爸爸去了天国, 终有一天我们会再次相聚

xiwangzairenjia

我也是看grace网站，里面有个真实案例讨论。医生说到，因为阿瓦斯汀要病人自己掏钱，加上疗效不确切，所以不建议加入。好像还提到说只有某些私人医疗保险才包括。可能每个州不同。

如果美国入了医保，估计欧洲也快了。这些大药厂一定不遗余力地推广药物的应用的。

说实在的，这些药这么贵，不如医保，也不一定个个美国病人用得起啊。

大鼻子

多谢Lily请我吃饭。又多了一个去广州的理由。另外，你说的那个医院我可能知道，以前去过。

爸爸的女儿

http://cancergrace.org/forums/index.php?topic=2606.0

It's value is not clear at all, and I don't request it.  Right now, the most we can really say about it is that the mutation, which is seen in about 20% of patients with lung adenocarcinoma and very few patients with squamous NSCLC, is correlated with NOT having an EGFR mutation.  In colon cancer, having this mutation (which is present in about 40-50% of colon cancers) is associated with NOT getting a benefit from the monoclonal antibody against EGFR erbitux (cetuximab), which is more established as a treatment for colon cancer than for lung cancer.  The association of K-RAS mutations with Erbitux in NSCLC has also been looked at, and the results pretty clearly show no association in the larger trials of Erbitux in lung cancer (it doesn't mean anything).  The K-RAS mutations are different between colon and lung cancer tumors, so it's not that surprising that the association isn't there in lung cancer even if it is for colon cancer.

   There are some people who use it for identifying patients who they think shouldn't get an oral EGFR tyrosine kinase inhibitor (like Tarceva, for instance) at all.  To be as frank as I can be, this is simply an erroneous way of thinking, even though some people at major cancer centers perpetuate this misinformation.  The evidence is clear that people with a K-RAS mutation are extremely unlikely to have an EGFR mutation or to have major tumor shrinkage with an oral EGFR inhibitor, but this absolutely does not mean that they get no benefit.  The people with a K-RAS mutation appear to do about the same as other people without an EGFR mutation.  Overall, as a population they show a modest benefit, a quite low probability of major tumor shrinkage, but a very real chance at minor tumor shrinkage or prolonged stable disease, and both of these situations can be associated with a survival benefit. There is no good evidence that the people with a K-RAS mutation get no benefit at all from an oral EGFR inhibitor.

   Because it doesn't appear to add any useful information beyond that of the EGFR mutation testing, I don't see any reason to order it right now.

-Dr. West

爸爸的女儿

第一段讲的是K-RAS突变对结肠癌的意义更大些。

第二段比较重要比较直白地讲K-RAS突变和服用EGFR靶向药的关系, 翻译如下：
有些人用这个（K-RAS突变）来界定病人根本上是否应该服用靶向药（例如特罗凯）。我尽可能直白地说，这是个错误的思考方式，尽管一些在大型癌症研究中心的人让人们记住了这个错误的信息。证据清楚地表明有K-RAS突变的人是极不可能有EGFR突变或者口服EGFR靶向药出现明显的肿瘤缩小，但是这明显地不意味着对他们没有任何好处。K-RAS突变的人和那些没有EGFR突变的人效果一样。总的来说，他们这群人会表现出温和的受益，很少可能肿瘤可以大幅缩小，但是非常有可能肿瘤稍微缩小或者延长了疾病稳定期， 而这两种情况均可被认为是受益的。没有好的证据显示K-RAS 突变的人服用EGFR靶向药完全没有好处。

因为看不到有什么额外有用的信息（EGFR突变测试之外），我不认为有理由要现在采用它（K-RAS测试）。

大鼻子

我想我爸爸也不用测K-RAS。直接试特吧。当然，Dr. West说的也不一定就是真理。我们只能让病人试试。

爱的力量

WEST也比较轻视CEA在肺腺癌病人上的作用，认为几乎不足以参考，除非结合人主观感受不适时进一步拍片。
WEST也不赞成过激治疗，对很多病人甚至建议不进展不治疗。

爸爸的女儿

不过，我觉得WEST讲得有道理是因为SATURN的实验报告里都不提K—RAS突变的病人使用特罗凯做维持治疗会如何，如果有反作用或者完全无效应该会提到的。只是强调EGFR突变和野生型的有效率有较大差异，也提到鳞癌也有一定有效率。
所以，二线治疗就像许多病友已经实践的，试一个月得了，有效就用，没效拉到。

[ 本帖最后由 爸爸的女儿 于 2010-1-31 00:34 编辑 ]

xiwangzairenjia

好像是这样的。