Effect of AGER on the biological behavior of non ‑small cell lung cancer H1299 cells.

Effect of AGER on the biological behavior of non‑small cell lung cancer H1299 cells. Mol Med Rep. 2020 May 22;: Authors: Wang Q, Zhu W, Xiao G, Ding M, Chang J, Liao H Abstract Advanced glycosylation end-product specific receptor (AGER) is a multi-ligand cell surface receptor abnormally expressed in lung cancer, and is a member of the immunoglobulin superfamily. Therefore, this study aimed to explore the effect of AGER on the biological behavior of non‑small cell lung cancer (NSCLC) H1299 cell line. A microarray‑based gene expression profiling analysis of the GSE27262 dataset from the Gene Expression Omnibus (GEO) database was conducted to identify differentially expressed genes, which were verified using The Cancer Genome Atlas (TCGA) database. The expression of AGER in the normal human lung BEAS‑2B cell line and NSCLC H1299 cell line was examined using reverse transcription‑quantitative PCR. Lentiviral interference and overexpression vectors of AGER were constructed and transfected into H1299 cells using Lipofectamine®. AGER expression and biological properties, including cell viability, apoptosis, migration and invasion abilities, in H1299 cells were investigated using MTT, flow cytometry, wound healing and Transwell assays. AGER was expressed at a low level in NSCLC tissues and H1299 cells (P
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research

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             Basel, 14 July 2020 - Roche (SIX: RO, ROG; OTCQX: RHHBY) and Blueprint Medicines Corporation (NASDAQ:BPMC), today announced the signing of a licensing and collaboration agreement providing exclusive rights to Roche for global co-development and commercialisation outside the United States (US), excluding Greater China*. In the US, Genentech, a member of the Roche Group, will obtain co-commercialisation rights to pralsetinib, Blueprint Medicine ’s investigational, once-daily oral precision therapy for the treatment of people with RET-altered ...
Source: Roche Media News - Category: Pharmaceuticals Source Type: news
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Future Oncology, Ahead of Print.
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Despite the relevant antitumor efficacy of immunotherapy in advanced non-small cell lung cancer (NSCLC), the results in patients whose cancer harbors activating epidermal growth factor receptor (EGFR) mutations are disappointing. The biological mechanisms underlying immune escape and both unresponsiveness and resistance to immunotherapy in EGFR-mutant NSCLC patients have been partially investigated. To this regard, lung cancer immune escape largely involves high amounts of adenosine within the tumor milieu with broad immunosuppressive effects. Indeed, besides immune checkpoint receptors and their ligands, other mechanisms ...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
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Source: Thoracic Cancer - Category: Cancer & Oncology Authors: Tags: CASE REPORT Source Type: research
D ‐dimer increases discontinuously after lung cancer surgery and applying risk‐stratified cutoff values of it makes for better venous thromboembolism (VTE) exclusion. AbstractBackgroundVenous thromboembolism (VTE) occurs at a high rate after lung cancer surgery and can be attributed to various clinical risk factors. Here, we aimed to determine whether early detection of perioperative D ‐dimer and risk‐stratified cutoff values would improve the diagnostic efficacy of VTE.MethodsIn this case ‐control study, D‐dimer results were acquired from 171 non‐small cell lung cancer (NSCLC) patients preoperatively and at ...
Source: Thoracic Cancer - Category: Cancer & Oncology Authors: Tags: ORIGINAL ARTICLE Source Type: research
Datta Epidemiologic studies have shown that vast majority of lung cancers (85–90%) are causally linked to tobacco smoking. Although much information has been gained about the effects of smoking on various signaling pathways, little is known about how deregulation of miRNAs leads to activation of oncogenes and inhibition of tumor suppressor genes in non-small cell lung cancer (NSCLC). Our previous study showed that smoking inhibits TGF-β-induced tumor suppressor functions through downregulation of Smad3 in lung cancer cells. In order to understand the upstream mechanism of downregulation of Smad3 by s...
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Source: Immunological Investigations - Category: Allergy & Immunology Tags: Immunol Invest Source Type: research
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