Molecular Oncology最新文献

{"title":"Classification of acute myeloid leukemia based on multi-omics and prognosis prediction value.","authors":"Yang Song, Zhe Wang, Guangji Zhang, Jiangxue Hou, Kaiqi Liu, Shuning Wei, Yan Li, Chunlin Zhou, Dong Lin, Min Wang, Hui Wei, Jianxiang Wang, Tao Cheng, Yingchang Mi","doi":"10.1002/1878-0261.70000","DOIUrl":"10.1002/1878-0261.70000","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a heterogeneous cancer, making outcomes prediction challenging. Several predictive and prognostic models are used but have considerable inaccuracy at individual level. We tried to increase prediction accuracy using a multi-omics strategy. We interrogated data from 1391 consecutive, newly diagnosed subjects with AML, integrating information on mutation topography, DNA methylation, and transcriptomics. We developed an unsupervised multi-omics classification system (UAMOCS) with these data. UAMOCS provides a multidimensional understanding of AML heterogeneity and stratifies subjects into three cohorts: (a) UAMOCS1 [high lymphocyte activating 3 (LAG3) expression, chromosome instability, myelodysplasia-related mutations]; (b) UAMOCS2 (monocytic-like profile, immune suppression and activated angiogenesis and hypoxia pathways); and (c) UAMOCS3 [CCAAT enhancer binding protein alpha (CEBPA) mutations and MYC pathway activation]. UAMOCS distinguishes overall survival rates across the cohorts (TCGA P = 0.042; GSE71014 P = 0.043; ihCAMs-AML, GSE102691 and GSE37642 all P < 0.001). The model's C-statistic is comparable to the 2022 ELN risk classification (0.87 vs 0.82; P = 0.162), but offers a more nuanced distinction between intermediate- and high-risk groups. When combined with high-throughput drug sensitivity testing, UAMOCS can accurately predict sensitivity to azacitidine (AZA) and venetoclax. The UAMOCS system is available as an R package. The UAMOCS system has the potential to redefine AML subtypes, enhance prognostic predictions, and guide treatment strategies based on patients' immune status and expected responses to therapies.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1836-1854"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382782","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":"CircCCNB1 inhibits vasculogenic mimicry by sequestering NF90 to promote miR-15b-5p and miR-7-1-3p processing in nasopharyngeal carcinoma.","authors":"Chunmei Fan, Fenghua Tan, Jie Wu, Zhaoyang Zeng, Wenjia Guo, He Huang, Wei Xiong","doi":"10.1002/1878-0261.13821","DOIUrl":"10.1002/1878-0261.13821","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is a kind of malignant tumor with high metastasis. Circular RNAs (circRNAs) are involved in tumor progression, but their functions and mechanisms are not well understood. Vasculogenic mimicry (VM) has been discovered as an alternative way to supply tumor nutrition and accelerate tumor progression, including NPC. We previously found that circCCNB1 (derived from cyclin B1) could inhibit the migration and invasion of NPC cells by binding to nuclear factor 90 (NF90), however, whether circCCNB1 has additional biological functions is still unclear. In this study, the effects of circCCNB1 binding to NF90 on the generation of miR-15b-5p and miR-7-1-3p were detected using qRT-PCR, western blotting, RNA pulldown, ribonucleoprotein immunoprecipitation and truncated experiments. VM formation assays were used to assess their biological functions. We found that circCCNB1 promoted the processing and generation of miR-15b-5p and miR-7-1-3p through competitive binding to NF90, thereby inhibiting the expression of calumenin (CALU), kinesin family member 1B (KIF1B), RNA polymerase III subunit G (POLR3G), ultimately decreasing the VM of NPC cells. This study not only reveals a new function of circCCNB1 in NPC, but also provides new insights for targeting angiogenesis therapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1876-1893"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441525","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":"CINs of the cytoplasm: dissecting dsRNA signaling in chromosomal instability.","authors":"Aglaia Skolariki, Rose L Jady-Clark, Eileen E Parkes","doi":"10.1002/1878-0261.70047","DOIUrl":"10.1002/1878-0261.70047","url":null,"abstract":"<p><p>Chromosomal instability (CIN), a pervasive feature of cancer, promotes tumor evolution and inflammatory signaling, yet its influence on innate immune sensing remains incompletely understood. Ruptured micronuclei, a direct byproduct of CIN arising from missegregated chromosomes, expose out-of-context double-stranded DNA that engages the cGAS-STING pathway. In their recent study, Sasaki et al. show that micronuclei are also a source of immunogenic double-stranded RNA (dsRNA), triggering MAVS-dependent type I interferon responses independently of STING. The authors show that micronuclei undergo aberrant transcription, producing dsRNA from nonexonic, transcriptionally accessible loci, with many species localizing near interferon-stimulated genes. This work suggests a feedforward loop in which type I interferon signaling reinforces its own activation through transcriptional dysregulation. Using MPS1 inhibition to induce acute CIN, the authors show that MAVS signaling promotes MHC Class I expression and immune cell recruitment. These findings reposition CIN as a dual trigger of innate immunity through cytoplasmic DNA and RNA sensing. Future work should define how these pathways integrate in the context of chronic CIN and evaluate strategies to target DNA and RNA sensing in immune-edited tumors.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1561-1564"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044419","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":"Etoposide-induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms.","authors":"Aditya Karunanithi Nivedita, Varda Shoshan-Barmatz","doi":"10.1002/1878-0261.13807","DOIUrl":"10.1002/1878-0261.13807","url":null,"abstract":"<p><p>Etoposide is an inhibitor of DNA topoisomerase II, an enzyme essential for DNA transcription, replication, and chromosome segregation. It is well accepted that etoposide triggers cell death due to DNA damage. Our results indicate that multiple molecular mechanisms contribute to etoposide-induced apoptosis, including the overexpression of the mitochondrial voltage-dependent anion channel 1 (VDAC1) and its oligomerization, forming a mega-channel that releases pro-apoptotic proteins, thereby activating apoptosis. Etoposide induces C-terminal truncation of VDAC1 (VDAC1-ΔC) via the proteolytic actions of calpain-1 and asparagine endopeptidase (AEP). A calpain-specific inhibitor effectively prevented etoposide-induced VDAC1-ΔC formation, apoptosis, and the nuclear translocation of apoptosis-inducing factor (AIF). Additionally, etoposide upregulates the expression levels of apoptosis regulators (p53, Bax, p21, AIF) and of the proteases calpain and AEP. Etoposide-induced apoptosis and VDAC1 truncation are cell-type dependent and associated with calpain levels and activity. Etoposide-induced VDAC1-ΔC formation and apoptosis are tightly linked: as both display similar patterns of concentration- and time-dependence, both are inhibited by calpain and AEP inhibitors, as well as the VDAC1 oligomerization inhibitor VBIT-4, and are dependent on intracellular Ca²⁺. These findings highlight the complexity of etoposide's actions in different cellular contexts, suggest possible mechanisms of resistance, offer potential biomarkers for guiding etoposide treatment in cancer patients, and propose targeting VDAC1 and calpain as promising therapeutic strategies in cancer therapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1855-1875"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374375","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":"Enhancing patient engagement in cancer research: a focus on patient-centric approaches to scientific discovery.","authors":"Estela Cepeda, Marina Reguero, Vanesa Abón, Marta Puyol","doi":"10.1002/1878-0261.70004","DOIUrl":"10.1002/1878-0261.70004","url":null,"abstract":"<p><p>Patient engagement in healthcare and research empowers patients to actively participate in decision-making, treatment planning, and research design, fostering better treatment outcomes and relevance. However, barriers, such as power imbalances, structural limitations, a lack of awareness, and socioeconomic disparities, often hinder meaningful involvement, particularly for marginalized groups. Overcoming these challenges requires inclusive frameworks and infrastructures to promote collaboration among patients, researchers, and other stakeholders. Initiatives like the Patient Engagement Open Forum or World Cancer Research Day underscore the importance of patient-centered approaches. By fostering trust, transparency, and shared decision-making, a more inclusive and impactful healthcare and research ecosystem can be achieved.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1549-1552"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468746","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":"Strategies to reduce the cancer burden and improve access to effective and affordable cancer interventions in Europe.","authors":"Anton Berns, Ulrik Ringborg, Julio Celis, Bengt Jönsson, Michael Baumann","doi":"10.1002/1878-0261.70058","DOIUrl":"10.1002/1878-0261.70058","url":null,"abstract":"<p><p>The development of new anticancer treatments, their clinical evaluation and introduction into the healthcare system need improvement. New drugs and cell therapies often come with significant costs for society while only marginally improving patients' survival and health-related quality-of-life. Therefore, bold, innovative clinical trials with critical assessment of the efficacy and cost-effectiveness of new preventive measures and medical treatments are needed to ensure that patients and society benefit. Drug development programmes controlled by pharma should be complemented with initiatives such as stop studies, dose reduction, combination and repurposing trials. These should be validated in academia-initiated trials supported by societal funds. Special attention should be devoted to paediatric and rare adult cancers. Comprehensive Cancer Centres (CCCs) covering the entire cancer research continuum, present throughout the EU, are critical for this. More of such centres must be established concomitantly with a robust accreditation methodology to ensure that they meet appropriate quality standards. It is crucial that funding for these initiatives, now temporarily and partially provided by the EU Cancer Mission and Europe's Beating Cancer Plan, is secured for a much longer period.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1553-1560"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120255","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":"Targeted metabolomics reveals novel diagnostic biomarkers for colorectal cancer.","authors":"Zuojian Hu, Fenglin Shen, Yang Liu, Ziqing Zhong, Yongling Chen, Zhiyuan Xia, Cuiju Mo, Hongxiu Yu","doi":"10.1002/1878-0261.13791","DOIUrl":"10.1002/1878-0261.13791","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a prevalent malignant tumor worldwide, with a high mortality rate due to its complex etiology and limited early screening techniques. This study aimed to identify potential biomarkers for early detection of CRC utilizing targeted metabolite profiling of platelet-rich plasma (PRP). Based on multiple reaction monitoring (MRM) mode, liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis identified metabolites in PRP collected from patients with CRC (n = 70) and healthy controls (n = 30). A total of 302 metabolites were identified and quantified in this study, including various categories such as lipids, lipid mediators, amino acids, and derivatives, organic acids and derivatives, nucleotides and derivatives, alkaloids, carbohydrates, vitamins and derivatives, and others. The differential analysis revealed that five carbohydrates and organic acids (lactose, glycerol-3-phosphate, 2-hydroxyglutaric acid, isocitric acid, and citric acid) involved in the carbohydrate metabolism pathway displayed consistent upregulation within PRP derived from patients with CRC. To further validate the abundance of differential metabolites, 10 pairs of CRC tissues, adjacent tissues, and matched PRP were collected. Ultimately, five carbohydrate metabolites were validated in PRP, and compared with carcinoembryonic antigen (CEA) and cancer antigen 19-9 (CA199), the five carbohydrate metabolites significantly improved the specificity of differentiating patients with CRC from healthy controls. Furthermore, the diagnostic efficacy of the combined five-carbohydrate metabolite panel was superior to that of individual metabolites, CEA and CA199. The sensitivity, specificity, and AUC of the metabolite panel in distinguishing patients with CRC from healthy controls were 90.00%, 96.67%, and 0.961 (95% CI 0.922-0.998), respectively. Collectively, metabolomics was used to identify and validate differential metabolites in the PRP of CRC, which may serve as potential early screening markers for patients with CRC.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1737-1750"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927635","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":"Respiratory complex I-mediated NAD⁺ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21^Cip1 expression by SIRT3 and SIRT7.","authors":"Masato Higurashi, Kazunori Mori, Hidetsugu Nakagawa, Momoko Uchida, Fumihiro Ishikawa, Motoko Shibanuma","doi":"10.1002/1878-0261.13808","DOIUrl":"10.1002/1878-0261.13808","url":null,"abstract":"<p><p>The role of the electron transport chain (ETC) in cell proliferation control beyond its crucial function in supporting ATP generation has recently emerged. In this study, we found that, among the four ETC complexes, the complex I (CI)-mediated NAD⁺ regeneration is important for cancer cell proliferation. In cancer cells, a decrease in CI activity by RNA interference (RNAi) against NADH:ubiquinone oxidoreductase core subunit V1 (NDUFV1) arrested the cell cycle at the G₁/S phase, accompanying upregulation of p21^Cip1 cyclin-dependent kinase inhibitor expression. Mechanistically, a decrease in the NAD⁺/NADH ratio downregulated SIRT3 and SIRT7 function, which suppressed p21^Cip1 expression at the translational and transcriptional levels, respectively, resulting in the upregulation of the antiproliferative molecule. Importantly, high expression levels of the core subunits of CI correlated with poor prognosis in patients with the hormone receptor(+)/human epidermal growth factor receptor 2(-) (HR+/HER2-) subtype of breast cancer. Therefore, NDUFV1 and SIRT3/7 have emerged as promising therapeutic targets against this breast cancer subtype.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1775-1796"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053054","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":"Obesity alters the fitness of peritumoral adipose tissue, exacerbating tumor invasiveness in renal cancer through the induction of ADAM12 and CYP1B1.","authors":"Sepehr Torabinejad, Caterina Miro, Annarita Nappi, Francesco Del Giudice, Annunziata Gaetana Cicatiello, Serena Sagliocchi, Lucia Acampora, Federica Restolfer, Melania Murolo, Emery Di Cicco, Federico Capone, Ciro Imbimbo, Monica Dentice, Felice Crocetto","doi":"10.1002/1878-0261.13782","DOIUrl":"10.1002/1878-0261.13782","url":null,"abstract":"<p><p>Obesity exacerbates the risk and aggressiveness of many types of cancer. Adipose tissue (AT) represents a prevalent component of the tumor microenvironment (TME) and contributes to cancer development and progression. Reciprocal communication between cancer and adipose cells leads to the generation of cancer-associated adipocytes (CAAs), which in turn foster tumor invasiveness by producing paracrine metabolites, adipocytokines, and growth factors. Interfering with the crosstalk between CAAs and cancer cells is of key relevance in the prevention of tumor progression. The present study aimed to analyze the contribution of peritumoral AT in renal cell carcinoma (RCC) progression in lean versus overweight or obese patients. By isolating human adipose-derived stromal/stem cells from the three groups of patients and performing conditioned medium studies with RCC cells along with in vivo xenograft experiments, we found that peritumoral adipocytes from the three groups show a distinct expression profile of genes. In particular, ADAM metallopeptidase domain 12 (ADAM12) and cytochrome P450 family 1 subfamily B member 1 (CYP1B1) were found to be upregulated in obesity and their silencing reduced RCC cell invasiveness. In conclusion, high ADAM12 and CYP1B1 expressions in the peritumoral adipocytes boost tumor invasiveness and may serve as an indicator of poor prognosis in RCC.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1612-1632"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979220","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":"Integration of single-cell and bulk RNA-sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer.","authors":"Zhuofan Mou, Lorna W Harries","doi":"10.1002/1878-0261.13804","DOIUrl":"10.1002/1878-0261.13804","url":null,"abstract":"<p><p>Prognostic transcriptomic signatures for prostate cancer (PCa) often overlook the cellular origin of expression changes, an important consideration given the heterogeneity of the disorder. Current clinicopathological factors inadequately predict biochemical recurrence, a critical indicator guiding post-treatment strategies following radical prostatectomy. To address this, we conducted a meta-analysis of four large-scale PCa datasets and found 33 previously reported PCa-associated genes to be consistently up-regulated in prostate tumours. By analysing single-cell RNA-sequencing data, we found these genes predominantly as markers in epithelial cells. Subsequently, we applied 97 advanced machine-learning algorithms across five PCa cohorts and developed an 11-gene epithelial expression signature. This signature robustly predicted biochemical recurrence-free survival (BCRFS) and stratified patients into distinct risk categories, with high-risk patients showing worse survival and altered immune cell populations. The signature outperformed traditional clinical parameters in larger cohorts and was overall superior to published PCa signatures for BCRFS. By analysing peripheral blood data, four of our signature genes showed potential as biomarkers for radiation response in patients with localised cancer and effectively stratified castration-resistant patients for overall survival. In conclusion, this study developed a novel epithelial gene-expression signature that enhanced BCRFS prediction and enabled effective risk stratification compared to existing clinical- and gene-expression-derived prognostic tools. Furthermore, a set of genes from the signature demonstrated potential utility in peripheral blood, a tissue amenable to minimally invasive sampling in a primary care setting, offering significant prognostic value for PCa patients without requiring a tumour biopsy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1811-1835"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458668","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}