Project description:Genome-Wide Screening of Genomic Alterations and Transcriptional Modulation in Non-Smoking Female Lung Cancer in Taiwan Sixty-one pairs of cancer and normal lung tissue specimens from non-smoking females were collected at National Taiwan University Hospital and Taichung Veterans General Hospital. The selection criteria of clinical specimens depend on pathology report, physical examination and cigarette-smoking history. Surgical lung tissue specimens were immediately snap-frozen in liquid N2 and stored at -80 °C. Surgical specimens would be further processed for RNA and DNA extraction. Only those samples passed quality controls were processed for gene expression profiling analysis and single nucleotide polymorphism (SNP) analysis respectively.
Project description:Although smoking is the major risk factor for lung cancer, only 7% of female lung cancer patients in Taiwan have a history of cigarette smoking, extremely lower than those in Caucasian females. This report is a comprehensive analysis of the molecular signature of non-smoking female lung cancer in Taiwan.
Project description:Although smoking is the major risk factor for lung cancer, only 7% of female lung cancer patients in Taiwan have a history of cigarette smoking, extremely lower than those in Caucasian females. This report is a comprehensive analysis of the molecular signature of non-smoking female lung cancer in Taiwan. RNA was extracted from paired tumor and normal tissues for gene expression analysis.
Project description:The incidence of non-smoking female patients with non-small cell lung cancer (NSCLC) is increasing in recent decades. However, the pathogenesis of patients is unclear and early diagnosis biomarkers are in urgent need. In this study, 136 non-smoking female subjects (65 patients with NSCLC, 6 patients with benign lung tumors and 65 healthy controls) were enrolled, and their metabolic profiling were investigated using a pseudotargeted gas chromatography-mass spectrometry.
Project description:A chemopreventive effect of aspirin (ASA) on lung cancer risk is supported by epidemiologic and preclinical studies. We conducted a randomized, double-blind, placebo controlled study in current heavy smokers to compare modulating effects of intermittent versus continuous low dose ASA on gene signatures of smoking and lung cancer from nasal brushings. Fifty-four participants were randomized to intermittent ASA (ASA 81 mg daily for one week alternating with placebo daily for one week) or continuous ASA (81 mg daily) for 12 weeks. The primary endpoint was modulation of a smoking gene signature in nasal brushings. Other [JB1] endpoints included modulation of nasal and bronchial gene signatures for smoking, lung cancer and chronic obstructive pulmonary disease (COPD) and changes in cyclooxygenase (COX)- and 5-lipoxygenase (LOX)-mediated arachidonic acid (ARA) metabolism. Low dose ASA intervention caused minimal changes in smoking and lung cancer gene signature scores in nasal epithelium of current heavy smokers. The small sample size of the intervention groups may have limited the ability to detect modulation of the gene signatures. Low dose ASA lowered urinary prostaglandin E metabolite, a marker of COX-mediated ARA metabolic pathway with no change in urinary leukotriene E4, a marker of 5-LOX-mediated pathway. Exploratory genomic analysis showed that ASA intervention induced wide-ranging genomic changes in the nasal epithelium, including modulation of the arachidonic acid pathway and wound healing. A companion study is underway using ASA plus zileuton to test dual suppression of COX- and 5-LOX-mediated pathways on these gene signature scores in current heavy smokers.