哦明白了，祝愿你家有效，也给你贴个原来我发的帖子
对了你家bkm120对血象有打击么，能抗感染同时用吗
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有关egfr我也查过，尤其是看易瑞沙能不能用于肾癌，不过临床试验一般结果都不好，比如这个http://www.ncbi.nlm.nih.gov/pubmed/14578682
刚刚看到这个文章http://www.ncbi.nlm.nih.gov/pubmed/19371940 不知道是不是原因
如果这个是真的说不定肺癌那边联合易瑞沙和bkm120，我们也可以试一下。
Activated Akt prevents antitumor activity of gefitinib in renal cancer cells.
Kuroda K1, Horiguchi A, Sumitomo M, Asano T, Ito K, Hayakawa M, Asano T.
Author information
Abstract
OBJECTIVES:
To investigate the mechanism of gefitinib resistance in renal cell carcinoma (RCC) cells. Although epidermal growth factor receptor (EGFR) is frequently overexpressed in RCC, gefitinib, a tyrosine kinase inhibitor of EGFR, has only a limited antitumor effect on RCC.
METHODS:
The effects of gefitinib on the activation status of EGFR and kinases downstream in its signaling cascade were examined in three gefitinib-resistant RCC cell lines: SKRC-44, KU20-01, and 786-O. The changes in signaling cascades and cell survival that were induced by gefitinib in combination with either the phosphatidylinositol 3-kinase inhibitor LY294002 or the knockdown of Akt expression by transient transfection with Akt small interfering RNA were examined in 786-O cells.
RESULTS:
Gefitinib alone did not significantly reduce cell viability in any of the examined cell lines. Although in each line, the phosphorylation of EGFR and extracellular signal-regulated kinase was inhibited by 0.1 muM gefitinib, the phosphorylation of Akt was constitutive and was not inhibited by even 10 muM gefitinib. In 786-O cells, the phosphorylation of both extracellular signal-regulated kinase and Akt was inhibited by gefitinib used in combination with either LY294002 or the knockdown of Akt expression, and the viability of 786-O cells was suppressed significantly by gefitinib used in combination with LY294002 (P < .0001) or Akt small interfering RNA (P = .0044).
CONCLUSIONS:
Constitutively activated Akt might prevent the antitumor efficacy of gefitinib in renal cell carcinoma, and the therapeutic effectiveness of gefitinib might be improved by inhibiting Akt activation. |
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