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lipid profile levels in adenocarcinoma of the lung

Zoe Hall, Zsuzsanna Ament, Catherine H Wilson, Deborah L Burkhart, Tom Ashmore, Albert Koulman, Trevor Littlewood, Gerard I Evan, Julian L Griffin
MYC-mediated pathogenesis in lung cancer continues to attract interest for new therapeutic strategies. In this study, we describe a transgenic mouse model of KRAS-driven lung adenocarcinoma that affords reversible activation of MYC, used here as a tool for lipidomic profiling of MYC-dependent lung tumors formed in this model. Advanced mass spectrometric imaging and surface analysis techniques were used to characterize the spatial and temporal changes in lipid composition in lung tissue. We found that normal lung tissue was characterized predominantly by saturated phosphatidylcholines and phosphatidylglycerols, which are major lipid components of pulmonary surfactant...
August 15, 2016: Cancer Research
E Louis, P Adriaensens, W Guedens, K Vanhove, K Vandeurzen, K Darquennes, J Vansteenkiste, C Dooms, E de Jonge, M Thomeer, L Mesotten
BACKGROUND: Accumulating evidence has shown that cancer cell metabolism differs from that of normal cells. However, up to now it is not clear whether different cancer types are characterized by a specific metabolite profile. Therefore, this study aims to evaluate whether the plasma metabolic phenotype allows to discriminate between lung and breast cancer. PATIENTS AND METHODS: The proton nuclear magnetic resonance spectrum of plasma is divided into 110 integration regions, representing the metabolic phenotype...
January 2016: Annals of Oncology: Official Journal of the European Society for Medical Oncology
Peter Mazzone, Xiaofeng Wang, Mary Beukeman, Qi Zhang, Meredith Seeley, Robert Mahoney, Tracy Holt, Kirk Pappan
Lung Cancer Posters ISESSION TYPE: Original Investigation PosterPRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PMPURPOSE: Determine if differences exist in the profile of small molecule metabolites in the serum of patients with stage I-III non-small cell lung cancer when compared to matched controls.METHODS: Serum of patients with biopsy confirmed untreated stage I-III non-small cell cancer and at risk controls was collected. 2 controls were selected for each lung cancer patient through propensity matching that included age, gender, smoking history, COPD, DM, and lipids...
October 1, 2014: Chest
Kojiro Yano
Inhibitors of lipid metabolic pathways, particularly drugs targeting the mevalonate pathway, have been suggested to be valuable in enhancing the effectiveness of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) and these compounds may also be effective in patients with inherent or acquired resistance to EGFR-TKIs. The present study examined gene expression profiles in lung adenocarcinoma to characterize the interaction between growth factor signals and lipid metabolic pathways at the transcriptional level...
April 2012: International Journal of Molecular Medicine
Arne Warth, Thomas Muley, Michael Meister, Esther Herpel, Anita Pathil, Hans Hoffmann, Philipp A Schnabel, Christian Bender, Andreas Buness, Peter Schirmacher, Ruprecht Kuner
BACKGROUND: Aquaporins (AQPs) have been recognized to promote tumor progression, invasion, and metastasis and are therefore recognized as promising targets for novel anti-cancer therapies. Potentially relevant AQPs in distinct cancer entities can be determined by a comprehensive expression analysis of the 13 human AQPs. METHODS: We analyzed the presence of all AQP transcripts in 576 different normal lung and non-small cell lung cancer (NSCLC) samples using microarray data and validated our findings by qRT-PCR and immunohistochemistry...
2011: BMC Cancer
H Bartsch, S Petruzzelli, S De Flora, E Hietanen, A M Camus, M Castegnaro, K Alexandrov, M Rojas, R Saracci, C Giuntini
Cigarette smoking is the strongest risk factor for lung cancer, but genetically determined variations in the activities of pulmonary enzyme that metabolize tobacco-derived carcinogens may affect individual risk. To investigate whether these enzymes (e.g., CYP1A-related) can serve as markers for carcinogen-DNA damage, lung tissue specimens were taken during surgery from middle-aged men with either lung cancer or non-neoplastic lung disease. Phase I [aryl hydrocarbon hydroxylase (AHH), ethoxycoumarin O-deethylase (ECOD)] and phase II (epoxide hydrolase, UDP-glucuronosyltransferase, glutathione S-transferase) enzyme activities, glutathione and malondialdehyde contents were determined in lung parenchyma and/or bronchial tissues; some samples were also analyzed for DNA adducts, using 32P-postlabeling...
November 1992: Environmental Health Perspectives
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