Cancer Science最新文献

{"title":"TERT Promoter Mutations Are Preferentially Associated With the ERBB2 G776-Altered Subtype of HER2-Mutant NSCLC.","authors":"Akihiro Yoshimura, Juichiro Yoshida, Chieko Takumi, Koichi Takayama","doi":"10.1111/cas.70504","DOIUrl":"10.1111/cas.70504","url":null,"abstract":"<p><p>HER2-mutant non-small cell lung cancer (NSCLC) comprises molecularly heterogeneous tumors with diverse ERBB2 mutation subtypes, and HER2-directed therapies have increased the need for refined molecular stratification. However, subtype-specific co-occurring genomic alterations remain incompletely characterized. We performed a two-stage clinicogenomic analysis to identify and validate recurrent co-mutations in HER2-mutant NSCLC. A public MSK-IMPACT lung adenocarcinoma cohort was used for discovery, and a nationwide Japanese real-world cohort from the Center for Cancer Genomics and Advanced Therapeutics was used for validation. In the MSK-IMPACT cohort of 2201 lung adenocarcinomas, TERT mutations were significantly enriched in ERBB2-mutant tumors compared with ERBB2-wild-type tumors (odds ratio, 2.40; 95% confidence interval, 1.12-4.70; p = 0.017). This association was reproduced in the independent validation cohort, where 16 of 174 HER2-mutant NSCLC cases harbored concurrent TERT mutations, all of which were promoter-region variants. Among the evaluated clinicogenomic variables, the ERBB2 mutation subtype was the only factor significantly associated with TERT mutation status. The ERBB2 G776-altered subtype remained independently associated with TERT mutation after multivariable adjustment (adjusted odds ratio, 7.49; 95% confidence interval, 1.81-31.0; p = 0.006). In a small exploratory subset of trastuzumab deruxtecan-treated patients (n = 52; TERT-mutated, n = 5), no statistically robust differences in treatment outcomes were observed according to TERT mutation status. TERT promoter mutations are recurrent co-mutations in HER2-mutant NSCLC and are preferentially associated with the ERBB2 G776-altered subgroup. These findings support ERBB2 subtype-aware molecular stratification and highlight previously underappreciated genomic heterogeneity within HER2-mutant NSCLC.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13470766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148726883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quizartinib Resistance Mutations and Treatment Outcomes in Relapsed or Refractory FLT3-ITD-Positive AML.","authors":"Yuichiro Semba, Toshihiro Miyamoto, Senji Kasahara, Yoshikane Kikushige, Takahiro Maeda, Goichi Yoshimoto, Shuichi Ota, Akio Saito, Yuho Najima, Hiroki Hosoi, Daigo Niiya, Koji Kato, Koji Nagafuji, Takashi Akasaka, Tomohiko Kamimura, Atsushi Takita, Maiko Narahara, Tadashi Toki, Koichi Iwanaga, Koji Yonemoto, Mine Harada, Koichi Akashi","doi":"10.1111/cas.70485","DOIUrl":"10.1111/cas.70485","url":null,"abstract":"<p><p>Quizartinib is a FMS-like tyrosine kinase 3 (FLT3) inhibitor indicated for FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukemia (AML). We aimed to evaluate quizartinib resistance mechanisms, in addition to efficacy and safety outcomes, in patients with relapsed or refractory FLT3-ITD-positive AML. This multicenter, single-arm study in Japan (jRCTs071200015) enrolled 18 patients between May 2020 and December 2022. Of these, 15 patients received oral quizartinib (up to 53 mg once daily) for up to 12 cycles of 28 days each, then were followed for 12 months. The primary endpoint was to evaluate the type and rate of quizartinib resistance mutations; secondary endpoints included composite complete remission (CRc) rate, overall response rate (ORR), hematopoietic stem cell transplantation (HSCT) rate, relapse-free survival (RFS), overall survival (OS), and adverse events (AEs). Among seven evaluable patients, acquired mutations were detected in four patients (NF1 [R2616X], CSF3R [Q754X], NRAS [G13R], and FLT3 [D835Y] in one patient each), while loss of FLT3-ITD was observed in two patients. In efficacy analyses (n = 15), CRc rate was 66.7% (95% confidence interval [CI], 38.4-88.2), ORR was 73.3% (44.9-92.2), and median OS was 13.6 months (5.4-not evaluable). Three patients (20.0%) received HSCT directly after quizartinib; in these patients, median RFS was 8.5 months (95% CI, 6.2-not evaluable). Grade ≥ 3 non-hematologic AEs and grade 1 QT prolongation were each reported in three patients (20.0%). These data offer additional information on potential resistance mechanisms in patients with relapsed or refractory FLT3-ITD-positive AML. Trial Registration: Japan Registry of Clinical Trials (jRCTs071200015).</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13464453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Request for Clarification on Data Presentation in Table 2, Figures 3 and 4 of Onuki et al. (Cancer Science 2020).","authors":"Junying Zhang","doi":"10.1111/cas.70503","DOIUrl":"10.1111/cas.70503","url":null,"abstract":"<p><p>This Letter requests clarification of two data presentation issues in Onuki et al. (Cancer Science 2020): a numerical discrepancy in Table 2 and the unspecified age range in Figure 3 that may explain the 1000-case difference with Figure 4.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13464451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"scRNA-Seq in Gastric Cancer Reveals Macrophage-Derived C1q as a Diagnostic Marker.","authors":"Saisai Gong, Yupeng Zhao, Sheng Yang, Tong Liu, Chengyun Li, Yun Zhou, Geyu Liang","doi":"10.1111/cas.70495","DOIUrl":"10.1111/cas.70495","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) and the complement system play pivotal roles in reshaping the chronic inflammatory microenvironment and driving malignant transformation. Although C1QA⁺ TAMs have been identified in multiple tumor types, their role in gastric cancer (GC) remains unexplored. Single-cell RNA sequencing (scRNA-seq) was performed on paired tumor tissues and adjacent tissues from three treatment-naïve patients to map macrophage heterogeneities. To evaluate the clinical and translational value of C1q, immunohistochemistry (IHC) was conducted on 100 GC samples, and C1q concentrations were measured via ELISA in plasma from a multi-center cohort of 240 patients and 100 GC tissue. Additionally, the effects of C1q-mediated THP-1-derived macrophages on the malignant behaviors of GC cells were investigated using in vitro migration. Transcriptomic analysis of 56,151 single cells successfully identified a distinct pro-inflammatory subset: C1QA⁺ TAMs. IHC staining demonstrated that C1q and CD163 were highly co-expressed in compromised tissues, and their elevated expression significantly correlated with poor patient prognosis. Multi-center plasma analysis revealed that elevated circulating C1q levels robustly enhanced clinical diagnostic accuracy. In vitro functional assays confirmed that C1q significantly primed M2 macrophage polarization, thereby accelerating the migration of GC cells. We first identified and functionally validated the C1QA⁺ TAM subset as a key driver of microenvironmental remodeling. C1q serves as a crucial mediator of macrophage polarization and holds strong promise as a novel, non-invasive biomarker for the early diagnosis.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased Expression by a Chemically Modified siRNA to PTBP1 Seriously Affects Warburg Effect in Colorectal Cancer Cells.","authors":"Keita Matsumoto, Hirokatsu Hayashi, Yoshihisa Tokumaru, Seito Fujibayashi, Noriki Mitsui, Masahide Endo, Takeshi Horaguchi, Yuji Hatanaka, Ryoma Yokoi, Chika Mizutani, Masashi Kuno, Masahiro Fukada, Ryuichi Asai, Itaru Yasufuku, Yuta Sato, Jesse Yu Tajima, Yoshihiro Tanaka, Remi Nakashima, Yukihiro Akao, Nobuhisa Matsuhashi","doi":"10.1111/cas.70491","DOIUrl":"10.1111/cas.70491","url":null,"abstract":"<p><p>Cancer cells preferentially rely on aerobic glycolysis, known as the Warburg effect, to support growth and survival. We previously demonstrated that polypyrimidine tract-binding protein 1 (PTBP1) maintains PKM2 dominance by regulating pyruvate kinase isoform splicing, sustaining the Warburg phenotype. PTBP1 suppression shifts metabolism toward PKM1 dominance, enhancing oxidative phosphorylation, reactive oxygen species (ROS) production, apoptosis, and antitumor immunity. Thirteen chemically modified siR-PTBP1 derivatives targeting either the coding region or the 3'-untranslated region (3'-UTR) of PTBP1 mRNA were synthesized and evaluated in colorectal cancer cell lines. Cytotoxicity, protein expression, oxidative stress, and metabolic alterations were assessed using cell-based assays, immunoblotting, and metabolomic analysis. siRNA stability was evaluated following nuclease exposure and quantified by TaqMan RT-qPCR. siRNAs targeting the 3'-UTR more effectively suppressed PTBP1 expression and increased the PKM1/PKM2 ratio than coding-region-targeting siRNAs. Among them, derivative 2-6 showed the strongest cytotoxicity with oxidative stress and apoptosis. Metabolomic profiling demonstrated altered glycolytic flux and preserved pentose phosphate pathway intermediates with activated redox responses, while adenylate and guanylate energy charges remained viable, indicating metabolic stress without energy collapse. Tricarboxylic acid cycle metabolites were elevated, consistent with enhanced oxidative phosphorylation. Derivative 2-6 showed resistance to nuclease-mediated degradation. Direct PKM2 knockdown did not induce comparable cytotoxicity. Chemically modified siR-PTBP1, particularly derivative 2-6, induces a metabolically vulnerable state characterized by oxidative imbalance, leading to apoptosis. These findings identify PTBP1 as a key regulator of the Warburg effect and support siRNA-based metabolic targeting as a therapeutic strategy.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological Considerations on Neutrophil-Macrophage Crosstalk in Gastric Cancer Under Chemo Immunotherapy.","authors":"Haitao You, Shunxiong Tang","doi":"10.1111/cas.70493","DOIUrl":"10.1111/cas.70493","url":null,"abstract":"","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Five-Year Trends in Biomarker Testing and Targeted Therapy for NSCLC: A Patient-Initiated Nationwide Survey in Japan.","authors":"Satoshi Ikeda, Kazuo Hasegawa, Takayuki Takahama, Kenta Kachi, Akihiro Yanagisawa, Sachiko Kawakami, Masashi Yoshida, Miyuki Sakai, Sachiko Watanabe, Kazuhiko Nakagawa","doi":"10.1111/cas.70499","DOIUrl":"10.1111/cas.70499","url":null,"abstract":"<p><p>Although multigene testing for advanced non-small cell lung cancer (NSCLC) is reimbursed in Japan, optimizing its real-world clinical impact remains challenging. This study updates nationwide testing trends and evaluates the treatment gap between diagnostic results and first-line therapeutic interventions. We conducted a retrospective cohort study using the Diagnosis Procedure Combination database (April 2019 to May 2024). The analysis included 24,047 patients with Stage IV NSCLC across 300 hospitals who underwent diagnostic lung biopsies. Comprehensive multigene testing shifted significantly; testing for ≥ 5 genes rose sharply from late 2021, followed by a marked increase in 6-7 gene testing from mid-2023. Testing for rare drivers (MET, RET, KRAS, HER2) increased substantially. However, approximately 30% of patients remained untested regardless of region or age. While the proportion of patients receiving first-line targeted therapy plateaued at just under 30%, the use of targeted therapies for rare drivers showed a steady increase. In conclusion, multigene testing has rapidly replaced single-gene testing in Japan, narrowing the diagnostic gap for rare oncogenic drivers. Nevertheless, the persistent 30% untested rate emphasizes the need for better shared decision-making to ensure all patients receive comprehensive biomarker evaluation.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148686206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircHECTD1 Promotes Cholangiocarcinoma Progression Through Interaction With SFPQ to Induce Autophagy.","authors":"Shouwen Zhao, Shanshan Jiang, Xutong Wang, Kai Cui, Zhilei Cao, Le Zhang, Zhiqiang Wei, Yuping Ma, Han Hao, Kunpeng Zhang, Jiamin Zhang, Tianyu Dong","doi":"10.1111/cas.70498","DOIUrl":"10.1111/cas.70498","url":null,"abstract":"<p><p>Cholangiocarcinoma (CCA) constitutes a highly malignant tumor type demonstrating rising global incidence rates. Circular RNAs (circRNAs), characterized by their covalently bonded single-stranded loop configuration, have been identified as functional regulators across various cancer types. Previous studies have suggested circHECTD1's involvement in tumor processes, but its specific contributions and molecular pathways in CCA progression, particularly regarding autophagy regulation, remain unclear. Experimental data demonstrated significant upregulation of circHECTD1 in CCA cell lines, along with notable stability against RNase-mediated breakdown. From a functional perspective, increased circHECTD1 expression stimulated tumor cell growth, motility, invasive capacity, and autophagy processes, while triggering autophagosome formation. Mechanistically, circHECTD1 served as a molecular platform for the splicing factor SFPQ (proline- and glutamine-rich), facilitating SFPQ's binding to the ATG12 promoter regulatory region and enhancing the expression of ATG12 mRNA, resulting in increased transcriptional activity and enhanced mRNA durability, which in turn stimulated the autophagic process. When SFPQ was experimentally downregulated, this effect was diminished. Conversely, when autophagy was pharmacologically inhibited, the oncogenic effects mediated by circHECTD1 were effectively counteracted. These observations suggest that circHECTD1 plays a crucial role in the progression of CCA by forming a complex with SFPQ, which subsequently enhances both the transcription of ATG12 and the stability of ATG12 mRNA, thereby promoting autophagy and tumor progression.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13451654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148690143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Daraxonrasib and Beyond: Pan-RAS Inhibition, Resistance, and Next-Generation Strategies.","authors":"Ryo Honda","doi":"10.1111/cas.70497","DOIUrl":"10.1111/cas.70497","url":null,"abstract":"<p><p>RAS proteins have long been considered difficult therapeutic targets, but allele-selective inhibitors established the clinical tractability of mutant RAS. Daraxonrasib (RMC-6236), an oral pan-RAS inhibitor, has now extended this concept by targeting multiple mutant and wild-type RAS proteins. In the randomized phase III RASolute 302 trial, daraxonrasib substantially improved survival over chemotherapy in previously treated metastatic pancreatic ductal adenocarcinoma while maintaining manageable toxicity, thereby establishing a clinically useful therapeutic window for pan-RAS inhibition. Nevertheless, epithelial toxicity and acquired resistance, including mutations affecting ternary-complex formation and mechanisms associated with increased KRAS abundance, remain important challenges. This review discusses the mechanistic and clinical development of daraxonrasib and examines emerging strategies designed to improve the depth, durability, and selectivity of RAS suppression. These include pan-KRAS inhibitors, targeted RAS degraders, RAS-cleaving protein biologics, and tumor-directed delivery systems. Together, these approaches may reshape the treatment of RAS-driven cancers across tumor types and disease stages.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13444396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148680781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LAMC2⁺ Epithelial Cells Drive Bladder Cancer Progression and Predict Immunotherapy Response via SERPINB3/STAT3/CD44 Axis.","authors":"Yutong Chen, Yunzhong Jiang, Zezhong Yang, Minxuan Jing, Wentai Wu, Jiale He, Lu Wang, Minghai Ma, Yaodong Zhang, Min Wang, Jianpeng Li, Yuanchun Pu, Bingliang He, Yanjia Liu, Kaibo Mi, Hang Liu, Mengzhao Zhang, Jinhai Fan","doi":"10.1111/cas.70492","DOIUrl":"10.1111/cas.70492","url":null,"abstract":"<p><p>Laminin subunit gamma 2 (LAMC2) is a molecule related to the extracellular matrix. It plays a vital role in many cancers. But its effect in bladder cancer (BCa) is still undefined. This study was aimed at exploring the biological function, downstream mechanism, and therapeutic potential of LAMC2 in BCa. We combined single-cell RNA sequencing data from 13 BCa samples and data from TCGA-BLCA, GSE13507, and IMvigor210 cohorts. Bioinformatics analyses were carried out, including epithelial cell subclustering, pathway enrichment, GSVA, HdWGCNA, and RNA sequencing. The expression of LAMC2 in BCa tissues was confirmed through immunohistochemistry and immunofluorescence. Then shRNA was used to knock down LAMC2 in 5637 and T24 cells to test its effects in vitro and in vivo. These results were also tested in a xenograft tumor model. Potential inhibitors of LAMC2 were screened by molecular docking and in vitro experiments. We found that LAMC2 was enriched in a malignant epithelial cell subgroup and was linked to higher tumor grade, advanced tumor stage, poor prognosis and inferior response to immunotherapy. LAMC2 regulated bladder cancer cell proliferation, migration, and invasion through the SerpinB3/STAT3/CD44 axis based on the results of in vitro and single-cell analysis. Diosmetin was found to suppress LAMC2-related signaling in bladder cancer cells, providing a new strategy for BCa treatment.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}