Oncology Research最新文献

{"title":"Correlation of senescence-related gene FEN1 on neuroblastoma progression and cisplatin chemotherapy sensitivity.","authors":"Youyang Hu, Yishu Luo, Tianyue Xie, Yuehua Chen, Jun Zhao, Weichao Ji, Zhiwei Yan, Sitong Qiu, Kexin Gao, Haixia Zhu, Limin Ma, Qiyou Yin","doi":"10.32604/or.2025.060021","DOIUrl":"10.32604/or.2025.060021","url":null,"abstract":"<p><strong>Objective: </strong>Neuroblastoma (NB) is frequently associated with high-risk pediatric cases that demonstrate limited response to cisplatin, contributing to a poor prognosis. Recent studies have explored the role of tumor cell senescence in increasing sensitivity to this chemotherapy agent. This study aims to identify genes related to cell senescence in children diagnosed with NB, evaluate their influence on cisplatin sensitivity, and investigate potential strategies to enhance the efficacy of chemotherapy.</p><p><strong>Methods: </strong>Gene expression profiles and clinical data were obtained for 498 NB patients from the GEO database (GSE49710). The study focused on identifying genes that were differentially expressed between stage IV and other stages, particularly those linked to cell senescence and cisplatin resistance. To analyze the prognostic significance of these differentially expressed genes, we employed LASSO regression and multivariate Cox proportional hazards models. Transcriptomic and proteomic analyses of 15 NB specimens revealed a significant correlation between Flap endonuclease-1 (FEN1) expression levels and both cellular senescence and sensitivity to cisplatin. We quantified FEN1 expression and cisplatin IC50 values in four different NB cell lines. The influence of FEN1 knockdown and overexpression on NB cell proliferation, invasion, and migration was evaluated using cloning assays, transwell assays, and scratch assays. Furthermore, we utilized Western blotting to analyze senescence-associated proteins p21 and proliferating cell nuclear antigen (PCNA), thereby evaluating the role of FEN1 in cellular senescence. The impact of FEN1 on cisplatin sensitivity was investigated via the CCK-8 cell counting assay. Additionally, we investigated how FEN1 inhibitors might impact NB cell proliferation and enhance the therapeutic efficacy of cisplatin treatment.</p><p><strong>Results: </strong>FEN1 was found to be highly expressed in stage IV NB and showed a strong association with cisplatin sensitivity, establishing it as a critical molecular marker linked to poor patient prognosis. Notably, elevated FEN1 expression correlated with reduced sensitivity to cisplatin, as evidenced by higher IC50 values. In the SH-SY5Y cell line, FEN1 knockdown led to significant reductions in cell proliferation, invasion, and migration, along with an increase in β-galactosidase staining-indicative of senescence. This knockdown also resulted in elevated levels of the p21 protein and decreased expression of PCNA, concurrently lowering cisplatin IC50 values. Conversely, FEN1 overexpression in the SK-N-SH cell line resulted in enhanced cell proliferation, invasion, and migration. This overexpression was associated with reduced β-galactosidase staining, decreased levels of p21, and increased expression of PCNA, ultimately resulting in higher cisplatin IC50 values. Importantly, FEN1 inhibitors alone significantly impeded NB cell proliferation, and their","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1695-1708"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560719","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}

{"title":"Retraction: Inhibition of Proliferation, Migration, and Invasion by Knockdown of Pyruvate Kinase-M2 (PKM2) in Ovarian Cancer SKOV3 and OVCAR3 Cells.","authors":"","doi":"10.32604/or.2025.068988","DOIUrl":"https://doi.org/10.32604/or.2025.068988","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14685034103671.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1801-1802"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560653","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}

{"title":"Correction: MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma.","authors":"Fang Chen, Dongqiang Yang, Yuhua Ru, Shan Cao, Aishe Gao","doi":"10.32604/or.2025.064363","DOIUrl":"https://doi.org/10.32604/or.2025.064363","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3727/096504018X15426763753594.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1799-1800"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560717","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}

{"title":"SIK2 inhibitor SIC-19 enhances the sensitivity of PARP inhibitors in triple-negative breast cancers and pancreatic cancers.","authors":"Qian Li, Shunpeng Zhu, Mingxian Zhu, Fang Wang, Jinhua Zhou","doi":"10.32604/or.2025.062539","DOIUrl":"10.32604/or.2025.062539","url":null,"abstract":"<p><strong>Objectives: </strong>Our previous research demonstrated that SIC-19, an innovative inhibitor of salt-inducible kinase 2 (SIK2), effectively reduces SIK2 protein levels through the ubiquitin-proteasome pathway and exhibits synthetic lethal effects with poly ADP-ribose polymerase (PARP) inhibitors in ovarian cancer. However, the role of SIC-19 in triple-negative breast cancer (TNBC) and pancreatic cancer (PC) remains poorly defined. This study aims to investigate whether SIC-19 combined with PARP inhibitors can induce synthetic lethal effects in TNBC and PC.</p><p><strong>Methods: </strong>Cell lines with high SIK2 expression were identified through Western blot analysis. The combination's impact was evaluated using Cell Counting Kit-8 (CCK8), clone formation, and apoptosis assays, as well as <i>in vivo</i> xenograft models.</p><p><strong>Results: </strong>Our findings indicated that the IC50 of SIC-19 was inversely correlated with endogenous SIK2 expression in TNBC and PC cell lines. SIC-19 modulates the homologous recombination repair pathway by suppressing levels of RAD50-pS635, thereby enhancing the sensitivity of TNBC and PC cells, as well as xenografts, to PARP inhibitors.</p><p><strong>Conclusion: </strong>These results underscore the potential of combining PARP inhibitors in combination with SIK2 inhibitors as a novel therapeutic approach to increase PARP inhibition's effectiveness in treating TNBC and PC. This innovative combination therapy represents a promising approach for overcoming resistance mechanisms and improving the outcomes for patients with these challenging malignancies.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1757-1767"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560654","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}

{"title":"Clinically proven natural products against breast cancer, with mechanistic insights.","authors":"Md Mahmudul Hasan, Shah Md Wasin, Mishu Rahman, Eva Azme, Md Saqline Mostaq, Md Mahedi Hasan Nahid, Nor Mohammad, Farjana Afrin Tanjum, Md Anamul Haque, Md Ashiq Mahmud, Mohammad Nurul Amin","doi":"10.32604/or.2025.062778","DOIUrl":"10.32604/or.2025.062778","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer still stands to be the foremost contributor to cancer-related incidence and mortality in women globally accounting for about 14% of all female cancer-related deaths worldwide. This research seeks to illustrate the mechanisms and clinical findings of natural products against breast cancer treatment.</p><p><strong>Methodology: </strong>Required data for this review article was retrieved employing several readily obtainable search databases, including Web of Science^® (Thomson Reuters, USA), PubMed^® (U.S. National Library of Medicine, USA), and SciVerse Scopus^® (Elsevier Properties S.A., USA), taking into consideration certain search terms like \"breast cancer,\" \"natural products against breast cancer,\" and \"Clinically proven natural products in the treatment of breast cancer\" and so on.</p><p><strong>Results: </strong>Several natural products, namely Omega-3 fatty acids, dietary isothiocyanates, curcumin, green tea, flaxseed, limonene, and others, were found to modulate crucial pathways in breast cancer cells. These substances suppressed angiogenesis by downregulating the vascular endothelial growth factor (VEGF), promoted apoptosis by activating caspase enzymes, and prevented cell proliferation by controlling cyclin-dependent kinases. Clinical studies demonstrated improved outcomes in patients receiving these natural products with standard treatment procedures.</p><p><strong>Discussion: </strong>The findings underscore the multifaceted functions of natural products in breast cancer therapy, highlighting their potential to increase the efficacy of conventional treatments while reducing adverse effects. Further exploration of synergistic actions and optimal dosages is needed.</p><p><strong>Conclusion: </strong>Clinically proven natural products represent a potential avenue for breast cancer treatment with their mechanistic insights that facilitate their incorporation into treatment regimens. To maximize clinical applications, future inquiries should center on elucidating the full spectrum of these anticancer functions.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1611-1632"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560716","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}

{"title":"Plasticity of myeloid-derived suppressor cells in cancer and cancer therapy.","authors":"Jiajia Lv, Xiaoyou Zhong, Lin Wang, Weifei Fan","doi":"10.32604/or.2025.060063","DOIUrl":"10.32604/or.2025.060063","url":null,"abstract":"<p><p>The tumor microenvironment (TME) is a complex and dynamic network comprised of tumor cells, surrounding cellular components, various signaling molecules, and the stroma. Myeloid-derived suppressor cells (MDSCs) are pivotal players in the immunosuppressive landscape of the TME, effectively hindering antitumor immune responses and facilitating tumor progression. Originating from pathologically activated myeloid precursors and relatively immature myeloid cells, MDSCs retain plasticity to further differentiate into other myeloid cells, such as macrophages or dendritic cells, which underpins their heterogeneity and adaptability in response to the TME. In this review, we delve into the plasticity of MDSCs in the tumor microenvironment and illuminate the underlying mechanisms that enable them to modulate immune responses. Furthermore, we explore the implications of MDSCs plasticity for cancer therapy, particularly its role in enhancing the efficiency of combination treatments.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1581-1592"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560651","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}

{"title":"Research review of the mechanism and clinical application prospects of tertiary lymphoid structures in the immune micro-environment of gastrointestinal tumors.","authors":"Jiang Zhu","doi":"10.32604/or.2025.058957","DOIUrl":"10.32604/or.2025.058957","url":null,"abstract":"<p><p>Changes in the intestinal immune micro-environment of the gastrointestinal tract are indispensable in the occurrence and development of gastrointestinal cancer. Tertiary lymphoid structure (TLS) is an immune cell aggregation structure found around gastrointestinal cancer in recent years. More and more research proves that tertiary lymphoid structure plays a key biological role and clinical value in disease progression, patient prognosis, and adjuvant treatment. This review aims to explore the research progress, biological significance, and potential clinical applications of TLSs in gastrointestinal tumors. The formation, development, and interaction of TLSs with tumor microenvironment have been reviewed and analyzed in recent years. Meanwhile, this review not only evaluates the clinical value of TLSs as prognostic biomarkers and predictors of treatment response but also explores their role in guiding the formulation of immunotherapy strategies for gastrointestinal tumors. In addition, this review points out the main problems in the current research of TLSs and looks forward to their future development, especially their broad application prospects in the diagnosis, treatment, and prognostic evaluation of gastrointestinal tumors.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1571-1580"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560652","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}

{"title":"Unlocking the potential of tumor-targeting peptides in precision oncology.","authors":"Hafiz Muhammad Rehman, Sidra Ahmad, Azeem Sarwar, Hamid Bashir","doi":"10.32604/or.2025.062197","DOIUrl":"10.32604/or.2025.062197","url":null,"abstract":"<p><p>Targeted cancer therapy has emerged as a promising alternative to conventional chemotherapy, which is often plagued by poor selectivity, off-target effects, and drug resistance. Among the various targeting agents in development, peptides stand out for their unique advantages, including minimal immunogenicity, high tissue penetration, and ease of modification. Their small size, specificity, and flexibility allow them to target cancer cells while minimizing damage to healthy tissue selectively. Peptide-based therapies have shown great potential in enhancing the efficacy of drug delivery, improving tumor imaging, and reducing adverse effects. With cancer responsible for millions of deaths worldwide, the development of peptide-based therapeutics offers new hope in addressing the limitations of current treatments. As detailed studies on different aspects of targeting peptides are crucial for optimizing drug development, this review provides a comprehensive overview of the literature on tumor-targeting peptides, including their structure, sources, modes of action, and their application in cancer therapy-both as standalone agents and in fusion drugs. Additionally, various computational tools for peptide-based tumor-targeting drug design and validation are explored. The promising results from these studies highlight peptides as ideal candidates for targeted cancer therapies, offering valuable insights for researchers and accelerating the discovery of novel anti-tumor peptide base drug candidates.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1547-1570"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560658","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}

{"title":"ETV1 transcriptional manipulation of KIFC1 regulates the progression of pancreatic cancer.","authors":"Fangfang Hu, Zhibin Bai, Yang Wang, Haodong Tang, Jiahua Zhou","doi":"10.32604/or.2025.059631","DOIUrl":"10.32604/or.2025.059631","url":null,"abstract":"<p><strong>Background: </strong>Kinesin-14 family protein 1 (KIFC1) is abnormally overexpressed in various cancers, and the transcription factor ETS variant 1 (ETV1) is an oncogenic transcription factor in tumors. The potential binding sites on the KIFC1 promoter by ETV1 were observed; however, no evidence supports that ETV1 targets KIFC1. Aims: This study aimed to investigate the relationship between KIFC1 and ETV1, and their effects and mechanisms in pancreatic cancer.</p><p><strong>Methods: </strong>Pan-cancer analysis of KIFC1 expression was performed in GEPIA2 database. KIFC1 expression levels were determined by immunohistochemistry (IHC) in our pancreatic cancer cohort. The correlation between KIFC1 expression and prognosis, tumor mutation burden, tumor purity, mismatch repair, and high-frequency tumor mutated genes was analyzed using a series of bioinformatic tools. ETV1 targeting of KIFC1 promoter transcription was determined using luciferase reporter assay. KIFC1 knockdown and ETV1 overexpression were used to determine the role of the ETV1/KIFC1 axis in cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of pancreatic cancer cells <i>in vitro</i> and tumor growth <i>in vivo</i>.</p><p><strong>Result: </strong>KIFC1 expression was increased in clinical specimens and pancreatic cancer cell lines and positively correlated with tumor mutation burden, tumor purity, mismatch repair, and KRAS and TP53 mutations. High KIFC1 expression was significantly associated with poor prognosis. Knockdown of KIFC1 suppressed the proliferation, migration, and invasion of pancreatic cancer cells and tumor growth. ETV1 overexpression increased KIFC1 expression and affected KIFC1 transcription. ETV1 overexpression reversed the role of KIFC1 knockdown in inhibiting cell proliferation, invasion, migration, and EMT, as validated <i>in vivo</i>.</p><p><strong>Conclusions: </strong>KIFC1 serves as a tumor activator in pancreatic cancer by promoting proliferation, migration, invasion, and tumor growth, which may be partly manipulated by ETV1.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1723-1737"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560722","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}

{"title":"IL1A: a novel prognostic biomarker and potential therapeutic target for renal clear cell carcinoma.","authors":"J I Zeng, Xueteng Meng, Yuan Zhang, Jun Li, Taotao Ma, Cheng Huang","doi":"10.32604/or.2025.061978","DOIUrl":"10.32604/or.2025.061978","url":null,"abstract":"<p><strong>Background: </strong>Renal cell carcinoma (RCC) is a prevalent malignancy characterized by a rising incidence and significant mortality. Interleukins (ILs) are crucial in regulating immune cell trafficking and exhibit anti-tumor properties. However, limited research has explored the expression levels and prognostic significance of interleukins in RCC.</p><p><strong>Methods: </strong>In this comprehensive study, we performed a detailed analysis of interleukins in RCC patients using multiple bioinformatics tools, including Oncomine, UALCAN, GEPIA, Kaplan-Meier plotter, cBioPortal, GeneMANIA, TRRUST, STRING, and Linked Omics.</p><p><strong>Results: </strong>Our analysis demonstrated a significant upregulation in the transcriptional levels of IL4, IL7, IL15, IL16, IL23A, IL26, and IL32 were significantly upregulated in RCC tissues, indicating their potential involvement in the pathogenesis of this malignancy. In contrast, IL1A, IL11, and IL27 were downregulated, indicating their potential function as tumor suppressors. Significant correlations were identified between the expression levels of IL11, IL23A, IL27, IL32, and the pathological stage of RCC patients. The expression levels of IL1A, IL4, IL11, IL15, IL16, IL23A, IL26, IL27, and IL32 were significantly correlated with improved prognosis. The differentially expressed interleukins primarily function in cytokine-cytokine receptor interactions and immune response-regulating signaling pathways. homeobox A10 (HOXA10), v-myb myeloblastosis viral oncogene homolog (avian) (MYB), v-rel reticuloendotheliosis viral oncogene homolog A (avian) (RELA), and nuclear factor of kappa light polypeptide gene enhancer in B-cells 1(NFKB1) are key transcription factors for ILs, while LCK proto-oncogene (LCK), LYN proto-oncogene (LYN), spleen associated tyrosine kinase (SYK), Janus kinase 3 (JAK3), and FER tyrosine kinase (FER) are IL targets. IL expression significantly correlated with the infiltration of six distinct immune cell types. IL1A potentially exerts an anti-tumor effect in RCC prognosis by inducing neutrophil extracellular traps (NETs). Additionally, NFKB1 may positively regulate IL1A, providing a rationale for further <i>in vivo</i> and clinical studies.</p><p><strong>Conclusion: </strong>In conclusion, our study demonstrates the potential role of IL 1A in the prognosis of RCC and establishes a theoretical foundation for subsequent <i>in vivo</i> and clinical investigations.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1739-1755"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560723","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}