The 2nd European Lung Cancer Congress was held in Geneva, Switzerland on April 28, 2010, and presented many highlights against the backdrop of the ever-deepening and concrete concept of individualized cancer treatment. The short-term goal of turning lung cancer into a “chronic disease” will gradually become a reality, as lung cancer treatments become more abundant and effective, and the survival time of lung cancer has been significantly improved. In this paper, we will summarize the conference participants. The importance of detecting EGFR mutations to improve the efficacy of EGFR-TKI drugs (gefitinib and erlotinib) has been confirmed by several studies represented by IPASS. Gene mutation testing has moved from the laboratory to clinical practice and is progressing towards the goal of achieving individualized therapy. In his keynote speech, Prof. P, A, Bunn pointed out the challenges we are currently facing: known mutation types are only expressed in a small number of patients and these patients will eventually develop acquired resistance, and there is no effective treatment for patients with K-ras mutations, so finding new targets for Therefore, it is important to find new targets for treatment and develop new drugs. The incidence of EML4/ALK fusion gene, a newly discovered oncogene, is about 4% in non-small cell lung cancer patients with ALK gene rearrangement forming a fusion gene with EML4, mostly in the non-smoking young population. A phase III trial of PF-02341066 for second-line treatment of patients with ALK mutations is already underway, and the future of ALK-TKI drugs is promising. Patients with resistance to EGFR-TKI drugs have been shown to be associated with secondary mutations in EGFR (T790M). For this new target, irreversible TKI drugs are entering phase III clinical studies, and inhibitors specific for the T790M mutation will also receive attention. In addition, many downstream signaling proteins activated by oncogenes such as MAPK, AKT, mTOR, etc. will also become new therapeutic targets, while inhibitors of functional building blocks of tumor cell mitosis such as Aurora B and PLK-1 have also completed in vitro trials and entered phase I clinical studies. Inhibitors of MMP, FAK and SFK are also available to target the invasion of tumor cells into surrounding normal tissues, and inhibitors of these factors are entering clinical trials. The status of targeted therapy in the first line of advanced non-small cell lung cancer has been widely recognized. the ECOG-4599 study and the AVAiL study are randomized clinical trials of Avastin (recombinant human anti-vascular endothelial growth factor monoclonal antibody) in combination with chemotherapy. The FLEX study demonstrated that the addition of cetuximab to chemotherapy also significantly prolonged survival. The IPASS study in Asian patients demonstrated that non-smoking or lightly smoking Asian patients with advanced lung adenocarcinoma treated with gefitinib monotherapy had superior progression-free survival, objective effectiveness rate (ORR) and quality of life compared to paclitaxel/carboplatin chemotherapy, and overall survival was similar between the two groups. However, Professor Scagliotti from Italy said “no” to the first-line application of targeted therapy in this meeting. He suggested that the two large studies of chemotherapy in combination with Avastin were flawed, with ECOG-4599 achieving a significant difference in survival but with 15 treatment-related deaths that called into question the safety of Avastin. convincing. Although the FLEX study achieved a significant advantage of 1 or 2 months of OS extension, the PFS of the two groups was equal, which is not a satisfactory result at a high cost. For the study of first-line application of EGFR-TKI, Prof. Scagliotti, on the other hand, pointed out that the benefit population of EGFR-TKI drugs is mostly female, non-smoking, adenocarcinoma and Asian population, while there is no significant difference between first- or second-line treatment with erlotinib even for patients with detectable EGFR gene mutation. It is clear that the combination of vascular targeting agents with chemotherapy requires rigorous patient screening, and patients in the bleeding-risk population must be excluded in order to improve efficacy while ensuring safety. A detailed analysis of the IPASS study results showed that the advantage of PFS in both groups changed over time. In the early stage of treatment, the chemotherapy group had a better PFS than the gefitinib group, while the gefitinib group showed a PFS advantage in the later stage. A stratified analysis of the IPASS study showed that patients with EGFR mutations treated with gefitinib had a significantly better PFS than chemotherapy, whereas patients with wild-type EGFR had an increased risk of disease progression with gefitinib. The efficiency of gefitinib treatment was 71.2% in EGFR mutation-positive patients and 1.1% in EGFR wild-type patients, while the efficiency of paclitaxel/carboplatin chemotherapy was 47.3% in EGFR mutation-positive patients and 23.5% in wild-type patients. Thus, the key to the selection of first-line targeted drugs is how to screen for EGFR mutations more accurately, conveniently and effectively, which is the basic guarantee of clinical benefit of first-line EGFR-TKI therapy. Blind use of targeted drugs in patients with unknown EGFR mutation status will increase the risk of disease progression in EGFR wild-type patients. 3. Predictive value of biomarkers – molecular staging is seen The greatest significance of individualized therapy is that it can significantly improve remission rates and disease control and reduce unnecessary overtreatment and harmful treatment. To achieve this goal, a molecular staging and target staging system for lung cancer should be established in addition to our routinely applied clinicopathological staging, and individualized treatment plans should be designed along these lines for each patient’s characteristics. Reviewing this conference, it is easy to see that biological markers have become essential elements to guide clinical individualized treatment of lung cancer from targets of clinical translational research, and are developing towards more refined and clinical functions. Biological markers are often closely related to disease regression and overall survival time, and these markers are also predictive markers of clinical efficacy of drugs, such as EGFR mutations, K-ras mutations, BRCA1-RNA, microRNAs, etc. are currently known. In his presentation, Prof. Mack from USA proposed the use of serum proteomics to detect genetic mutations in lung cancer patients and to guide individualized treatment. The results of serum proteomics in the BR and 21 studies by Carbone et al. were a highlight of the conference. The BR and 21 studies confirmed the status of erlotinib as a second-line treatment for advanced NSCLC, and the use of serum proteomics to measure EGFR and KRAS mutations in patients confirmed that patients with EGFR mutations had better outcomes with erlotinib. Taron from Spain reported that BRCA1RNA is not only a prognostic marker but also a predictive marker, and that patients with high BRCA1 expression are sensitive to anti-microtubule drugs but not to platinum, whereas the opposite is true for patients with low expression. Based on this finding, Taron et al. conducted a preliminary study in which BRCA1 RNA levels were measured in patients preparing for postoperative adjuvant chemotherapy and divided into a low-expression group receiving GP regimen chemotherapy, a medium-expression group receiving DP regimen chemotherapy, and a high-expression group receiving D monotherapy, showing that patients had DFS and OS of 22 and 43 months, respectively, with no significant differences between the three groups. This led to the conclusion that the selection of chemotherapy regimens based on BRCA1 RNA levels is feasible. The relationship between CXCR4 overexpression and prognosis of metastatic NSCLC was reported by Otsuka et al. from Canada and also received high attention in this meeting. high CXCR4 expression was shown to be associated with tumor cell migration, invasion and adhesion in in vitro experiments. By screening the tissue specimens of 832 patients that met the criteria for immunohistochemical detection, CXCR4 high expression was found in 10,7%, and the median survival was only 2,7 months significantly lower than that of 6,1 months in the control group. The study also suggested that this index was associated with squamous carcinoma, smoking patients and brain metastasis, which is an indicator of poor prognosis.