Given the complexity and redundancy of the PI3 K signaling network, PI3 K pathway inhibition may be most useful in combination with either chemotherapy or other targeted therapies, such as MEK inhibitors, anti-angiogenic therapy, and hormonal therapy, in appropriately selected OC patients. Here, we discuss the relevance of the PI3 K pathway in OC and provide an up-to-date review of clinical trials of novel PI3 K inhibitors Raf抑制剂 alone or in combination with cytotoxics and novel therapies in OC. In addition, the challenges of drug resistance and predictive

biomarkers are addressed.
目的:研究隐丹参酮对Akt活性的影响及其在抑制HepG2细胞生长中的作用。方法:Western印迹检测隐丹参酮对Akt磷酸化的影响;CCK-8法检测隐丹参酮与MK2206或PP242联合用药对HepG2的生长抑制作用。结果:Western印迹证明隐丹参酮处理能够增强HepG2细胞Akt的磷酸化,同时发现隐丹参酮对Akt的增强作用依赖于mTORC2的活性;通过MK2206或PP242抑制Akt的反馈激活,能够明显促进隐丹参酮对HepG2细胞的生长抑制作用。结论:通过抑制Akt的反馈激活能够增强隐丹参酮的抗肿瘤作用,为隐丹参酮肿瘤治疗的临床应用联合用药提供了理论基础。
Head and neck squamous cell carcinoma is the sixth most common cancer in the world with approximately650000 new cases diagnosed annually.Next-generation molecular techniques and results from phase 2 of the Cancer

Genome Atlas becoming available have PFTα溶解度 drastically improved our current knowledge on the genetics basis of head and neck squamous cell carcinoma.New insights and new perspectives on the mutational landscape implicated in head and neck squamous cell carcinoma provide improved tools for prognostication.More importantly,depend on the patient’s tumor subtypes and prognosis,deescalated or more aggressive therapy maybe chosen to achieve greater potency while minimizing the toxicity of therapy.This paper aims to review our current

knowledge on the genetic mutations and altered molecular pathways in head and neck squamous cell carcinoma.Some of the most common mutations in head and neck squamous cell carcinoma reported by the cancer genome atlas including TP53,NOTCH1,Rb,CDKN2 A,Ras,PIK3 CA and EGFR are described here.Additionally,the emerging role of epigenetics and the role of human papilloma virus in head and neck squamous cell carcinoma are also discussed RAD001 in this review.The molecular pathways,clinical applications,actionable molecular targets and potential therapeutic strategies are highlighted and discussed in details.
目的:观察爱罗咳喘宁对慢性阻塞性肺疾病(chronic obstructive pulmonarydisease,COPD)大鼠模型支气管和肺组织中p38丝裂原活化蛋白激酶(p38mitogen activatein kinase,p38MAPK)、肿瘤坏死因子-α(tumor necrosis factor alpha,TNF-α)、及水通道蛋白5(aquaporin 5,AQP5)基因表达的影响,探讨爱罗咳喘宁方对COPD炎症及气道高分泌的作用及机制。方法:采用脂多糖(lipopolysaccharide,LPS)加烟雾诱导COPD大鼠模型,随机将大鼠分为正常组、模型组、爱罗咳喘宁低、中、高剂量组。正常组、模型组灌胃生理盐水(15.52 m L·kg-1·d-1),爱罗咳喘宁口服液低、中、高剂量组分别灌胃(7.75,15.52,31.