Molecular Oncology最新文献

{"title":"Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation.","authors":"Elena Genova, Michele Montrone, Uday Rangaswamy, Francesco Diversi, Irene Schiavo, Denise Ferrarini, Roberta Di Florio, Irene Longo, Michele Coscia, Nicola Zamboni, Giorgia Demontis, Lisa Veghini, Vincenzo Corbo, Remo Sanges, Paul Heppenstall","doi":"10.1002/1878-0261.70233","DOIUrl":"10.1002/1878-0261.70233","url":null,"abstract":"<p><p>Neuronal innervation of the pancreas has historically been characterized using marker-based classification and physiological studies, but its transcriptomic landscape remains only partially explored. A detailed molecular profile of pancreatic sensory neurons could provide insights into their role in health and disease, particularly in pancreatic ductal adenocarcinoma (PDAC), where neural remodeling influences tumor progression and pain signaling. Wild-type and PDAC mice were injected with the retrotracer Fast Blue into pancreatic or cancerous tissue. Dorsal root ganglia were dissociated, and Fast Blue-positive sensory neurons were isolated, lysed, and analyzed using single-cell RNA sequencing. Data were validated using immunofluorescence, organoid cultures and qPCR. We performed transcriptomic profiling of sensory neurons innervating the pancreatic head and tail under normal and cancer conditions. Our analysis identified neurofilament-containing neurons as the predominant sensory subtype in both contexts, while non-peptidergic neurons were underrepresented in tumor-associated innervation. Differential gene expression analysis revealed a unique subset of genes upregulated in sensory neurons innervating pancreatic tumors, many linked to mitochondrial activity. Further validation also revealed the presence of transcripts transferred via extracellular vesicles (including the Pdx1-CreERT2 transgene from the KPC mouse model), suggesting a novel mechanism of tumor-neuron interaction. Our findings provide a detailed characterization of pancreatic and pancreatic ductal adenocarcinoma sensory innervation. We identified tumor-derived RNA within sensory neurons in the PDAC mouse model, suggesting an extracellular vesicle-mediated RNA transfer mechanism that may remodel sensory signaling and open new prospects for diagnostic and therapeutic innovation in PDAC. Impact statement Transcriptomic profiling of pancreatic sensory neurons reveals shifts in neuronal populations, tumor-specific mitochondrial gene upregulation, and potential extracellular vesicle-mediated transcript transfer. Circulating tumor transcripts in KPC mice provide a reference for pancreatic innervation, tumor-nerve interactions, and therapeutic targets.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1726-1741"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473902","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":"RETRACTION: Mechanism of p27 Upregulation Induced by Downregulation of Cathepsin B and Upar in Glioma.","authors":"","doi":"10.1002/1878-0261.70288","DOIUrl":"10.1002/1878-0261.70288","url":null,"abstract":"<p><strong>Retraction: </strong>S. Gopinath, K. Alapati, R. R. Malla, C. S. Gondi, S. Mohanam, D. H. Dinh, and J. S. Rao, \"Mechanism of p27 Upregulation Induced by Downregulation of Cathepsin B and Upar in Glioma,\" Molecular Oncology 5, no. 5 (2011): 426-437, https://doi.org/10.1016/j.molonc.2011.07.004. The above article, published online on 26 July 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor in Chief, Kevin Ryan; the Federation of European Biochemical Societies; and John Wiley and Sons Ltd. Following publication, concerns were raised by a third party regarding the duplications of image elements Figure 7, as well as duplicated western blot bands between Figures 4C and 6B, between Figures 1C and 4C, within Figure 3A and within Figure 6A. Internal investigation confirmed the duplications in these figures and additionally identified undeclared splice marks within Figures 2D and 4C, duplicated western blot bands between Figure 3A and Figure 4A of a previous publication with shared authors (DOI: 10.1371/journal.pone.0011668) where the same bands were presented in a different scientific context. The retraction has been agreed because the concerns were determined to affect the authenticity and reliability of the data and results presented. The authors have been informed of the retraction decision where possible; however, current contact details could not be verified.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1892"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199283","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":"Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.","authors":"Giulia Schiavoni, Antonella Palmese, Stefano Scalera, Laura Cipriani, Davide Mascolo, Patrizia Vici, Teresa Arcuri, Lorena Filomeno, Eriseld Krasniqi, Giovanni Blandino, Giulia Bon, Marcello Maugeri-Saccà","doi":"10.1002/1878-0261.70232","DOIUrl":"10.1002/1878-0261.70232","url":null,"abstract":"<p><p>Breast cancer, the most frequently diagnosed cancer in women globally, is a heterogeneous disease with distinct subtypes requiring distinct therapeutic approaches. Regardless of molecular subtyping, breast cancer stem cells significantly contribute to tumor heterogeneity, distant dissemination, and therapeutic resistance. The Hippo pathway is a key regulator of organogenesis and tissue development, and its deregulation is common in breast cancer and linked to cancer stem cell features across several cancer types. Dysfunctional pathway activity leads to the aberrant activation of Hippo downstream effectors, the Yes-associated protein (YAP) and its paralog transcriptional co-activator with PDZ-binding motif (TAZ), which promote epithelial-to-mesenchymal transition, growth factor-independent proliferation, and maintenance of the breast cancer stem cells' niche. This review summarizes the regulation of the Hippo pathway, emphasizing its significant role in coordinating stemness-related mechanisms in breast cancer. An overview of how the Hippo pathway fuels stemness in triple-negative breast cancer, the most aggressive BC subtype, is then provided. We also discuss how the activation of stem cell-like properties, driven by dysregulation of the Hippo pathway, contributes to the development of resistance to current therapies across the spectrum of breast cancer subtypes.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1667-1693"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521466","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":"Interrogating the immune landscape of microsatellite stable RAS-mutated colon cancer.","authors":"Rodrigo Dienstmann, Eduardo García-Galea, Alice O'Farrell, Zak Kinsella, Maxime Meylan, Florent Petitprez, Ingrid Arijs, Tom Venken, Hari Ps, Adrian Lärkeryd, Ian Miller, Janick Selves, Nadja Meindl-Beinker, Fiorella Ruiz-Pace, Elena Élez, Raquel Comas-Navarro, Frank Lincoln, Dirk Fey, Gift Nyamundanda, Aoife Nolan, Joern Lewin, Raquel Perez-Lopez, Jonathan Briody, Kathleen Bennett, Walter Kolch, David Matallanas, Alexander Kel, Enrique Arenas, Joaquín Arribas, Bart Ghesquière, Josep Tabernero, Julie Meilleroux, Deborah McNamara, Ray McDermott, Marvin Lim, Mary O'Reilly, Brian Bird, Lisa Stack, Lucia Moloney, Patrick Morris, Keith Egan, Maciej Milewski, Lars Scheuer, Joachim Behringer, Georg Bolz, Ramon Salazar, Cristina Santos, Andrea Ruiz, Orla Casey, Verena Murphy, Matthias Ebert, Livio Trusolino, Diether Lambrechts, Anguraj Sadanandam, Catherine Sautès-Fridman, Jochen Prehn, Paolo Nuciforo, Jacques Fieschi, Florence Monville, Darran O'Connor, Wolf Fridman, Annette Byrne","doi":"10.1002/1878-0261.70225","DOIUrl":"10.1002/1878-0261.70225","url":null,"abstract":"<p><p>To explore the immune microenvironment of RAS-mutated (RASmt) microsatellite stable (MSS) colon cancer (CC), we retrospectively performed whole exome sequencing, RNA sequencing, and robust digital pathology analyses and studied immune markers in a cohort of 161 patients treated with standard-of-care therapies with early stage disease (both fresh frozen and formalin-fixed paraffin-embedded [FFPE] samples) or 121 patients with metastatic setting (primary tumor FFPE samples). Only a small proportion of cases exhibited a highly infiltrated immune microenvironment, with a strong association between Immunoscore^® (IS)-high (13% of the samples) and Tumor Lymphocytes Infiltrating Score (TuLIS)-high scores (25% of the samples). Immunoscore Immune-Checkpoint (ISIC)-high tumors (52% of the samples) shared a similar microenvironment composition to IS-high and TuLIS-like high tumors and displayed higher mutational burdens than ISIC-low tumors. In conclusion, a substantial proportion of MSS RASmt CCs exhibit high ISIC scores, meriting evaluation in prospective trials of immunotherapy-based combination regimens.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1713-1725"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147284518","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":"COMP-PMEPA1 axis promotes epithelial-to-mesenchymal transition in breast cancer cells.","authors":"Konstantinos S Papadakos, Gilar Gorji-Bahri, Lejla Gradjan, Julia Zajac, Kacper Gil, Yvonne Thokozile Nduku, Anna M Blom","doi":"10.1002/1878-0261.70221","DOIUrl":"10.1002/1878-0261.70221","url":null,"abstract":"<p><p>Epithelial-to-mesenchymal transition (EMT), driven by cues from the tumor microenvironment, is a critical initiator of metastatic progression. In breast cancer patients, elevated expression of cartilage oligomeric matrix protein (COMP) is associated with shorter survival and increased metastatic risk. Here, we investigated the role of COMP in regulating EMT in breast cancer. Breast cancer cells treated with recombinant COMP or engineered to overexpress COMP exhibited a marked decrease in the epithelial marker CDH1 and an increase in mesenchymal markers such as VIM and VCAN. Consistent with these in vitro findings, COMP-expressing xenograft tumor tissues showed enhanced EMT characteristics. Functionally, COMP promoted increased migration and invasion of breast cancer cells in both autocrine and paracrine manners, dependent on its thrombospondin (TSP) and C-terminal domains. We further identified protein TMEPAI (encoded by gene PMEPA1) as a functional COMP-binding partner that mediates COMP-induced EMT, primarily through interaction with the TSP domain of COMP. Mechanistically, COMP shifted transforming growth factor beta (TGFβ) signaling from canonical phosphorylated mothers against decapentaplegic homolog 2/3 (pSMAD2/3) activation toward pSMAD1/5, likely through its interaction with PMEPA1. This study suggests the COMP-PMEPA1 axis as a new driver of EMT in breast cancer models.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1780-1799"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194992","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":"Cell-cycle-specific lesion evolution rather than inhibition of double-strand-break repair underpins cisplatin radiosensitization.","authors":"Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis","doi":"10.1002/1878-0261.70240","DOIUrl":"10.1002/1878-0261.70240","url":null,"abstract":"<p><p>DNA double-strand breaks (DSBs) generated from collisions of DNA replication forks with cisplatin-induced interstrand crosslinks underpin cisplatin cytotoxicity. Yet, the impact of cell-cycle-dependent cisplatin-DNA adduct (CDA) formation on cell cycle progression and interactions with DNA replication remain incompletely characterized. Also, although cisplatin enhances tumor response to ionizing radiation (IR), the underpinning radiosensitizing mechanisms remain unresolved. Here, we close this void and analyze CDAs (GpG crosslinks) and DSB (γH2AX foci) induction and repair in a strictly cell-cycle-dependent manner. We report for the first time that CDAs form in a dose- and time-dependent manner in all cell cycle phases, whereas DSBs emerge only in S-phase. Repair of IR-induced DSBs remains largely unaffected by CDAs in G₁, S, and G₂ phases, but is inhibited when S-phase-treated cells progressed to G₂. Radiosensitization occurs after prolonged cisplatin exposure, likely owing to G₂-phase accumulation and lesion evolution from S-phase, thus impairing repair of IR-induced DSBs. Cisplatin fails to radiosensitize quiescent (G₀) cells. In summary, CDA formation is similar across the cell cycle, but DSBs form only in S-phase. Whereas CDAs fail to interfere with repair of IR-induced DSBs, progression-dependent repair disruptions cause radiosensitization. Elucidation of the underpinning mechanisms may help to design improved cisplatin-radiation schedules for more efficacious therapies.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1814-1834"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486501","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":"Weakening the nuclear envelope: Lamin B receptor in melanoma metastasis.","authors":"Francesca Lorenzini, Maria Caterina Mione","doi":"10.1002/1878-0261.70281","DOIUrl":"10.1002/1878-0261.70281","url":null,"abstract":"<p><p>Nuclear envelope fragility has been identified as a hallmark of the metastatic process. Indeed, cancer cells undertake a challenging journey through diverse environments during metastasis, notably squeezing through narrow spaces and dense collagen matrices. In their report, Baird et al. identify a key player in nuclear fragility in confined cancer cell migration: the Lamin B receptor. Its overexpression and clustering in specific regions of the nuclear envelope increase nuclear distortion and fragility, rendering nuclei more susceptible to rupture with consequent chromatin extrusion and genomic instability. Elucidating the mechanisms underlying this process, particularly the receptor's sterol reductase activity, represents a promising step towards the identification of novel therapeutic targets.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1663-1666"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199361","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":"Pre-analytical optimization of cell-free DNA and extracellular vesicle-derived DNA for mutation detection in liquid biopsies.","authors":"Jonas Dohmen, Lucrezia De Santis, Bret M Stephens, Vincent Bernard, Jörg C Kalff, Lara Braun, Phillipp Leyendecker, Johannes Röttgen, Daniel Weissinger, Anirban Maitra, Paola A Guerrero, Alexander Semaan","doi":"10.1002/1878-0261.70222","DOIUrl":"10.1002/1878-0261.70222","url":null,"abstract":"<p><p>Liquid biopsies enable noninvasive tumor profiling and longitudinal disease monitoring. Their analytical performance is strongly influenced by pre-analytical factors, yet direct comparisons between cell-free DNA (cfDNA) and extracellular vesicle-derived DNA (evDNA) remain scarce. We prospectively evaluated four pre-analytical variables: processing delay, storage temperature, tube type, and plasma input volume, on cfDNA and evDNA from cancer patient plasma (n = 244) using ddPCR, Qubit, and TapeStation. Key findings were validated in archived plasma samples (n = 723). In the prospective cohort, cfDNA concentrations increased after 24 h and evDNA after 48 h at room temperature, while retrospective analysis revealed earlier changes (cfDNA: 6 h; evDNA: 24 h). Storage conditions influenced both analytes, as short-term refrigeration (4 °C) better preserved DNA quality than -80 °C freezing, while extracted DNA remained stable at -80 °C. Acid citrate dextrose (ACD) and K₂EDTA tubes performed similarly under prompt processing. Higher plasma volumes improved evDNA, but not cfDNA, for mutation detection. evDNA demonstrates greater resilience than cfDNA under suboptimal conditions. Standardized workflows and prompt processing are essential to ensure reliable mutation detection in clinical liquid biopsy applications.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1762-1779"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147271547","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":"Correction to \"Human papillomavirus (HPV)-18 E6 oncoprotein interferes with the epithelial cell polarity Par3 protein\".","authors":"","doi":"10.1002/1878-0261.70278","DOIUrl":"10.1002/1878-0261.70278","url":null,"abstract":"","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1890"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150448","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":"E2A selectively regulates TGF-β-induced apoptosis in KRAS-mutant non-small cell lung cancer.","authors":"Sergei Chuikov, Shiva Krishna Katkam, Zhefan Wang, Venkateshwar G Keshamouni","doi":"10.1002/1878-0261.70236","DOIUrl":"10.1002/1878-0261.70236","url":null,"abstract":"<p><p>Transforming growth factor-β (TGF-β) regulates epithelial homeostasis by inducing growth arrest and apoptosis during early carcinogenesis; however, these tumor-suppressive functions are frequently lost in advanced nonsmall cell lung cancer (NSCLC) despite intact signaling. We identify the transcription factor E2A as a critical mediator of resistance to TGF-β-induced apoptosis in mutant KRAS-driven NSCLC. TGF-β induces E2A expression in a SMAD3-dependent manner in NSCLC cells harboring mutant KRAS, but not in those with wild-type KRAS. Silencing E2A restores TGF-β-induced apoptosis in mutant KRAS cell lines without affecting epithelial-mesenchymal transition. E2A depletion promotes mitochondrial apoptosis through mitochondrial outer membrane permeabilization, caspase-3 activation, and regulation of BCL-2 family and inhibitor-of-apoptosis proteins. In contrast, wild-type KRAS NSCLC cells fail to upregulate E2A in response to TGF-β and remain resistant to apoptosis following E2A silencing. Knockdown of mutant KRAS abrogates the pro-apoptotic effects of E2A silencing, establishing KRAS dependency. E2A silencing enhances radiation-induced growth inhibition, likely through increased sensitivity to TGF-β signaling. E2A is overexpressed in lung adenocarcinoma and is significantly elevated in tumors harboring mutant KRAS. These findings identify E2A as a context-specific suppressor of TGF-β-mediated apoptosis and a potential therapeutic target in mutant KRAS NSCLC.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1877-1888"},"PeriodicalIF":4.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499443","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}