Therefore, gene screening on the basis of other genes may improve its detection rate. No significant difference was found between patients with and without genes mutation in sex and smoking status (p > 0.05), but they as a whole had a significant difference in age (51 versus 61, p = 0.032). The patients with fusion genes are younger than those without mutations, which is in concordance with other reports [11], [18], [29] and [30]. In the absence of EML4-ALK targeted therapy, patients have a similar prognosis whether ALK was fusion positive or not [7], but other data indicate that

the prognosis is controversial [12] and [31]. Here, we observed that patients with fusion genes had a clinical beta-catenin inhibitor benefit in ORR, DCR and median PFS than those without mutations. Although they were not significantly different, which may due to the limitation of the sample numbers, the results showed a positive response in the patients harboring fusion genes. In addition, the new targeted medicines for ALK, ROS1 and RET have been come into the market or in clinical trials. For example, crizotinib was approved by US FDA in 2011 for the treatment of patients with

locally APO866 advanced or metastatic ALK-positive NSCLC and it was available in the market of China since June 2013. Sunitinib, sorafenib and vandetanib could effectively inhibit RET positive lung cancer cells [21]. In this study, we demonstrated that CB samples could be an option to substitute tissues to detect ALK, ROS1 and RET fusion genes in lung cancer patients. Patients with fusion gene mutation may have a better clinical response than those without mutations, which needed to be confirmed by a large sample study. “
“Ovarian cancer is the leading cause of death from gynecological malignancies [1]. Each year, more than 190,000 new cases of ovarian cancer are diagnosed worldwide, which Cytidine deaminase accounts for approximately 4% of all cancers diagnosed in women [2]. Efforts to develop screening

or diagnostic tools for early detection of ovarian cancer have not been successful; therefore, a significant number of patients are diagnosed in advanced stages, requiring cytoreductive and systemic therapies such as palliative surgery and chemotherapy, respectively. However, despite an initial favorable response to chemotherapy [3] and [4], the heterogeneity and genetic instability of ovarian cancer cells [5] often leads to the development of drug resistance [6] and [7], resulting in increased cancer-related mortality. The prognosis of patients with advanced ovarian cancer has not improved over the last few decades [8], and the development of novel therapeutic strategies is therefore of critical importance [9]. Targeting relatively more homogenous and genetically stable host organ microenvironments is a new strategy that was introduced to overcome the drug resistance of tumor cells and produce better therapeutic outcomes [10] and [11].