No abstract available.
Small Cell Lung Carcinoma*

No abstract available.
Small Cell Lung Carcinoma*

No abstract available.
Small Cell Lung Carcinoma*

No abstract available.
Carcinoma, Non-Small-Cell Lung*

No abstract available.
Carcinoma, Non-Small-Cell Lung*

No abstract available.
Carcinoma, Squamous Cell* ; Lung Neoplasms* ; Lung* ; Small Cell Lung Carcinoma*

Introduction: Specific mutations in the epidermal growth factor receptor (EGFR) characterize a subgroup of nonsmall cell lung cancer (NSCLC) patients that may be highly responsive to receptor inhibitor therapy. 18F-FDG PET/CT scans can map the glucose metabolism and treatment response of NSCLC. Therefore, we aimed to assess the pattern of metabolic response and outcome of inoperable NSCLC treated with epidermal growth factor receptor (EGFR) inhibitors, using 18F-FDG PET/CT scan. Methods: A retrospective study of inoperable NSCLC patients on EGFR inhibitor treatment that were referred for wholebody18F-FDG PET/CT scans was conducted based on cases scanned from January 2011 to June 2014. Comparison was made among serial attenuation-corrected fused PET/CT images for all study patients throughout the course of their treatment. Comparison based on PERCIST criteria was categorized into 4 levels ie. complete response (CMR), partial response (PMR), stable disease (SMD), progressive metabolic disease (PMD). Results: Overall, there were 5 patients identified, mean age: 57.4 years old +/- 2.9 years; The median survival time from initiation of EGFR inhibitor treatment to death was 17 months. Two patients showed initial partial metabolic response (PMR), two had progressive metabolic disease (PMD) and one had complete metabolic response (CMR) after the initiation of treatment. The patient with initial CMR had relapse and PMD 5 months later. Majority of patients eventually succumbed to their illness. Conclusions: Wholebody18F-FDG PET/CT is able to assess metabolic treatment response of NSCLC towards EGFR inhibitor treatment.
Lung Neoplasms ; Carcinoma, Non-Small-Cell Lung

Background and Objectives: Cell lines serve as invaluable tools in studying lung cancer biology and developing new therapies to combat the disease. However, commercially available cell lines are typically of Caucasian origin and may be less representative of the local genetic background. To address this, our lab previously immortalized cells from pleural fluid of a Filipino non-small cell lung cancer (NSCLC) patient via CDK4 transduction. Copy number variations (CNVs) are a type of genetic variation which may affect physiology and disease by disrupting gene function or altering gene expression, and in cancer, these may be associated with patient outcomes. CNV profiling can be valuable for understanding the biology of our immortalized cells and identifying genes that could serve as potential targets for diagnostic, prognostic, and therapeutic interventions. This study aimed to characterize previously immortalized NSCLC-derived cells, GL01, in comparison with an established lung adenocarcinoma (LUAD) cell line, A549, through whole-genome microarray-based copy number profiling. Methods: DNA was extracted from GL01 and A549 cells using a commercially-available silica-based DNA extraction kit. DNA extracts were quantified and normalized for microarray analysis. Whole-genome copy number profiling was done using the OncoScan CNV Plus Assay following the manufacturer’s protocols, and data was analyzed using the Chromosome Analysis Suite software. Functional analysis of genes identified to be involved in copy number aberrations was done using the PANTHER Classification System. Results: Copy number aberrations span 1,592,737,105 bp in GL01 and 1,715,708,552 bp in A549, with a high degree of concordance between the two. Largescale and focal copy number aberrations previously identified to be recurrent in various LUAD cohorts were present in both GL01 and A549. Focal copy number aberrations associated with previously described lung cancer-related genes involve the PDE4D gene in GL01 and the SKIL and CDKN2A/CDKN2B genes in both GL01 and A549. PANTHER Pathway analysis of genes positively correlated with mRNA expression showed that the ubiquitin proteasome pathway was significantly overrepresented in both GL01 (FDR p = 0.000074) and A549 (FDR p = 0.000075), with 20 genes involved. Additionally, the KRAS:p.G12C/S:c.34G>T/A somatic mutation variant was detected in both GL01 and A549. Conclusion This study provides a method for identifying potentially clinically-relevant genes associated with a sample’s copy number aberrations and the pathways they represent, providing personalized mechanistic, prognostic, and therapeutic insights into the cancer biology of our cells.
carcinoma, non-small cell lung ; adenocarcinoma of lung

No abstract available.
Drug Therapy, Combination* ; Small Cell Lung Carcinoma*

No abstract available.
Camptothecin ; Recurrence ; Small Cell Lung Carcinoma