For decades,cancer researchers have focused on genomic and transcriptomic analyses.The completion of the Human Genome Project has opened the 通常 door to the post-genome era and oncoproteomics.Proteins play a critical role in tumorigenesis and influence the differences between normal cells and malignant cells.This report proposes

the concept that cancer is a proteomic disease.This concept is based on examining protein expression profiles,post-translational modifications,and protein-protein interactions in carcinogenesis using recent advances in comparative,functional and structural proteomics.This approach provides a new way of viewing carcinogenesis,presents new clues in biomarker discovery for cancer diagnosis and therapy,and reveals important scientific findings and their significance to clinical applications.
Pancreatic cancer is the fourth most common cause of cancer deaths worldwide. Although recent therapeutic developments for patients with pancreatic cancer have provided survival benefits, the outcomes for patients with pancreatic cancer remain unsatisfactory. Molecularly targeted cancer therapy has advanced in the past decade with the use of a number of pathways as candidates of therapeutic Alisertib体内 targets. This review summarizes

the molecular features of this refractory disease while focusing on the recent clinical and experimental findings on pancreatic cancer. It also discusses the data supporting current standard clinical outcomes, and offers conclusions that may improve the management of pancreatic cancer in the future.
胰腺癌是一种恶性程度极高的消化道肿瘤,虽然经过数十年的研究,其中位生存期仍仅为6个月,5年生存率不足5%[1]。在西方国家,胰腺癌是导致肿瘤病人死亡的第四大原因,且其发病率呈逐年上升趋势,预计未来10年内将成为肿瘤病人死亡的第二大原因[2]。此外,虽然胰腺癌手术切除率有明显提高,围手术期病死率及并发症发生率显著下降,但治疗效果仍无明显改善[3]。因此,需迫切寻求对胰腺癌有
目的观察AKT-GSK-3β信号转导通路对化疗后肝癌细胞凋亡的影响,进一步探讨该通路在肝癌细胞化疗敏感性中的调控作用。方法应用细胞培养与Western

点击此处 blot技术,检测肝癌细胞化疗后凋亡情况并分析其与AKT-GSK-3β信号通路活化的关系,通过特异性阻断信号通路方法,对AKT-GSK-3β通路调节肝癌细胞化疗敏感性进行验证。结果肝癌细胞经奥沙利铂化疗后发生凋亡,表现为BAX蛋白表达增加和Bcl-2蛋白表达减少,同时AKT-GSK-3β通路磷酸化激活。阻断该通路后,化疗后肝癌细胞凋亡明显增加。结论 AKT-GSK-3β信号途径可以下调肝癌细胞化疗敏感性,与其化疗效果有密切联系。
PI3K/AKT途径作为细胞内重要的信号转导通路之一,通过磷酸化多种底物,从而发挥着抗凋亡、促增殖的关键作用。许多恶性肿瘤中存在该通路的持续激活,如白血病、淋巴瘤、肺癌、胃癌、乳腺癌等。本文就PI3K/AKT信号通路在急性早幼粒细胞白血病中的作用作一综述。
磷脂酰肌醇-3-激酶(phosphatidylinositol-3-kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)和哺乳动物雷帕霉素蛋白(mammalian target of rapamycin,m TOR)信号通路对许多生理和病理过程是至关重要的,如细胞增殖、血管生成、新陈代谢、分化和存活,因此,被认为是癌症的主调节器。有研究表明,PI3K信号通路的异常活化与多种实体瘤和血液恶性肿瘤的发生、进展及耐药相关,靶向PI3K途径作为治疗策略成为肿瘤研究的热点。现将PI3K/Akt/m TOR信号通路组成及其功能、PI3K/
恶性肿瘤的发生是一个涉及多因素、多基因的多阶段病理过程.以往的研究主要集中在基因组和转录组分析.随着人类基因组计划的完成,肿瘤研究开始进入”后基因组时代”,肿瘤蛋白质组学应运而生.