太好了至少有了新的思路和希望。
可能是用数学模型的方法分析了各种药物联用的作用，但是用什么样的组合最好，一是不能过早的告诉公众，二是没有经过临床验证的过程，所以，需要等待。但是有常识有胆识的病友可以根据此理论自行试验，也许能摸出一片生天呢
东南偏东2013 发表于 2013-11-11 15:38 static/image/common/back.gif
可能是用数学模型的方法分析了各种药物联用的作用，但是用什么样的组合最好，一是不能过早的告诉公众，二是 ...
这个是论文的摘要
Sorafenib/Regorafenib and Phosphatidyl Inositol 3 Kinase/Thymoma Viral Proto-Oncogene Inhibition Interact to Kill Tumor Cells
Mol Pharmacol October 2013 84:562-571; published ahead of print July 22, 2013,
Abstract
The present studies were undertaken to determine whether the multikinase inhibitors sorafenib/regorafenib cooperated with clinically relevant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral proto-oncogene (AKT) inhibitors to kill tumor cells. In liver, colorectal, lung, breast, kidney, and brain cancer cells, at clinically achievable doses, sorafenib/regorafenib and the PI3K inhibitor acetic acid (1S,4E,10R,11R,13S,14R)-phenanthren-11-yl ester (PX-866) cooperated in a greater than additive fashion to kill tumor cells. Cells lacking phosphatase and tensin homolog were as sensitive to the drug combination as cells expressing the protein. Similar data were obtained using the AKT inhibitors perifosine and 8--9-phenyl-1,2,4-triazolo naphthyridin-3(2H)-one hydrochloride (MK2206). PX-866 treatment abolished AKT/glycogen synthase kinase 3 (GSK3) phosphorylation, and cell killing correlated with reduced activity of AKT and mammalian target of rapamycin (mTOR). Expression of activated AKT and to a lesser extent activated mTOR reduced drug combination lethality. Expression of B-cell lymphoma–extra large or dominant negative caspase 9, but not cellular FLICE (FADD-like IL-1b–converting enzyme)-inhibitory protein short, protected cells from the drug combination. Treatment of cells with PX-866 increased protein levels of p62, lysosome-associated membrane protein 2 (LAMP2), and microtubule-associated protein light chain (LC) 3 and LC3II that correlated with a large increase in LC3–green fluorescent protein (GFP) vesicle numbers. Exposure of PX-866 treated cells to sorafenib reduced p62 and LAMP2 levels, decreased the ratio of LC3 to LC3II, and reduced LC3-GFP vesicle levels. Knockdown of Beclin1 or autophagy-related 5 suppressed drug toxicity by ∼40%. In vivo, sorafenib and PX-866 or regorafenib and MK2206 cooperated to suppress the growth of established HuH7 and HCT116 tumors, respectively. Collectively our data demonstrate that the combination of sorafenib family kinase inhibitors with inhibitors of the PI3K/AKT pathway kills tumor cells in vitro and in vivo.
用的是多吉美（索拉菲尼）/瑞格菲尼联合PX-866（PI3K抑制剂）和MK2206（AKT抑制剂）作的体外细胞实验
提到了两种自噬相关的基因：Beclin1和agt5：
Knockdown of Beclin1 or autophagy-related 5 suppressed drug toxicity by ∼40%
敲减Beclin1和atg5抑制了大约40%的药物毒性
这句话不知道怎么理解
即使这理论正确，真能治愈，但自行用现有的药按这理论来联合，将过不了一个瓶颈，就是剂量。假设用多吉美+瑞戈非尼+BKM120+某种药，那么每天的剂量如何设计？各1/4量？那么低的药浓度如何抑制肿瘤靶点？各1/2的量？仍浓度嫌低，且副作用估计也不轻；各3/4的量？这会靠谱，但副作用叠加可能已经很厉害；各足量，想也不敢想……
憨豆精神 发表于 2013-11-12 22:21 static/image/common/back.gif
即使这理论正确，真能治愈，但自行用现有的药按这理论来联合，将过不了一个瓶颈，就是剂量。假设用多吉美+瑞 ...
谢谢憨豆叔！我是想参照肺癌病人联用BKM120的做法。现阶段靠我们自己去试一个联合用药治愈癌症肯定不行，但通过尝试联合用药延长药物的有效期值得考虑。
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