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

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

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.
Carcinoma, Non-Small-Cell Lung* ; Humans

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

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

Summary Lung cancer remains a top cause of new cases and deaths from malignancies globally and locally. The development of targeted therapy for advanced non-small cell lung cancer (NSCLC), particularly adenocarcinoma, promises to improve survival significantly among suitable patients as compared to chemotherapy. About 50% of NSCLC patients have some driver mutations that can be treated by targeted therapy. The most common mutation is that involving EGFR which is found in as much as 90% of patients with driver mutations, most especially in those with adenocarcinoma, in women and never-smokers and those of East Asian ancestry. This is followed by patients with ALK or ROS1 rearrangements in another 5% each. Proper molecular profiling is, however necessary at the outset to identify patients who are suitable for targeted treatment. Fortunately, in the Philippines, testing for EGFR, ALK and ROS1 mutations are possible with several of the tyrosine kinase inhibitor drugs (TKIs) that target these mutations also available. A smaller proportion of patients have BRAF mutations (<5%) but the drug needed to treat this is not available commercially in our country. There are other mutations in advanced NSCLC which are considered potential drug targets for treatment. However, developing a clinically acceptable drug for use in lung cancer has been less successful. KRAS mutations, for example, can be as common as EGFR mutations (and sometimes more so) but no suitable drug for lung cancer has been identified yet. This is also true for METex14, HER2, VEGF, and others that are less common. Clinical studies continue to be done involving these target molecules. These biomarkers have sometimes found usefulness as indicators of poor prognosis and/or likelihood of developing drug resistance but for the most part, have remained in the realm of research. Immunotherapy was not included as a topic in this article. The search continues for new molecules to be used in targeted therapy for lung cancer. Development of drug resistance to TKIs, often inevitable and just a matter of time, continue to drive these development efforts. The remaining approximately 50% of NSCLC with no driver mutations also push efforts to search for appropriate drugs that will be good for them – including immunotherapy. Studies are also being done to look at various combinations of targeted therapy with chemotherapy and even immunotherapy. It will not be an overstatement to say that the future of lung cancer, especially NSCLC is rapidly evolving and will be creating data that may be very different from what we know at present. Clinicians who encounter and/or treat lung cancer should keep abreast of this rapidly changing information in properly advise their patients on suitable therapies. This is particularly true in financially constrained settings such as the Philippines where even just the cost of testing for these mutations can already be a significant barrier to whether or not to use targeted therapy.
Carcinoma, Non-Small-Cell Lung ; Mutation

Many clinical trials of molecular target drugs have been done against advanced lung cancer, however, majority did not meet the primary endpoint. Positive studies of EGFR-TKI such as BR21 and Interest used unselected populations of non-small cell lung cancer. It was quite difficult to explain why they were positive. In the present review, the difficulties of clinical trial design in molecular target drugs were discussed based on the differences of the magnitude of antitumor activity and the target tumor cell population between cytotoxic drugs and molecular target therapy
Carcinoma, Non-Small-Cell Lung ; Lung ; Lung Neoplasms

BACKGROUND: Lung cancer in younger patients seems to be a more aggressive disease and their prognosis may be worse than that of older patients. Abnormal p53 expression in primary lung cancer may be an independent prognostic factor for poor prognosis. This study was conducted to determine the difference of abnormal p53 mutation in patients with primary non-small cell lung cancer (NSCLC) under 45 years of age and 55 years old or greater. METHOD: The present study was performed to compare the clinical and pathological features of primary NSCLC between patients younger than 45 years old and older than 55 years old and to evaluate the difference of abnormal p53 mutation between two groups. Immunohistochemical detection of abnormal p53 mutation was assessed in all primary NSCLC specimens by pathologist. RESULTS: Positive nuclear staining of p53 mutation was found in 76.0% of younger patients and in 76.9% of older patients with variable intensity of staining. And there was no significant coorelation between abnormal p53 mutation according to the disease stage or histologic subtype. CONCLUSION: In this investigation, these were no difference in p53 mutation between two groups.
Carcinoma, Non-Small-Cell Lung ; Humans ; Lung Neoplasms ; Middle Aged ; Prognosis ; Small Cell Lung Carcinoma*