现代实用医学2012年3月第24卷第3期
・281・
作者单位：318000浙江省台州，台州市中心医院
通信作者：曹学全，Email:caoxuequan@126
PI3K
p85
在胃癌组织中的表达，探讨其与胃癌发生的关系及其临床意义。方法
采用免疫
组化EnVision 法检测PI3K
p85
蛋白阳性表达率为80%(48/60)，正常胃黏膜组织为10%（2/20），差异有统计学意义(蛋白表达与胃癌临床分期、浸润深度及淋巴结转移有关( 均＞0.05)。结论
PI3K
p85
Modern Practical Medicine,March 2012,Vol.24,No.3
・282・
临床病理特征例数
PI3K
贝芙美
p85
ÖµÐÔ±ðÄÐ3226(81.25)0.067
0.796
女28
22(78.57)
年龄(岁)≥604033(82.50)0.469
0.494
南猴王＜6020
15(75.00)
组织学分级高中分化3526(74.28) 1.714
0.190
低分化25
22(88.00)
TNM 分期Ⅰ及Ⅱ期3120(64.52)9.611
0.002
Ⅲ及Ⅳ期29
28(96.55)
浸润深度浅肌层1812(66.67)7.727
0.021
深肌层2216(72.27)外膜20
20(100.00)
淋巴结转移有2727(100.00)12.273
0.000
无
33
21(63.64)
表1PI3K
p85
基因在
iSH2区域的缺失和变异能导致PI3K 的活化[2]
。据报道，PI3K 、Akt 和NF-ka-ppaB/p65等信号蛋白在非小细胞肺癌、大肠癌和前列腺腺癌中亦存在持续活化以及表达量增高[8-10]。
有关PI3K
p85
在由正常大肠黏膜
组织、腺瘤组织到大肠癌组织的演进过程中其蛋白阳性表达量依次升高，差异有显著统计学意义。本研究结果显示PI3K
p85
与胃癌的恶性转化有关，通
过今后进一步的研究对癌前病变中PI3K p85
蛋白表达与胃癌生物学特性的关系。结果显示PI3K5612号台风
p85
£¼
0.05)，而与患者性别，年龄及病理分型无关(洛仑兹力
均
蛋
白过表达的病例，其肿瘤恶性程度高，更易出现浸润和转移，并且预后较差。与文献[11]报道一致。有研究显示[12]，通过RNA 干扰技术抑制PI3K p85
的干预可能为肿瘤
靶向提供新的靶点。参考文献：
[1]蔗糖浓硫酸
OsakiM,OshimuraM,Ito H.PI3K-Aktpathway:its functions and alterations in human cancer [J ].Apoptosis,2004,9(6):667-676.
[2]
Philp AJ,Campbell IG,Leet C,et al.The phosphatidylinositol3'-kinase p85alpha gene is an oncogene in human ovarian and colon tumors [J ].Cancer Res,2001,61(20):7426-7429.
[3]Carter JH,Douglass LE,Deddens JA,et al.Pak-1expression increases with pro-
gression of colorectal carcinomas to meta-stasis [J ].Clin Cancer Res,2004,10(10):3448-3456.
[4]
Geering B,Cutillas PR,Nock G,et al.Class IA phosphoinositide 3-kinase sar-eobligate p85-p110hetered iners [J ].Proc
Natl Acad Sci USA.2007,104(19):7809-7814.
[5]
Solit DB,Basso AD,Olshen AB,et al.In-hibition of heart shock protein in 90func-tion down-regulates Akt kinase and sensi-tizes tumors to taxol [J ].Cancer Res,2003,
62(9):2139-2144.
[6]
Gershtein ES,Scherbakov AM,Shat-shkaya VA,et al.Phosphatidy linositol3-kinase/AKT signaling pathway compon-ents in human breast cancer:clinicopathol-ogical correlations [J ].Anticancer Res,2007,27(4A ):1777-1782.
[7]
Chang F,Lee JT,Navolanic PM,et al.In-volvement of PI3K/Aktpathway in cell cycle progression,apoptosis,and neoplas-
tictransformation:a target for cancer chemotherapy [J ].Leukemia,2003,17(3):590-603.
[8]
沈阳音乐学院南校区地址Lee SH,Kim HS,Park WS,et al.Non-small cell lung cancers frequently express phosphorylated Akt;an immunohisto-chemical study [J ].APMIS,2002,110(7-8):587-592.
[9]Itoh N,Semba S,Ito M,et al.Phosphoryl-ation of Akt/PKB is required for sup-pression of cancer cell apoptosis and tum-or progre-ssion in human colorectal car-cinoma [J ].Cancer,2002,94(12):3127-3134.[10]Shukla S,Maclennan GT,Marengo SR,et
al.Constitutive activation of PI3K-Akt and NF-kappaB during prostate cancer progression in autochthonous transgenic mouse model [J ].Prostate,2005,64(3):224-239.
[11]Rychahou PG,Jackson LN,Silva SR,et
al.Targeted molecular therapy of the PI3K pathway:therapeutic significance of PI3K subunit targeting in colorectal carcin-oma [J ].AnnSurg,2006,243(6):833-842.[13]Fu Y ,Zhang Q,Kang C,et al.Inhibitory
effects of adenovirus mediated Akt1and PIK3R1shRNA on the growth of malig-nant tumor cells in vitro and in vivo [J ].Cancer Biol Ther,2009,8(11):1002-1009.
收稿日期：2011-11-09（本文编辑：姜晓庆）
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