Medical Oncology最新文献

{"title":"Analysis of possible effects of recombinant antimicrobial peptide TP4 on colon cancer line HT-29.","authors":"Seda Kılınç, Mert Karaoğlan, Mehmet Kuzucu","doi":"10.1007/s12032-025-02937-5","DOIUrl":"https://doi.org/10.1007/s12032-025-02937-5","url":null,"abstract":"<p><p>Tilapia piscidin 4 (TP4) is a 25-amino-acid cationic antimicrobial peptide derived from Nile tilapia (Oreochromis niloticus). TP4 has demonstrated strong antimicrobial activity against a broad range of pathogens and exhibits additional biological functions, including wound healing and anticancer activity. In a previous study, recombinant TP4 peptide was produced in the Pichia pastoris KM71H expression system and purified by Ni-NTA affinity chromatography. The aim of this study was to evaluate and compare the cytotoxicity of recombinant TP4 against HT-29 colon cancer and HGF-1 healthy gingival fibroblast cells.The antimicrobial activity of TP4 was first assessed using minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) assays, confirming its efficacy. Subsequently, the cytotoxic effects of TP4 on HT-29 and HGF-1 cells were further analyzed using the MTT, lactate dehydrogenase (LDH), total antioxidant/oxidant status (TAS/TOS), and malondialdehyde (MDA) assays. TP4 disrupted the antioxidant balance in both cell types, with a significant increase in the oxidant levels and a marked decrease in the antioxidant levels in HT-29 cells. The IC₅₀ values of TP4 were determined to be 15 μg/mL for HT-29 cells and 25 μg/mL for HGF-1 cells. Apoptosis assays, including Annexin V & Dead Cell, RT-qPCR, and ELISA, revealed that TP4 induced apoptosis predominantly in HT-29 cells, as evidenced by the upregulation of BAX and CASP3 and the downregulation of the BCL-2. In conclusion, TP4 exhibited selective and potent apoptotic effects on HT-29 colon cancer cells, suggesting its potential as a novel therapeutic agent for colon cancer treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"356"},"PeriodicalIF":2.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675254","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":"Ursolic acid affects autophagy and apoptosis of breast cancer through PLK1 via AKT/mTOR signaling pathway.","authors":"Kehong Yang, Zhuzhu Xie, Shiao Liu, Ruilong Xu, Jie Mao, Wenjing Feng, Xinya Zhao, Yuqi Dai, Ying Zou, Rongkang Qian, Ronghua Qian","doi":"10.1007/s12032-025-02917-9","DOIUrl":"https://doi.org/10.1007/s12032-025-02917-9","url":null,"abstract":"<p><p>Breast cancer poses a significant threat to women's health globally, exhibiting the greatest incidence and fatality rates among female cancers. Chemotherapy is frequently employed in the clinical management of breast cancer. While the majority of patients require novel chemotherapeutic agents due to treatment resistance. We sought to examine the impact of ursolic acid (UA) on apoptosis and autophagy levels in breast cancer through Polo-like Kinase 1 (PLK1) via the AKT/mTOR signaling pathway. Tamoxifen (TAM) and adriamycin (ADM) served as positive control agents. In vitro experiments, the MTT assay was utilized to evaluate the viability of MCF-7/MDA-MB-231 cells, flow cytometry and JC-1 staining to analyze apoptosis, electron microscopy and MDC staining to scrutinize autophagy, and Western blot (WB) to measure the expression of pertinent proteins. In vivo research utilized the BALB/c mouse breast cancer model established with 4T1, comparing the volume and weight of transplanted tumors across several groups. Tumor necrosis was identified using HE staining, anti-apoptotic protein Bcl-2 expression was assessed via IHC labeling, and protein expression was evaluated using WB. UA suppressed tumor proliferation in BALB/c mice models of breast cancer. Tumor proliferation was markedly suppressed in the TAM and medium/high-dose UA cohorts. HE staining demonstrated significant necrosis, while IHC/WB analysis validated that UA or UA combined with Volasertib may reduce levels of Bcl-2, PLK1, p-AKT/AKT, and p-mTOR/mTOR, in conjunction with increased LC3 II/I. In conclusion, the study revealed that UA may affect the apoptosis and autophagy of breast cancer through PLK1 via AKT/mTOR signaling pathway.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"358"},"PeriodicalIF":2.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682784","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":"Integrating scRNA-seq and spatial transcriptomics to explore the implication of G6PD on immune microenvironment in lymphatic metastasis of breast cancer.","authors":"Hongsen Liu, Mengting Chen, Bo Hong, Ruijin Liang, Lijie Fan, Yun Qian","doi":"10.1007/s12032-025-02943-7","DOIUrl":"https://doi.org/10.1007/s12032-025-02943-7","url":null,"abstract":"<p><p>Breast cancer is among the most prevalent malignancies, with lymph node metastasis strongly linked to worse prognostic outcomes. Despite this, the mechanisms underlying the formation of an immunosuppressive microenvironment that drives lymph node metastasis remain poorly understood. By profiling 118,127 cells from eight patients with breast cancer alongside their metastatic axillary lymph nodes through single-cell sequencing and spatial transcriptomics, this study uncovered the activation of the pentose phosphate pathway during the metastatic process. The expression level of G6PD in breast cancer tumor tissues was significantly higher than that in adjacent tissues. Furthermore, high G6PD expression was associated with poorer prognosis. G6PD was more highly expressed in metastatic lymph nodes, which exhibited an immunosuppressive microenvironment induced by CD4 Treg cells, and the expression of G6PD was positively correlated with immune cell infiltration by Treg cells. Clinical evaluation further demonstrated a significant correlation among G6PD expression, lymph node metastasis, and malignancy. Additionally, clinical drug response data revealed that patients resistant to chemotherapy also had higher G6PD expression. These findings establish G6PD as a molecular marker for predicting the risk of lymph node metastasis and prognosis in breast cancer. This study discovered elevated expression of G6PD in breast cancer, as well as the formation of an immunosuppressive microenvironment mediated by Treg cells in breast cancer lymph node metastatic tissues, emphasizing the critical role of G6PD in promoting lymph node metastasis by driving Treg cell infiltration.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"355"},"PeriodicalIF":2.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675255","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":"Noncoding RNAs as mechanistic regulators and therapeutic modulators of YAP/TAZ signaling in colorectal cancer.","authors":"Mehrnaz Mostafavi, Elham Dehbashi, Faraz Rahmani Khajeh, Masoumeh Nouri, Mahdis Kadkhodaei Eliaderani, Nahal Aghajamal Avval, Moein Ghasemi, Dina Seyedi, Malihe Sharafi, Reza Morovatshoar, Sepide Javankiani, Alireza Azani, Farzad Sadri, Qumars Behfar","doi":"10.1007/s12032-025-02934-8","DOIUrl":"https://doi.org/10.1007/s12032-025-02934-8","url":null,"abstract":"<p><p>Colorectal cancer (CRC) continues to represent a significant global health challenge due to its high incidence and mortality rates. Among the signaling pathways implicated in CRC, the Hippo pathway has gained considerable attention for its evolutionarily conserved role in regulating cellular proliferation, programmed cell death, and organ size control. The recent studies have revealed that alterations in this pathway contribute not only to tumor initiation but also to metastasis and therapy resistance. Emerging evidence underscores the pivotal involvement of noncoding RNAs (ncRNAs)-including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs)-in modulating this pathway, particularly through the regulation of its core effectors, Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ). The intricate crosstalk between ncRNAs and Hippo signaling components suggests a multilayered regulatory mechanism that warrants further investigation. This review provides mechanistic insights into the dynamic crosstalk between ncRNAs and the YAP/TAZ axis, highlighting their roles in tumor progression, metastasis, and chemoresistance. Considering these intricate interactions, this review further emphasizes the emerging therapeutic and biomarker potential of ncRNAs, offering novel perspectives for both targeted intervention and early diagnosis in CRC management.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"357"},"PeriodicalIF":2.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675256","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":"Epigenetic dysregulation in cancer: mechanisms, diagnostic biomarkers and therapeutic strategies.","authors":"Komal Imran, Muhammad Javed Iqbal, Muhammad Mushtaq Ahmed, Ammara Khalid, Hernán Cortés, Octavio Daniel Reyes-Hernández, Gabriela Figueroa-González, Gerardo Leyva-Gómez, Luca Falzone, Massimo Libra, Federica Longo, Javad Sharifi-Rad, Daniela Calina","doi":"10.1007/s12032-025-02905-z","DOIUrl":"https://doi.org/10.1007/s12032-025-02905-z","url":null,"abstract":"<p><p>The disruption of the epigenetic patterns and its impact on gene expression is recognized as a critical factor in the initiation and progression of cancer. Altered patterns of DNA methylation, histone modifications, and non-coding RNA expression are distinctive features of tumorigenesis. These dynamic shifts in the epigenetic landscape during oncogenic transformation are intricately linked to tumor heterogeneity, the sustained capacity for self-renewal, and the ability to undergo multi-lineage differentiation. The abnormal reprogramming of cancer stem cells presents a formidable challenge in cancer treatment and drug resistance. However, the reversible nature of epigenetic modifications holds significant potential for developing novel cancer treatments through the targeted inhibition of epigenetic modifiers. Utilizing this approach as a standalone therapy or combined with other anticancer treatments has yielded promising outcomes. In this review, we emphasize the central role of epigenetic dysregulation in cancer pathogenesis, epigenetic changes in the cancer genome, and the latest advancements in cancer therapy, particularly the potential of epigenetic factors as biomarkers for early detection and their application in current cancer treatment modalities.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"359"},"PeriodicalIF":2.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682783","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":"Dynamic ubiquitination networks in liver cancer: decoding E3 ligases and deubiquitinases as gatekeepers of therapeutic resistance.","authors":"Nuo Xu, Yun Tong, Kexin Ma, Lihan Jiang, Wenjie Zheng","doi":"10.1007/s12032-025-02912-0","DOIUrl":"https://doi.org/10.1007/s12032-025-02912-0","url":null,"abstract":"<p><p>Patients with advanced hepatocellular carcinoma are treated using conventional therapeutic approaches and a variety of molecularly targeted drugs. Nevertheless, therapeutic resistance emerges because of the high heterogeneity of the malignancy, often restricting the effectiveness of these interventions. Therefore, therapeutic resistance represents a significant obstacle in managing liver cancer. Ubiquitination and deubiquitination, essential regulatory mechanisms, regulate the activity of diverse proteins and are pivotal in determining tumor therapeutic resistance. In this review, we focus on the enzymes involved in ubiquitination and deubiquitination in hepatocellular carcinoma, examining their associated phenotypes. Furthermore, we synthesize findings from a range of studies to elucidate the mechanisms of therapeutic resistance in hepatocellular carcinoma and highlight the critical role of ubiquitination and deubiquitination enzymes in these processes. Finally, we explore the therapeutic potential of targeting the ubiquitination and deubiquitination systems to enhance drug efficacy in liver cancer treatment significantly.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"352"},"PeriodicalIF":2.8,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667933","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":"Synthetic oleanolic acid derivative, RTA-408, overcome in TMZ-resistant glioblastoma cells by inducing apoptosis and G1 cell cycle arrest.","authors":"Kuan-Ting Lee, Ann-Shung Lieu, Chih-Lung Lin, Yi-Chiang Hsu, Tai-Hsin Tsai","doi":"10.1007/s12032-025-02875-2","DOIUrl":"https://doi.org/10.1007/s12032-025-02875-2","url":null,"abstract":"<p><p>Glioblastoma is the most malignant primary brain tumor. It is characterized by high cellular heterogeneity, which contributes to its high chemoresistance and recurrence rate. To investigate the anticancer effect of RTA-408 on TMZ-resistant glioblastoma, we developed 2 TMZ-resistant cell lines, GBM841R and U-87MGR. Our findings revealed that RTA-408 (Omaveloxolone) effectively inhibited growth, induced cytotoxicity, and reduced colony formation in TMZ-resistant glioblastoma cells. RTA-408 treatment also induced dose-dependent cell cycle arrest, increasing the proportion of cells in the G1 phase while reducing that of those in the G2/M phase. Moreover, RTA-408 enhanced apoptosis and caspase-3 activation in TMZ-resistant cells. Next-generation sequencing revealed that RTA-408 modulated the expression of Nrf2-Keap1-ARE downstream genes in both TMZ-resistant and TMZ-sensitive glioblastoma cells. Western blot analysis revealed that RTA-408 modulated apoptosis-related protein expression and inhibited reactive oxygen species production, thereby reducing oxidative stress in TMZ-resistant glioblastoma cells. These findings indicate that RTA-408 is not only a promising alternative for TMZ-sensitive glioblastoma but also a first-line treatment option for TMZ-resistant glioblastoma.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"353"},"PeriodicalIF":2.8,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667960","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":"A novel naphthoquinone compound triggers DNA damage-induced apoptosis on cholangiocarcinoma through upregulation of BAX.","authors":"Gizem Bulut, Merve Kayis, Dilan Gezer, Zeliha Gokmen, Zelal Adiguzel, Chiara Raggi, Engin Ulukaya","doi":"10.1007/s12032-025-02927-7","DOIUrl":"https://doi.org/10.1007/s12032-025-02927-7","url":null,"abstract":"<p><p>Cholangiocarcinoma (CCA), a devastating malignancy originating from the bile ducts, is of significant clinical importance due to its rising incidence and poor prognosis. Quinones as being naturally occurring compounds and their frequent utility in anticancer drug development studies seem to be potential sources for the discovery of new chemotherapeutics. In this study, a synthetic naphthoquinone derivative newly synthesized and previously published by our group, named as MK13, has been tested against intrahepatic-CCA (iCCA) cell lines (CCLP1 and HUCCT1). Cell viability was measured with the MTT assay at the doses of 1.56-50 µM for 48 h treatment. Cell death was showed both morphologically with fluorescent double staining and biochemically with flow cytometry analysis of phosphatidylserine translocation. Oxidative stress and DNA damage were also measured with flow cytometry and gene expressions were interpreted via qPCR analysis. MK13 resulted in a strong reduction (about 80%) in viability, especially against CCLP1 cells when compared with doxorubicin. Cell death resulted from apoptosis was shown to be triggered by severe DNA damage that is independent of oxidative stress. Apoptosis was confirmed at molecular level with the upregulation of BAX, a pro-apoptotic BH-3 only protein, and DR5, a cell surface death receptor. MK13 seems to be a promising anticancer compound against iCCA and deserves further attention for in vivo proof-of-concept studies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"354"},"PeriodicalIF":2.8,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675253","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":"Harnessing the oral-systemic axis: A novel frontier in cancer management.","authors":"Anjana Parmar, Palwinder Kaur, Mandeep Kaur, Palakurthi Yanadaiah","doi":"10.1007/s12032-025-02921-z","DOIUrl":"https://doi.org/10.1007/s12032-025-02921-z","url":null,"abstract":"<p><p>The human body harbors numerous microorganisms, including bacteria, fungi, viruses, and bacteriophages, which are primarily found in the oral cavity and are considered the largest microbiological reservoir. The oral microbiota has a profound influence on the human body and health. An imbalance between the bacteria and their hosts may cause local oral and dental difficulties. The recent research has indeed underscored the significant role of oral microbial dysbiosis in the development of various systemic and long-term diseases, potentially culminating in cancer by triggering oncogenic processes in the body. The analogy of activated pathways depends on the involvement of a specific subset of microbial species or consortia within the oral cavity. This review explains the pivotal role of oral microbial dysbiosis in cancer pathogenesis. It also specifies the role of specific oral pathogens and associated mechanisms through which dysbiotic oral microbiota contribute to oncogenic processes. As a rational and innovative approach, the review features various phytotherapeutics that are found to be active against pathogenic oral microbes and also show activity against systemic cancers. This review aims to emphasize the oral-systemic axis by highlighting phytotherapies known for their cancer management properties, which have shown activity against oral microbes and are linked to the pathogenesis of the respective cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"348"},"PeriodicalIF":2.8,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667934","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":"Symplocamide A as marine-derived proteasome inhibitor: a promising scaffold for targeted cancer therapy.","authors":"Humeyra Cavdar Dincturk, Aysenur Betul Bilgin, Deniz Günal Köroğlu, Celale Kirkin Gozukirmizi, Gulay Ozkan, Esra Capanoglu, William N Setzer, Dietrich Büsselberg, Daniela Calina, Javad Sharifi-Rad","doi":"10.1007/s12032-025-02870-7","DOIUrl":"https://doi.org/10.1007/s12032-025-02870-7","url":null,"abstract":"<p><p>Symplocamide A (Sym A), a 3-amino-6-hydroxy-2-piperidone (Ahp)-containing cyclodepsipeptide derived from the marine cyanobacterium Symploca sp., has emerged as a promising candidate in anticancer research. With potent serine protease and proteasome inhibition, Sym A has demonstrated nanomolar cytotoxicity across several cancer cell lines, including lung and neuroblastoma models. This review critically assesses the anti-cancer mechanisms, pharmacokinetic properties, synthetic approaches, and translational limitations of Symplocamide A, highlighting its potential and challenges as a therapeutic agent in oncology. A systematic literature review was performed using PubMed, Scopus, Web of Science, Google Scholar, and the TRIP database, incorporating studies published until March 2025. Articles were selected based on predefined inclusion criteria focusing on Sym A's anticancer activity, mechanisms of action, bioavailability, synthesis, and toxicity profiles. Sym A exhibits selective cytotoxicity toward various cancer cell lines, notably inhibiting chymotrypsin with over 200-fold greater potency than trypsin. Structural analysis underscores the role of Ahp and brominated tyrosine residues in target affinity and stability. Pharmacokinetic modeling indicates favorable intestinal absorption and drug-likeness, although brain penetration is limited. Synthetic production remains inefficient, with low overall yield. No in vivo or clinical studies have yet been reported. Toxicological concerns are heightened by its structural similarity to cyanotoxins, necessitating cautious evaluation. Symplocamide A demonstrates high preclinical anticancer potential through protease inhibition and favorable bioavailability traits. Nonetheless, its clinical translation is hindered by synthesis challenges, the absence of in vivo validation, and undefined toxicity. Further studies are warranted to evaluate its therapeutic window, optimize synthetic accessibility, and assess safety in vivo.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"351"},"PeriodicalIF":2.8,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667959","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}