Plasma MiRNA Alterations Between NSCLC Patients Harboring Del19 And L858R EGFR Mutations

Lung cancer is the leading cause of cancer related death worldwide.Non-small-cell lung cancer(NSCLC)which consists of heterogeneous classes of tumors represents approximately 85%of all new lung cancer diagnoses.Smoking remains important while air pollution becomes more and more severe.Most patients are diagnosed with advanced-stage for inadequate prevention awareness and unclear symptoms and so on.Although the best way to cure lung cancer is surgery,few patients could really benefit from it due to reason listed above.Classical chemotherapy offers limited benefit while suffering complex adverse effects.Based on recognition of driver mutations,treatment paradigm for NSCLC patients has been shifted.Accurate staging of the cancer is required to determine the optimal management strategy,which includes surgery,radiochemotherapy,immunotherapy and targeted approaches with anti-angiogenic monoclonal antibodies or tyrosine kinase inhibitors if tumours harbour oncogene mutations.Several of these driver mutations have been identified(for example,in epidermal growth factor receptor(EGFR)and anaplastic lymphoma kinase(ALK),and therapy continues to advance to tackle acquired resistance problems.Patients could get clearly better benefit with less adverse effects.However,recently exon 19 deletion mutation(Del 19)of epidermal growth factor receptor(EGFR)clearly shows better clinical benefit over single-point substitution mutation L858R in exon 21(L858R).The aim of this study was to investigate the difference by analyzing the expression of plasma microRNAs of NSCLC patients with EGFR mutation Del19 or L858R.MiRNA microarray of plasma from patients' blood identified 79 mapped,network-eligible miRNAs(fold>5),of which 76 were up regulated and 3 were down.Among analysis,MYC,Argonaute2(AG02),Y-box binding protein 1(YBX1),cyclin E1(CCNE1)were involved in organismal abnormalities and cancer.Our findings provide information on the epigenetic signature of the two major sensitive mutations among NSCLC and add to the understanding of mechanisms underlying the different outcomes.