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Lung Cancer Imaging with Fluorescence Endoscopy
Published in Mary-Ann Mycek, Brian W. Pogue, Handbook of Biomedical Fluorescence, 2003
Georges Wagnières, Annette McWilliams, Stephen Lam
The overall 5-year survival rate is around 14% for non-small cell carcinoma and 5% for small cell carcinoma [2]. The only patients who achieve long-term survival are those with resectable early-stage disease. Patients with early stage (stage 0 or IA) non-small cell lung cancer have a 5-year survival rate of 80% [8,9], A number of endobronchial therapies, such as photodynamic therapy, electrocautery, and laser therapy, have been developed in the last two decades that can eradicate small, preinvasive lung cancer in the central airways [10–12]. Unfortunately, the majority of patients present with advanced, inoperable disease (stage III/IV) and do not benefit from these treatments. Thus, there is an urgent need to develop and validate methods that can detect and localize early, preinvasive lung cancer.
Application of constrained coefficient fuzzy linear programming in medical electrical impedance tomography
Published in Applied Mathematics in Science and Engineering, 2022
Mingliang Ding, Xiaotong Li, Shuaibo Zhao
In order to verify the performance of the CCFLP optimization algorithm, we established four typical lung cancer (squamous cell carcinoma, adenocarcinoma, large cell carcinoma, small cell carcinoma) models according to the distribution of different lung cancer cells for simulation study. Among them, most of the adenocarcinomas are located in the periphery of the lung, with consistent cell size. Squamous cell carcinomas often occupy the centre of the lung, which is a central lung cancer with no hierarchy. Small cell carcinomas are located in the centre of the lung, with consistent size, and cytological specimens show syncytial-like cell clusters or single tumour cells arranged in a linear pattern. And large cell carcinomas are often arranged in a palisade pattern.
Carnosic acid exhibits antiproliferative and proapoptotic effects in tumoral NCI-H460 and nontumoral IMR-90 lung cells
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Amanda Cristina Corveloni, Simone Cristine Semprebon, Adrivanio Baranoski, Bruna Isabela Biazi, Thalita Alves Zanetti, Mário Sérgio Mantovani
The cell lines IMR-90 (Non-Tumor Human Fibroblast) and NCI-H460 (Non–Small-Cell Carcinoma of the Human Lung) were obtained from the Cell Bank of Rio de Janeiro. Cells were grown in DMEM (Dulbecco’s Modified Eagle Medium, Gibco®, Cat. No. 11995–081) with pyruvate and L-glutamine (Gibco®, Cat. No. 11995–081) supplemented with 10% fetal bovine serum (FBS) (Gibco®, Cat. No. 11995–081) containing 0.1% antibiotic/antimycotic (Invitrogen, Cat. No. 15240096) and maintained in a humid atmosphere at 37°C containing 5% CO2. The cells were mycoplasma-free and, under these conditions, cell viability remained at 90%.
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Lung cancer is the leading cause of cancer-related death worldwide with 18% of all cancer deaths (IARC 2020). There are four histological types of lung cancer: three non-small cells lung cancer (NSCLC) – adenocarcinoma, squamous cell carcinoma, large cell carcinoma – and one small cell carcinoma (IARC 2020). Type 3 EMT is largely recognized as fundamental to confer an invasive and metastatic phenotype to tumor cells. This specificity relies on the incomplete or partial conversion of epithelial cells into mesenchymal cells, expressing both markers, such that cancerous cells undergo mesenchymal epithelial transition (MET) at the metastatic sites (Brabletz et al. 2018). Cells originating from EMT may acquire a resistance to apoptosis and a circulating tumor cell phenotype (Francart et al. 2018). All these abilities promote cancer progression (Kalluri and Weinberg 2009; Mittal 2016; Nieto et al. 2016; Thiery et al. 2009). EMT involvement in cancer pathways is well-known and TGF-β (SMAD2/3), MAPK, IL-6, Wnt, SHH and Notch are all involved (Kalluri and Weinberg 2009; Mittal 2016; Xiao and He 2010). These pathways target several transcription factors, SNAI and ZEB with particular affinity. These latter exert a direct impact on E-cadherin expression. TWIST, Goosecoid and FOXC2 also display the ability to suppress E-cadherin expression, but indirectly (Manshouri et al. 2019; Xiao and He 2010). The purpose of EMT signaling cascades is to inhibit epithelial markers and induce mesenchymal markers. In that way, many markers were detected and the most often used are a decrease of E-cadherin and ZO-1 and an elevation of vimentin, N-cadherin, fibronectin, αSMA and MMPs expression (Polette et al. 2007, 2004; Xiao and He 2010). MicroRNA, primarily the miR200 family, regulate EMT tumor progression by targeting ZEB1 and ZEB2 and vice versa (Xiao and He 2010; Zhang and Ma 2012). One of the main elements influencing EMT is the tumor microenvironment. Growth factors (EGF, FGF, HGF and TGF-β), degrading ECM enzymes (MMP) and ECM proteins (type 1 collagen) exert a great influence on EMT progression (Jung, Fattet, and Yang 2015; Kalluri and Zeisberg 2006). Tumor-derived exosomes which contain inducers of EMT provide autocrine and paracrine signals of EMT in tumors which are self-sustained (Syn et al. 2016).