EGFR 野生型 ，易和特，用还是不用？

我比较关心的问题，精力有限不全部翻译了。

从结论来看：  试验组结果是作为2线治疗不如化疗的效力。 我觉得中位的无进展生存解释了为什么那么多人吃了几个月说“耐药”的原因，
隐约感觉那些盲吃的人（包括我自己） 都是在摸瞎走。真正有效的应该都在1年以上有效。


EGFR inhibitors for wild-type EGFR NSCLC: to use or not to use?
Jacek Jassem aEmail Address, Rafał Dziadziuszko a
Gefitinib and erlotinib—EGFR tyrosine kinase inhibitors—were the first molecularly targeted drugs used to treat advanced non-small-cell lung cancer (NSCLC). The positive results of BR.21—a phase 3 study comparing erlotinib with placebo in patients with NSCLC in whom first-line or second-line chemotherapy had failed—paved the way for the widespread use of these drugs.1 When BR.21 was started, EGFR mutations in NSCLC had not yet been identified, therefore the study included molecularly unselected patients. The discovery and characterisation of EGFR mutations in 2004 was a key example of oncogene addiction, associated with high efficacy of biomarker-driven treatment.2, 3 As a result, EGFR tyrosine kinase inhibitors are now the treatment of choice for patients with EGFR-mutated tumours (about 10% of all NSCLCs in white populations). Although EGFR tyrosine kinase inhibitors are generally more efficacious than chemotherapy for these patients,4—6 the value of these compounds in second-line and third-line treatment of patients with wild-type or unknown EGFR mutation status is still controversial. Almost all of the data about efficacy for use in these populations are based on retrospective subset analyses of clinical studies comparing EGFR tyrosine kinase inhibitors with chemotherapy or placebo. These studies included genotypically heterogeneous populations of patients, most of whom had unknown EGFR mutation status.
In The Lancet Oncology, Marina Garassino and colleagues7 present results of the TAILOR phase 3 study, comparing erlotinib with docetaxel for treatment of advanced NSCLC in patients with wild-type EGFR tumours for whom first-line platinum-based chemotherapy has failed. The investigators showed the superiority of chemotherapy versus the EGFR tyrosine kinase inhibitor. Median overall survival was 8·2 months (95% CI 5·8—10·9) with chemotherapy versus 5·4 months (4·5—6·8) with erlotinib (adjusted hazard ratio 0·73, 95% CI 0·53—1·00; p=0·05).
We commend the investigators for their effort: the study was independent, well designed, and correctly interpreted. By contrast with the ambiguity of previous subgroup analyses, the message is clear and could change clinical practice: the efficacy of EGFR tyrosine kinase inhibitors is very limited for second-line treatment of wild-type EGFR NSCLC.
The study population of TAILOR included a large proportion of adenocarcinomas (69%) and many participants were non-smokers (22%)—both associated with an increased likelihood of EGFR mutation. However, even in these subgroups, chemotherapy provided greater benefit than erlotinib. Hence, clinical and pathological features cannot be thought of as surrogates of EGFR status when selecting patients for treatment with EGFR tyrosine kinase inhibitors. Instead, in patients whose molecular subtype is unknown, every effort should be made to obtain a tumour sample for EGFR genotyping. If getting a sample is difficult, a potential alternative might be liquid biopsy using circulating lung cancer cells or free tumour DNA in the plasma.8, 9
The TAILOR study was started in 2007, when establishing EGFR status was not routinely done for patients with advanced NSCLC. At present, most potential candidates for treatment with EGFR tyrosine kinase inhibitors undergo EGFR testing as a part of their initial pathology diagnosis. This approach has resulted in a change in the use of erlotinib and gefitinib in patients with EGFR-positive tumours, from second-line or third-line to first-line treatment. Thus, most patients in whom primary chemotherapy fails have EGFR wild-type tumours, and the question addressed in TAILOR is even more relevant.
Do the results mean that chemotherapy remains the only option for patients with wild-type EGFR disease? Not necessarily. Within the past decade, several molecular changes (mutations, gene rearrangements, and amplifications) have been identified that drive NSCLC growth and survival, many of which are promising therapeutic targets. These abnormalities include gene rearrangements in ALK, ROS1, RET, and NTRK1; mutations in HER2 and BRAF; and amplification of MET. Overall, potential therapeutic targets exist for more than 50% of adenocarcinomas and around 33% of squamous-cell carcinomas, and the numbers are continuously increasing.10 Because most mutations in NSCLC are mutually exclusive with other genetic abnormalities, further molecular subtyping of wild-type EGFR tumours might identify additional patients suitable for alternative therapies. The clinical application of biomarker-driven therapeutic strategies will also be helped by the introduction of high-throughput multiplex genotyping, which will enable simultaneous sequencing and measuring copy numbers of hundreds of genes from only nanograms of cancer cell DNA.
Although these advances will probably reduce the proportion of patients who need chemotherapy, it will remain the main treatment option for advanced NSCLC. The TAILOR study will contribute to more rational use of chemotherapy and EGFR tyrosine kinase inhibitors in the treatment of NSCLC, based on its molecular profile.

期待基因检测不准吧，老爸已经用了21天了

有人能翻译下吗，头晕，看不懂...

感觉不管是什么型的都要试一试吧