Oncogenesis最新文献

{"title":"CENPF (+) cancer cells promote malignant progression of early-stage TP53 mutant lung adenocarcinoma.","authors":"Yanlu Xiong, Jie Lei, Miaomiao Wen, Yongfu Ma, Jinbo Zhao, Yahui Tian, Zitong Wan, Xiaoyan Li, Jianfei Zhu, Wenchen Wang, Xiaohong Ji, Ying Sun, Jie Yang, Jiao Zhang, Shaowei Xin, Yang Liu, Lintao Jia, Yong Han, Tao Jiang","doi":"10.1038/s41389-025-00546-5","DOIUrl":"https://doi.org/10.1038/s41389-025-00546-5","url":null,"abstract":"<p><p>The prevention and precise treatment of early-stage lung adenocarcinoma (LUAD) characterized by small nodules (stage IA) remains a significant challenge for clinicians, which is due largely to the limited understanding of the oncogenic mechanisms spanning from preneoplasia to invasive adenocarcinoma. Our study highlights the pivotal role of cancer cells exhibiting high expression of centromere protein F (CENPF), driven by TP53 mutations, which become increasingly prevalent during the transition from preneoplasia to invasive LUAD. Biologically, cancer cells (CENPF+) exhibited robust proliferative and stem-like capabilities, thereby propelling the malignant progression of early-stage LUAD. Clinically, autoantibodies against CENPF in the serum and elevated cancer cells (CENPF+) in tissue correlated positively with the progression of early-stage LUAD, especially those in stage IA. Our findings suggest that cancer cells (CENPF+) play a central role in orchestrating the malignant evolution of LUAD and hold potential as a novel biomarker for early-stage detection and management of the disease.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"14 1","pages":"5"},"PeriodicalIF":5.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567034","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":"STAG2 expression imparts distinct therapeutic vulnerabilities in muscle-invasive bladder cancer cells.","authors":"Sarah R Athans, Henry Withers, Aimee Stablewski, Katerina Gurova, Joyce Ohm, Anna Woloszynska","doi":"10.1038/s41389-025-00548-3","DOIUrl":"10.1038/s41389-025-00548-3","url":null,"abstract":"<p><p>Expression of stromal antigen 2 (STAG2), a member of the cohesin complex, is associated with aggressive tumor characteristics and worse clinical outcomes in muscle invasive bladder cancer (MIBC) patients. The mechanism by which STAG2 acts in a pro-oncogenic manner in bladder cancer remains unknown. Due to this elusive role of STAG2, targetable vulnerabilities based on STAG2 expression have not yet been identified. In the current study, we sought to uncover therapeutic vulnerabilities of muscle invasive bladder cancer cells based on the expression of STAG2. Using CRISPR-Cas9, we generated isogenic STAG2 wild-type (WT) and knock out (KO) cell lines and treated each cell line with a panel of 312 anti-cancer compounds. We identified 100 total drug hits and found that STAG2 KO sensitized cells to treatment with PLK1 inhibitor rigosertib, whereas STAG2 KO protected cells from treatment with MEK inhibitor TAK-733 and PI3K inhibitor PI-103. After querying drug sensitivity data of over 4500 drugs in 24 bladder cancer cell lines from the DepMap database, we found that cells with less STAG2 mRNA expression are more sensitive to ATR and CHK inhibition. In dose-response studies, STAG2 KO cells are more sensitive to the ATR inhibitor berzosertib, whereas STAG2 WT cells are more sensitive to PI3K inhibitor PI-103. These results, in combination with RNA-seq analysis of STAG2-regulated genes, suggest a novel role of STAG2 in regulating PI3K signaling in bladder cancer cells. Finally, synergy experiments revealed that berzosertib exhibits significant synergistic cytotoxicity in combination with cisplatin against MIBC cells. Altogether, our study presents evidence that berzosertib, PI-103, and the combination of berzosertib with cisplatin may be novel opportunities to investigate as precision medicine approaches for MIBC patients based on STAG2 tumor expression.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"14 1","pages":"4"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537380","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":"Proteomic meta-analysis unveils new frontiers for biomarkers research in pancreatic carcinoma.","authors":"Federica Di Marco, Maria Concetta Cufaro, Verena Damiani, Beatrice Dufrusine, Erika Pizzinato, Fabio Di Ferdinando, Gianluca Sala, Rossano Lattanzio, Enrico Dainese, Luca Federici, Peter Ponsaerts, Vincenzo De Laurenzi, Ilaria Cicalini, Damiana Pieragostino","doi":"10.1038/s41389-025-00547-4","DOIUrl":"10.1038/s41389-025-00547-4","url":null,"abstract":"<p><p>Pancreatic carcinoma (PC) is the sixth leading cause of cancer death in both sexes in 2022, responsible for almost 5% of all cancer deaths worldwide; it is characterized by a poor prognosis since most patients present with an unresectable and metastatic tumor. To date, the decreasing trend in mortality rates related to the most common cancers has contributed to making pancreatic cancer a serious public health problem. In the last few years, scientific research has led to many advances in diagnostic approaches, perioperative management, radiotherapy techniques, and systemic therapies for advanced disease, but only with modest incremental progress in PC patient outcomes. Most of the causes of this high mortality are, unfortunately, late diagnosis and an important therapeutic resistance; for this reason, the most recent high-throughput proteomics technologies focus on the identification of novel biomarkers and molecular profiling to generate new insights in the study of PC, to improve diagnosis and prognosis and to monitor the therapies progress. In this work, we present and discuss the integration of results from different revised studies on protein biomarkers in a global proteomic meta-analysis to understand which path to pursue scientific research. In particular, cancer signaling, inflammatory response, and cell migration and signaling have emerged as the main pathways described in PC, as well as scavenging of free radicals and metabolic alteration concurrently highlighted new research insights on this disease. Interestingly, from the study of upstream regulators, some were found to be shared by collecting data relating to both biological fluid and tissue biomarkers, side by side: specifically, TNF, LPS, p38-MAPK, AGT, miR-323-5p, and miR-34a-5p. By integrating many biological components with their interactions and environmental relationships, it's possible to achieve an in-depth description of the pathological condition in PC and define correlations between concomitant symptoms and tumor genesis and progression. In conclusion, our work may represent a strategy to combine the results from different studies on various biological samples in a more comprehensive way.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"14 1","pages":"3"},"PeriodicalIF":5.9,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11830788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433559","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":"Subtype-specific role for Jagged1 in promoting or inhibiting breast tumor formation.","authors":"Wen-Cheng Chung, Wei Wang, Lavanya Challagundla, Charles D Moore, Sean E Egan, Keli Xu","doi":"10.1038/s41389-025-00545-6","DOIUrl":"10.1038/s41389-025-00545-6","url":null,"abstract":"<p><p>Notch signaling is altered in breast cancer. Recent studies highlighted both tumor-suppressive and oncogenic roles for Notch in this tissue. The function of Jagged1, the most highly expressed Notch ligand in the mammary gland, is not well defined. Here we report that deletion of Jagged1 in the mammary epithelium of virgin mice led to expansion of the mammary stem cell (MaSC) compartment and defective luminal differentiation associated with decreased expression of the progesterone receptor (PR). In contrast, deletion of Jagged1 in alveolar cells of pregnant mice had no effect on alveolar and lactogenic differentiation or post-lactational involution. Interestingly, deletion of Jagged1 promoted mouse mammary tumor formation from luminal cells but suppressed them from basal cells, associated with downregulation of Notch target genes Hey1 and Hey2, respectively. In agreement with mouse experiments, high expression of JAG1 and HEY1 are associated with better overall survival among patients with luminal tumors, whereas high expression of JAG1 and HEY2 are both associated with worse overall survival in basal subtype of human breast cancer. These results identified Jagged1 as an important regulator of mammary epithelial hierarchy and revealed differential roles of Jagged1-mediated Notch signaling in different subtypes of breast cancer arising from distinct cell types.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"14 1","pages":"2"},"PeriodicalIF":5.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075172","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":"Targeting fucosyltransferase FUT8 as a prospective therapeutic approach for DLBCL.","authors":"Hao Xu, Qi Li, Yuchen Zhang, Chuan He, Xinyun Zhang, Zhiming Wang, Meifang Zhao, Yali Chai, Wenzhuo Zhuang, Bingzong Li","doi":"10.1038/s41389-025-00544-7","DOIUrl":"10.1038/s41389-025-00544-7","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) is characterized by its aggressive nature and resistance to standard chemotherapy, necessitating the development of new therapeutic approaches. The emergence of natural products and their derivatives has notably influenced cancer treatment, making morusinol, a medicine-derived monomer, a promising candidate. Here, we showed that morusinol exerted antitumor effects on DLBCL in vitro by inducing apoptosis and cell cycle arrest. Impressively, morusinol treatment exhibited potent tumor growth inhibition in vivo, proving both well-tolerated and safe in mouse models. Moreover, our investigation identified FUT8, a fucosyltransferase, as a potential target for morusinol. FUT8's role as an oncogene in DLBCL and its correlation with poor survival further underscored its significance. Furthermore, our screening efforts involving clinical and preclinical drugs unveiled a compelling synergistic effect between chidamide and morusinol. Additionally, morusinol's ability to hinder M2-like polarization of tumor-associated macrophages suggested its potential in immune response modulation within DLBCL. Collectively, morusinol showcased substantial promise as an anti-tumor agent for potential clinical application in DLBCL management, potentially augmenting established therapeutic strategies. Moreover, our findings offered promising prospects for natural products to effectively leverage its therapeutic advantages. Working model: The role of Morusinol in treating DLBCL.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"14 1","pages":"1"},"PeriodicalIF":5.9,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11779920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067151","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":"P4HB maintains Wnt-dependent stemness in glioblastoma stem cells as a precision therapeutic target and serum marker.","authors":"Zheng Yuan, Hongbo Jing, Yilin Deng, Meichen Liu, Tao Jiang, Xiong Jin, Weiwei Lin, Yang Liu, Jinlong Yin","doi":"10.1038/s41389-024-00541-2","DOIUrl":"10.1038/s41389-024-00541-2","url":null,"abstract":"<p><p>Glioblastoma stem cells (GSCs) are pivotal in the recurrence and drug resistance of glioblastoma multiforme (GBM). However, precision therapeutic and diagnostic markers for GSCs have not been fully established. Here, using bioinformatics and experimental analysis, we identified P4HB, a protein disulfide isomerase, as a serum marker that maintains stemness in GSCs through the Wnt/β-catenin signaling pathway. Transcriptional silencing of P4HB induces apoptosis and diminishes stem cell-like characteristics in GSCs. Treatments with the chemical CCF624 or the China National Medical Products Administration (NMPA)-approved securinine significantly prolonged survival in patient-derived xenograft mouse models, underscoring P4HB's potential as a therapeutic target and presenting an expedited path to clinical application through drug repurposing. Additionally, elevated P4HB levels in patient serum were found to correlate with disease progression, underscoring its utility as a biomarker and its promise for precision medicine.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"42"},"PeriodicalIF":5.9,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11585657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695675","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 Note: MEK inhibitors induce apoptosis via FoxO3a-dependent PUMA induction in colorectal cancer cells.","authors":"Lin Lin, Dapeng Ding, Yanmei Jiang, Yan Li, Shijun Li","doi":"10.1038/s41389-024-00543-0","DOIUrl":"10.1038/s41389-024-00543-0","url":null,"abstract":"","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"41"},"PeriodicalIF":5.9,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11582311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687604","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":"Identification of pancreatic cancer-specific protease substrates for protease-dependent targeted delivery.","authors":"Etienne J Slapak, Danny A Zwijnenburg, Jan Koster, Maarten F Bijlsma, C Arnold Spek","doi":"10.1038/s41389-024-00542-1","DOIUrl":"10.1038/s41389-024-00542-1","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) presents significant challenges due to the inadequacy of existing chemotherapeutics, which often result in toxicity-dependent dose limitations and premature cessation of therapy. Targeted delivery of therapeutic molecules offers a promising solution. Given that PDAC is marked by a desmoplastic reaction with extensive aberrant protease activity, protease-dependent targeted delivery could minimize off-target toxicities and is of increasing interest. The efficacy of targeted delivery hinges on the specificity of the substrates used; insufficient specificity can lead to off-target effects, reducing the advantage over non-targeted methods. Here, we employ an unbiased library approach to screen over 7 million peptide substrates for proteolytic cleavage by PDAC cell lysates, identifying 37 substrates enriched by at least 500-fold after three rounds of selection. As systemically administered targeted delivery depends on the absence of substrate cleavage in circulation, the peptide library was also screened against whole blood lysates, and enriched substrates were removed from the PDAC-enriched dataset to obtain PDAC-specific substrates. In vitro validation using FRET-peptides showed that 13 of the selected 15 substrates are cleaved by a panel of PDAC cell line lysates. Moreover, evaluation against healthy murine organ and human blood lysates to assess off-target cleavage revealed that the identified substrates are indeed PDAC-specific and that several substrates may be superior with respect to PDAC specificity over the CAPN2-responsive substrate, which has recently shown preclinical potential in targeted therapy, but future animal models should address the potential superiority. Overall, we thus identified substrates with high selectivity and sensitivity for PDAC that could be employed in protease-dependent targeted therapies.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"40"},"PeriodicalIF":5.9,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11579016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142682267","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":"Sertraline/chloroquine combination therapy to target hypoxic and immunosuppressive serine/glycine synthesis-dependent glioblastomas.","authors":"Anaís Sánchez-Castillo, Kim G Savelkouls, Alessandra Baldini, Judith Hounjet, Pierre Sonveaux, Paulien Verstraete, Kim De Keersmaecker, Barbara Dewaele, Benny Björkblom, Beatrice Melin, Wendy Y Wu, Rickard L Sjöberg, Kasper M A Rouschop, Martijn P G Broen, Marc Vooijs, Kim R Kampen","doi":"10.1038/s41389-024-00540-3","DOIUrl":"10.1038/s41389-024-00540-3","url":null,"abstract":"<p><p>The serine/glycine (ser/gly) synthesis pathway branches from glycolysis and is hyperactivated in approximately 30% of cancers. In ~13% of glioblastoma cases, we observed frequent amplifications and rare mutations in the gene encoding the enzyme PSPH, which catalyzes the last step in the synthesis of serine. This urged us to unveil the relevance of PSPH genetic alterations and subsequent ser/gly metabolism deregulation in the pathogenesis of glioblastoma. Primary glioblastoma cells overexpressing PSPH and PSPH^V116I showed an increased clonogenic capacity, cell proliferation, and migration, supported by elevated nucleotide synthesis and utilization of reductive NAD(P). We previously identified sertraline as an inhibitor of ser/gly synthesis and explored its efficacy at suboptimal dosages in combination with the clinically pretested chloroquine to target ser/gly^high glioblastoma models. Interestingly, ser/gly^high glioblastomas, including PSPH^amp and PSPH^V116I, displayed selective synergistic inhibition of proliferation in response to combination therapy. PSPH knockdown severely affected ser/gly^high glioblastoma clonogenicity and proliferation, while simultaneously increasing its sensitivity to chloroquine treatment. Metabolite landscaping revealed that sertraline/chloroquine combination treatment blocks NADH and ATP generation and restricts nucleotide synthesis, thereby inhibiting glioblastoma proliferation. Our previous studies highlight ser/gly^high cancer cell modulation of its microenvironment at the level of immune suppression. To this end, high PSPH expression predicts poor immune checkpoint therapy responses in glioblastoma patients. Interestingly, we show that PSPH amplifications in glioblastoma facilitate the expression of immune suppressor galectin-1, which can be inhibited by sertraline treatment. Collectively, we revealed that ser/gly^high glioblastomas are characterized by enhanced clonogenicity, migration, and suppression of the immune system, which could be tackled using combined sertraline/chloroquine treatment, revealing novel therapeutic opportunities for this subgroup of GBM patients.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"39"},"PeriodicalIF":5.9,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625213","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":"Condensate remodeling reorganizes innate SS18 in synovial sarcomagenesis.","authors":"Pengli Li, Ziwei Zhai, Yixin Fan, Wei Li, Minjing Ke, Xiaoxi Li, Huiru Gao, Yu Fu, Zhaoyi Ma, Wenhui Zhang, Hongyan Yi, Jin Ming, Yue Qin, Bo Wang, Junqi Kuang, Duanqing Pei","doi":"10.1038/s41389-024-00539-w","DOIUrl":"10.1038/s41389-024-00539-w","url":null,"abstract":"<p><p>SS18-SSX onco-fusion protein formed through aberrant chromosomal translocation t (X, 18; p11, q11), is the hallmark and plays a critical role in synovial sarcomagenesis. The recent works indicated that both the pathological SS18-SSX tumorigenic fusion and the corresponding intrinsic physiological SS18 protein can form condensates but appear to have disparate properties. The underlying regulatory mechanism and the consequent biological significance remain largely unknown. We show that the physical properties of oncogenic fusion protein SS18-SSX condensates within cells undergo alterations compared to the proto-oncogene protein SS18. By small-molecule screening and mutant assay, we identified the recognition of H2AK119ub histone modification could account for the distinctive properties of SS18-SSX1 condensates. Notably, we show that SS18-SSX1 condensates have impact on SS18 condensates and hijack that in a phase separation manner, resulting in the relocation of protein SS18 to the H2AK119ub modification targeted by SS18-SSX1. Consequently, this leads to the downregulation of tumor suppressor genes occupied by SS18 physiologically, like CAV1 and DAB2. These results reveal the underlying mechanism of genomic disorder and tumorigenesis caused by the remodeling of oncoprotein SS18-SSX1 condensates at the macroscopic level.</p>","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"38"},"PeriodicalIF":5.9,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11519567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522592","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}