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| 1 | Whether Probiotic Supplementation Benefits Rheumatoid Arthritis Patients: A Systematic Review and Meta-Analysis显示文摘Gut and oral microflora are important factors in the pathogenesis and development of rheumatoid arthritis(RA). Recent studies have shown that probiotic supplements have beneficial consequences on experimental arthritis in rats. However, results from randomized clinical trials on the effects of probiotics have not been consistent. The aim of this study was to systematically review the existing evidence for the effects of probiotic intervention in RA. We included randomized controlled trials(RCTs) of RA patients receiving stable treatment with disease-modifying anti-rheumatic drugs(DMARDs) that:(1) were combined with additional probiotic supplements or(2) were combined with either no additional supplements or only a placebo treatment. Statistical analysis was performed using Review Manager 5.3.3.Six randomized clinical trials were eligible for inclusion in the meta-analysis, with 249 participants in total. The results showed that the probiotic intervention treatment has not yet achieved significant improvement in the American College of Rheumatology 20% improvement criteria(ACR20) score and the disease activity score in 28 joints(DAS28). The laboratory index C-reactive protein(CRP)(mg·L–1) was significantly reduced in the intervention group. The expression of inflammatory cytokines tumor necrosis factor(TNF)-α and interleukine(IL)-1β was also significantly reduced, while IL-10 expression increased in the probiotic intervention groups. This article is the first systematic review and meta-analysis providing a comprehensive assessment of the benefits of treating RA with probiotics. We found that probiotic supplementation may show a limited improvement in RA therapy in existing reports because of a lack of sufficiently high-quality work on the part of clinicians. More multi-centered, large-sample RCTs are needed in order to evaluate the benefits of probiotics in RA treatment. | Hudan Pan Runze Li Ting Li Jun Wang Liang Liu | 2017 | Engineering2017，3，1： | 7 |
| 2 | Integrated genomic analysis identifies deregulated JAK/STAT-MYC-biosynthesis axis in aggressive NK-cell leukemia显示文摘好攻击的 NK 房间白血病(ANKL ) 是在从亚洲的人之中是更流行的 NK 房间瘤的一种稀罕形式并且中央并且南美洲。病人们通常在天以内死到月,甚至在收到迅速的治疗学的管理以后。这里,我们由集成整个染色体执行了 ANKL 的第一全面研究, transcriptome 并且定序指向,象功能的试金一样的 cytokine 数组。在 JAK-STAT 小径的变化在 48% 被识别(14/29 ) ANKL 病人,当细胞外的 STAT3 激发器 IL10 被 56 褶层的一般水准提高时(P < 0.0001 ) 在检查的所有病人的血浆。另外的经常变异的基因包括的 TP53 (34%) , TET2 (28%) , CREBBP (21%) 和 MLL2 (21%) 。耐心的 NK 白血病房间在多重新陈代谢的小径显示出 STAT3 phosphorylation, MYC 表示和 transcriptional 活动的突出的激活。机能上地, STAT3 激活和 MYC 表示为 ANKL 房间的增长和幸存是批评的。发信号的 STAT 调整了发信号的 MYC 抄写节目,和两 STAT, MYC 抄写被要求维持核苷酸合成和 glycolysis 的激活。一起, JAK-STAT 小径在 ANKL 为 genomic 改变和 IL10 刺激代表一个主要目标。这最新发现的 JAK/STAT-MYC-biosynthesis 轴可以在对待白血病的这种子类型为新奇治疗学的策略的发展提供机会。 | Liang Huang Dan Liu Na Wang Shaoping Ling Yuting Tang Jun Wu Lingtong Hao Hui Luo Xuelian Hu Lingshuang Sheng Lijun Zhu Di Wang Yi Luo Zhen Shang Min Xiao Xia Mao Kuangguo Zhou Lihua Cao Lili Dong Xinchang Zheng Pinpin Sui Jianlin He Shanlan Mo Jin Yan Qilin Ao Lugui Qiu Hongsheng Zhou Qifa Liu Hongyu Zhang Jianyong Li Jie Jin Li Fu Weili Zhao Jieping Chen Xin Du Guoliang Qing Hudan Liu Xin Liu Gang Huang Ding Ma Jianfeng Zhou Qian-fei Wang | 2018 | Cell Research2018，28，2： | 5 |
| 3 | Targeting oncogenic Myc as a strategy for cancer treatment显示文摘The MYC family oncogene is deregulated in>50%of human cancers,and this deregulation is frequently associated with poor prognosis and unfavorable patient survival.Myc has a central role in almost every aspect of the oncogenic process,orchestrating proliferation,apoptosis,differentiation,and metabolism.Although Myc inhibition would be a powerful approach for the treatment of many types of cancers,direct targeting of Myc has been a challenge for decades owing to its“undruggable”protein structure.Hence,alternatives to Myc blockade have been widely explored to achieve desirable anti-tumor effects,including Myc/Max complex disruption,MYC transcription and/or translation inhibition,and Myc destabilization as well as the synthetic lethality associated with Myc overexpression.In this review,we summarize the latest advances in targeting oncogenic Myc,particularly for cancer therapeutic purposes. | Hui Chen Hudan Liu Guoliang Qing | 2018 | Signal Transduction and Targeted Therapy2018，3，1： | 5 |
| 4 | Regulation of cancer cell metabolism:oncogenic MYC in the driver’s seat显示文摘Cancer cells must rewire cellular metabolism to satisfy the demands of unbridled growth and proliferation.As such,most human cancers differ from normal counterpart tissues by a plethora of energetic and metabolic reprogramming.Transcription factors of the MYC family are deregulated in up to 70%of all human cancers through a variety of mechanisms.Oncogenic levels of MYC regulates almost every aspect of cellular metabolism,a recently revisited hallmark of cancer development.Meanwhile,unrestrained growth in response to oncogenic MYC expression creates dependency on MYC-driven metabolic pathways,which in principle provides novel targets for development of effective cancer therapeutics.In the current review,we summarize the significant progress made toward understanding how MYC deregulation fuels metabolic rewiring in malignant transformation. | Yang Dong Rongfu Tu Hudan Liu Guoliang Qing | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 2 |
| 5 | Deciphering the pharmacological mechanism of Guan-Jie-Kang in treating rat adjuvant-induced arthritis using omics analysis显示文摘Traditional Chinese medicine (TCM) formulas have attracted increasing attention worldwide in the past few years for treating complex disease including rheumatoid arthritis. However, their mechanisms are complex and remain unclear. Guan-Jie-Kang (GJK), a prescription modified from “Wu Tou Decoction,” was found to significantly relieve arthritis symptoms in rats with adjuvant-induced arthritis after 30-day treatment, especially in the 24 g/kg/day group. By analyzing 1749 targets related to 358 compounds in the five herbs of GJK, we identified the possible anti-arthritis pathways of GJK, including the calcium signaling and metabolic pathways. Bone damage levels were assessed by micro-computed tomography, and greater bone protective effect was observed with GJK treatment than with methotrexate. Receptor activator of nuclear factor kB ligand (RANKL)-RANK signaling, which is related to calcium signaling, was significantly regulated by GJK. Moreover, a target metabolomics assay of serum was conducted;17 metabolic biomarkers showed significant correlations with treatment. An integrated pathway analysis revealed that pyruvate metabolism, purine metabolism, and glycolysis metabolism were significantly associated with the effects of GJK in arthritis treatment. Thus, this study establishes a new omics analytical method integrated with bioinformatics analysis for elucidating the multi-pathway mechanisms of TCM. | Hudan Pan Yanfang Zheng Zhongqiu Liu Zhongwen Yuan Rutong Ren Hua Zhou Ying Xie Liang Liu | 2019 | Frontiers of Medicine2019，13，5： | 1 |
| 6 | MYC in T-cell acute lymphoblastic leukemia: functional implications and targeted strategies显示文摘T-cell acute lymphoblastic leukemia(T-ALL)is an aggressive hematological cancer that frequently occurs in children and adolescents,which results from the transformation of immature T-cell progenitors.Aberrant cell growth and proliferation of T-ALL lymphoblasts are sustained by activation of strong oncogenic drivers.Mounting evidence highlights the critical role of the NOTCH1-MYC highway toward the initiation and progression of T-ALL.MYC has been emphasized as a primary NOTCH1 transcriptional target impinging in leukemia-initiating cell activity particularly responsible for disease onset and relapse.These findings lay a foundation of T-ALL as an ideal disease model for studying MYC-mediated cancer.The biology of MYC deregulation in T-ALL supports innovative strategies for therapeutic targeting of MYC.To summarize the relevant literature and data in recent years,we here provide a comprehensive overview of the functional importance of MYC in T-ALL development,and the molecular mechanisms underlying MYC deregulation in T-ALL.Finally,we illustrate the innovative MYC-targeted approaches that have been evaluated in pre-clinical models and shown significant efficacy.Given the complexity of T-ALL molecular pathogenesis,we propose that a combination of anti-MYC strategies with conventional chemotherapies or other targeted/immunotherapies may provide the most durable response,especially for those patients with relapsed and refractory T-ALL. | Qilong Li Sa Pan Ting Xie Hudan Liu | 2021 | Blood Science2021，3，3： | 0 |
| 7 | Polo样激酶1通过PLK1-Myc反馈激活信号环路稳定癌蛋白Myc并促进肿瘤细胞生长存活显示文摘癌基因MYCN(编码N-Myc)在癌症中出现扩增突变预示不良预后和复发耐药。众多细胞水平和模式动物研究表明,干预癌蛋白N-Myc的表达或活性能够显著甚至完全抑制肿瘤发生和发展。 | Daibiao Xiao Ming Yue Hexiu Su Ping Ren Jue Jiang Feng Li Yufeng Hu Haining Du Hudan Liu 卿国良 | 2017 | 科学新闻2017，19，4： | 0 |
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