Human pathology最新文献

{"title":"Upgrade risk in intraductal papillomas: A retrospective analysis of real-world data and predictive model development","authors":"Jenni Kotola ,&nbsp;Anselm Tamminen","doi":"10.1016/j.humpath.2026.106097","DOIUrl":"10.1016/j.humpath.2026.106097","url":null,"abstract":"<div><h3>Background</h3><div>In current practice, the traditional strategy of excising all IDPs has been replaced by more selective management. However, criteria for selecting patients for surveillance remain unclear, and no widely accepted predictive model exists.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed real-world data from 325 cases of IDPs diagnosed via core needle biopsy (CNB) at a tertiary teaching hospital between 2010 and 2023. We assessed upgrade rates to malignancy and evaluated potential predictive factors. Two previously published models were applied to our cohort, and a new model was developed based on our data.</div></div><div><h3>Results</h3><div>Overall, 17% (55/325) of IDPs were upgraded to malignancy. Among lesions without atypia on CNB (n = 215), the upgrade rate was 8.8% (19/215), compared to 40% (23/58) in those with atypia (p &lt; 0.001). Previously suggested models yielded modest results when applied to our study population. First model would have spared 11% (24/215) of patients from surgery, while the second model would have spared 17% (36/215), with one missed upgrade. Our model identified all upgraded cases and would have spared 33% (72/215) of non-atypical IDPs from surgery.</div></div><div><h3>Conclusions</h3><div>Atypia on CNB is a strong predictor of upgrade to malignancy. Existing models showed limited utility in reducing unnecessary surgeries. Our proposed model demonstrated improved performance and may support more individualized management of IDPs.</div></div>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":"172 ","pages":"Article 106097"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354708","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":"Clinical, pathologic, and molecular profiles of sarcomatoid and rhabdoid differentiated clear cell renal cell carcinoma: A series of 21 tumors","authors":"Yue Yu ,&nbsp;Yingjing Wang ,&nbsp;Xiao Cheng,&nbsp;Xuan Chen,&nbsp;Wei Zhao,&nbsp;Suying Wang,&nbsp;Huizhi Zhang","doi":"10.1016/j.humpath.2026.106099","DOIUrl":"10.1016/j.humpath.2026.106099","url":null,"abstract":"<div><div>Clear cell renal cell carcinoma (ccRCC) with sarcomatoid and/or rhabdoid differentiation—distinct dedifferentiation phenotypes—exhibits high aggressiveness and poor prognosis. Despite recent advances, their clinicopathologic and molecular characteristics remain incompletely defined. This study analyzed 21 such cases, predominantly in males (19 patients), with a median age of 64 years (range: 29 – 83 years) and average tumor size of 6.1 cm (range: 3.5 – 14 cm). Among these, 14 cases showed sarcomatoid differentiation, 11 cases exhibited rhabdoid differentiation, and four cases demonstrated both types simultaneously. Most tumors (16/21, 76.19%) exhibited necrosis. Two patients presented with synchronous pulmonary metastases at diagnosis, and six developed distant metastases (bone/lung/liver/brain) 4 - 30 months postoperatively. Next-generation sequencing revealed that 90.5% (19/21) of samples harbored <em>VHL</em> gene alterations, which represent the initial driver mutation in ccRCC development. Additionally, chromatin remodeling genes showed enriched abnormalities, including <em>PBRM1</em> (52.4%, 11/21), <em>BAP1</em> (33.3%, 7/21) and <em>SETD2</em> (19.0%, 4/21), suggesting a potential role for these genes in the transformation to sarcomatoid and/or rhabdoid morphology. Notably, 28.6% of tumors had TSC/MTOR pathway alterations, and <em>TP53</em> mutations (33.3%) were significantly associated with poor prognosis (p = 0.049). No statistically significant differences in driver mutation prevalence or prognosis were observed between sarcomatoid and rhabdoid differentiation. These findings highlight the value of molecular stratification in elucidating pathogenesis and guiding targeted therapy for this aggressive ccRCC subtype, particularly emphasizing TP53 as a prognostic biomarker and TSC/MTOR alterations as potential therapeutic targets.</div></div>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":"172 ","pages":"Article 106099"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365039","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":"Epigenetic profiling of biphenotypic sinonasal sarcoma across fusion variants and high-grade transformation","authors":"Yuri Merlotti Gomes ,&nbsp;João Víctor Alves de Castro ,&nbsp;Nicolai Merlotti Gomes ,&nbsp;Rodrigo Fonseca Abreu ,&nbsp;Leslie Domenici Kulikowski ,&nbsp;Beatriz Martins Wolff ,&nbsp;Clóvis Antonio Pinto ,&nbsp;Antonio G. Nascimento ,&nbsp;Ronaldo Nunes Toledo ,&nbsp;Anders Meyer ,&nbsp;Igor Lima Fernandes ,&nbsp;Cristovam Scapulatempo Neto ,&nbsp;Philipp Jurmeister ,&nbsp;David Capper ,&nbsp;Josephine K. Dermawan ,&nbsp;Karen J. Fritchie ,&nbsp;Stephania Martins Bezerra ,&nbsp;Felipe D'Almeida Costa","doi":"10.1016/j.humpath.2026.106076","DOIUrl":"10.1016/j.humpath.2026.106076","url":null,"abstract":"<div><div>Biphenotypic sinonasal sarcoma (BSS) is a rare mesenchymal neoplasm characterized by dual neural and myogenic differentiation, recurrent <em>PAX3</em> gene rearrangements, and low-grade morphology. High-grade transformation has been described, posing significant diagnostic challenges due to overlap among sinonasal tumors. DNA methylation profiling has emerged as a powerful diagnostic tool for sinonasal neoplasms, although BSS was not included in previous cohorts. In this study, we investigated the DNA methylation profile of BSS and its relationship with fusion type and high-grade transformation. Fourteen BSS samples were retrospectively collected from four academic institutions. All cases underwent genome-wide methylation profiling using the Illumina Infinium MethylationEPIC array, and available clinical, radiological, histopathologic, and immunohistochemical data were reviewed. RNA sequencing was performed when sufficient material was available. Methylation profiles were analyzed using t-distributed stochastic neighbor embedding (t-SNE) and compared with a reference cohort of sinonasal tumors. The median patient age was 52.7 years, with a female predominance (M:F ratio 1:2.25). The most common fusion was <em>PAX3</em>::<em>MAML3</em> (6/12, 50.0%), followed by <em>PAX3</em>::<em>FOXO1</em> and other rare rearrangements, including <em>PAX3</em>::<em>NCOA2</em>, <em>PAX3</em>::<em>YAP1</em>, and <em>FUS</em>::<em>POU2AF3</em>, detected in one case each (1/12, 8.3%). Most importantly, all BSS samples formed a cohesive epigenetic group upon dimensionality reduction, clearly separated from other sinonasal tumors. No specific clustering was seen among different fusion types or tumor grade. Our findings support that BSS represents a unique and molecularly distinct sinonasal sarcoma with a characteristic DNA methylation signature, independent of gene fusion partners or histologic progression, providing a valuable tool for the classification of challenging cases.</div></div>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":"172 ","pages":"Article 106076"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258258","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 role of advanced molecular diagnostics in informing targeted therapies for AML.","authors":"Jennifer Marvin-Peek, Sanam Loghavi, Ghayas C Issa, Naval G Daver, Tapan M Kadia, Farhad Ravandi, Courtney D DiNardo","doi":"10.1016/j.humpath.2026.106179","DOIUrl":"10.1016/j.humpath.2026.106179","url":null,"abstract":"<p><p>The application of advanced molecular diagnostics has transformed the clinical management of patients with acute myeloid leukemia (AML), a heterogeneous disease characterized by a diverse genomic landscape. Comprehensive molecular profiling is now central to diagnosis, risk stratification, therapeutic decision-making and disease monitoring. While conventional diagnostic approaches including karyotyping, fluorescence in situ hybridization (FISH) and quantitative polymerase chain reaction (qPCR) remain essential, advances in next-generation sequencing have enabled the rapid and broad identification of recurrent genomic alterations, many of which are now directly targetable. These developments have accelerated the integration of genotype-directed treatment strategies into routine clinical practice. Expansion sequencing capabilities, including whole-exome and whole-genome approaches is further enhancing the detection of clinically relevant alterations, refining disease classification and offers the possibility of a single diagnostic platform that can detect all relevant alterations. At the same time, increasingly sensitive molecular techniques for measurable residual disease (MRD) assessment are providing new opportunities to dynamically evaluate treatment response and guide post-remission strategies. The growing volume and complexity of molecular data present ongoing challenges in interpretation, necessitating careful integration with clinical context and continued validation in prospective studies. Collectively, advances in molecular diagnostics are reshaping AML management to promote an adaptive, precision-based approach aimed at improving patient outcomes.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106179"},"PeriodicalIF":2.6,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148137896","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":"Optical genome mapping in myeloid neoplasms.","authors":"Guilin Tang, Qing Wei, Melanie Klausner, Ying S Zou, Gokce A Toruner","doi":"10.1016/j.humpath.2026.106176","DOIUrl":"10.1016/j.humpath.2026.106176","url":null,"abstract":"<p><p>We summarize the technical principles of optical genome mapping (OGM) and evaluate its current clinical applications across myeloid neoplasms, with emphasis on acute myeloid leukemia and myelodysplastic syndromes. We highlight evidence demonstrating high concordance with standard cytogenetic methods, while also showing incremental diagnostic yield through detection of cryptic abnormalities and/or refinement complex rearrangements. We further discuss clinically relevant cytogenomic abnormalities that may be underrecognized by conventional cytogenetics, including chromoanagenesis, KMT2A partial tandem duplication and cryptic rearrangements involving genes such as NUP98 and MECOM. We also address practical considerations for implementation of OGM in a clinical cytogenetic laboratory, including pre-analytical DNA quality requirements, assay sensitivity, bioinformatic interpretation and workflow integration. Current data support OGM as a complementary component of genomic workups rather than a replacement for all existing assays. As analytical standards mature and outcome-linked evidence expands, OGM has strong potential to improve genomic risk stratification, refine disease classification and advance precision diagnostics in myeloid neoplasms.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106176"},"PeriodicalIF":2.6,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148101374","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":"Multimodal measurable residual disease detection in acute myeloid leukemia: From technology to clinical integration.","authors":"George Mason, Ameya Hanamshet, Jad Othman","doi":"10.1016/j.humpath.2026.106175","DOIUrl":"10.1016/j.humpath.2026.106175","url":null,"abstract":"<p><p>Measurable residual disease (MRD) is an increasingly vital tool in predicting the risk of relapse in patients with acute myeloid leukemia (AML), with a growing role in directing therapeutic choices. The vast phenotypic and genomic heterogeneity of AML precludes a universal MRD assay, thereby requiring multiple complementary assays with unique advantages and limitations. This review aims to provide hematologists and pathologists with guidance in the selection, use and interpretation of MRD testing across multiple modalities. Assay characteristics, laboratory considerations and MRD targets are reviewed, accompanied by case-based discussions.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106175"},"PeriodicalIF":2.6,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148101417","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":"Advances in digital pathology and artificial intelligence in the diagnosis of myeloid neoplasms.","authors":"Pravin Patel, Olga Pozdnyakova","doi":"10.1016/j.humpath.2026.106178","DOIUrl":"10.1016/j.humpath.2026.106178","url":null,"abstract":"<p><p>Recent advances in digital pathology and artificial intelligence (AI) are transforming our ability to diagnose myeloid neoplasms, including acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and myeloproliferative neoplasms (MPN). Modern AI systems now achieve expert-level performance across peripheral blood smear assessment, bone marrow aspirate and biopsy interpretation, flow cytometry, cytogenetics, and next-generation sequencing; with many platforms surpassing 90% accuracy and enabling detection of subtle morphologic and immunophenotypic signatures beyond human perception. Moreover, AI tools increasingly integrate multimodal inputs to support classification, risk stratification, and treatment predictions, often outperforming conventional methods. These systems augment pathologists by streamlining workflows, enhancing consistency, reducing interobserver variability, and accelerating turnaround times, paving the way for advanced precision diagnostics in hematopathology. However, challenges remain in clinical adoption, including cost, security, regulatory oversight, and validation across diverse populations. Despite these hurdles, early regulatory successes such as digital peripheral blood smear morphology analyzers illustrate the feasibility of real-world implementation. Broader adoption will however require coordinated efforts among developers, laboratories, pathologists, and regulatory agencies to ensure safety, transparency, and interoperability.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106178"},"PeriodicalIF":2.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054233","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":"Non-langerhans cell histiocytosis: A growing category of emerging entities.","authors":"Melissa Delio, Cassandra Duarte, Bradford J Siegele, L Jeffrey Medeiros, Zenggang Pan","doi":"10.1016/j.humpath.2026.106177","DOIUrl":"10.1016/j.humpath.2026.106177","url":null,"abstract":"<p><p>Histiocytoses are uncommon and comprise a diverse group of disorders of myeloid-derived cells with a macrophage or dendritic cell phenotype. They encompass a large number of subtypes, including Langerhans cell histiocytosis (LCH) and non-LCH. LCH is most common and perhaps best understood. The non-LCH in the current World Health Organization Classification of Hematolymphoid Tumors (WHO-HAEM5) includes Erdheim-Chester disease, juvenile xanthogranuloma, Rosai-Dorfman disease, ALK⁺ histiocytosis, and histiocytic sarcoma. Due to the rarity of non-LCH, there is a lack of awareness, knowledge and experience among general pathologists in the diagnosis of these entities, often resulting in significant delays or even misinterpretation. These histiocytic neoplasms also exhibit clinical, pathological and molecular heterogeneity. Given that these neoplasms all resemble histiocytes to some degree, there is substantial morphologic overlap between these entities, reactive histiocytes, and some non-histiocytic neoplasms. The diagnostic process can be further complicated by unusual morphologic features, such as epithelioid and spindle cell cytology, a marked inflammatory reaction, and prominent fibrosis. Beginning in 2010 with the discovery of BRAF mutations in LCH, our biologic understanding of histiocytic neoplasms greatly expanded with recognition of the importance of the mitogen activated protein kinase (MAPK) pathway in pathogenesis. The biologic spectrum of histiocytic neoplasms continues to expand, in large part driven by discovery of novel molecular genetic aberrations, suggesting that additional non-LCH or modifications to the classification of these entities may be included to future editions of the WHO classification. In this article, we systemically review the clinicopathologic and molecular genetic features of each type of non-LCH. We also provide differential diagnoses and diagnostic algorithms to assist pathologists in establishing the diagnosis of these entities.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106177"},"PeriodicalIF":2.6,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054337","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":"Single cell sequencing in acute myeloid leukemia: Linking genotype to functional phenotype for precision risk stratification and treatment decisions.","authors":"Annabelle J Anandappa, Wenbin Xiao, Linde A Miles","doi":"10.1016/j.humpath.2026.106174","DOIUrl":"https://doi.org/10.1016/j.humpath.2026.106174","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by clonal expansion of myeloid precursor cells. The pathologic evaluation of AML integrates multiple levels of characterization, including morphology of cells circulating in peripheral blood and bone marrow, identification of blast lineage by immunohistochemistry and flow cytometry immunophenotyping, and genetic studies including karyotype, fluorescence in-situ hybridization, and next generation sequencing (NGS). NGS analysis is utilized routinely to define the mutational landscape of AML, which informs risk stratification and choice of therapy. However, the current methods of immunophenotypic classification in clinical practice use a relatively small number of surface markers to coarsely determine hematopoietic lineage, and bulk sequencing approaches are largely unable to accurately capture clonal complexity, resolve mutational order, and distinguish residual leukemia from clonal hematopoiesis. Single-cell sequencing techniques have transformed our understanding of normal and malignant hematopoiesis by moving beyond the classical hematopoietic hierarchy to define transitional cell states, thereby unraveling clonal complexity with unprecedented resolution. Single-cell multi-omic approaches that span genomics, transcriptomics, proteomics, epigenomics, and metabolomics have the potential to unravel the vast disease heterogeneity in AML, address the discordance between genetic subtypes and functional phenotypes, and improve risk stratification. The latest frontier, spatial single-cell techniques apply these multi-omic approaches to study cells in situ, offering new insights into the bone marrow microenvironment. Here, we review how single cell sequencing technologies have been utilized to study AML throughout the course of disease, including initial diagnosis, assessment of measurable residual disease in remission, and clonal evolution at relapse, and we look ahead to future applications that may impact clinical practice.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106174"},"PeriodicalIF":2.6,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054317","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":"TSC gene-associated lesions of the lung.","authors":"Fatime Szalai, Ildiko Krencz, Charles D Burger, Anna Kornafeld, Andras Khoor","doi":"10.1016/j.humpath.2026.106173","DOIUrl":"https://doi.org/10.1016/j.humpath.2026.106173","url":null,"abstract":"<p><p>Pathogenetic alterations of tumor suppressor genes TSC1 and TSC2 are responsible for the development of tuberous sclerosis complex (TSC) and various sporadic diseases, including sporadic lymphangioleiomyomatosis (LAM). TSC can be inherited and non-inherited and is characterized by indolent tumor formation in multiple organs. The most important pulmonary manifestation of TSC is LAM. It affects the majority of female and a small subset of male patients, heavily impacting their quality of life and survival. It is a cystic lung disease, which is now considered a PEComa-type neoplasm. In addition to the TSC-associated form (TSC-LAM), LAM can also occur sporadically (S-LAM), almost exclusively in women. Both forms present with proliferation of immature smooth muscle cells, resulting in cystic destruction of the pulmonary parenchyma and emergence of respiratory symptoms, including dyspnea and pneumothorax. Currently, sirolimus is the only FDA-approved treatment option for LAM patients; however, a subgroup of patients either do not respond or tolerate therapy. Recently published data has shed light on the heterogeneity of LAM and the importance of the tumor microenvironment, which may serve as new aspects for future research. Other TSC gene-associated lesions of the lung include multifocal micronodular pneumocyte hyperplasia (MMPH) and non-LAM PEComa (clear cell sugar tumor). While MMPH may not be progressive or require clinical treatment, it might require differentiation from atypical adenomatous hyperplasia or lepidic adenocarcinoma of the lung.</p>","PeriodicalId":13062,"journal":{"name":"Human pathology","volume":" ","pages":"106173"},"PeriodicalIF":2.6,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054386","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}