Project description:We performed RNA-seq using 19 human surgically-resected lung adenocarcinomas to investigate of difference between EGFR-mutated and wild-type lung adenocarcinomas.
Project description:We have examined the both miRNA and mRNA expression profiles in 155 lung adenocarcinoma samples with known EGFR mutation status (52 mutated and 103 wild-type cases). An integrative analysis was performed to identify the unique miRNA-mRNA regulatory network in EGFR-mutated lung adenocarcinoma.
Project description:We have examined the both miRNA and mRNA expression profiles in 155 lung adenocarcinoma samples with known EGFR mutation status (52 mutated and 103 wild-type cases). An integrative analysis was performed to identify the unique miRNA-mRNA regulatory network in EGFR-mutated lung adenocarcinoma.
Project description:Expression profiles of 18,175 unique genes and three major genetic changes, p53, EGFR and K-ras, were investigated in 149 patients with non-small cell lung cancer (NSCLC), including 90 patients with adenocarcinomas (AD) to determine their relationships with various clinicopathologic features and Gene Ontology (GO) terms. Keywords: Disease state analysis Expression profiles in 149 patients with NSCLC, 9 patients with SCLC and 5 for normal lung tissue.
Project description:Purpose: To characterize microRNA signatures for tolerance, persistence and resistance to EGFR tyrosine kinase inhibitors (TKIs) in human lung cancer. Methods: microRNA profiles of gefitinib- and osimertinib-tolerant cells in PC9 and HCC827 cells were generated by deep microRNA sequencing using Illumina. In addition, microRNA profiles of PC9 subpopulations cells with characterizations of persistence and resistance to gefitinib were generated by deep microRNA sequencing. The mappable reads were aligned to the human genome and miRbase using Bowtie. Results: We identified a specific microRNA profile distinguishing tolerance, persistence and resistance to gefitinib or osimertinib from parental human lung cancer cells with mutated EGFR. The expressions of those microRNAs in lung cancer cells were validated by qRT-PCR. Functionally, knocking down top-upregulated microRNAs reduced the tolerance, persistence and resistance to gefitinib or osimertinib in those tolerant and resistant cells. Conversely, overexpression of those microRNAs enhanced the tolerance and resistance to EGFR inhibition in cells sensitive to gefitinib and osimertinib. Conclusions: Our work identifies a panel of microRNAs that mediate EGFR-TKI tolerance and resistance in lung cancer. Our study provides potential non-coding targets to improve the efficacy of EGFR-TKIs therapy in cancer pagtients.
Project description:The lung adenocarcinoma has an increased incidence in smokers. The molecular target therapy has been developed for lung adenocarcinoma patients harboring EGFR gene mutation. However, the treatment options for the patients without mutation are currently limited. Thus, analysis of EGFR gene mutation status at early stage is important strategy to classify patients for effective treatments and improving prognosis. This study aimed to identify microRNA (miRNAs) signature in relation to mutation status in EGFR gene in early stage of lung adenocarcinoma male patients with smoking history. MiRNA profiles were assessed by microarray in paired plasma and tissue pooled from 10 EGFR wild type (EGFR-wt) and 10 EGFR mutated (EGFR-mut) patients.
Project description:The lung adenocarcinoma has an increased incidence in smokers. The molecular target therapy has been developed for lung adenocarcinoma patients harboring EGFR gene mutation. However, the treatment options for the patients without mutation are currently limited. Thus, analysis of EGFR gene mutation status at early stage is important strategy to classify patients for effective treatments and improving prognosis. This study aimed to identify microRNA (miRNAs) signature in relation to mutation status in EGFR gene in early stage of lung adenocarcinoma male patients with smoking history. MiRNA profiles were assessed by microarray in paired plasma and tissue pooled from 10 EGFR wild type (EGFR-wt) and 10 EGFR mutated (EGFR-mut) patients.
Project description:Expression profiles of 18,175 unique genes and three major genetic changes, p53, EGFR and K-ras, were investigated in 149 patients with non-small cell lung cancer (NSCLC), including 90 patients with adenocarcinomas (AD) to determine their relationships with various clinicopathologic features and Gene Ontology (GO) terms. Keywords: Disease state analysis
