Project description:Circular RNAs (circRNAs) play important roles in tumorigenesis, including lung cancer. However, the expression profile and clinical value of circRNAs in lung adenocarcinoma remains unclear. This study aimed to establish the circular RNA expression profile of lung adenocarcinoma tissue and determine its potential diagnostic and prognostic value.
Project description:To determine the circRNA expression profile in lung adenocarcinoma compared with adjacent normal tissues, we used circRNA microArray analysis form Arraystar to examine the expression of circRNAs in lung adenocarcinoma compared with adjacent normal tissues
Project description:The model is based on publication:
Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification
Abstract:
Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.
Project description:microRNA expression profiling of Stage I Lung Adenocarcinoma and non-tumor adjacent tissues. The Nanostring nCounter Human miRNA Expression Assay Kit version 1.6 (Nanostring, Seattle, WA) was used to obtain microRNA profiles of tumor and adjacent non-tumor tissues excised from Stage I Lung Adenocarcinoma patients. Total cellular RNA was extracted from tumor and matching adjacent non-tumor lung using miRNA Kit (QIAGEN), according to the manufacturer’s instructions, and 100 ng were used for hybridization to Nanostring nCounter Human miRNA Expression Assay Kit version 1.6 (Nanostring, Seattle, WA) following processing protocol recommended by the manufacturer.
Project description:Genome wide DNA methylation profiling of tumor samples with lung adenocarcinoma patients. The Illumina HumanMethylation27 BeadChip array was used to obtain DNA methylation profiles across approximately 27,578 CpGs in lung cancer samples. Samples included tumor samples with lung adenocarcinoma.
Project description:This dataset is the mRNA expression for Stage I Lung Adenocarcinoma and non-tumor adjacent tissues also characterized by Genome-wide DNA methylation profiling. Total cellular RNA was extracted from tumor and matching adjacent non-tumor lung and hybridized to Illumina HumanRef-8 v3 Expression Beadchip arrays.
Project description:microRNA expression profiling of Stage I Lung Adenocarcinoma and non-tumor adjacent tissues. The Nanostring nCounter Human miRNA Expression Assay Kit version 1.6 (Nanostring, Seattle, WA) was used to obtain microRNA profiles of tumor and adjacent non-tumor tissues excised from Stage I Lung Adenocarcinoma patients.
Project description:Microarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients. 28 brain metastasis samples: 19 from Marc Ladanyi 9 from William L. Gerald