and p53 signaling pathways in cancer.","authors":"Rachel Shoemaker, Mo-Fan Huang, Ying-Si Wu, Cheng-Shuo Huang, Dung-Fang Lee","doi":"10.1093/narcan/zcae037","DOIUrl":"10.1093/narcan/zcae037","url":null,"abstract":"The p53 tumor suppressor gene governs a multitude of complex cellular processes that are essential for anti-cancer function and whose dysregulation leads to aberrant gene transcription, activation of oncogenic signaling and cancer development. Although mutations can occur at any point in the genetic sequence, missense mutations comprise the majority of observed p53 mutations in cancers regardless of whether the mutation is germline or somatic. One biological process involved in both mutant and wild-type p53 signaling is the N 6-methyladenosine (m6A) epitranscriptomic network, a type of post-transcriptional modification involved in over half of all eukaryotic mRNAs. Recently, a significant number of findings have demonstrated unique interactions between p53 and the m6A epitranscriptomic network in a variety of cancer types, shedding light on a previously uncharacterized connection that causes significant dysregulation. Cross-talk between wild-type or mutant p53 and the m6A readers, writers and erasers has been shown to impact cellular function and induce cancer formation by influencing various cancer hallmarks. Here, this review aims to summarize the complex interplay between the m6A epitranscriptome and p53 signaling pathway, highlighting its effects on tumorigenesis and other hallmarks of cancer, as well as identifying its therapeutic implications for the future.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 3","pages":"zcae037"},"PeriodicalIF":3.4,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11426327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel insights into the role of bisphenol A (BPA) in genomic instability. 关于双酚 A (BPA) 在基因组不稳定性中作用的新见解。

IF 3.4

NAR cancer Pub Date : 2024-09-24 eCollection Date: 2024-09-01 DOI: 10.1093/narcan/zcae038

Anastasia Hale, George-Lucian Moldovan

引用次数: 0

Intrinsic PARG inhibitor sensitivity is mimicked by TIMELESS haploinsufficiency and rescued by nucleoside supplementation. TIMELESS 单倍体缺失可模拟 PARG 抑制剂的内在敏感性，并通过补充核苷来挽救这种敏感性。

IF 3.4

NAR cancer Pub Date : 2024-07-16 eCollection Date: 2024-09-01 DOI: 10.1093/narcan/zcae030

Camilla Coulson-Gilmer, Samantha Littler, Bethany M Barnes, Rosie M Brady, Holda A Anagho, Nisha Pillay, Malini Dey, William Macmorland, Daniel Bronder, Louisa Nelson, Anthony Tighe, Wei-Hsiang Lin, Robert D Morgan, Richard D Unwin, Michael L Nielsen, Joanne C McGrail, Stephen S Taylor

{"title":"Intrinsic PARG inhibitor sensitivity is mimicked by TIMELESS haploinsufficiency and rescued by nucleoside supplementation.","authors":"Camilla Coulson-Gilmer, Samantha Littler, Bethany M Barnes, Rosie M Brady, Holda A Anagho, Nisha Pillay, Malini Dey, William Macmorland, Daniel Bronder, Louisa Nelson, Anthony Tighe, Wei-Hsiang Lin, Robert D Morgan, Richard D Unwin, Michael L Nielsen, Joanne C McGrail, Stephen S Taylor","doi":"10.1093/narcan/zcae030","DOIUrl":"10.1093/narcan/zcae030","url":null,"abstract":"A subset of cancer cells are intrinsically sensitive to inhibitors targeting PARG, the poly(ADP-ribose) glycohydrolase that degrades PAR chains. Sensitivity is accompanied by persistent DNA replication stress, and can be induced by inhibition of TIMELESS, a replisome accelerator. However, the nature of the vulnerability responsible for intrinsic sensitivity remains undetermined. To understand PARG activity dependency, we analysed Timeless model systems and intrinsically sensitive ovarian cancer cells. We show that nucleoside supplementation rescues all phenotypes associated with PARG inhibitor sensitivity, including replisome speed and fork stalling, S-phase completion and mitotic entry, proliferation dynamics and clonogenic potential. Importantly nucleoside supplementation restores PARG inhibitor resistance despite the continued presence of PAR chains, indicating that sensitivity does not correlate with PAR levels. In addition, we show that inhibition of thymidylate synthase, an enzyme required for dNTP homeostasis, induces PARG-dependency. Together, these observations suggest that PARG inhibitor sensitivity reflects an inability to control replisome speed and/or maintain helicase-polymerase coupling in response to nucleotide imbalances.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 3","pages":"zcae030"},"PeriodicalIF":3.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11249981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141629663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CRISPR-Cas9 for selective targeting of somatic mutations in pancreatic cancers. 用于选择性靶向胰腺癌体细胞突变的 CRISPR-Cas9。

IF 3.4

NAR cancer Pub Date : 2024-06-19 eCollection Date: 2024-06-01 DOI: 10.1093/narcan/zcae028

Selina Shiqing K Teh, Kirsten Bowland, Eitan Halper-Stromberg, Akhil Kotwal, Alexis Bennett, Alyza Skaist, Jacqueline Tang, Fidel Cai, Antonella Macoretta, Hong Liang, Hirohiko Kamiyama, Sarah Wheelan, Ming-Tseh Lin, Ralph H Hruban, Chien-Fu Hung, Michael Goldstein, Robert B Scharpf, Nicholas J Roberts, James R Eshleman

{"title":"CRISPR-Cas9 for selective targeting of somatic mutations in pancreatic cancers.","authors":"Selina Shiqing K Teh, Kirsten Bowland, Eitan Halper-Stromberg, Akhil Kotwal, Alexis Bennett, Alyza Skaist, Jacqueline Tang, Fidel Cai, Antonella Macoretta, Hong Liang, Hirohiko Kamiyama, Sarah Wheelan, Ming-Tseh Lin, Ralph H Hruban, Chien-Fu Hung, Michael Goldstein, Robert B Scharpf, Nicholas J Roberts, James R Eshleman","doi":"10.1093/narcan/zcae028","DOIUrl":"10.1093/narcan/zcae028","url":null,"abstract":"Somatic mutations are desirable targets for selective elimination of cancer, yet most are found within noncoding regions. We have adapted the CRISPR-Cas9 gene editing tool as a novel, cancer-specific killing strategy by targeting the subset of somatic mutations that create protospacer adjacent motifs (PAMs), which have evolutionally allowed bacterial cells to distinguish between self and non-self DNA for Cas9-induced double strand breaks. Whole genome sequencing (WGS) of paired tumor minus normal (T-N) samples from three pancreatic cancer patients (Panc480, Panc504, and Panc1002) showed an average of 417 somatic PAMs per tumor produced from single base substitutions. Further analyses of 591 paired T-N samples from The International Cancer Genome Consortium found medians of ∼455 somatic PAMs per tumor in pancreatic, ∼2800 in lung, and ∼3200 in esophageal cancer cohorts. Finally, we demonstrated 69-99% selective cell death of three targeted pancreatic cancer cell lines using 4-9 sgRNAs designed using the somatic PAM discovery approach. We also showed no off-target activity from these tumor-specific sgRNAs in either the patient's normal cells or an irrelevant cancer using WGS. This study demonstrates the potential of CRISPR-Cas9 as a novel and selective anti-cancer strategy, and supports the genetic targeting of adult cancers.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 2","pages":"zcae028"},"PeriodicalIF":3.4,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11195629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141447921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs. 微卫星断裂诱导复制产生高度突变的染色体外环状DNA。

IF 3.4

NAR cancer Pub Date : 2024-06-08 eCollection Date: 2024-06-01 DOI: 10.1093/narcan/zcae027

Rujuta Yashodhan Gadgil, S Dean Rider, Resha Shrestha, Venicia Alhawach, David C Hitch, Michael Leffak

{"title":"Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.","authors":"Rujuta Yashodhan Gadgil, S Dean Rider, Resha Shrestha, Venicia Alhawach, David C Hitch, Michael Leffak","doi":"10.1093/narcan/zcae027","DOIUrl":"10.1093/narcan/zcae027","url":null,"abstract":"Extrachromosomal circular DNAs (eccDNAs) are produced from all regions of the eucaryotic genome. We used inverse PCR of non-B microsatellites capable of forming hairpin, triplex, quadruplex and AT-rich structures integrated at a common ectopic chromosomal site to show that these non-B DNAs generate highly mutagenized eccDNAs by replication-dependent mechanisms. Mutagenesis occurs within the non-B DNAs and extends several kilobases bidirectionally into flanking and nonallelic DNA. Each non-B DNA exhibits a different pattern of mutagenesis, while sister clones containing the same non-B DNA also display distinct patterns of recombination, microhomology-mediated template switching and base substitutions. Mutations include mismatches, short duplications, long nontemplated insertions, large deletions and template switches to sister chromatids and nonallelic chromosomes. Drug-induced replication stress or the depletion of DNA repair factors Rad51, the COPS2 signalosome subunit or POLη change the pattern of template switching and alter the eccDNA mutagenic profiles. We propose an asynchronous capture model based on break-induced replication from microsatellite-induced DNA double strand breaks to account for the generation and circularization of mutagenized eccDNAs and the appearance of genomic homologous recombination deficiency (HRD) scars. These results may help to explain the appearance of tumor eccDNAS and their roles in neoantigen production, oncogenesis and resistance to chemotherapy.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 2","pages":"zcae027"},"PeriodicalIF":3.4,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11161834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141297689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The shaping of mRNA translation plasticity by RNA G-quadruplexes in cancer progression and therapy resistance. 在癌症进展和抗药性过程中，RNA G-四联体对 mRNA 翻译可塑性的影响。

NAR cancer Pub Date : 2024-05-31 eCollection Date: 2024-06-01 DOI: 10.1093/narcan/zcae025

Anne Cammas, Alice Desprairies, Erik Dassi, Stefania Millevoi

引用次数: 0

Non-canonical mRNA translation initiation in cell stress and cancer. 细胞应激和癌症中的非规范 mRNA 翻译启动

NAR cancer Pub Date : 2024-05-31 eCollection Date: 2024-06-01 DOI: 10.1093/narcan/zcae026

Mélanie Mahé, Tiffany Rios-Fuller, Olga Katsara, Robert J Schneider

{"title":"Non-canonical mRNA translation initiation in cell stress and cancer.","authors":"Mélanie Mahé, Tiffany Rios-Fuller, Olga Katsara, Robert J Schneider","doi":"10.1093/narcan/zcae026","DOIUrl":"10.1093/narcan/zcae026","url":null,"abstract":"The now well described canonical mRNA translation initiation mechanism of m7G 'cap' recognition by cap-binding protein eIF4E and assembly of the canonical pre-initiation complex consisting of scaffolding protein eIF4G and RNA helicase eIF4A has historically been thought to describe all cellular mRNA translation. However, the past decade has seen the discovery of alternative mechanisms to canonical eIF4E mediated mRNA translation initiation. Studies have shown that non-canonical alternate mechanisms of cellular mRNA translation initiation, whether cap-dependent or independent, serve to provide selective translation of mRNAs under cell physiological and pathological stress conditions. These conditions typically involve the global downregulation of canonical eIF4E1/cap-mediated mRNA translation, and selective translational reprogramming of the cell proteome, as occurs in tumor development and malignant progression. Cancer cells must be able to maintain physiological plasticity to acquire a migratory phenotype, invade tissues, metastasize, survive and adapt to severe microenvironmental stress conditions that involve inhibition of canonical mRNA translation initiation. In this review we describe the emerging, important role of non-canonical, alternate mechanisms of mRNA translation initiation in cancer, particularly in adaptation to stresses and the phenotypic cell fate changes involved in malignant progression and metastasis. These alternate translation initiation mechanisms provide new targets for oncology therapeutics development.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 2","pages":"zcae026"},"PeriodicalIF":0.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141201327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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