Cancer gene therapy最新文献

{"title":"Reprogramming the tumor microenvironment via TFF3 targeting: a potential novel avenue to boost CAR-T cell therapy in solid tumors","authors":"Arman Rahimi, Ghasem Solgi, Mehrnoush Safarzadeh, Pantea Mohammadi, Mohsen Rastegari-Pouyani","doi":"10.1038/s41417-026-01040-9","DOIUrl":"10.1038/s41417-026-01040-9","url":null,"abstract":"CAR-T cell therapy has shown great success in hematological malignancies. However, this immunotherapeutic strategy faces critical challenges in solid tumors mainly due to the key hurdles brought about by the hostile tumor microenvironment (TME). Effective CAR-T cell therapy in solid tumors is hampered by low tumor infiltration of the administered T cells due to the dense fibrotic nature of the TME and its aberrant vasculature. Also, solid tumors shape a highly immunosuppressive milieu in which the cytotoxic activity and persistence of functional CAR-T cells are abolished. Trefoil factor family (TFF) peptides, especially TFF3, have recently drawn a lot of attention due to their pro-tumor activities. Based on the recent evidence, TFF3 is upregulated in solid tumors where it plays roles in chemotherapy resistance, increased survival, and proliferation of cancer cells, expansion of the immunosuppressive cells and enhanced angiogenesis, which contributes to the aberrant tumor vasculature. In this review, we explore how TFF3 signaling contributes to tumor progression and immune escape, and how its inhibition might reshape the tumor microenvironment (TME) to better support CAR-T cell activity. Mounting evidence suggests that blocking TFF3 could help reduce immunosuppression, restore more normal blood vessel structure, and disrupt the pro-fibrotic and tumor-promoting interactions driven by cancer stem cells (CSCs). At the same time, since TFF3 plays an important role in protecting mucosal tissues and promoting repair after injury, its inhibition needs to be approached carefully. We also discuss strategies to selectively block TFF3 within tumors while minimizing unwanted effects on healthy tissues. Gaining a deeper understanding of how TFF3 contributes to therapy resistance may open up new opportunities to enhance CAR-T cell treatment in solid tumors, either through combination therapies or as a preconditioning step before CAR-T cell infusion.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 4","pages":"492-503"},"PeriodicalIF":6.4,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263222","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":"Hepatitis B virus–induced hepatocellular carcinoma: HBx-associated epigenetic mechanisms and therapeutic opportunities","authors":"Atahar Husein, Azfar Jamal, Mohammad Azhar Kamal, Yaser E. Alqurashi, Esam S. Al-Malki, Mohammed M. Naiyer, Syed Arif Hussain, Mohiuddin Khan Warsi","doi":"10.1038/s41417-026-01051-6","DOIUrl":"10.1038/s41417-026-01051-6","url":null,"abstract":"Chronic hepatitis B virus (HBV) infection is a major etiological factor in the development of hepatocellular carcinoma (HCC), a cancer that causes a large number of cancer-related deaths around the world. Although antiviral treatments are effective, the risk of HCC remains because studies using advanced sequencing have shown that liver cells still carry integrated viral DNA, experience ongoing inflammation, and undergo lasting changes in epigenetic regulation. HBV maintains its genome in liver cells as a chromatin-like cccDNA structure, and with the help of the HBx protein, it manipulates the cell’s chromatin machinery to support viral gene expression and disrupt normal control of enhancers, DNA methylation, and Polycomb regulation. These alterations enhance transcriptional plasticity and, in the context of chronic liver injury and additional somatic mutations, may contribute to malignant transformation. This review highlights recent mechanistic studies that have suggested a pathway linking HBV persistence to chromatin dysfunction. Further, it outlines an emerging therapeutic opportunity with chromatin-directed drugs, as well as rational combinations of these drugs with immunotherapy for HBV-related HCC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 5","pages":"612-623"},"PeriodicalIF":6.4,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249455","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":"Mesenchymal stem cell-mediated delivery boosts the efficacy of suicide gene therapy based on retroviral replicating vectors in peritoneally disseminated cancer","authors":"Shuji Kubo, Yuya Takeuchi, Emiko Sonoda-Fukuda, Nao Ogawa, Shugo Shinoda, Akiko Nakano-Doi, Takayuki Nakagomi, Soichiro Funaki, Noriyuki Kasahara","doi":"10.1038/s41417-026-01047-2","DOIUrl":"10.1038/s41417-026-01047-2","url":null,"abstract":"Retroviral replicating vectors (RRVs) hold promise for cancer gene therapy but face limitations due to their relatively low titers and susceptibility to inactivation by body fluids, limiting their application to intratumoral delivery. To overcome these challenges and target metastatic cancers, we investigated the use of tumor-homing mesenchymal stem cells (MSCs) as RRV carriers in a clinically relevant model of malignant peritoneal mesothelioma. MSCs derived from adipose tissue, bone marrow, and umbilical cord demonstrated significant migration toward mesothelioma cells and were permissive to RRV infection and production. MSCs transferred RRVs to tumor cells more effectively in direct co-culture than in Transwell assays. Using peritoneally disseminated cancer models, we confirmed that MSCs enhanced RRV transfer, even under ascites-mimicking conditions. In vivo biomolecular imaging and flow cytometry revealed markedly reduced RRV transduction under ascites conditions; however, MSC/RRV delivery significantly enhanced intratumoral viral transmission. Furthermore, while both direct RRV and MSC/RRV treatments were effective in non-ascites models, MSC/RRV delivery achieved superior antitumor efficacy in ascites-mimicking models, resulting in robust tumor suppression and prolonged survival. These findings highlight the potential of MSCs to overcome the limitations of RRV and suggest that MSC-based RRV-mediated suicide gene therapy represents a promising strategy for peritoneally disseminated cancers complicated by cancerous ascites.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 8","pages":"909-918"},"PeriodicalIF":6.4,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01047-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Tumor-suppressive role of CNTNAP2 in glioma: Dual regulation of the NDN-ERK axis and M2 macrophage polarization","authors":"Yu Wu, Weiwei Zou, Shiqi Xia, Ti Zhang, Fan Yao, Yangqin Li, Xiaoqian Liu, Qian Peng, Xiao-Liang Xing","doi":"10.1038/s41417-026-01046-3","DOIUrl":"10.1038/s41417-026-01046-3","url":null,"abstract":"Cancer constitutes a persistent major global health burden, which underscores the urgent demand for innovative biomarkers and therapeutic targets. While the Contactin-associated protein (CNTNAP) family has been associated with tumor development, the pan-cancer role of CNTNAP2 is still poorly characterized. Researchers performed a comprehensive pan-cancer analysis of CNTNAP2 based on The Cancer Genome Atlas (TCGA) datasets to evaluate its expression profile and clinical relevance, and conducted functional experiments in U118MG glioblastoma cells and CNTNAP2-deficient mouse tissues to verify its biological function. The results identified CNTNAP2 as a dual diagnostic (AUC > 0.9) and prognostic biomarker for glioma, with low expression levels correlating to worse overall survival. In vitro assays showed that CNTNAP2 knockdown enhanced the proliferation and migration of U118MG cells, while its overexpression inhibited these malignant phenotypes. Mechanistically, CNTNAP2 deficiency triggered excessive activation of the ERK signaling pathway and downregulated its key downstream target Necdin (NDN), and pharmacological inhibition of ERK reversed the oncogenic effects caused by CNTNAP2 silencing. Further analysis demonstrated elevated M2 macrophage infiltration in glioma, and CNTNAP2 expression was closely correlated with M2 macrophage polarization; high CNTNAP2 expression also corresponded to lower TIDE scores, suggesting improved immunotherapy response. Collectively, CNTNAP2 acts as a tumor suppressor in glioma via the NDN-ERK axis, suppressing tumor progression and M2 macrophage polarization, making it a promising diagnostic, prognostic biomarker and potential therapeutic target for glioma.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 7","pages":"810-820"},"PeriodicalIF":6.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01046-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TP53 mutation at codon 179 metabolically reprograms cancer cells to promote invasion","authors":"Debina Sarkar, Gaurav C. Gyanwali, Jaishree Patel, Polina Shevchuk, Aaron Jeffs, Adele G. Woolley, Selena Wang, Maryam Sardari, Apeksha Bhandarkar, Halima Siddiqui, Magdalena Ratajska, Makhdoom Sarwar, Srinivasaraghavan Kannan, Chandra S. Verma, Catherine J. Drummond, Cushla McKinney, Jisha Antony, Sally P. McCormick, Antony Braithwaite, Sunali Mehta","doi":"10.1038/s41417-026-01045-4","DOIUrl":"10.1038/s41417-026-01045-4","url":null,"abstract":"Mutations in the tumour suppressor, TP53, are prevalent in human cancers yet their functional implications remain unclear. Through comprehensive pan-cancer database analysis, we identified H179 mutations in TP53 as significantly associated with poor disease-free survival across multiple cancer types. Functional studies in lung, ovarian, and prostate cancer cells over-expressing the p53H179R/Y mutants revealed that these mutants are not only defective in tumour-suppressive functions but also actively promote tumour progression. These mutants drive metabolic reprogramming by increasing neutral lipid levels through de novo fatty acid synthesis (p53H179R/Y) and fatty acid uptake (p53H179Y), accompanied by increased lipid droplets and APOE expression, collectively promoting enhanced invasiveness relative to p53-null cells. Our findings demonstrate that TP53 missense mutations are not functionally equivalent to TP53 loss. Notably, H179 mutations act as oncogenic drivers, and our data highlight APOE and lipid metabolism as potential therapeutic targets, underscoring the clinical relevance of precise TP53 mutation characterisation.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 7","pages":"775-794"},"PeriodicalIF":6.4,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01045-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GOT1 promotes endometrial cancer progression by regulating ferroptosis through the STAT3-GPX4 axis and attenuating medroxyprogesterone acetate sensitivity","authors":"Yiran Li, Yuting Shen, Wen Lu","doi":"10.1038/s41417-026-01044-5","DOIUrl":"10.1038/s41417-026-01044-5","url":null,"abstract":"Ferroptosis plays a critical role in tumor development and treatment response, but its regulatory mechanisms in endometrial cancer (EC) are not well understood. This study aimed to identify ferroptosis-related genes in EC and explore their roles and mechanisms. Differentially expressed genes from EC datasets were intersected with ferroptosis-related gene sets to identify key candidates. The functional role of GOT1 was studied using in vitro assays, while transcriptomic and proteomic profiling were integrated to explore downstream pathways. Immunohistochemistry (IHC) was performed on 35 EC samples and 11 adjacent normal tissues. GOT1’s contribution to medroxyprogesterone acetate (MPA) resistance was evaluated both in vitro and in vivo. GOT1 expression was significantly elevated in EC tissues and correlated with poor prognosis. Silencing GOT1 impaired EC cell proliferation and migration, increasing intracellular Fe²⁺, lipid ROS, and 4-HNE levels. IHC confirmed elevated GOT1, STAT3, GPX4, TFRC, TFAP4, and PAX8 in EC tissues. Transcriptome data showed that GOT1 knockdown reduced GPX4 and altered metabolism pathways. Overexpression of GPX4 reversed the ferroptosis and growth inhibition caused by GOT1 depletion. Proteomic analysis revealed that GOT1 physically interacts with STAT3 and functionally enhances STAT3-dependent transcription, thereby indirectly promoting GPX4 expression. GOT1 overexpression reduced EC cell sensitivity to MPA in vitro and in vivo, whereas GOT1 inhibition partially restored MPA responsiveness. It contributes to EC progression and ferroptosis resistance via the STAT3–GPX4 axis, diminishing MPA efficacy. GOT1 may serve as potential biomarker and therapeutic target to enhance ferroptosis-based strategies in EC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 7","pages":"795-809"},"PeriodicalIF":6.4,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01044-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The paradox of miR-107 in oncology: dual roles as a tumor suppressor and oncomiR","authors":"Mamdouh A. Ragab, Nevine Fathy, Yasmin M. Attia, Eman A. Amer, Sally A. Fahim","doi":"10.1038/s41417-026-01042-7","DOIUrl":"10.1038/s41417-026-01042-7","url":null,"abstract":"MicroRNAs (miRNAs) are central post-transcriptional regulators that shape oncogenic and tumor-suppressive networks through RNA-induced silencing complex (RISC)–mediated repression of target mRNAs. Among these, hsa-miR-107—a member of the miR-16 family encoded within an intron of the PANK1 gene—has emerged as a particularly paradoxical regulator in cancer. Accumulating evidence indicates that miR-107 cannot be classified as a single-function miRNA; instead, it behaves as a context-dependent “molecular switch” whose impact is dictated by tissue-specific target availability, tumor stage, and the surrounding regulatory landscape. This review synthesizes mechanistic and translational data explaining how miR-107 exerts opposing roles as both a tumor suppressor and an oncomiR. In tumor-suppressive contexts, miR-107 integrates into stress-response circuitry via a p53/PANK1/miR-107 axis, repressing HIF-1β, impairing HIF-1 complex formation, and reducing VEGF-driven angiogenesis. miR-107 also restricts proliferation and invasion by targeting cell-cycle kinases (e.g., CDK6 and CDK8), suppressing NOTCH2 signaling in glioma, and attenuating pro-survival PI3K/AKT signaling indirectly in NSCLC through BDNF repression. Conversely, in aggressive cancers, miR-107 promotes malignancy through “meta-oncogenic” disruption of global miRNA biogenesis by targeting DICER1, enabling EMT programs via loss of miR-200 family activity. It also activates PI3K/AKT signaling through direct repression of PTEN (notably in bladder cancer) and enhances metastatic behavior in colorectal cancer by co-silencing metastasis suppressors such as DAPK and KLF4. A distinctive layer of complexity is added by miR-107-mediated miRNA–miRNA interaction, exemplified by direct destabilization of the tumor-suppressive let-7 family in advanced breast cancer. Therefore, the review highlights higher-order regulation by lncRNA competing endogenous RNA (ceRNA) “sponges” that sequester miR-107 (e.g., LINC00662, UASR1, H19, MFI2-AS1), thereby rewiring downstream oncogenic pathways. We discuss emerging clinical implications of miR-107 as a biomarker and as a therapeutic lever for reversing multidrug resistance, while outlining key challenges for safe, context-aware miRNA-based interventions.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 7","pages":"888-896"},"PeriodicalIF":6.4,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01042-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical landscape and development of universal CAR-T cell therapies","authors":"Jincai Zhou","doi":"10.1038/s41417-026-01043-6","DOIUrl":"10.1038/s41417-026-01043-6","url":null,"abstract":"","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 7","pages":"884-887"},"PeriodicalIF":6.4,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052893","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":"Single-nucleus and spatial transcriptomics analyses reveal interplay between evolutionary dynamics and energy metabolism in primary cardiac lymphoma","authors":"Xiaojuan Wei, Qianbing Zhang, Pengjun Liao, Sichu Liu, Xinmiao Jiang, Ling Huang, Su Yao, Hui Yuan, Kezhen Li, Wenyu Li, Liwei Hao, Sipei Wu","doi":"10.1038/s41417-026-01031-w","DOIUrl":"10.1038/s41417-026-01031-w","url":null,"abstract":"Primary cardiac lymphoma (PCL), a rare B-cell non-Hodgkin’s lymphoma, has shown a rising incidence, yet the lack of clarity regarding its molecular basis continues to hinder the development of effective targeted therapies. In this study, we utilized single-nucleus RNA sequencing and Visium CytAssist spatial transcriptomics in two patients with PCL to examine the metabolic and immune landscape of PCL. Our data implicate chromosomal instability (CIN) as a potential driver of disease progression, likely by modulating cellular sensitivity to metabolic stress. Single-cell analysis identified five distinct malignant B-cell states, including a B3 subset defined by subclonal diversification and enriched fatty acid metabolism-MAPK signaling. NFYA was also noted as a transcription factor potentially involved in this lipid reprogramming. Spatial observations suggest that B3 cells may contribute to an immunosuppressive microenvironment, with the CD44-LGALS9 axis acting as a possible mediator of endothelial cell remodeling and T-cell suppression. Ultimately, this study provides fresh insights into the clonal evolution and metabolic adaptations of PCL. These findings suggest that fatty acid metabolic reprogramming and CD44-LGALS9-mediated immune evasion play roles in tumor maintenance within the cardiac environment, offering a preliminary basis for future targeted therapeutic intervention.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 5","pages":"571-587"},"PeriodicalIF":6.4,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004787","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":"The role of STAT3 in regulating ferroptosis in cancer: molecular mechanisms and targeted therapeutic perspectives","authors":"Xianglin Jiang, Yatsu Lam, Zhi Li, Zeting Yuan, Peihao Yin","doi":"10.1038/s41417-026-01037-4","DOIUrl":"10.1038/s41417-026-01037-4","url":null,"abstract":"Cancer is still a big health problem and a growing issue worldwide. Colorectal cancer (CRC), as a highly prevalent malignancy worldwide, faces critical challenges in overcoming therapy resistance and recurrence. Beyond classical cell death pathways like apoptosis, targeting alternative forms of programmed cell death (PCD) may provide novel strategies to circumvent current therapeutic limitations. Ferroptosis—an iron-dependent, lipid peroxidation-driven form of PCD—exerts dual roles in tumor modulation, with the STAT3 signaling pathway identified as its central regulatory hub. This review systematically elucidates the molecular mechanisms by which STAT3 suppresses ferroptosis in tumor cells through regulating glutathione peroxidase 4 (GPX4), iron metabolism genes (like TFR1, FTH1), and oxidative stress pathways. Furthermore, it explores how natural products (like baicalein, ginsenoside Rh3) and synthetic inhibitors (like W1131) targeting STAT3 inhibition modulate this signaling axis to induce ferroptosis across diverse tumor cell types. Nevertheless, off-target effects, drug resistance, and interference with physiological processes pose significant challenges for the clinical translation of STAT3 inhibitors. This review provides insights into addressing these unresolved issues.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 5","pages":"601-611"},"PeriodicalIF":6.4,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147873466","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}