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| 1 | Genomic landscape of gastric cancer: molecular classification and potential targets显示文摘Gastric cancer imposes a considerable health burden worldwide, and its mortality ranks as the second highest for all types of cancers. The limited knowledge of the molecular mechanisms underlying gastric cancer tumorigenesis hinders the development of therapeutic strategies. However, ongoing collaborative sequencing efforts facilitate molecular classification and unveil the genomic landscape of gastric cancer. Several new drivers and tumorigenic pathways in gastric cancer, including chromatin remodeling genes, Rho A-related pathways, TP53 dysregulation, activation of receptor tyrosine kinases, stem cell pathways and abnormal DNA methylation, have been revealed. These newly identified genomic alterations await translation into clinical diagnosis and targeted therapies. Considering that loss-of-function mutations are intractable, synthetic lethality could be employed when discussing feasible therapeutic strategies. Although many challenges remain to be tackled, we are optimistic regarding improvements in the prognosis and treatment of gastric cancer in the near future. | Jiawei Guo Weiwei Yu Hui Su Xiufeng Pang | 2017 | Science China(Life Sciences)2017，60，2： | 6 |
| 2 | Triptolide suppresses pancreatic cancer cell proliferation by inhibiting hedgehog signaling pathway activity显示文摘Dear Editor,Pancreatic cancer (PCa) is a high-grade gastrointestinal malignancy more commonly occurring in elderly populations with lower than 5% overall 5-year survival rate (Hidalgo, 2010). PCa responds poorly to most chemotherapeutic agents, and therefore it is imperative to develop novel therapeutic agents that have anti-cancer activities against PCa. | Juanjuan Feng Mingjin Rao Man Wang Lin Liang Zhi Chen Xiufeng Pang Weiqiang Lu Zhenliang Sun | 2019 | Science China(Life Sciences)2019，62，10： | 6 |
| 3 | Small molecule 1′-acetoxychavicol acetate suppresses breast tumor metastasis by regulating the SHP-1/STAT3/MMPs signaling pathway显示文摘 | Jieqiong Wang Li Zhang Guoliang Chen Jing Zhang Zhenxi Li Weiqiang Lu Mingyao Liu Xiufeng Pang | 2014 | Breast Cancer Research and Treatment2014，，2： | 2 |
| 4 | The greedy nature of mutant RAS: a boon for drug discovery targeting cancer metabolism?显示文摘地岬 oncogene 变化经常在人的癌症被检测。在调停地岬的 tumorigenesis 之中,驾驶 KRAS 的癌症是经常诊断的大多数并且对当前的治疗抵抗。尽管有超过三十年集中的努力,仍然为变异的地岬蛋白质没有特定的治疗。当试着堵住那些生长得很好的下游的小径时,例如 RAF-MAPK 小径和 PI3K-AKT 小径,注意在新陈代谢的小径和可行性上对地岬的潜在的效果被给予了为指向这些小径。最近的研究证明了那地岬不仅支持氧气的 glycolysis 和夫酸安新陈代谢 reprograming 提供精力,而且它也便于分叉的新陈代谢小径, autophagy,和 macropinocytosis。这些改变为肿瘤生长产生积木并且在肿瘤房间加强抗氧化剂防卫。所有这些新陈代谢的变化遇见地岬驱动的癌症的不同要求,从正常房间使他们不同。确实,一些成就被做了通过指向特定的新陈代谢在现出症状之前的潜的模型给换新电线禁止肿瘤生长。尽管仍然有阐明的一条长路改变的新陈代谢的风景,我们相信特定的新陈代谢的酶或小径能治疗学地为地岬驱动的癌症的选择抑制被指向。 | Jing Lv Jieqiong Wang Siyu Chang Mingyao Liu Xiufeng Pang | 2016 | Acta Biochimica et Biophysica Sinica2016，48，1： | 1 |
| 5 | Acetyl-11-keto-β-boswellic acid inhibits prostate tumor growth by suppressing vascular endothelial growth factor receptor 2-mediated angiogenesis显示文摘 | Xiufeng Pang Zhengfang Yi Xiaoli Zhang | 2009 | Cancer Research2009，69，14： | 1 |
| 6 | A combination therapy for KRAS-mutant lung cancer by targeting synthetic lethal partners of mutant KRAS显示文摘The KRAS gene is frequently mutated in multiple cancer types,but it fell off the drug discovery radar for many years because of its inherent 'undruggable' structure and undefined biological properties.As reported in the paper entitled 'Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK' in Nature Communications,we performed a synthetic lethal screening with a combinatorial strategy on a panel of clinical drugs;we found that combined inhibition of polo-like kinase 1 and RhoA/Rho kinase markedly suppressed tumor growth in mice.An increase in the expression of the tumor suppressor P21^(WAF1/CIP1) contributed to the synergistic mechanism of the combination therapy.These findings open a novel avenue for the treatment of KRAS-mutant lung cancer. | Xiufeng Pang Mingyao Liu | 2016 | Chinese Journal of Cancer2016，35，11： | 1 |
| 7 | Celastrol suppresses angiogenesis-mediated tumor growth through inhibition of AKT/mammalian target of rapamycin pathway显示文摘 | Xiufeng Pang Zhengfang Yi Jing Zhang | 2010 | Cancer Research2010，70，5： | 1 |
| 8 | Celastrol Suppresses angiogenesis-mediated tumor growth through inhibition of AKT/Mammalian target of rapamycin pathway显示文摘 | Xiufeng Pang Zhengfang Yi Jing Zhang | | 0，，05： | 1 |
| 9 | Evaluation of the relative differences in building energy simulation results显示文摘Building energy modeling,also known as building energy simulation,has developed rapidly in recent years and plays a crucial role in building life-cycle analysis.It can be employed in the design phase to predict the energy consumption of different design schemes and evaluate various control and retrofitting measures at the operation stage.In such simulations,it is commonly understood and accepted that the simulated relative differences are more reliable than the predictions of absolute energy results.However,whether this common understanding is true is yet to be thoroughly investigated.In this study,we investigate the simulated relative differences and the extent to which they are affected by the degree of model input deviation.Simulation and Monte Carlo approaches are adopted for the analysis.The results indicate that the simulated relative differences are not as reliable as expected,and the outputs strongly depend on the degree of the model input deviation.When the degree of deviation is less than 15%or the model inputs are within reasonable ranges,the simulated relative differences match the baseline obtained using Monte Carlo simulations.Moreover,the model’s error indicators meet the requirements of the ASHRAE Guideline 14–2014 when the degree of input deviation is below 15%. | Dan Wang Xiufeng Pang Wei Wang Chuan Wan Gang Wang | 2022 | Building Simulation2022，15，11： | 0 |
| 10 | Targeting metabolic vulnerability in mitochondria conquers MEK inhibitor resistance in KRAS-mutant lung cancer显示文摘MEK is a canonical effector of mutant KRAS;however,MEK inhibitors fail to yield satisfactory clinical outcomes in KRAS-mutant cancers.Here,we identified mitochondrial oxidative phosphorylation(OXPHOS)induction as a profound metabolic alteration to confer KRAS-mutant non-small cell lung cancer(NSCLC)resistance to the clinical MEK inhibitor trametinib.Metabolic flux analysis demonstrated that pyruvate metabolism and fatty acid oxidation were markedly enhanced and coordinately powered the OXPHOS system in resistant cells after trametinib treatment,satisfying their energy demand and protecting them from apoptosis.As molecular events in this process,the pyruvate dehydrogenase complex(PDHc)and carnitine palmitoyl transferase IA(CPTIA),two rate-limiting enzymes that control the metabolic flux of pyruvate and palmitic acid to mitochondrial respiration were activated through phosphorylation and transcriptional regulation.Importantly,the co-administration of trametinib and IACS-010759,a clinical mitochondrial complex I inhibitor that blocks OXPHOS,significantly impeded tumor growth and prolonged mouse survival.Overall,our findings reveal that MEK inhibitor therapy creates a metabolic vulnerability in the mitochondria and further develop an effective combinatorial strategy to circumvent MEK inhibitors resistance in KRAS-driven NSCLC. | Juanjuan Feng Zhengke Lian Xinting Xia Yue Lu Kewen Hu Yunpeng Zhang Yanan Liu Longmiao Hu Kun Yuan Zhenliang Sun Xiufeng Pang | 2023 | Acta Pharmaceutica Sinica B2023，13，3： | 0 |
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