Medical OncologyPub Date : 2024-12-14DOI: 10.1007/s12032-024-02580-6
Sushmita Ghosh, Arpana Sharma, R Suresh Kumar, Vilas Nasare
{"title":"Sorcin: mechanisms of action in cancer hallmarks, drug resistance and opportunities in therapeutics.","authors":"Sushmita Ghosh, Arpana Sharma, R Suresh Kumar, Vilas Nasare","doi":"10.1007/s12032-024-02580-6","DOIUrl":"10.1007/s12032-024-02580-6","url":null,"abstract":"<p><p>Soluble resistant related calcium binding protein (Sorcin) plays an important role in tumor progression, angiogenesis, metastasis, and multidrug resistance. Differential expression of Sorcin across different cancers significantly correlates with key clinicopathological characteristics and survival outcomes, underscoring its potential as a prognostic marker. Its involvement in drug-resistant cancers further advert Sorcin as a promising therapeutic target. This review summarizes the mechanistic role of Sorcin in cancer, its contribution to drug resistance, clinical relevance, and the current and emerging therapeutic approaches aimed at translating Sorcin-targeted therapies into clinical practice.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"29"},"PeriodicalIF":2.8,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-13DOI: 10.1007/s12032-024-02577-1
Ali G Alkhathami, Harikumar Pallathadka, Sejal Shah, Subbulakshmi Ganesan, Abhishek Sharma, Seema Devi, Yasser Fakri Mustafa, Mohammed Qasim Alasheqi, Abed J Kadhim, Ahmed Hussein Zwamel
{"title":"LncRNAs in modulating cancer cell resistance to paclitaxel (PTX) therapy.","authors":"Ali G Alkhathami, Harikumar Pallathadka, Sejal Shah, Subbulakshmi Ganesan, Abhishek Sharma, Seema Devi, Yasser Fakri Mustafa, Mohammed Qasim Alasheqi, Abed J Kadhim, Ahmed Hussein Zwamel","doi":"10.1007/s12032-024-02577-1","DOIUrl":"10.1007/s12032-024-02577-1","url":null,"abstract":"<p><p>Paclitaxel (PTX) is widely used for treating several cancers, including breast, ovarian, lung, esophageal, gastric, pancreatic, and neck cancers. Despite its clinical utility, cancer recurrence frequently occurs in patients due to the development of resistance to PTX. Resistance mechanisms in cancer cells treated with PTX include alterations in β-tubulin, the target molecule involved in mitosis, activation of molecular pathways enabling drug efflux, and dysregulation of apoptosis-related proteins. Long non-coding RNAs (lncRNAs), which are RNA molecules longer than 200 nucleotides without protein-coding potential, serve diverse regulatory roles in cellular processes. Increasing evidence highlights the involvement of lncRNAs in cancer progression and their contribution to PTX resistance across various cancers. Consequently, lncRNAs have emerged as potential therapeutic targets for addressing drug resistance in cancer treatment. This review focuses on the current understanding of lncRNAs and their role in drug resistance mechanisms, aiming to encourage further investigation in this area. Key lncRNAs and their associated pathways linked to PTX resistance will be summarized.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"28"},"PeriodicalIF":2.8,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-12DOI: 10.1007/s12032-024-02578-0
Xiaoe He, Jiayin Guo, Yanrui Bai, Hui Sun, Jing Yang
{"title":"Salmonella-based therapeutic strategies: improving tumor microenvironment and bringing new hope for cancer immunotherapy.","authors":"Xiaoe He, Jiayin Guo, Yanrui Bai, Hui Sun, Jing Yang","doi":"10.1007/s12032-024-02578-0","DOIUrl":"10.1007/s12032-024-02578-0","url":null,"abstract":"<p><p>Immunotherapy has revolutionized cancer treatment, yet its effectiveness is limited by immunosuppressive tumor microenvironment (TME). To overcome this challenge, innovative strategies to effectively modulate the TME are urgently needed. Over the past decades, bacteria-mediated cancer immunotherapy has recaptured increasing attention, driven by advances in synthetic biology, genetic engineering and our knowledge of host-pathogen interactions. Among various bacterial species, Salmonella has emerged as a leading candidate with significant therapeutic potential due to its broad-spectrum anti-tumor activity, tumor-targeting ability, immunomodulatory effects, oncolytic properties, genetic programmability, and engineering flexibility. These characteristics enable Salmonella to reshape the immunosuppressive TME, thereby enhancing anti-tumor efficacy. This review elaborates the regulatory effects of Salmonella on key components of the TME, the versatile engineering strategies for optimizing Salmonella's ability to modulate the TME, and recent advancements in combination cancer therapies. We also summarize current clinical applications and discuss challenges of developing safer and more effective Salmonella-based cancer immunotherapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"27"},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-09DOI: 10.1007/s12032-024-02549-5
Shengyuan Fu, Yao Guo, Zhiyong Peng, Dengyang Zhang, Zhiguang Chang, Yan Xiao, Qi Zhang, Liuting Yu, Chun Chen, Yun Chen, Yuming Zhao
{"title":"Progression and perspectives in disease modeling for Juvenile myelomonocytic leukemia.","authors":"Shengyuan Fu, Yao Guo, Zhiyong Peng, Dengyang Zhang, Zhiguang Chang, Yan Xiao, Qi Zhang, Liuting Yu, Chun Chen, Yun Chen, Yuming Zhao","doi":"10.1007/s12032-024-02549-5","DOIUrl":"10.1007/s12032-024-02549-5","url":null,"abstract":"<p><p>Juvenile myelomonocytic leukemia (JMML) is a rare myeloproliferative neoplasm occurring in infants and young children. JMML has been shown to be resistant to all conventional cytotoxic chemotherapy drugs, and current curative therapies still rely on hematopoietic stem cell transplantation, which carries a high risk of relapse post-transplantation. This underscores the urgent need for novel treatment strategies. However, the rarity of JMML poses a major limitation for research, as it is difficult to collect substantial primary research material. To gain a deeper insight into the underlying biological mechanisms of JMML, researchers are continuously improving and developing preclinical research models to better emulate the disease. Therefore, this review aims to delineate the various experimental models currently employed in JMML, including patient-derived cell-based models, cell models, and animal models. We will discuss the characterization of these models in the context of JMML, hoping to provide a valuable reference for researchers in this field.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"25"},"PeriodicalIF":2.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-09DOI: 10.1007/s12032-024-02567-3
Zainab Lafi, Sina Matalqah, Ebaa Abu-Saleem, Nisreen Asha, Hala Mhaidat, Sherine Asha, Lara Al-Nashash, Hussein S Janabi
{"title":"Metal-organic frameworks as nanoplatforms for combination therapy in cancer treatment.","authors":"Zainab Lafi, Sina Matalqah, Ebaa Abu-Saleem, Nisreen Asha, Hala Mhaidat, Sherine Asha, Lara Al-Nashash, Hussein S Janabi","doi":"10.1007/s12032-024-02567-3","DOIUrl":"10.1007/s12032-024-02567-3","url":null,"abstract":"<p><p>The integration of nanotechnology into cancer treatment has revolutionized chemotherapy, boosted its effectiveness while reduced side effects. Among the various nanotherapeutic approaches, metal-organic frameworks (MOFs) stand out as promising carriers for targeted chemotherapy, with the added benefit of enabling combination therapies. MOFs, composed of metal ions or clusters linked by coordination bonds, tackle critical issues in traditional cancer treatments, such as poor stability, limited efficacy, and severe side effects. Their key advantages include customizable size and shape, diverse compositions, controlled porosity, large surface areas, ease of modification, and biocompatibility. This review highlights recent advancements in the use of MOFs for cancer therapy, showcasing their role in both monotherapies and combination strategies. Additionally, it explores the future potential and challenges of MOF-based platforms in tumor treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"26"},"PeriodicalIF":2.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-07DOI: 10.1007/s12032-024-02575-3
Hao Zhou, Wenqiong Xiang, Guangyu Zhou, Fernando Rodrigues-Lima, Fabien Guidez, Li Wang
{"title":"Metabolic dysregulation in myelodysplastic neoplasm: impact on pathogenesis and potential therapeutic targets.","authors":"Hao Zhou, Wenqiong Xiang, Guangyu Zhou, Fernando Rodrigues-Lima, Fabien Guidez, Li Wang","doi":"10.1007/s12032-024-02575-3","DOIUrl":"10.1007/s12032-024-02575-3","url":null,"abstract":"<p><p>Despite significant advancements in the research of the pathogenesis mechanisms of Myelodysplastic Neoplasm (MDS) in recent years, there are still many gaps to fill. The advancement of metabolomics studies has led to a research booming in clarifying the impact of metabolic abnormalities during the pathogenesis of MDS. The present review primarily focuses on the dysregulated metabolic pathways, exploring the influences on the pathogenesis of MDS and their roles during the course of the disease. Furthermore, we discuss the potential of relevant metabolic pathways as therapeutic targets, along with the latest metabolic-related treatment drugs and approaches.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"23"},"PeriodicalIF":2.8,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Betulinic acid and oleanolic acid modulate CD81 expression and induce apoptosis in triple-negative breast cancer cells through ROS generation.","authors":"Dian Yuliartha Lestari, Gondo Mastutik, Indri Safitri Mukono","doi":"10.1007/s12032-024-02574-4","DOIUrl":"https://doi.org/10.1007/s12032-024-02574-4","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by a lack of hormones receptors and the HER2 receptor, making it unresponsive to targeted therapy. Triterpenoids such as betulinic acid (BA) and oleanolic acid (OA) have anticancer effects by inducing apoptosis in TNBC cells. CD81 is a tetraspanin that affects the growth and metastasis of cancer cells. To examine the effect of BA and OA on the viability of TNBC cell line (MDA-MB 231) by analyzing the CD81 expression, intracellular ROS, and apoptosis. The MDA-MB 231 cells was cultured and treated by BA and OA. The viability cell was evaluated by the CCK8 assay. This study analyzed the binding of BA and OA with CD81 using molecular docking and evaluated CD81 expression, intracellular ROS, and apoptosis by flow cytometry. The result showed that BA and OA inhibited viability of MDA-MB-231 cells. BA and OA bind to CD81 in silico, with binding affinities of 9.0 kcal/mol for BA and 7.2 kcal/mol for OA. Flow cytometry results revealed that BA can downregulate CD81 expression. BA and OA also increased intracellular ROS levels and induced apoptosis. These findings suggest that BA and OA, especially BA, can modulate CD81 expression and promote apoptosis in TNBC cells through the generation of ROS, thereby offering a potential therapeutic strategy for the treatment of TNBC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"24"},"PeriodicalIF":2.8,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cedrus atlantica extract inhibits melanoma progression by suppressing epithelial-mesenchymal transition and inducing mitochondria-mediated apoptosis.","authors":"Hong-Wei Gao, Kai-Fu Chang, Xiao-Fan Huang, Meng-Chiao Lee, Nu-Man Tsai, Tze-Ho Chen","doi":"10.1007/s12032-024-02573-5","DOIUrl":"https://doi.org/10.1007/s12032-024-02573-5","url":null,"abstract":"<p><p>Melanoma has a low incidence, accounting for less than 5% of skin cancers; however, it is the most lethal cancer, primarily because of its high potential for metastasis and resistance to different treatments. Natural products can sensitize melanoma to chemotherapy and overcome drug resistance. Previous studies have reported Cedrus atlantica extract has various pharmacological benefits such as anti-inflammatory, antioxidant, antibacterial, and analgesic properties. This study aimed to explore the effects of C. atlantica extract (CAt) against melanoma in vitro and in vivo. The effects of CAt on B16F10 cell viability, proliferation, migration, invasion, and apoptosis were detected using MTT, colony formation, wound-healing, Boyden chamber, and TUNEL assays. Semi-quantitative RT-PCR and western blotting were used to measure mRNA and protein expression, respectively. Results revealed that CAt selectively decreased the viability of B16F10 cells and inhibited colony formation in a dose-dependent manner. CAt reduces cell migration and invasion by regulating epithelial-mesenchymal transition-associated proteins (Snail, E-cadherin, and vimentin). Moreover, CAt enhanced the Bax/Bcl-2 ratio and the expression of cleaved-caspase-9, caspase-3, and PARP1, resulting in the activation of mitochondria-mediated apoptosis. In an in vivo study, CAt significantly inhibited tumor growth and prolonged the lifespan of mice at a well-tolerated dose. Importantly, the combination of CAt and 5-fluorouracil (5-FU) exhibited synergistic growth suppression and attenuated the development of 5-FU resistance. Overall, the findings suggest that CAt holds promise as a potential drug or adjuvant to improve melanoma treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"22"},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-12-04DOI: 10.1007/s12032-024-02568-2
Moein Shirzad, Abdolreza Daraei, Hossein Najafzadehvarzi, Nazila Farnoush, Hadi Parsian
{"title":"Co-culture system of breast cancer and normal cells to investigate inflammation: using doxorubicin encapsulated in adipose-derived exosomes.","authors":"Moein Shirzad, Abdolreza Daraei, Hossein Najafzadehvarzi, Nazila Farnoush, Hadi Parsian","doi":"10.1007/s12032-024-02568-2","DOIUrl":"https://doi.org/10.1007/s12032-024-02568-2","url":null,"abstract":"<p><p>Doxorubicin (DOX) chemotherapy for breast cancer is an effective treatment option, but it also has disadvantages. Exosomes (EXOs) have safely and successfully transported DOX and reduced its adverse effects; however, its use is still being explored. In this study, a co-culture system of malignant and non-malignant breast cells was used to generate an in vitro model reflecting the in vivo cellular microenvironment, and the effects of this treatment were investigated by examining inflammatory genes. Extracellular matrices (EXOs) were extracted from mesenchymal stem cells derived from human adipose tissue by ultracentrifugation. Later, Western blotting, dynamic light scattering (DLS) and transmission electron microscopy methods were used to examine the properties of the EXO. DOX was encapsulated in the EXOs by sonication and the loading rate was measured by spectrophotometry. In the current study, a co-culture system was used to investigate the cytotoxic effects of free DOX and DOX encapsulated in EXOs (EXO-DOX) on various breast cell lines, including MCF-7, MCF-10A, MDA-MB-231, and A-MSC. Additionally, the expression levels of inflammatory cytokines (IL-1β, IL-6, IL-10, and TNF-α) were examined. Methylthiazolyldiphenyl-tetrazolium bromide assay demonstrated that free DOX showed the highest cytotoxicity against MCF-10A cells, followed by MCF-7 cells. Conversely, EXO-DOX indicated a greater effect on MCF-7 cells and had a lower IC<sub>50</sub> compared to MDA-MB-231 cells. Free DOX significantly downregulated the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), particularly in MCF-7 and MCF-10A cells, while concurrently upregulating IL-10 expression. EXO-DOX induced a more significant alteration in cytokine expression than the control and free DOX treatment groups. The co-culture system revealed a synergistic effect of free DOX on cancer cells while simultaneously mitigating the toxic effects of DOX on normal cells. This study suggests that EXO-DOX has promising potential as a targeted drug delivery system that could potentially improve therapeutic efficacy and minimize off-target toxicity.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"21"},"PeriodicalIF":2.8,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2024-11-30DOI: 10.1007/s12032-024-02563-7
Xiyu Zhao, Victor Yang, Mohammed Ullah, Mark Schuweiler, Jonathan Zou, Austin Chen, Shuhan Jia, Padmini Ranasinghe
{"title":"The physician payments Sunshine Act and medical oncology: a seven-year financial analysis.","authors":"Xiyu Zhao, Victor Yang, Mohammed Ullah, Mark Schuweiler, Jonathan Zou, Austin Chen, Shuhan Jia, Padmini Ranasinghe","doi":"10.1007/s12032-024-02563-7","DOIUrl":"https://doi.org/10.1007/s12032-024-02563-7","url":null,"abstract":"<p><p>The integration of pharmaceutical and medical device companies with clinical practice is under scrutiny due to financial incentives that may influence oncology care. The Physician Payments Sunshine Act mandates transparency in these financial relationships. This study examines the trends in non-research payments to oncology specialists between 2017 and 2023, analyzing amounts, reasons, and variations by subspecialty and region. We conducted a retrospective analysis of the Centers for Medicare and Medicaid Services Open Payments database, focusing on U.S.-based hematology, medical oncology, and hematology-oncology specialists. Payments were categorized by amount, purpose, and payment type, with temporal and geographic comparisons. Data analysis was conducted in Rstudio (version 2022.07.0) with Kruskal-Wallis, Mann-Whitney U, and Chi-square tests to assess statistical significance across specialties, regions, and payment periods. Between 2017 and 2023, 2,158,140 payments totaling $601,567,196.10 were made to 19,585 U.S.-based hematology, medical oncology, and hematology-oncology specialists. Hematology-oncology received the highest total payment amount ($393,169,915.10) and transaction count (1,700,202), while hematology had the highest median payment ($23.05) compared to hematology-oncology ($18.12) and medical oncology ($19.5). Payment patterns demonstrated seasonal peaks, particularly in Q1 and Q4, and increased markedly during major oncology conferences (ASCO, ASH). Analysis by geographic region revealed that the South consistently received the highest total payments, peaking at $36.8 million in 2023, while the Northeast had the highest median payment values, reaching $22.87 in 2023. The COVID-19 pandemic corresponded with lasting shifts in payment patterns, with median payment values rising significantly during the pandemic period and remaining elevated post-COVID across all specialties. Additionally, the distribution of payments by type revealed that direct cash payments and consulting fees were the most prominent, with hematology-oncology showing the greatest reliance on high-value cash transactions, while stock payments featured prominently in hematology. Sensitivity analyses confirmed these patterns as robust, with minimal variance observed when excluding extreme values, further validating consistent trends across specialties, regions, and periods. This study reveals specialty- and region-specific variations in oncology-related payments, with significant increases during key conferences and the COVID-19 pandemic. These findings underscore the importance of continued transparency and scrutiny in industry-oncology financial interactions to mitigate potential conflicts of interest in oncology care.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"20"},"PeriodicalIF":2.8,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}