Project description:Analysis of gene expression profiling in osteotropic Lewis Lung carcinoma cells. The osteotropic lung cancer cell sublines were established throuth in vivo selection. The gene expression profiling of parental and osteotropic sublines was identified through microarray analysis.
Project description:Chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer, suggesting that COPD stroma favors cancer initiation. Therefore, we used proteomics and polysome-profiling to identify gene expression programs that distinguish stroma of patients harboring lung cancer from those that do not, with varied COPD severities. This profiling unveiled distinct COPD-dependent cancer-associated gene expression programs predominantly manifesting as alterations in mRNA translation. Mechanistically, such programs are downstream of the mammalian target of rapamycin pathway in mild COPD and pathological extracellular matrix in more severe COPD; and both programs parallel activation of distinct pro-cancer fibroblast-derived secretomes. Therefore, depending upon COPD severity, the lung stroma can exist in two states favoring cancer initiation, which likely result in distinct disease entities.
Project description:Mechanisms of resistance and sensitivity to the multi-targeted kinase inhibitor dasatinib are unknown. We previously found that lung cancer cells with kinase-inactivating BRAF mutations are sensitive to dasatinib and undergo senescence whereas cells with wild type BRAF are resistant. To better understand mechanisms underlaying the differential sensitivity of lung cancer cells to dasatinib, we performed gene expression profiling of lung cancer cells with (sensitive) and without (resistant) kinase-inactivating BRAF mutations