A variety of cytotoxic agents,either alone or in combination,have been evaluated,although primarily in the context of small single-arm or retrospective studies.Most regimens have been associated with median progression-free survival rates in the range of 2-4 mo and overall survival rates between 4-8mo,highlighting the very poor prognosis of patients who are candidates

for such treatment.Targeted therapies studied in this chemotherapy-refractory setting,meanwhile,have produced even worse efficacy results.In the current article,we review the clinical evidence for treatment of refractory disease,primarily Romidepsin分子量 in patients who have progressed on front-line gemcitabine-based chemotherapy.In the process,we highlight the limitations of the available data to date as well as some of the challenges in designing appropriate 很少 clinical trials in this salvage setting,including how to select an appropriate control arm given the absence of a wellestablished reference standard,and the importance of incorporating predictive biomarkers and quality of life measures whenever possible into study design.
磷脂肌醇3-激酶(phosphoinositide-3

kinase,PI3K)-蛋白激酶B(protein kinase B,PKB,又称AKT)-雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号通路不仅与细胞的增殖、存活及迁移密切相关,其与肿瘤的发生和发展也具有相关性。近年来,以该通路作为抗肿瘤治疗的靶点已成为研究的热点。本文就胃癌中PI3K/AKT/mTOR信号通路的调节、相关蛋白的表达情况以及针对该通路的靶向药物治疗的研究作综述,并就今后胃癌中该通路可能的研究方向作展望。
SEMA3B是近年发现的一种抑癌基因。早期研究中人类SEMA3B蛋白最多的是其在神经系统中表达,在神经系统的发育及轴突引导作用中特征性变化而被发现。近期研究认为SEMA3B涉及多种生物学途径,与NRP1和NRP2受体结合使VEGF作用下调,从而抑制肿瘤的血管形成;还可通过介导p53或上调IGFBP-6而抑制抗细胞凋亡通路。目前,SEMA3B基因在肿瘤发生发展中的作用机制研究尚不明确,需要进一步深入研究。
Gastric

cancer(GC)is one of the most common malignancies and remains the second leading cause of cancer-related death worldwide.There is an increasing understanding of the roles that genetic and epigenetic alterations play in GCs.Recent studies using nextgeneration sequencing(NGS)have revealed a number of potential 所以 cancer-driving genes in GC.Whole-exome sequencing of GC has identified recurrent somatic mutations in the chromatin remodeling gene ARID1A and alterations in the cell adhesion gene FAT4,a member of the cadherin gene family.Mutations in chromatin remodeling genes(ARID1A,MLL3 and MLL)have been found in 47%of GCs.Whole-genome sequencing and whole-transcriptome sequencing analyses have also discovered novel alterations in GC.