E17K substitution in AKT1 in prostate cancer.
E17K substitution in AKT1 in prostate cancer.
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DOI：
10.1038/sj.bjc.6605673
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发表时间：
2010-05-11
影响因子：
8.8
通讯作者：
中科院分区：
文献类型：
--
作者：
磷脂酰肌醇3-激酶(PI3K)-AKT通路在许多癌症中被激活。AKT1和PI3K调节和催化亚基的突变热点已在多种肿瘤类型中被检测到。在AKT1中，E17K替换导致AKT1的激活不依赖于PI3K。对原发和复发前列腺癌标本进行了AKT1突变分析以及PIK3CA和PIK3R1突变热点分析。我们发现，在前列腺癌中，AKT1(E17K)的患病率为1.4%。这种突变似乎与良好的临床病程有关，但它与特定的肿瘤生长模式无关。在前列腺癌中未发现PIK3CA或PIK3R1的激活突变。AKT1基因的E17K替换在前列腺癌中很少见。它似乎与良好的临床结果有关，但与肿瘤的特定组织学无关。
The phosphatidylinositol 3-kinase (PI3K)–AKT pathway is activated in many cancers. Mutational hotspots in AKT1 and in the regulatory and catalytic subunits of PI3K have been detected in multiple tumour types. In AKT1, the E17K substitution leads to a PI3K-independent activation of AKT1. A mutational profiling of AKT1 and of the mutational hotspots in PIK3CA and PIK3R1 was carried out in samples from primary and recurrent prostate tumours. We show that, in prostate cancer, AKT1(E17K) had a prevalence of 1.4%. The mutation seemed to be associated with a favourable clinical course but it was not associated with a specific tumour growth pattern. Activating mutations in PIK3CA or PIK3R1 were not found in prostate cancer. The E17K substitution in AKT1 is rare in prostate cancer. It seems associated with a favourable clinical outcome but not with a specific histology of the tumour.
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影响因子：
8.8
作者：
Davies, M. A.;Stemke-Hale, K.;Tellez, C.;Calderone, T. L.;Deng, W.;Prieto, V. G.;Lazar, A. J. F.;Gershenwald, J. E.;Mills, G. B.
通讯作者：
Mills, G. B.
影响因子：
8.8
作者：
通讯作者：
--
影响因子：
50.3
作者：
Wang, SY;Gao, J;Wu, H
通讯作者：
Wu, H
影响因子：
--
作者：
Zilberman, Dorit E.;Cohen, Yoram;Rechavi, Gideon
通讯作者：
Rechavi, Gideon
DOI：
10.1126/science.1164382
发表时间：
2008-09-26
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Parsons DW;Jones S;Zhang X;Lin JC;Leary RJ;Angenendt P;Mankoo P;Carter H;Siu IM;Gallia GL;Olivi A;McLendon R;Rasheed BA;Keir S;Nikolskaya T;Nikolsky Y;Busam DA;Tekleab H;Diaz LA Jr;Hartigan J;Smith DR;Strausberg RL;Marie SK;Shinjo SM;Yan H;Riggins GJ;Bigner DD;Karchin R;Papadopoulos N;Parmigiani G;Vogelstein B;Velculescu VE;Kinzler KW
通讯作者：
Kinzler KW