Molecular Oncology最新文献

{"title":"Longitudinal circulating tumor DNA profiling in patients with advanced endometrial cancer using an off-the-shelf targeted NGS panel.","authors":"Carlos Casas-Arozamena, Karin Teien Lande, Eva Diaz, Ana Vilar, Juan Cueva, Efigenia Arias, Victoria Sampayo, Alicia Abalo, Nerea González, Eva Colás, Antonio Gil-Moreno, Miguel Abal, Gema Moreno-Bueno, Therese Sørlie, Kristina Lindemann, Laura Muinelo-Romay","doi":"10.1002/1878-0261.70246","DOIUrl":"10.1002/1878-0261.70246","url":null,"abstract":"<p><p>Intratumor heterogeneity presents a major challenge in precision oncology for endometrial cancer (EC). Circulating tumor DNA (ctDNA) offers a minimally invasive method to monitor tumor evolution and therapeutic resistance. In this retrospective study, we evaluated a tumor-agnostic NGS panel to detect and track ctDNA in 18 EC patients and directly compared its performance with a tumor-informed ddPCR approach. ctDNA was detected by NGS in over 60% of plasma samples, while ddPCR showed higher positivity rates in paired samples (71.9% vs 62.5%), with overall concordance of 65.7% and fair agreement (Cohen's kappa = 0.23). The cfDNA-NGS panel identified a broad spectrum of alterations, including relapse-specific mutations indicative of clonal evolution, but showed lower sensitivity for low-frequency variants compared with ddPCR. Discordant cases, including false-negative results in both approaches, highlight the impact of assay sensitivity, target selection, and biological factors on ctDNA detection. ctDNA dynamics correlated with disease progression and treatment response, although detection was limited in cases with brain metastases. These findings support the utility of tumor-agnostic ctDNA monitoring in advanced EC and highlight the importance of assay quality and careful interpretation to address limitations such as clonal hematopoiesis and technical sensitivity.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776325","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":"DNA methylation and expression of MAPRE3 affect overall survival of early-stage non-small cell lung cancer patients.","authors":"Chao Chen, Jiancheng Cheng, Ruili Hou, Xiaoyuan Zheng, Li Su, Maria Moksnes Bjaanæs, Anna Karlsson, Maria Planck, Johan Staaf, Åslaug Helland, Manel Esteller, David C Christiani, Feng Chen, Xiaofei Cao, Ruyang Zhang","doi":"10.1002/1878-0261.70260","DOIUrl":"https://doi.org/10.1002/1878-0261.70260","url":null,"abstract":"<p><p>The MAPRE3 gene is aberrantly expressed in several cancers. We profiled DNA methylation in tumor tissues from early-stage non-small cell lung cancer (NSCLC) patients and assessed associations with overall survival (OS). Significant CpG probes were validated in The Cancer Genome Atlas (TCGA). The methylation level of cg12821679_MAPRE3 showed significant associations with OS in lung squamous cell carcinoma (LUSC) (HR = 0.32, P = 6.55 × 10^-7), but it was not observed in lung adenocarcinoma (LUAD). In LUSC, MAPRE3 expression was significantly correlated with cg12821679_MAPRE3 (r = 0.17, P = 2.96 × 10^-3) and potential trans-regulated genes were enriched in the Nicotine addiction pathway. Additionally, MAPRE3 expression showed significant associations with OS in both LUAD and LUSC (LUAD: HR_{low vs high} = 2.28, P = 2.40 × 10^-3; LUSC: HR_{low vs high} = 1.61, P = 0.0244). The association between smoking cessation and overall survival was significantly modified by MAPRE3 expression (HR_interaction = 0.69, P = 0.0282). Smoking cessation improved OS only in patients with high MAPRE3 expression (HR = 0.56, P = 2.82 × 10^-3). We conclude MAPRE3 may predict NSCLC prognosis and influence the prognostic benefit of smoking cessation.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776342","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":"EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.","authors":"Donovan Pineau, Leonor Garcia, Hugo Arnold, Antonija Hanžek, Maialen Arrieta, Laurent R Gauthier, Christine Granotier-Beckers, François D Boussin, Amaury Herbet, Marie Hautière, Valentin Asei-Ceschino, Clémentin Jacques, Laura Brard, Thomas Harnois, Valérie Coronas, Bruno Constantin, Aurélien Chatelier, Jean Chemin, Serge Urbach, Martial Seveno, Szimonetta Hideg, Chantal Ripoll, Kasandra Aguilar-Cázarez, Min Zheng, Guo-Hao Huang, Sheng-Qing Lv, Lei Zhang, Philippe Rondard, Laurent Prezeau, Jean-Philippe Pin, Hugues Duffau, Luc Bauchet, Valérie Rigau, Franck Denat, Charles Truillet, Didier Boquet, Jean-Philippe Hugnot","doi":"10.1002/1878-0261.70223","DOIUrl":"https://doi.org/10.1002/1878-0261.70223","url":null,"abstract":"<p><p>Diffuse gliomas are primary brain tumors including glioblastomas (GB), astrocytomas, and oligodendrogliomas, the latter two harboring IDH1 mutations and exhibiting slower progression. Gliomas display cellular plasticity, with transitions between astrocyte-like, oligodendrocyte-like, progenitor-like, and mesenchymal-like states driven by genetic alterations and microenvironmental signals. The proneural-to-mesenchymal transition (PMT), associated with increased malignancy, is tightly regulated by the tumor microenvironment, notably through cytokine signaling and non-tumor cell interactions. Endothelins (ET-1, ET-2, ET-3), vasoactive peptides mainly produced by vascular cells, signal through the G-protein-coupled receptors EDNRA and EDNRB and were previously suggested to promote glioma proliferation based on serum-based models. Here, we revisited endothelin signaling using eleven serum-free glioma lines and tumor samples. Multi-omics and electrophysiological analyses identified EDNRB as the predominant receptor, enriched in astrocyte-like cells, increased by BMPs or growth factor withdrawal, and repressed by interferons, IL-6 family cytokines, endothelins, and Hippo/YAP signaling. EDNRA was confined to a perivascular tumor subpopulation and induced by Notch signaling selectively in GB. Functionally, endothelins reduced proliferation while promoting migration and PMT via EDNRB-dependent Ca²⁺ signaling, ERK/STAT3 activation, and apamin-sensitive SK2/SK3 potassium channel activity. Collectively these findings establish endothelin signaling as an important regulator of glioma cell plasticity and behavior.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776307","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":"Circulating tumor cell viability during and after radiotherapy mirrors treatment response in cancer patients.","authors":"Yvonne Goy, Jana Löptien, Cornelia Coith, Afroditi Nanou, Katharina Hintelmann, Pinnschmidt Hans, Cordula Petersen, Klaus Pantel, Sabine Riethdorf, Kerstin Borgmann, Harriet Wikman","doi":"10.1002/1878-0261.70261","DOIUrl":"https://doi.org/10.1002/1878-0261.70261","url":null,"abstract":"<p><p>The response to radiotherapy (RT) is influenced by the individual DNA repair capacity of both the tumor cells and the host. In this study, we assessed whether circulating tumor cell (CTC) enumeration, kinetics, and CTC viability (i.e., the apoptotic rate) could provide a more accurate tool for monitoring and stratifying the RT response. We analyzed CTCs and tumor-derived extracellular vesicles (tdEVs) during RT in 71 lung (n = 35) and breast (n = 36) cancer patients receiving RT treatment for brain (n = 54) and bone (n = 19) metastases. The DNA repair capacity of the host was assessed by ex vivo irradiation of peripheral blood mononuclear cells (PBMCs). RT treatment did not seem, in most cases, to cause a short-term release of CTCs. We found that both the number and apoptotic rate of CTCs before and after RT treatment is a powerful indicator of poor prognosis. Additionally, the fraction of apoptotic CTCs correlated with RT response and patient outcome. This study demonstrated that the RT response is associated with tumor-specific traits, which can be accessed via easily accessible liquid biopsy approaches.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776154","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":"CCDC80 suppresses high-grade serous ovarian cancer migration via negative regulation of B7-H3.","authors":"Aya Saleh, Nitzan Medina-Itzhaki, Milena Chekov, Eden Gal-Swisa, Roba Gabesh-Wahabi, Inbar Savyon, Inna Naroditsky, Hilary A Kenny, Basem Fares, Lina Korsensky, Einav Girsh, Liron Berger, Ruth Perets","doi":"10.1002/1878-0261.70235","DOIUrl":"https://doi.org/10.1002/1878-0261.70235","url":null,"abstract":"<p><p>Paired box protein Pax-8 (PAX8) is a critical lineage marker and master regulator of transcription in high-grade serous ovarian carcinoma (HGSC)-the most common subtype of epithelial ovarian cancer-driving cell proliferation and migration and resisting apoptosis. This study aimed to elucidate the mechanism of action of PAX8 in this disease. By performing an unbiased analysis of PAX8-regulated genes, we discovered two PAX8-regulated genes-coiled-coil domain-containing protein 80 (CCDC80) and cluster of differentiation 276 (CD276) antigen (also known as B7-H3)-that mediate PAX8 activity and play key cancer cell autonomous roles in this disease. Our findings indicate that PAX8 negatively regulates CCDC80, a novel cell autonomous tumor suppressor in HGSC. We demonstrate that CCDC80, localized to the nucleus, significantly reduces HGSC tumor growth and metastasis in vivo in a mouse model. Notably, CCDC80 exerts its function by suppressing the expression of the immune checkpoint protein B7-H3. However, in HGSC, B7-H3 is predominantly cytoplasmic and promotes HGSC proliferation and migration independent of its immune role. Additionally, PAX8 positively regulates B7-H3 expression in a CCDC80-independent manner, underscoring the multifaceted oncogenic role of PAX8. This study highlights the complex regulatory network involving PAX8, CCDC80, and B7-H3 in HGSC progression. Targeting this signaling pathway may provide a novel therapeutic strategy to improve treatment outcomes for patients with epithelial ovarian cancer. B7-H3, which is currently targeted in clinical trials, shows promise as HGSC target for therapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729389","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":"CD47 promotes mitogen-activated protein kinase and epithelial-to-mesenchymal transition molecular programs to drive prometastatic phenotypes in non-small cell lung cancer.","authors":"Asa P Y Lau, Lilian G Zhai, Ryunosuke Hoshi, Zackary Rousseau, Abraam Zakhary, Yin Fang Wu, Rola M Saleeb, Heyu Ni, Kelsie L Thu","doi":"10.1002/1878-0261.70237","DOIUrl":"https://doi.org/10.1002/1878-0261.70237","url":null,"abstract":"<p><p>CD47 is best known for its role in tumor immune evasion; however, studies in diverse cell models indicate that it also has cell autonomous, tumor-promoting functions which are cell type- and context-specific. Motivated by the prognostic and therapeutic significance of CD47 and the limited knowledge regarding its roles beyond immune evasion in non-small cell lung cancer (NSCLC), we sought to define the cellular and molecular processes driven by intrinsic CD47 signaling in NSCLC. Transcriptome profiling of CD47 wild-type and knockout NSCLC cells implicated its regulation of genes enriched for signatures of mitogen-activated protein kinase (MAPK) signaling and epithelial-to-mesenchymal transition (EMT). A significant positive association between CD47 and MAPK/EMT expression signatures was also evident in large cohorts of NSCLC cell lines and tumor tissues. Functional studies indicated that CD47 does not regulate cell proliferation in NSCLC cells like it does in other cancer types. Instead, CD47 regulates cell adhesion and migration through an ERK and EMT axis, validating our transcriptomic findings. Moreover, CD47 loss-of-function significantly diminished the ability of NSCLC cells to metastasize in vivo, demonstrating the physiological relevance of cell-intrinsic CD47 signaling in lung cancer cells. Our data reveal a novel role for CD47 in relaying signals through ERK to promote EMT expression programs and prometastatic phenotypes in NSCLC. Although additional mechanistic studies are needed to further decipher the CD47-ERK-EMT signaling pathway, our findings reinforce the therapeutic potential of CD47, rationalizing further research to develop CD47 blockade as a multimodal therapy for NSCLC.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729451","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":"Molecular cancer prevention: Intercepting disease.","authors":"Charlotte Grieco, Tej Pandya, Charles Swanton","doi":"10.1002/1878-0261.70258","DOIUrl":"https://doi.org/10.1002/1878-0261.70258","url":null,"abstract":"<p><p>Over several decades, therapeutic advances have transformed oncology, yet for many tumour types, survival improvements have been incremental, with substantial treatment-related morbidity. A decisive pivot in oncology, from treating established malignancy to intercepting and preventing carcinogenesis, could deliver far greater population impact. Delivering this shift requires further mechanistic understanding of tumour initiation, validated biomarkers of premalignant progression and redesigned prevention trials in at-risk populations. Regulatory and commercial frameworks must evolve to enable scalable molecular prevention. Such trials must deliver tolerable side effect profiles and rely on biologically validated surrogate endpoints rather than traditional survival outcomes. Cancer interception should be established as a core pillar of oncological management, alongside early detection and the therapeutic management of established disease, together creating an opportunity to reduce global disease burden at a scale that decades of therapeutic progress in advanced cancer have yet to achieve.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717396","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":"Metastasis on pause: How dormant tumor cells stay hidden within the tumor microenvironment and evade immune surveillance.","authors":"Kanishka Tiwary, Jose Javier Bravo-Cordero","doi":"10.1002/1878-0261.70259","DOIUrl":"https://doi.org/10.1002/1878-0261.70259","url":null,"abstract":"<p><p>Metastasis remains the leading cause of cancer-related mortality. Even after major advances in early detection and systemic therapies, long-term disease recurrence frequently arises from the presence of dormant disseminated tumor cells (DTCs) at distant sites. Dormant DTCs disseminate from the primary tumor and reside in secondary organs in a reversible quiescent state characterized by minimal proliferation, enabling resistance to therapies that target actively dividing cells. Despite their inactivity, dormant DTCs are far from inert. Dormant DTCs dynamically interact with the surrounding tumor microenvironment (TME), including stromal, vascular, and immune components, to establish niches that maintain quiescence while limiting immune detection. While the mechanisms by which proliferating cancer cells evade immune surveillance have been extensively studied, the processes governing immune regulation, immune-mediated dormancy, and immune evasion of dormant DTCs remain incompletely integrated across literature. In this review, we explore recent advances describing how microenvironmental cues and immune pressures converge on tumor cell-intrinsic programs to sustain dormancy, promote immune tolerance, and enable long-term survival of DTCs across different organs and cancer types. We further discuss conditions that disrupt this equilibrium and drive escape from dormancy, as well as emerging therapeutic strategies aimed at eliminating or controlling dormant DTCs by targeting dormancy-specific immune and microenvironmental interactions.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699087","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":"Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2-COL3A1 axis.","authors":"Iryna Horak, Iva Staniczková Zambo, Matěj Přikryl, Peter Múdry, Danica Zapletalová, Jarmila Navrátilová, Jiří Navrátil, Jan Šmarda, Liudmyla Drobot, Petr Beneš, Lucia Knopfová","doi":"10.1002/1878-0261.70245","DOIUrl":"https://doi.org/10.1002/1878-0261.70245","url":null,"abstract":"<p><p>Osteosarcoma is the most common malignant bone tumor, primarily affecting adolescents and young adults. Patients with metastases have a low survival rate, making the identification of prognostic markers crucial. The adaptor protein CIN85 is involved in various signaling pathways that regulate cell differentiation, adhesion, and motility. Its overexpression is associated with poor prognosis in multiple cancers. However, the role of CIN85 in osteosarcoma progression has not yet been explored. This study shows that CIN85 expression is higher in osteosarcoma than in normal bone tissue and further increased in metastatic lesions relative to primary tumors. CIN85 overexpression increases cell migration and Matrigel invasion, whereas silencing CIN85 suppresses these behaviors. Functional annotation and enrichment analyses of the CIN85-driven transcriptome suggest that CIN85 regulates migration, adhesion, and extracellular matrix organization in osteosarcoma. CIN85 affects MMP2 and COL3A1 gene expression and activates Akt/mTOR signaling. Knockdown of MMP2 and COL3A1 or pharmacological inhibion of Akt/mTOR signaling abrogates CIN85-induced motility. This study demonstrates that elevated CIN85 expression contributes to osteosarcoma migration and metastasis, highlighting its potential as a therapeutic target.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717411","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":"Proteasome inhibitor, ixazomib prevents topoisomerase-I degradation and reverses irinotecan resistance in colorectal cancer.","authors":"Yuho Ebata, Koji Ando, Hirofumi Hasuda, Koshi Mimori, Elizabeth C Unan, Siddhartha Pulukuri, Aahana Tiku, Allison Berger, Eiji Oki, Ajit Bharti, Tomoharu Yoshizumi","doi":"10.1002/1878-0261.70256","DOIUrl":"https://doi.org/10.1002/1878-0261.70256","url":null,"abstract":"<p><p>Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge. We previously showed that camptothecin induces ubiquitin-proteasome pathway (UPP)-mediated topoI degradation. In this study, we investigated whether inhibition of UPP could prevent topoI degradation and restore camptothecin sensitivity. SN-38, an active metabolite of irinotecan, induced topoI degradation in irinotecan-resistant colorectal cancer cell lines, which was suppressed by ixazomib. The combination significantly enhanced cytotoxicity, colony inhibition, and reduced IC₅₀ values compared with SN-38 alone. Mechanistically, ixazomib prevented proteasome-mediated degradation of ubiquitinated topoI, restoring its stability. In vivo, the combination significantly suppressed tumor growth in a DLD-1 xenograft model compared with SN-38 alone. These findings indicate that UPP-dependent topoI degradation is a key mechanism underlying irinotecan resistance in colorectal cancer. Pharmacological inhibition of the proteasome effectively prevents topoI loss and restores irinotecan sensitivity, suggesting that proteasome inhibitors such as ixazomib may serve as promising therapeutic partners for camptothecin-based chemotherapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690684","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}