0%)高于在正常肺组织中的表达水平(阳性率0 0%,P0 05)。结论 Hsp90AB1在NSCLC组织中高表达,并且其表达水平与

0%)高于在正常肺组织中的表达水平(阳性率0.0%,P0.05)。结论 Hsp90AB1在NSCLC组织中高表达,并且其表达水平与肺癌的病理类型及肺腺癌患者总生存期相关。
目的研究人前列腺癌组织中热休克蛋白90(HSP90)、糖蛋白96(gp96)的表达及其临床意义。方法收集我院2010年4月至2014年4月间确诊的前列腺癌组织标本56例(其中新鲜组织16例),同期入院的良性前列腺增生组织标本25例(其中新鲜组织8例)作为对照组。同时收集每例患者完整的临床病理资料。运用实时定量聚合酶链反应(qRT-PCR)和免疫组织化学(IHC)方法分别检测前列腺癌和前列腺增生组织中HSP90、gp96在mRNA和蛋白水平的表达情况及其与患者临床病理资料之间的相关性。结果前列腺癌组织中HSP90、gp96在mRNA水平(P<0.05)及蛋白水平(P<0.01)的表达均明显高于良性前列腺增生组织,且HSP90与gp96表达两者间存在关联性(P<0.01)。结合患者临床病理相关参数分析显示,Gleason评分≥7分的中高危组与7分以下的低危组之间HSP90、gp96的阳性表达率均有显著差异(P<0.05),且gp96的表达还与患者T分期密切相关(P<0.01)。但HSP90、gp96的表达与患者年龄、前列腺体积、血清tPSA值、淋巴结转移均无关。结论前列腺癌组织中HSP90、gp96在mRNA和蛋白水平均明显高表达,对于前列腺癌的发生发展可能起到促进作用,可作为判断前列腺癌恶性程度的指标。
正电子发射计算机断层显像(PET)具有灵敏度高、可定量等优点,是当前发展迅速的分子显像技术。~(89)Zr是一种新型正电子显像核素,半衰期及能量适中,适于大分子生物活性物质的标记及临床应用。本文对~(89)Zr的生产、标记方法以及~(89)Zr标记化合物的研究进展进行综述。
Signaling

VX-770化学结构 pathways of gastric carcinogenesis and gastric cancer progression are being avidly studied to seek optimal treatment of gastric cancer. Among t h e m, h e p a t o c y t e g r o w t h f a c t o r( H G F) / c- M E T, phosphoinositide 3-kinase(PI3K)/Akt/mammalian target of rapamycin(m TOR) and janus kinase

2/signal transducer and activator of transcription 3(JAK2/STAT3) pathways have been widely investigated. Their aberrant expression or mutation has been significantly associated with advanced stage PCI-24781供应商 or poor prognosis of gastric cancer. Recently, aberrations of immune checkpoints including programmed cell death-1/programmed cell death ligand-1(PD-1/PD-L1) have GABA Receptor inhibitor been suggested as an important step in the formation of a microenvironment favorable for gastric cancer. Accomplishments in basic research have led to the development of novel agents targeting these signaling pathways. However, phase Ⅲ studies of selective anti-HGF/c-MET

antibodies and m TOR inhibitor failed to show significant benefits in terms of overall survival and progression-free survival. Few agents directly targeting STAT3 have been developed. However, this target is still critical issue in terms of chemoresistance, and SH2-containing protein tyrosine phosphatase 1 might be a significant link to effectively inhibit STAT3 activity. Inhibition of PD-1/PD-L1 showed durable efficacy in phase Ⅰ studies, and phase Ⅲ evaluation is warranted. Therapeutic strategy to concurrently inhibit multiple tyrosine kinases is a reasonable option, however, lapatinib needs to be further evaluated to identify good responders. Regorafenib has shown promising effectiveness in prolonging progression-free survival in a phase Ⅱ study. In this topic highlight, we review the biologic roles and outcomes of clinical studies targeting these signaling pathways.

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