Mutation Research-Reviews in Mutation Research最新文献

{"title":"Mechanisms, treatment strategies and predictive biomarkers of drug resistance in acute myeloid leukemia","authors":"Jianjian Zhuang ,&nbsp;Yue Li ,&nbsp;Yingqiong Zhang ,&nbsp;Yiling Huang ,&nbsp;Yijia Han ,&nbsp;Nengming Lin ,&nbsp;Yangling Li","doi":"10.1016/j.mrrev.2025.108578","DOIUrl":"10.1016/j.mrrev.2025.108578","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults, and its incidence increases with age and is more common in elderly population. The current treatment methods for AML mainly include chemotherapy, targeted therapy, immunotherapy and hematopoietic stem cell transplantation, among which chemotherapy and targeted therapy are the most common methods. Combined therapy further enhances the therapeutic effect of AML and reduces drug toxicity. At present, drug resistance is a common problem in the treatment of AML. Gene mutations and treatment-induced mutations are the main causes of drug resistance in AML, and drug resistance is also generated during the interaction between tumor microenvironment and AML. Real-time monitoring of tumor markers such as the most common gene mutations and the changes of novel biomarkers, provides certain reference value for the occurrence of AML and the prevention of drug resistance in the process of AML diagnosis and treatment. Finally, a new direction in the future diagnosis and treatment of AML is proposed based on the current diagnosis and treatment status.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"797 ","pages":"Article 108578"},"PeriodicalIF":4.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145726920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling oral cancer’s molecular blueprint: A novel classification to guide precision therapy","authors":"Manoj Pandey ,&nbsp;Pooja Singh ,&nbsp;Mridula Shukla ,&nbsp;Monika Rajput ,&nbsp;Ruhi Dixit","doi":"10.1016/j.mrrev.2025.108580","DOIUrl":"10.1016/j.mrrev.2025.108580","url":null,"abstract":"<div><div>Oral cancer poses a significant health challenge in Southeast Asia, with a high incidence and mortality. Despite extensive genomic research, a molecular classification for this disease is lacking. This study aimed to address this gap by proposing a molecular classification of oral cancer based on genetic alterations. We conducted a comprehensive literature search on PubMed, identifying 8176 articles related to oral cancer genomics. From these, we selected studies focusing on genomics and compiled a list of 48 genes implicated in carcinogenesis, cross-referencing our findings with the TCGA database. Using cluster analysis and gene ontology, we grouped these genes by function and interactions, and then constructed protein-protein interaction networks to develop our proposed classification. Our results categorize the genes into five main groups: cell-cycle dysregulation (including growth activation and apoptotic dysregulation), immune-mediated, xenobiotic metabolism-associated, inflammatory pathway activation, and viral protein activation. Cell-cycle dysregulation was the most frequently studied, affecting over 60 % of cases, with TP53 being the most common alteration. While immune-mediated and inflammatory pathways are recognized for their therapeutic relevance, xenobiotic and viral mechanisms remain less explored. This review provides the first molecular classification of oral cancer, identifying five key carcinogenic pathways. This framework is expected to improve our understanding of the molecular diversity of oral cancer and guide the development of targeted therapies, especially for understudied pathways like xenobiotic metabolism and inflammation.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"797 ","pages":"Article 108580"},"PeriodicalIF":4.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145840815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of alterations in lamin A on genome integrity","authors":"Alannah J. DiCintio,&nbsp;Alan S. Waldman","doi":"10.1016/j.mrrev.2025.108577","DOIUrl":"10.1016/j.mrrev.2025.108577","url":null,"abstract":"<div><div>The maintenance of the genome in eukaryotic cells is dependent on the proper maintenance of the structure and function of the nuclear envelope which encases the genome. The nuclear envelope in higher eukaryotic cells is composed of the outer nuclear membrane, the inner nuclear membrane, and the nuclear lamina which resides just inside of the inner nuclear membrane. The nuclear lamina provides mechanical support to the nuclear envelope, plays essential roles in transport of molecules between the cytoplasm and the nucleus, and is pivotal in regulating global chromatin structure and three-dimensional nuclear architecture. Proper functioning of the nuclear lamina plays roles in regulating the cell cycle, transcription, RNA splicing, chromatin organization, DNA replication, and DNA repair. The nuclear lamina is conserved in metazoans and is composed of a meshwork of interwoven proteins called lamins, as well as lamin associated proteins. The protein known as lamin A is a vital constituent of the nuclear lamina. Alterations in lamin A, particularly those associated with disruptions in posttranslational processing of lamin A by zinc metallopeptidase ste24, have been linked to a variety of genetic disorders that give rise to genome instability and accelerated aging. This review will concentrate primarily on what has been learned about the dependency of effective DNA repair and DNA replication on a functional nuclear lamina, with particular emphasis on how modifications in the protein lamin A may corrupt a cell’s ability to maintain genome stability.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"797 ","pages":"Article 108577"},"PeriodicalIF":4.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145685863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA: Bridging cellular senescence and chronic inflammation in aging and beyond","authors":"Shimeng Wang ,&nbsp;Fanglong Wu ,&nbsp;Hongmei Zhou","doi":"10.1016/j.mrrev.2026.108587","DOIUrl":"10.1016/j.mrrev.2026.108587","url":null,"abstract":"<div><div>Aging is a progressive and irreversible physiological process driven by a complex network of interrelated molecular and cellular mechanisms. Among these, cellular senescence and chronic inflammation, as two core hallmarks of aging, are interlinked and jointly promote the development and progression of aging. However, the precise molecular crosstalk between these two processes remains unclarified. Mitochondrial DNA (mtDNA), as the only cytoplasmic DNA, has recently emerged as a pivotal \"bridge\" linking cellular senescence and chronic inflammation through various mechanisms. Anchored on the unique characteristics of mtDNA, this review systematically elucidates its central roles in mitochondrial dysfunction and oxidative stress, with a particular emphasis on the dynamic changes of mtDNA within the cytosol and extracellular space that construct and amplify the cellular “inflammation–senescence” coupling network. Furthermore, we propose a conceptual framework linking mtDNA mutation/damage to the cellular senescence and the propagation of chronic inflammation. Finally, we discuss the therapeutic potential of targeting mtDNA dynamics and highlight key challenges and future directions in this emerging field, offering novel insights for mitigating aging and age-related diseases.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"797 ","pages":"Article 108587"},"PeriodicalIF":4.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147481888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotype-phenotype correlations in biallelic carriers of FANCM protein truncating variants: A systematic literature review","authors":"Gisella Figlioli ,&nbsp;Amandine Billaud ,&nbsp;Paolo Peterlongo","doi":"10.1016/j.mrrev.2025.108559","DOIUrl":"10.1016/j.mrrev.2025.108559","url":null,"abstract":"<div><div>The <em>FANCM</em> gene is involved in the Fanconi Anemia (FA) DNA repair pathway. Although germline biallelic pathogenic variants in genes of this pathway cause the recessive FA syndrome, the role of <em>FANCM</em> in FA or FA-like has been questioned. Biallelic <em>FANCM</em> protein truncating variants (PTVs) have been primarily linked to infertility and cancer, suggesting the gene causes a clinically distinct phenotype. Four literature databases were systematically searched from inception to June 2024 to identify published articles describing individuals carrying biallelic PTVs in <em>FANCM</em>. Twenty articles describing 40 carriers of biallelic <em>FANCM</em> PTVs were identified. We established genotype-phenotype correlations and found that women carrying biallelic combinations of the C-terminal p.Gln1701* and p.Gly1906Alafs*12 PTVs showed infertility, chromosome fragility, breast cancer, and chemotoxicity. Men carrying the same PTVs combinations showed infertility only. Carriers of biallelic combinations including a single N-terminal PTV showed chromosome fragility, infertility, and early onset breast cancer and/or squamous cell carcinoma, and pediatric hematological cancers, often associated with severe chemotoxicity. Our findings indicate that <em>FANCM</em> biallelic PTVs may cause a novel recessive syndrome which is distinct from FA and characterized by infertility, chromosome fragility, cancer and chemotoxicity. While infertility is always observed, the severity of chromosome fragility, cancer predisposition and chemotoxicity seem to depend on <em>FANCM</em> PTVs position and the sex of the carrier. Larger analyses are warranted to consolidate these findings.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"Article 108559"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of methylglyoxal protein modifications in DNA damage and chromosomal instability: Emerging molecular mechanisms.","authors":"Leigh Donnellan, Michael Fenech, Varinderpal S Dhillon, Clifford Young, Peter Hoffmann, Permal Deo","doi":"10.1016/j.mrrev.2025.108558","DOIUrl":"10.1016/j.mrrev.2025.108558","url":null,"abstract":"<p><p>Methylglyoxal (MGO) is a highly reactive metabolite formed from glycolysis that can form advanced glycation endproducts (AGEs) on proteins and DNA. It has been well established that MGO induces DNA double strand breaks as a result of modifications on deoxyguanosine residues. However, recent studies shed new light on the genotoxic properties of MGO by its ability to cause chromosomal mis-segregation events, and other forms of chromosomal instability. These outcomes open a new avenue in which protein modifications, rather than DNA modifications, result in DNA damage. Herein, we present several hypotheses on how modification of proteins by MGO might cause these chromosome mis-segregation events based on identified protein modification sites from proteomic studies. These include various cell cycle proteins, such as those involved in sister chromatid cohesion, centrosome formation and histone proteins. Overall, recent studies implicate MGO in whole chromosome loss events, amongst other chromosomal instability events, suggesting it as a key player in cancer development and progression.</p>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"108558"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144805125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic roles of long non-coding RNAs in DNA damage response and genome stability","authors":"Li Wu ,&nbsp;Lingli Wang ,&nbsp;Jingyu Hou ,&nbsp;Zhengping Shao ,&nbsp;Jun Yang ,&nbsp;Xiangwei Gao","doi":"10.1016/j.mrrev.2025.108562","DOIUrl":"10.1016/j.mrrev.2025.108562","url":null,"abstract":"<div><div>To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions. First, some lncRNAs contain small open reading frames (sORFs) encoding functional micropeptides that actively participate in DDR pathways. Second, lncRNAs regulate R-loop homeostasis, a key mechanism for preserving genome integrity. Together, these findings expand our understanding of lncRNAs in the DDR, positioning them as both key mechanistic players and promising therapeutic targets.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"Article 108562"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145026489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The comet assay as a tool in human biomonitoring studies: Effects of confounding factors","authors":"Peter Møller ,&nbsp;Goran Gajski ,&nbsp;Marko Gerić ,&nbsp;Lisa Giovannelli ,&nbsp;Amaya Azqueta ,&nbsp;Anja Haveric ,&nbsp;Helga Stopper ,&nbsp;Ezgi Eyluel Bankoglu ,&nbsp;Andrew Collins ,&nbsp;Carina Ladeira","doi":"10.1016/j.mrrev.2025.108566","DOIUrl":"10.1016/j.mrrev.2025.108566","url":null,"abstract":"<div><div>The comet assay is widely used in human biomonitoring studies of environmental and occupational exposures. However, it is clear from multiple studies that various types of confounding factors might affect the direct relationship between exposure and DNA damage in the comet assay. In addition to common confounders such as age, sex, and smoking, other factors considered to be important determinants for background levels of DNA damage in the comet assay include exhaustive physical exercise, chronic diseases, medical treatment, and diet. These are typically controlled in biomonitoring studies by restriction or matching of subjects. Period effects (or seasonal variation) have been observed in a relatively large number of studies. There are various putative factors, which may cause period effects, including temporal variation in solar radiation, temperature, and air pollution. The present review describes the effects of these confounding factors in measurements of DNA strand breaks by the comet assay. In general, the literature does not indicate that any confounding factor is consistently associated with an increased level of DNA damage, measured by the comet assay. In this respect, it is important to balance the need to control for confounding with the risk of introducing in the statistical analysis a variable, which is influenced by exposure and outcome (i.e. collider bias). In addition, it is important that investigators describe procedures for controlling the effect of confounding factors in the selection of subjects and statistical analysis. Care should be taken in study design and statistical analysis to avoid unwanted effects of confounding factors.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"Article 108566"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The comet assay as a tool in human biomonitoring of exposure to heavy metals – A systematic review and meta-analysis","authors":"Peter Møller ,&nbsp;Ezgi Eyluel Bankoglu ,&nbsp;Helga Stopper ,&nbsp;Goran Gajski ,&nbsp;Marko Gerić ,&nbsp;Anja Haveric ,&nbsp;Amaya Azqueta ,&nbsp;Lisa Giovannelli ,&nbsp;Andrew Collins ,&nbsp;Carina Ladeira","doi":"10.1016/j.mrrev.2025.108567","DOIUrl":"10.1016/j.mrrev.2025.108567","url":null,"abstract":"<div><div>Exposure to heavy metals such as lead, arsenic and chromium is associated with genotoxicity and increased risk of cancer. In this systematic review and meta-analysis, we have assessed effects of heavy metal exposure on levels of DNA strand breaks in leukocytes, measured by the comet assay, in human biomonitoring studies. We distinguish between traditional toxic metals (lead), semi-metals/metalloids (arsenic), transition metals (chromium), and other heavy metals. The literature search led to 66 studies, which were assessed by meta-analysis. Using standardized mean difference and 95 % confidence interval (CI), the meta-analyses show increased levels of DNA strand breaks in subjects exposed to lead (1.99, 95 % CI: 1.47, 2.51), arsenic (1.36, 95 % CI: 0.94, 1.77), chromium/welding fume (2.03, 95 % CI: 1.48, 2.57), and other heavy metals (0.81, 95 % CI: 0.45, 1.18). Subgroup analysis indicates that all studies combined from middle-income countries have higher effect size (1.99, 95 % CI: 1.63, 2.35) than have studies from high-income countries (0.81, 95 % CI: 0.37, 1.26). The lower effect size in high-income countries may be due to differences in exposure levels, related to stricter regulation of emissions or more awareness/use of personal protective equipment in the working environment. Sensitivity analysis does not unequivocally link effect size to comet assay measurement bias, inferred by insufficient information on comet assay procedures, missing assay controls, non-blinded analysis of samples, or exposure misclassification. In conclusion, this systematic review and meta-analysis shows that exposure to heavy metals - lead, arsenic and chromium – is associated with increased levels of DNA strand breaks in human leukocytes.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"Article 108567"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145507686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mortality rate and causes of death in inborn errors of immunity: A systematic review and meta-analysis","authors":"Saba Fekrvand ,&nbsp;Zahra Hamidi Esfahani ,&nbsp;Mohammadmehdi Yarahmadi ,&nbsp;Ali Saeedi-Boroujeni ,&nbsp;Helia Salehi ,&nbsp;Ali Hakimelahi ,&nbsp;Amir Almasi-Hashiani ,&nbsp;Mahshid Rahmati ,&nbsp;Sanaz Afshar-Ghasemlou ,&nbsp;Najmeh Nameh Goshay Fard ,&nbsp;Fateme Tarighat Monfared ,&nbsp;Ehsan Khoshnezhad Afkham ,&nbsp;Nazanin Fathi ,&nbsp;Tannaz Moeini Shad ,&nbsp;Fateme Babaha ,&nbsp;Farzad Nazari ,&nbsp;Matineh Nirouei ,&nbsp;Amir Salehi Farid ,&nbsp;Negin Sanadgol ,&nbsp;Hosein Rafiemanesh ,&nbsp;Reza Yazdani","doi":"10.1016/j.mrrev.2025.108564","DOIUrl":"10.1016/j.mrrev.2025.108564","url":null,"abstract":"<div><h3>Background</h3><div>Patients with inborn errors of immunity (IEI) experience severe infectious and non-infectious complications, leading to an increased risk of mortality. Delayed diagnosis or misdiagnosis significantly contributes to the heightened mortality rates observed in IEI patients.</div></div><div><h3>Objectives</h3><div>This study systematically reviews the causes of mortality in IEI patients with a meta-analysis to determine the mortality rate among patients with various IEI.</div></div><div><h3>Methods</h3><div>Embase, ISI Web of Science, PubMed, and Scopus were searched (up to July 2024) using terms related to IEI and mortality.</div></div><div><h3>Results</h3><div>A total of 12,581 deceased IEI patients were included, with an overall reported mortality rate of 24.0 % (95 % confidence interval: 23.0–26.0 %) among all published IEI cases. This represents an approximately 27-fold higher mortality rate among IEI patients compared to the mean global mortality rate (24 % vs. 0.874 %). Severe combined immunodeficiency, chronic granulomatous disease, and ataxia-telangiectasia had the highest numbers of reported deceased cases (2304, 962, and 820 cases, respectively). However, familial hemophagocytic lymphohistiocytosis exhibited the highest mortality rate (49.0 %). The most common causes of death were infections, transplant-related mortality and non-infectious pulmonary complications, (3429, 2749, and 1141 cases), respectively. Among infectious causes of death, COVID-19 infection accounted for 10.8 % (370 cases).</div></div><div><h3>Conclusion</h3><div>This study identifies specific types of IEI with the highest mortality rates and numbers, alongside immune component defects most strongly associated with increased mortality. Patients with immune dysregulation, defects in cellular immunity, and phagocyte function were particularly linked to higher mortality rates, underscoring the urgent need for improved management strategies for these IEIs.</div></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"796 ","pages":"Article 108564"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}