International journal of oncology最新文献

{"title":"SUCLG1 promotes aerobic respiration and progression in plexiform neurofibroma.","authors":"Zifu Zhou, Qingfeng Li, Ran Huo","doi":"10.3892/ijo.2024.5716","DOIUrl":"10.3892/ijo.2024.5716","url":null,"abstract":"<p><p>Plexiform neurofibromas (PNFs) are benign tumors that affect 20‑50% of patients with type I neurofibromatosis (NF1). PNF carries a risk of malignancy. There is no effective cure for PNF. Its onset may be associated with genetic and metabolic abnormalities, but the exact mechanisms remain unclear. Succinate‑CoA ligase GDP/ADP‑Forming Subunit α(SUCLG1), a catalytic enzyme in the tricarboxylic acid cycle, is highly expressed in PNF. The present study aimed to explore the role of SUCLG1 in function and metabolism of PNF cells. SUCLG1 expression was verified using western blotting and immunofluorescence. After inducing SUCLG1 knockdown and overexpression, functional changes in PNF cells were assessed, as well as effects of SUCLG1 on cell respiration and glucose metabolism. Quantitative PCR, WB, electron microscopy and Flow cytometry demonstrated that SUCLG1 enhanced mitochondrial quality and promoted mitochondrial fusion, thereby driving proliferation and migration of tumor cells, inhibiting apoptosis and altering the cell cycle. A Seahorse assay showed that elevated SUCLG1 expression enhanced cell aerobic respiration without affecting the glycolytic process. This suggests that SUCLG1 upregulation in PNF does not trigger the Warburg effect associated with malignant tumors. This study also demonstrated the positive regulation of cellular function by promoting the expression level of the <i>SLC25A1</i> gene when SUCLG1 expression was elevated. In conclusion, SUCLG1 altered the mechanism of mitochondrial quality control to enhance cell aerobic respiration, thereby driving the pathogenesis of PNF. Thus, SUCLG1 can serve as a potential target in future therapeutic strategies.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs and their role in breast cancer metabolism (Review).","authors":"Wen Xuan Lee, Bann Siang Yeo, Rozi Mahmud, Geok Chin Tan, Mohamed Ibrahim Abdul Wahid, Yoke Kqueen Cheah","doi":"10.3892/ijo.2024.5713","DOIUrl":"10.3892/ijo.2024.5713","url":null,"abstract":"<p><p>Breast cancer (BC) continues to be the leading cause of cancer‑related mortality among women, placing a substantial disease burden on the global female population. MicroRNAs (miRNAs) are members of a large class of non‑coding RNAs capable of regulating gene expression at the post‑transcriptional level. With cases of early‑onset BC on the rise, miRNAs are promising biomarkers and therapeutic targets for early BC detection and treatment. Dysregulated miRNA expression is known to be closely linked to BC development and metastasis in cancer cells via metabolic reprogramming. Normal cellular metabolism is tightly regulated by various complex signaling pathways. Therefore, dysregulation of metabolism due to metabolic reprogramming is considered a hallmark of cancer. The present review delves into the crucial roles that miRNAs serve in disordered cellular metabolism of BC by targeting gene transcripts, key metabolic enzymes and transporter proteins responsible for regulating major cellular metabolism pathways. The future outlook and clinical implications of miRNAs as potential diagnostic, prognostic and therapeutic markers in BC metabolism are also discussed.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Sequential use of protein kinase inhibitors potentiates their toxicity to melanoma cells: A rationale to combine targeted drugs based on protein expression inhibition profiles.","authors":"Philippe G Aftimos, Murielle Wiedig, Mireille Langouo Fontsa, Ahmad Awada, Ghanem Ghanem, Fabrice Journe","doi":"10.3892/ijo.2024.5707","DOIUrl":"10.3892/ijo.2024.5707","url":null,"abstract":"<p><p>Following the publication of this article, a concerned reader drew to the Editor's attention that there appeared to be the duplication of a pair of western blots in each of Figs. 4 and 6, with the possibility of the bands in question having been resized in one of these cases. After having conducted an internal investigation, the Editorial Office also determined that there was a further instance of duplication of western bands comparing between Figs. 2 and 4. In all cases, the bands that had been re‑used were intended to show the results of differently performed experiments. After assessing the issues that have come to light with regard to the duplications of western blots in this paper, in view of the apparently misassembled data that has been identified in each of Figs. 2, 4 and 6, the Editor of <i>International Journal of Oncology</i> has determined that this paper should be retracted from the publication on the grounds of a lack of confidence in the presented data. Upon contacting the authors, they accepted the decision to retract this paper. The Editor apologizes to the readership for any inconvenience caused, and we also thank the reader for bringing this matter to our attention. [International Journal of Oncology 43: 919‑926, 2013; DOI: 10.3892/ijo.2013.2008].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of vascular endothelium and exosomes in cancer progression and therapy (Review).","authors":"Yonghao Dai, Yutong Yao, Yuquan He, Xin Hu","doi":"10.3892/ijo.2024.5712","DOIUrl":"10.3892/ijo.2024.5712","url":null,"abstract":"<p><p>Cancer poses a significant global health challenge and its progression is intricately connected to the interplay among various cell types and molecular pathways. In recent years, research has focused on the roles of vascular endothelial cells (VECs) and exosomes within the tumor microenvironment. Anomalies in tumor vascular integrity and function create a conducive milieu for cancer cell proliferation. Despite efforts in clinical anti‑angiogenic interventions, the anticipated outcomes remain elusive. VECs have the capability to transition into mesenchymal cells through endothelial‑to‑mesenchymal transition, thereby affecting cancer advancement. Exosomes are minute membrane‑bound vesicles generated by cells, serving as vital extracellular elements that facilitate cell‑to‑cell communication. They participate in modulating the tumor microenvironment, thereby influencing tumor progression, metastasis, drug resistance and angiogenesis. Additionally, exosomes serve as efficient carriers for drug delivery, as well as targeting and suppressing tumor cells. In summary, understanding the intricate and interconnected mechanisms of VECs and exosomes in cancer, encompassing tumor angiogenesis, microenvironment modulation and immune regulation, is crucial. A comprehensive exploration of these mechanisms may provide insight into cancer treatment and prevention and yield novel therapeutic targets.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Anti‑carcinogenic properties of omeprazole against human colon cancer cells and azoxymethane‑induced colonic aberrant crypt foci formation in rats.","authors":"Jagan M R Patlolla, Yuting Zhang, Qian Li, Vernon E Steele, Chinthalapally V Rao","doi":"10.3892/ijo.2024.5709","DOIUrl":"10.3892/ijo.2024.5709","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that certain of the in vitro image panels shown in Fig. 3B (featuring the effects of adding five different concentrations of omeprazole on acridine orange/ethidium bromide‑stained HCA‑7 cells) and Fig. 4 (showing western blotting experiments) on p. 173 and 174 respectively contained overlapping data panels, where results that were intended to represent the results of differently performed experiments had apparently been derived from the same original sources. Specifically, the image panels for 0 and 50 µM/ml omeprazole (Fig. 3Ba and Bb), and 100 and 200 µM/ml omeprazole (Fig. 3Bc and Bd), in Fig. 3B were strikingly similar; and the bands shown for p21 and cyclin A in Fig. 4A and B respectively were also similar, albeit each set of protein bands were turned through 180° relative to the other. After having examined their original data, the authors realized that these figures had been inadvertently assembled incorrectly. The revised versions of Figs. 3 (showing the data correctly for the 0, 100 and 300 µM/ml omeprazole experiments) and 4 (with the cyclin A data omitted) are shown on the next page. Note that the edits made to these figures do not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 40: 170‑175, 2012; DOI: 10.3892/ijo.2011.1214].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MYBBP1A‑mediated IGFBP4 promoter methylation promotes epithelial‑mesenchymal transition and metastasis through activation of NOTCH pathway in liver cancer.","authors":"Yujing Sun, Xiaoyu Weng, Wei Chen, Jiangzhen Ge, Bo Ding, Junnan Ru, Yunguo Lei, Xin Hu, Da Man, Shaobing Cheng, Ruoshu Duan, Jingjing Ren, Beng Yang","doi":"10.3892/ijo.2024.5710","DOIUrl":"10.3892/ijo.2024.5710","url":null,"abstract":"<p><p>Metastatic hepatocellular carcinoma (HCC) seriously threatens patients' prognosis. It was previously suggested that the insulin growth factor binding protein (IGFBP) family could serve as cancer suppressors in the development and metastasis of HCC. However, the role of IGFBP4 and its underlying molecular mechanism in HCC metastasis is elusive. In the present study, it was found that IGFBP4 is significantly downregulated in HCC, whose expression is positively correlated with the prognosis of patients with HCC. Overexpression of IGFBP4 restrained migration abilities and cancer metastasis of HCC cells both <i>in vitro</i> and <i>in vivo</i>. Furthermore, it was found that IGFBP4 represses HCC metastasis by inhibiting epithelial‑mesenchymal transition. Molecular mechanism studies showed that overexpression of IGFBP4 obviously suppresses NOTCH1 signaling in HCC. As for the upstream regulatory mechanism, it was revealed that downregulation of IGFBP4 in HCC was caused by CpG islands' hyper‑methylation‑dependent degradation mediated by MYBBP1A. Inhibition of MYBBP1A limited HCC metastatic ability and silence of IGFBP4 at the same time restored HCC metastatic potentials. Clinical data demonstrated that low expression of IGFBP4 was found in patients with HCC, especially with lymphatic metastasis. High MYBBP1A expression and low IGFBP4 expression in HCC were correlated with poor survival of patients with HCC. Summarily, in the present study, it was revealed that MYBBP1A/IGFBP4/NOTCH1 pathway could play a crucial role in the progression and metastasis of HCC, which stimulates novel therapeutic and diagnostic strategies against metastatic HCC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti‑angiogenic effect of <i>Bryopsis plumosa</i>‑derived peptide via aquaporin 3 in non‑small cell lung cancer.","authors":"Heabin Kim, Seung-Hyun Jung, Seonmi Jo, Jong Won Han, Moongeun Yoon, Jei Ha Lee","doi":"10.3892/ijo.2024.5711","DOIUrl":"10.3892/ijo.2024.5711","url":null,"abstract":"<p><p>Developing novel anti‑angiogenic agents with minimal toxicity is notably challenging for cancer therapeutics. The discovery and development of peptides, whether derived from natural sources or synthesized, has potential for developing anti‑angiogenic agents characterized by their ability to penetrate cancer cells, high specificity and low toxicity. The present study identified a <i>Bryopsis plumose</i>‑derived anticancer and anti‑angiogenesis marine‑derived peptide 06 (MP06). A 22‑amino acid peptide was synthesized and conjugated with fluorescein isothiocyanate (FITC‑MP06) for intracellular localization in H1299 non‑small cell lung cancer cells. Regulatory effects of this peptide on the viability, migration and self‑renewal of lung cancer cells was assessed. Furthermore, anti‑angiogenic effect of MP06 was investigated by monitoring vascular tube formation in human umbilical vein endothelial cells and a zebrafish model. Aquaporin (AQP)3, a membrane channel in various tissues, is involved in regulating stemness, epithelial‑mesenchymal transition (EMT) and angiogenesis. MP06 downregulated AQP3 expression. Consistently, AQP3 knockdown by RNA silencing downregulated its gene expression, leading to a decrease in stemness, EMT and angiogenesis properties in H1299 cells. MP06 could thus serve as a novel therapeutic target with anticancer and angiogenesis properties for non‑small cell lung cancer.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of ferroptosis by SIRT1 knockdown alleviates cytarabine resistance in acute myeloid leukemia by activating the HMGB1/ACSL4 pathway.","authors":"Qian Kong, Qixiang Liang, Yinli Tan, Xiangqin Luo, Yesheng Ling, Xiaofeng Li, Yun Cai, Huiqin Chen","doi":"10.3892/ijo.2024.5708","DOIUrl":"10.3892/ijo.2024.5708","url":null,"abstract":"<p><p>Resistance to cytarabine is a major obstacle to the successful treatment of acute myeloid leukemia (AML). The present study aimed to explore the mechanism by which sirtuin 1 (SIRT1) reverses the cytarabine resistance of leukemia cells. Cell viability was investigated using the EdU proliferation assay. The expression levels of molecules were determined by reverse transcription‑quantitative PCR, western blotting, and immunofluorescence staining. Flow cytometry was used to detect reactive oxygen species and apoptosis levels, The levels of superoxide dismutase, glutathione and malondialdehyde were examined by ELISA. Mitochondrial damage was investigated by transmission electron microscopy. Furthermore, tumor growth was evaluated in a xenograft model. The results revealed that SIRT1 expression was significantly upregulated in drug‑resistant leukemia cells. By contrast, knockdown of SIRT1 reversed cytarabine resistance in HL60 cells by promoting ferroptosis. Mechanistically, SIRT1 could regulate the translocation of HMGB1 from the nucleus to the cytoplasm in cytarabine‑resistant HL60 (HL60/C) cells. Furthermore, knockdown of HMGB1 inhibited the expression of ACSL4. In addition, knockdown of SIRT1 expression could inhibit the growth of HL60/C cells <i>in vivo</i> and reverse cytarabine resistance. In conclusion, the present results demonstrated that SIRT1 inhibition could be a promising strategy to overcome cytarabine resistance in AML.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non‑coding RNA‑mediated epigenetic modification of ferroptosis in non‑small cell lung cancer (Review).","authors":"Yumin Wang, Joshua S Fleishman, Yulin Li, Yuwei Cao, Haidong Wei, Zhe Zhang, Jichao Chen, Mingchao Ding","doi":"10.3892/ijo.2024.5714","DOIUrl":"10.3892/ijo.2024.5714","url":null,"abstract":"<p><p>Ferroptosis is a novel form of regulated cell death that plays a key role in inhibiting tumor malignancy. The ferroptosis signalling cascade provides new opportunities for lung cancer therapy. Non‑coding RNA (ncRNA)‑mediated epigenetic modification can influence the vulnerability of cancer cells to ferroptosis in non‑small‑cell lung cancer (NSCLC). The present review describes the core molecular mechanisms underlying ferroptosis and the role of epigenetic mechanisms in regulating ferroptosis in NSCLC, as well as developments in understanding the ncRNA‑induced mechanisms that affect ferroptosis in NSCLC. The present review aimed to enhance understanding of the epigenetic mechanisms mediated by ncRNAs that modulate ferroptosis in NSCLC, highlighting a novel therapeutic strategy for NSCLC via the ncRNA‑ferroptosis axis.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in leukemia management: Bridging diagnosis, prognosis and nanotechnology (Review).","authors":"Jingbo Li, Yingxue Wang, Chunli Dong, Lifu Luo","doi":"10.3892/ijo.2024.5700","DOIUrl":"10.3892/ijo.2024.5700","url":null,"abstract":"<p><p>Leukemia is a cancer that starts in blood stem cells in the bone marrow. Today, the proper diagnosis and prognosis of leukemia are essential in mitigating the morbidity and mortality associated with this malignancy. The advent of novel biomarkers, particularly those related to minimal residual disease, has paved the way for personalized therapeutic strategies and enables the quantitative assessment of patient responses to treatment regimens. Novel diagnostic and targeted drug delivery may be helpful for the improved management of leukemia. Genetic clinical parameters, such as chromosomal abnormalities, are crucial in diagnosing and guiding treatment decisions. These genetic markers also provide valuable prognostic information, helping to predict patient outcomes and tailor personalized treatment plans. In the present review, the studies on the diagnostic and prognostic parameters of leukemia were analyzed. The prognosis of leukemia was investigated in most of the studies, and the remaining were performed on diagnosis. The clinical and laboratory prognostic parameters were the most common, followed by diagnostic hematological parameters, diagnostic blood parameter studies, and diagnostic immunological parameters. Clinical and laboratory prognostic and hematologic parameters were the most extensively studied. The methods used to diagnose and prognose the leukemia cases in these studies were predominantly clinical hematology. Numerous surface proteins and receptors, including CD45, CD27, CD29, CD38, CD27, CD123, CD56 and CD25, react similarly in various kinds of leukemia, which are ideal for targeted drug delivery. Drug delivery to leukemia cells encounters several significant obstacles, including heterogeneity, that hinder the effectiveness of treatment. Nanocarriers play a critical role in targeted drug delivery for leukemia by enhancing the precision of treatments directed at surface proteins and receptors. Additionally, they can be functionalized with targeting drugs and antibodies to target specific tissues and cells.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}