Biochimica et biophysica acta. Reviews on cancer最新文献

{"title":"Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans","authors":"Donald W. Kufe","doi":"10.1016/j.bbcan.2026.189542","DOIUrl":"10.1016/j.bbcan.2026.189542","url":null,"abstract":"<div><div>The incidence of cancer in humans has been rising in association with extended life spans. Incidence rates of early onset cancers in humans &lt;55 years of age have also been increasing for unclear reasons. One potential contributory factor is an <strong>antagonistic pleiotropy</strong> in which certain genes that appeared in mammals to increase fitness for reproduction contribute to cancer susceptibility later in life. A related concept is an <strong>evolutionary mismatch</strong> in which humans have adapted to certain environmental and dietary factors that change over time and thereby increase cancer incidence. The <em>MUCIN 1</em> (<em>MUC1</em>) gene emerged in mammals and represents an example of antagonistic pleiotropy and evolutionary mismatch that is posited here as a contributing factor to the increasing incidence of cancer in humans. This Review focuses on the roles of MUC1 and the oncogenic M1C protein in reproductive fitness and barrier tissue protection that in settings of chronic inflammation promote pan-cancer progression and treatment resistance. Also highlighted are therapeutic approaches targeting MUC1 and M1C that are under clinical and pre-clinical development.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 2","pages":"Article 189542"},"PeriodicalIF":9.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential molecular mechanisms of malignant evolution in pulmonary nodules: From precancerous lesions to invasive adenocarcinoma","authors":"Guanyu Lu,&nbsp;Yan Li,&nbsp;Xiangliang Liu,&nbsp;Jiuwei Cui","doi":"10.1016/j.bbcan.2026.189529","DOIUrl":"10.1016/j.bbcan.2026.189529","url":null,"abstract":"<div><div>With the widespread implementation of lung cancer screening, the detection rate of pulmonary nodules has increased annually, and pulmonary nodules have become a global public health concern. Early identification of malignant pulmonary nodules and premalignant intervention represent important clinical challenges, requiring a deeper understanding of their evolutionary characteristics. The malignant evolution of pulmonary nodules results from multi-step, multi-factorial interactions between tumors and the host, primarily involving the evolution from precancerous lesions to invasive lung adenocarcinoma. With the continuous development of multi-omics technologies, researchers have been mapping the spatiotemporal atlas of tumor initiation and progression at the molecular level. Elucidating the molecular mechanisms of malignant evolution in pulmonary nodules involves a multi-perspective analysis of tumor cells, the microenvironment, and host factors. This integrated view facilitates the identification of key biomarkers and therapeutic targets. This review summarizes the early cellular and molecular events in the malignant evolution of pulmonary nodules, aiming to provide insights for early identification and precision treatment.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189529"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145936694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of in vitro and in vivo cancer models to study the impact of the tumor immune microenvironment on anticancer therapy","authors":"Rajat Gupta ,&nbsp;Raghu Radhakrishnan ,&nbsp;Shama Prasada Kabekkodu ,&nbsp;Sanjiban Chakrabarty","doi":"10.1016/j.bbcan.2025.189504","DOIUrl":"10.1016/j.bbcan.2025.189504","url":null,"abstract":"<div><div>The tumor microenvironment is a dynamic, heterogeneous cellular ecosystem that includes cancer cells, cancer-associated fibroblasts (CAFs), endothelial cells, and immune cells. Immortalized cancer cell lines specific to a particular cancer type have been extensively used to investigate the anticancer effects and functional aspects of novel drugs. However, cancer cell lines do not accurately mimic the complex multicellular nature of organs. Since species-specific differences in mouse models of human cancer impact the interpretation of therapeutic efficacy, efforts have been made to reduce and replace the use of animals in the drug development process. It is now acknowledged that existing tumor models may not adequately simulate the tumor microenvironment. This has led to an increasing need for complex tumor models that can accurately represent the tumor immune microenvironment (TIME). The Organ-on-Chip (OoC) device has features that enable high-throughput screening and repeatable drug testing procedures by accurately simulating the tumor microenvironment (TME). Furthermore, although animal models remain vital for systemic analysis, the interpretation of therapeutic efficacy is often hindered by species-specific differences in immune and physiological responses. This limitation has created a critical conceptual gap in preclinical research. We acknowledge the pressing need for complex tumor models that can accurately simulate the tumor immune microenvironment (TIME).</div><div>The immune system plays two key roles in cancer: fighting tumors and promoting the development of carcinogenesis. Recent advances have been made in understanding how the immune system contributes to cancer progression and the development of immune cell treatments for improved prognosis. In vivo and in vitro models have been created to investigate therapy resistance and the function of the tumor immune microenvironment (TIME) in anticancer therapy. This review provides a critical and balanced evaluation of the various in vitro (organoids, organ-on-chip, bioprinting) and in vivo (PDX, Humanized Mice) models utilized to study the TIME. We move beyond descriptive summaries to offer a functional comparison of these platforms, specifically delineating their utility in overcoming the clinical challenges of therapy resistance mechanisms and translational immunotherapy evaluations. This comparative approach demonstrates how advanced models, such as organ-on-chip (OoC), which enable dynamic control of the microenvironment and integration of multiple organs, can complement and refine the drug development process.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189504"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YY1: Master regulator of metabolic reprogramming in cancer","authors":"Rimsha Akram ,&nbsp;Rendy Hosea ,&nbsp;Fuqiang Zhao ,&nbsp;Andrzej Górecki ,&nbsp;Małgorzata Figiel ,&nbsp;Shourong Wu ,&nbsp;Vivi Kasim","doi":"10.1016/j.bbcan.2025.189505","DOIUrl":"10.1016/j.bbcan.2025.189505","url":null,"abstract":"<div><div>Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to fulfill increased bioenergetic and biosynthetic demands for survival and proliferation. These adaptations arise directly from oncogenic mutations or indirectly via adaptive responses to nutrient scarcity. In addition to supporting survival and biomass production, these metabolic shifts are closely associated with changes in gene expression, cellular differentiation, and the tumor microenvironment, thereby contributing to tumorigenesis and progression. Importantly, the recognition of metabolic dysregulation as a hallmark of malignancy revealed novel avenues for therapeutic intervention, as disrupting these pathways may impair energy generation and biosynthetic processes essential for tumor proliferation. In this review, we integrate data indicating that the transcription factor Yin yang 1 (YY1) is a central regulator of oncogenic metabolic reprogramming. Yin yang 2 (YY2) is a paralog of YY1 and performs distinct role in metabolism and redox regulation. Mechanistically, YY1 enhances aerobic glycolysis by diverting glycolytic flux toward lactate production. Furthermore, it modulates hepatic lipid homeostasis via direct transcriptional control of lipogenic enzymes and crosstalk with nutrient-sensing signaling cascades. Additionally, YY1 rewires amino acid metabolism to fuel tumorigenesis by supplying macromolecules and enabling epigenetic remodeling. Collectively, these findings highlight the equilibrium between YY1 and its paralog YY2 in sustaining redox homeostasis and tumor progression while positioning YY1 as a metabolic checkpoint that dynamically regulates these processes. Understanding these pathways will support development of YY1-directed inhibitors and combinatorial therapies to modulate metabolic reprogramming in cancer.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189505"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145703261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytes in glioblastoma tumor microenvironment","authors":"Shu Cui ,&nbsp;Fan Guan ,&nbsp;Xuetong Li ,&nbsp;Xinmiao Long ,&nbsp;Minghua Wu","doi":"10.1016/j.bbcan.2025.189518","DOIUrl":"10.1016/j.bbcan.2025.189518","url":null,"abstract":"<div><div>Glioblastoma (GBM) remains one of the most aggressive and lethal brain tumors in adults, characterized by extensive heterogeneity, robust therapeutic resistance, and a dismal prognosis despite maximal surgical resection, radiotherapy, and chemotherapy. A defining hallmark of GBM is its complex tumor microenvironment (TME), a dynamic ecosystem comprising immune cells, vascular networks, extracellular matrix, and various stromal components that collectively drive tumor progression and therapeutic evasion. Within this intricate niche, astrocytes, traditionally regarded as passive support cells in the central nervous system (CNS), have emerged as pivotal orchestrators of GBM pathogenesis. These cells undergo profound phenotypic reprogramming upon interaction with GBM cells, adopting diverse roles that encompass metabolic support, immune suppression, promotion of invasive growth, and induction of therapy resistance. Regulated by key signaling pathways and influenced by GBM-derived exosomes, blood-brain barrier disruption, and tumor-associated hypoxia, astrocytes exhibit remarkable plasticity and heterogeneity, including putative subtypes such as metabolic homeostasis, immune-inflammatory reactive, gliomagenic, and senescence-associated subtypes. Their ability to shape the TME through immunosuppressive axis activation, energy support, metabolic crosstalk, and intercellular communication via tunneling nanotubes (TNTs) and extracellular vesicles (EVs) underscores their critical role in GBM biology. This review focuses on the multifaceted contributions of astrocytes within the GBM microenvironment, exploring their phenotypic diversity, regulatory mechanisms, therapeutic potential as emerging targets to dismantle the pro-tumor niche as well as to improve patient outcomes and advances in technologies for investigating astrocytes in GBM.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189518"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding aberrant glycosylation in colorectal cancer: From Glycosyaltion characterization, expression regulation to potential clinical applications","authors":"Zihan Li ,&nbsp;Xichen Dong ,&nbsp;Jian Liu,&nbsp;Tao Wen","doi":"10.1016/j.bbcan.2025.189513","DOIUrl":"10.1016/j.bbcan.2025.189513","url":null,"abstract":"<div><div>Colorectal cancer (CRC) exhibits extensive alterations in glycosylation, characterized by remodeling of glycan chain structures, aberrant terminal modifications, and dysregulated glycosyltransferase activity. These alterations are intimately associated with malignant phenotypes, such as tumor invasion, migration and proliferation, and contribute to shaping an immunosuppressive tumor microenvironment (TME). In this review, we first delineate major glycosylation types implicated in CRC, including O-GalNAc glycosylation, O-GlcNAcylation, N-glycosylation, sialylation, glycosphingolipid, glycosaminoglycan, and other special antigens, and summarize the key enzymatic machinery governing their biosynthesis. We further explore how glycosylation reprogramming drives oncogenic signaling and cellular plasticity. Importantly, we highlight recent advances in CRC-specific glycosylation-based diagnostic, prognostic, and therapeutic strategies. By summarizing current mechanistic and translational insights, this review aims to establish a conceptual framework for elucidating CRC-specific glycosylation alterations and evaluating their clinical translational potential, with the goal of improving early diagnosis, prognostic assessment, and targeted therapeutic strategies.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189513"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145727769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting ferroptosis with flavonoids for cancer therapy: Mechanisms and opportunities","authors":"Guowei Gong ,&nbsp;Zhenxia Zhang ,&nbsp;Yuzhong Zheng","doi":"10.1016/j.bbcan.2025.189528","DOIUrl":"10.1016/j.bbcan.2025.189528","url":null,"abstract":"<div><div>Ferroptosis, an iron-dependent regulated cell death mechanism driven by lipid peroxidation, offers a novel therapeutic approach for cancer treatment. Flavonoids, a diverse group of polyphenolic compounds, demonstrate significant anticancer potential by modulating ferroptosis pathways, including iron metabolism, GPX4 inhibition, and lipid peroxidation. This study examines flavonoid-induced ferroptosis mechanisms and their therapeutic applications. A systematic review of preclinical and clinical studies evaluated flavonoid effects (quercetin, baicalein, luteolin) on ferroptosis in cancer models. Key mechanisms analyzed included iron pool modulation, GPX4/System Xc⁻ inhibition, and lipid peroxidation enhancement. Synergistic interactions with chemotherapy, immunotherapy, and radiotherapy were assessed. Flavonoids trigger ferroptosis by (1) elevating labile iron to form redox-active complexes that can disrupt homeostasis and amplify Fenton reactions, (2) suppressing GPX4 and System Xc⁻ leading to glutathione depletion and ROS elevation, and (3) upregulating ACSL4/LOX to intensify lipid peroxidation. Preclinical data confirm efficacy in resistant cancers (triple-negative breast cancer, glioblastoma, pancreatic adenocarcinoma) and synergy with standard therapies. Challenges like poor bioavailability and tumor heterogeneity highlight the need for advanced delivery systems (nanoparticles, prodrugs). Flavonoids are promising ferroptosis inducers for apoptosis-resistant cancers, leveraging multi-target mechanisms and emerging delivery technologies. Future research should prioritize clinical translation, biomarker identification, and optimized combination regimens to enhance therapeutic outcomes.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189528"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145881042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key methylation modifications in glioma stem cells","authors":"Lize Cai ,&nbsp;Xun Sun ,&nbsp;Rong Li ,&nbsp;Yifang Ping ,&nbsp;Shengqing Lv ,&nbsp;Juxiang Chen","doi":"10.1016/j.bbcan.2025.189527","DOIUrl":"10.1016/j.bbcan.2025.189527","url":null,"abstract":"<div><div>Glioblastoma (GBM), the most aggressive primary brain tumor in adults, is characterized by a poor prognosis with a median survival of approximately 15 months despite multimodal therapies. Its hallmark heterogeneity and cellular plasticity, driven by glioma stem cells (GSCs), which contribute to therapeutic resistance and tumor recurrence. GSCs, identified by markers such as CD133, CD15, and Nestin, exhibit self-renewal capacity, multilineage differentiation potential, and tumor-initiating ability. These cells demonstrate intrinsic resistance to radiation and chemotherapy, enhanced invasiveness, and the ability to remodel the tumor microenvironment through immune modulation and angiogenesis. Metabolic reprogramming in GSCs supports their aggressive phenotype by meeting bioenergetic demands. It also generates metabolites that drive epigenetic remodeling. Among epigenetic mechanisms, methylation of DNA, RNA, and proteins plays a critical role in regulating GSC plasticity, gene expression, and signaling pathways. This review explores the dynamics of methylation in GSCs, encompassing the latest research on DNA, RNA, and protein methylation within the field of GSCs. This review further provides insights for future research by proposing a hierarchical regulatory network of methylation in GSCs to deepen understanding of their unique characteristics. Furthermore, this review highlights the potential for developing additional methylation-related clinical markers to enhance diagnostic approaches.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189527"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aptamer-based strategies for glioblastoma: From SELEX to preclinical success","authors":"Abdullah Tahir Bayraç","doi":"10.1016/j.bbcan.2025.189524","DOIUrl":"10.1016/j.bbcan.2025.189524","url":null,"abstract":"<div><div>Glioblastoma presents a persistent therapeutic challenge due to extensive intratumoral heterogeneity and the blood-brain barrier. Nucleic acid aptamers offer an effective alternative to overcome these physiological obstacles where conventional modalities often have limited success. This review outlines the progression of aptamers from basic ligands to functional therapeutics, with a focus on targeting glioblastoma stem cells and engineering mechanisms for blood-brain barrier traversal. We discuss how recent biotechnological developments, including Cell-SELEX and AI-supported design, are solving earlier issues related to <em>in vivo</em> stability and conformational selectivity. Additionally, the article evaluates the shift toward multifunctional systems such as aptamer-drug conjugates and “drugtamers” designed for receptor-mediated transport. These advances indicate that next-generation aptamer platforms may overcome current translational limitations and enable more precise neuro-oncological treatments.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189524"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SF3B1 mutations in spliceosome-driven tumorigenesis: From splicing dysregulation to signaling network rewiring and therapeutic targeting","authors":"Ting Yang,&nbsp;Rui Qian,&nbsp;Xuanxuan Sun,&nbsp;Xin Hu,&nbsp;Youzhong Wan","doi":"10.1016/j.bbcan.2025.189521","DOIUrl":"10.1016/j.bbcan.2025.189521","url":null,"abstract":"<div><div>Splicing factor 3B subunit 1 (SF3B1), a core component of the U2 small nuclear ribonucleoprotein, has key functions in precursor messenger RNA (pre-mRNA) splicing and regulates gene expression by recognizing branch point sequences and coordinating spliceosome assembly. Mutations of <em>SF3B1</em> have been identified as high-frequency drivers in various tumor types. These include hotspot mutations such as K700E, which reshape the splicing factor network via abnormal interactions with SUGP1, DHX15, etc., resulting in activation of latent splicing sites. These changes in turn affect genes involved in RNA metabolism and the cell cycle and genomic stability, thereby triggering the downstream NF-κB, AKT, and p53 pathways to promote tumorigenesis. Clinically, <em>SF3B1</em> mutations occur in both hematological tumors (as in myelodysplastic syndrome) and solid tumors (such as breast cancer). Mutation-mediated splicing abnormalities thus represent targets for new therapeutic agents such as spliceosome inhibitor pladienolide B. However, although studies have advanced our understanding of these abnormalities from basic splicing changes to effects on signaling networks and potential clinical translation, various aspects need further exploration; these include mutation-specific functional heterogeneity, interactions with the tumor microenvironment, and mechanisms of drug resistance. This review systematically summarizes the functions of <em>SF3B1</em> mutations and their underlying molecular mechanisms in spliceosome-driven tumorigenesis, with the aim of providing a framework for better understanding of this process, as well as discussing prospects for new precision medicine diagnostic and treatment strategies.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1881 1","pages":"Article 189521"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}