MedComm – Oncology最新文献

{"title":"Fatty acids in cancer: Metabolic functions and potential treatment","authors":"Ao Du,&nbsp;Zhen Wang,&nbsp;Tengda Huang,&nbsp;Shuai Xue,&nbsp;Chuang Jiang,&nbsp;Guoteng Qiu,&nbsp;Kefei Yuan","doi":"10.1002/mog2.25","DOIUrl":"https://doi.org/10.1002/mog2.25","url":null,"abstract":"<p>Lipid metabolic reprogramming is one of the important metabolic characteristics of cancer cells. As major components of lipids, fatty acids provide energy and material basis for cancer cell survival. Abnormal fatty acid metabolism has been found in many cancers. Fatty acid uptake, transport, and synthesis are closely related to the pathogenesis of cancer. Meanwhile, fatty acid changes in the membrane structure of cancer cells and signal transduction mediated by signaling lipids are also helping cancer cells survive in the changing microenvironment. Some of these enzymes and metabolites involved in fatty acid metabolism are emerging as unique cancer biomarkers. Multiple studies have shown that disordered fatty acids can regulate tumor cell proliferation, metastasis, and drug resistance. Therefore, targeting fatty acid metabolism has become a promising treatment strategy. Here, we mainly present metabolic alterations of fatty acids, the basic components of lipids, in cancer. We discuss the cancer treatment based on fatty acid and fatty acid metabolism. These may provide a basis for a better understanding of lipid metabolic reprogramming in cancer, and also provide new ideas for cancer biomarker search, drug development, and combination therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.25","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50127649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morus alba derived Kuwanon-A combined with 5-fluorouracil reduce tumor progression via synergistic activation of GADD153 in gastric cancer","authors":"Jingjing Su,&nbsp;Abhimanyu Thakur,&nbsp;Guangzhao Pan,&nbsp;Jianglong Yan,&nbsp;Isha Gaurav,&nbsp;Sudha Thakur,&nbsp;Zhijun Yang,&nbsp;Alma Cili,&nbsp;Kui Zhang","doi":"10.1002/mog2.24","DOIUrl":"https://doi.org/10.1002/mog2.24","url":null,"abstract":"<p>Despite the application of conventional strategies including chemotherapy, radiotherapy, surgery, or immunotherapy, the mortality of gastric cancer (GC) patients remains high. Often, GC is not diagnosed until it has reached late stage, resulting in a missed surgical window. Therefore, a new therapeutic intervention for GC is necessary. Here, the combined application of Kuwanon-A (KA) and 5-fluorouracil (5-FU) was evaluated for its potential to combat GC for the first time. To determine the anticancer activity of KA (from <i>Morus alba</i>) along with 5-FU against GC, and their mechanism via GADD153, we examained anticancer potential of KA along with 5-FU via in vitro assays with GC cells, namely MKN-45, SGC-7901, HGC-27, and BGC-823, and in vivo assays with mouse xenograft of GC. KA alone could induce G2/M phase arrest and apoptosis in GC cells by activating GADD153 through the PERK/elF2α/ATF4 and IRE1/XBP1 signaling pathways, suggesting a critical role of increased endoplasmic reticulum stress in KA-induced apoptosis of GC cells. Moreover, the combination of KA and 5-FU showed an enhanced synergistic anticancer effect against GC both in vitro and in vivo. Conclusively, the combination of KA and 5-FU can act as an effective anticancer regimen in combating GC.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.24","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50137825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insight on the cellular and molecular basis of blood vessel formation: A specific focus on tumor targets and therapy","authors":"Nimish Mol Stephen,&nbsp;Udayawara Rudresh Deepika,&nbsp;Tehreem Maradagi,&nbsp;Tatsuya Sugawara,&nbsp;Takashi Hirata,&nbsp;Ponesakki Ganesan","doi":"10.1002/mog2.22","DOIUrl":"https://doi.org/10.1002/mog2.22","url":null,"abstract":"<p>The cellular and molecular switches that govern angiogenesis are considered therapeutic targets for several diseases like tumors and atherosclerosis. Thus, understanding the detailed molecular mechanisms underlying the formation of the new blood vessel is essential for developing novel therapeutic strategies. The formation of a new blood vessel (angiogenesis) is tightly regulated by balancing pro- and antiangiogenic molecules. Dysregulated angiogenesis contributes to the pathogenicity of several diseases, including tumors associated with uncontrolled vessel growth. Experimental and clinical studies emphasize that angiogenesis is a critical step for the transition of the tumor to a life-threatening malignancy. In recent years, angiogenesis has been targeted as one of the primary therapeutic goals for treating tumors, and rapid progress has been made by modulating its molecular regulators. Hence, the mechanisms of how blood vessel formation occurs could provide molecular insight into future angiogenic therapy. This review summarizes briefly the molecular players of blood vessel formation comprising vasculogenesis and angiogenesis and their role in tumor progression alongside antiangiogenic therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.22","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50124915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic virotherapy using neural stem cells as a novel treatment option for glioblastoma multiforme","authors":"Tanvir Ahmed","doi":"10.1002/mog2.23","DOIUrl":"https://doi.org/10.1002/mog2.23","url":null,"abstract":"<p>The most deadly and aggressive form of brain cancer is called a glioblastoma multiforme. Following diagnosis, the median duration of survival is only 14 months. It is imperative to develop cutting-edge therapeutic options because the results of conventional treatments are so poor. Replication-competent oncolytic viruses and replication-deficient viral vectors can be used to treat malignant tumors, an idea that has been around for more than a century. Cancer cells can be eliminated by any class. Oncolytic viruses are created with the specific purpose of locating, attacking, and multiplying in cancerous cells while bypassing normal brain tissue. Because of this, the viruses can kill tumors while protecting healthy brain cells. Getting the oncolytic virus reach tumor locations where it is needed is the biggest challenge. If neural stem cells were used as carrier cells to deliver oncolytic viruses to the right tumor locations, glioblastoma multiforme virotherapy will be significantly more efficient. The most recent advancements in the field of utilizing neural stem cells to deliver oncolytic viruses into glioblastoma tumors are the main focus of this review.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.23","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50156065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining an adenovirus encoding human endostatin and PD-1 blockade enhanced antitumor immune activity","authors":"Yaomei Tian,&nbsp;Qieyue Hu,&nbsp;Rui Zhang,&nbsp;Bailing Zhou,&nbsp;Daoyuan Xie,&nbsp;Yuanda Wang,&nbsp;Li Yang","doi":"10.1002/mog2.21","DOIUrl":"https://doi.org/10.1002/mog2.21","url":null,"abstract":"<p>Treatment with immune checkpoint inhibitors (ICIs) has recently achieved unprecedented clinical benefits, becoming a critical treatment for patients with cancer. However, a set of patients are resistant to immune checkpoint inhibitor therapy, likely due to the limited presence or lack of tumor-infiltrating lymphocytes in their tumors. Increasing data indicate that antiangiogenic therapy substantially reduces cancer-induced immunosuppression and is an effective way to enhance the efficacy of cancer immunotherapies by combination with ICIs. Endostatin, an angiogenesis inhibitor, has been widely used as an antiangiogenic therapy for cancer. We showed that combined therapy with an adenovirus encoding human endostatin, named Ad-E, and programmed cell death-1 (PD-1) blockade dramatically abrogated tumor growth, inhibited microvessel density, and promoted tumor apoptosis, compared to treatment with the single agents. Further investigation using flow cytometry showed that combined therapy significantly increased CD8⁺ T-cell infiltration into tumors and promoted the level of CD8⁺ IFN-γ⁺ T cells. Moreover, combined therapy effectively reduced the frequencies of CD11b⁺ F4/80⁺ tumor-associated macrophages (TAMs) and slightly increased M1/M2 ratio in the tumors. RNA-seq analysis of tumor tissue following combined therapy also demonstrated upregulated expression of genes associated with the antitumor immune response. These data support the rationale for combining antiangiogenic and ICIs for cancer therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.21","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50142850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New era for emerging therapeutic targeting human epidermal growth factor receptor 3 (HER 3) in advanced nonsmall cell lung cancer and metastatic breast cancer","authors":"Yasar Ahmed,&nbsp;Thamir Mahgoub,&nbsp;Maha Al Sindi,&nbsp;José J. Berenguer-Pina","doi":"10.1002/mog2.19","DOIUrl":"10.1002/mog2.19","url":null,"abstract":"<p>Human epidermal growth factor receptor 3 (HER3) is a member of the transmembrane receptor tyrosine kinase family. Upregulation of HER3 pathway has been implicated as a mechanism of resistance in solid tumors, particularly in estrogen receptor positive, HER2 positive breast cancer and epidermal growth factor (EGFR) mutant nonsmall cell lung cancer. Several studies suggest that HER3 overexpression represents a negative prognostic biomarker associated with poor survival. Preclinical and clinical studies of anti-HER3 investigational therapies suggest that expression of the HER3 ligand, neuregulin, may predict response to treatment. Despite its emergence as a key cancer therapeutic target, HER3 cannot be targeted with traditional tyrosine kinase inhibitors therapy due to its weak kinase activity. Monoclonal and bispecific antibodies targeting HER3 have been developed and tested in early phase trials. Objective responses were limited when first-generation HER3-specific monoclonal antibodies were investigated as monotherapies in phase 1 and 2 clinical trials for nonsmall cell lung cancer (NSCLC) and metastatic breast cancer (MBC). MBC and NSCLC HER3 specific antibody-drug conjugates have shown encouraging results in resistance in cancer cells, particularly in those that overexpress HER3. These agents have shown some promise in early phase trials in both NSCLC and MBC setting in heavily pretreated patients with varying degrees of response. It is unclear which subgroup of patients will truly benefit from targeting HER3 as these therapies are under investigation.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.19","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78116178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment and verification of a radiomics nomogram to predict distant metastasis in patients with descending type of nasopharyngeal carcinoma","authors":"Qin Yang,&nbsp;Yu Chen,&nbsp;Rui Huang,&nbsp;Wenya Yin,&nbsp;Shuang Zhang,&nbsp;Qianlong Tang,&nbsp;Xinyue Chen,&nbsp;Jinyi Lang,&nbsp;Gang Yin,&nbsp;Peng Zhang","doi":"10.1002/mog2.20","DOIUrl":"10.1002/mog2.20","url":null,"abstract":"<p>Distant metastasis is one of the main reasons for the failure of nasopharyngeal carcinoma (NPC) treatment, and descending type of nasopharyngeal carcinoma (type D NPC) is more prone to distant metastasis. Few people have explored the relationship between the radiomics characteristics of lymph nodes and the distant metastasis of type D NPC. Therefore, we establish a nomogram based on radiomics risk factors to predict distant metastasis in patients with type D NPC. This study retrospectively included 144 type D NPC (T1-2N2-3MO, AJCC 8th). 2600 features were extracted each from CT and MRI examinations conducted before treatment, respectively. Feature selection was performed by least absolute shrinkage and selection operator regression. A binary logistic regression model was used to construct a nomogram, and the C-index and calibration curve were used to evaluate the discrimination and accuracy of the nomogram. Combining CT and MRI radiomics features with a multimodal radiomics model, the average area under curve of the synthetic minority oversampling technique (SMOTE) data set was 0.873 (95% confidence interval [CI]: 0.797–0.949). The C-index in the training and validation sets of the original data set were 0.91 (95% CI: 0.848–0.972) and 0.815 (95% CI: 0.664–0.967); the sensitivity were 0.75 and 0.545, the specificity were 0.932 and 0.903, and the accuracy were 0.882 and 0.81. Therefore, we concluded that the multimodal radiomics model in predicting distant metastasis in descending type of NPC patients was good. The proposed model can provide a reference for precise treatment and prognosis prediction.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.20","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84823767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The landscape of TIGIT target and clinical application in diseases","authors":"Shu Rui,&nbsp;Xiangyu Kong,&nbsp;Jiaye Liu,&nbsp;Liying Wang,&nbsp;Xiaofei Wang,&nbsp;Xiuhe Zou,&nbsp;Xun Zheng,&nbsp;Feng Ye,&nbsp;Heng Xu,&nbsp;Zhihui Li,&nbsp;Han Luo","doi":"10.1002/mog2.18","DOIUrl":"10.1002/mog2.18","url":null,"abstract":"<p>Immune checkpoint blockade has dramatically altered the concept of cancer therapeutics over the past few years. Beyond the existing classical pathways, novel immune checkpoints, such as T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) structural domain (TIGIT), have also emerged in recent years and have promising therapeutic potential. Recent researches have provided ample evidence that TIGIT is extensively involved in various cancerous and noncancerous diseases such as chronic inflammation, autoimmune diseases, abnormal pregnancy status, and most recently coronavirus disease 2019. In contrast to the programmed cell death receptor 1 pathway which primarily affects T-cell function, targeting TIGIT pathway regulates multiple types of immunocytes but has fewer immune-related adverse events. Owing to its unique advantages and extensive involvement in diseases, extensive clinical trials blockade TIGIT or combine it with other targets are ongoing, and numerous phase II clinical trials have already seen promising results. In this review, we summarized the existing research on TIGIT in various diseases and discussed the perspective and challenges related to targeting this molecular for therapy, with an attempt to provide directions for subsequent studies.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.18","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88716740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor–neuron interactions: A novel concept contributor to glioblastoma invasion","authors":"Dongling Pei,&nbsp;Zhenyu Zhang,&nbsp;Long Zhang","doi":"10.1002/mog2.17","DOIUrl":"10.1002/mog2.17","url":null,"abstract":"<p>Recently, a study published in <i>Cell</i> by Venkataramani et al.<span>¹</span> demonstrated that neuronal (NEU), neural progenitor (NPC)-like, and nonmesenchymal (non-MES)-like glioblastoma cells (GBCs) could drive brain tumor cell invasion. Those astrocyte (AS)-unconnected, invasive GBCs (“unconnected^TUM/AC”) transitioned over time and infiltrated into other regions, largely consisting of tumor cell and AS-connected, stable GBCs (“connected^TUM/AC”). This work elegantly indicated that GBCs are not only connected with each other via gap junctions but are also connected with neurons. In addition, NEU activity drives glioma progression via glutamatergic neuron-to-brain tumor synaptic communication and nonsynaptic paracrine stimulation.<span>^{2, 3}</span> However, how these tumors integrate into complex NEU circuits remains unclear.</p><p>Glioblastomas are the most frequently occurring malignant type of primary brain tumor, comprising 12%–15% of all intracranial tumors. However, even with current standard therapies, the majority of patients succumb to the disease within 2 years of diagnosis.<span>⁴</span> Due to the high heterogeneity and invasion of glioblastoma, gross total resection, radiotherapy, and chemotherapy with DNA-alkylaing agent (temozolomide) are largely ineffective.<span>⁵</span> Suvà and co-workers<span>⁶</span> demonstrated that GBCs exist in four cellular states: NPC-like, oligodendrocyte progenitor (OPC)-like, AS-like, and MES-like states. Despite different subtypes, no specific treatment works more effectively. Thus, research into malignant gliomas is complex and challenging.</p><p>Increasing evidence has been found to illustrate the functional and synaptic integration of glioma into the brain network, facilitating brain tumor progression. The NEU activities function through gap junctions, neurotransmitters, ion channels, synapses, tumor microtubes (TMs), and NEU molecules to establish communication with glioma. As reported, there have been several recent discoveries that have described how neurons may form synaptic connections with brain tumor cells. Among cell–cell communication, gap junctions consisted of connexin proteins, which form conductive pores in the plasma membranes among adjacent NEU cells, increasing glioma cell invasiveness and migration.<span>^{7, 8}</span> γ-Aminobutyric acid and glutamate are the predominant neurotransmitters that impair glioma cell growth.<span>^{3, 9}</span> We aimed to provide a simplified explanation of crosstalk on neuron-glioma, found by Venkataramani.</p><p>To understand the rapid spread of malignant glioma, patient-derived human GBC cells were injected into mice via intracranial stereolocalization and the GBCs were separated into two subtypes: unconnected^TUM/AC GBCs and connected^TUM/AC GBCs. Connected^TUM/AC GBCs were found to be anatomically connected with other","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.17","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90223655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type I collagen homotrimers: A potential cancer-specific interventional target","authors":"Ying Zhou,&nbsp;Linzhu Zhang,&nbsp;Jiang Xie,&nbsp;Junhong Han","doi":"10.1002/mog2.16","DOIUrl":"10.1002/mog2.16","url":null,"abstract":"<p>Pancreatic cancer cell-derived homotrimer type 1 collagen plays an important role in the pathogenesis of pancreatic cancer. Homotrimer type 1 collagen produced by pancreatic cancer cells upregulated proliferation-related pathways through the integrin α3β1 axis. Deletion of homotrimer type 1 collagen in genetically engineered mouse models altered the intratumoral microbiome, increased T-cell infiltration, enhanced anti-PD-1 therapy, and ultimately inhibited tumor growth.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.16","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77168971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}