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10.1038/bjc.2017.270 http://scihub22266oqcxt.onion/10.1038/bjc.2017.270 C5674098!5674098 !28898237     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28898237 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nintedanib selectively inhibits the activation and tumour-promoting effects of fibroblasts from lung adenocarcinoma patients |pdf=|usr=}}{{28898237 }} gab.com Text Nintedanib selectively inhibits the activation and tumour-promoting effects of fibroblasts from lung adenocarcinoma patients JO: Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28898237 #FOAvip BACKGROUND: Nintedanib is a clinically approved multikinase receptor inhibitor to treat non-small cell lung cancer with adenocarcinoma (ADC) histology in combination with docetaxel, based on the clinical benefits reported on ADC but not on squamous cell carcinoma (SCC), which are the two most common histologic lung cancer subtypes. METHODS: We examined the potential role of tumour-associated fibroblasts (TAFs) in the differential effects of nintedanib in ADC and SCC. Because TAFs are largely quiescent and activated in histologic sections, we focused on the antifibrotic effects of nintedanib on TAFs stimulated with the potent fibroblast activator TGF-?1, which is upregulated in lung cancer. RESULTS: Nintedanib dose-dependently inhibited the TGF-?1-induced expression of a panel of pro-fibrotic activation markers in both ADC-TAFs and control fibroblasts derived from uninvolved lung parenchyma, whereas such inhibition was very modest in SCC-TAFs. Remarkably, nintedanib abrogated the stimulation of growth and invasion in a panel of carcinoma cell lines induced by secreted factors from activated TAFs in ADC but not SCC, thereby supporting that TGF-? signalling and aberrant TAF-carcinoma cross-talk is regulated by different mechanisms in ADC and SCC. CONCLUSIONS: These results reveal that nintedanib is an effective inhibitor of fibrosis and its associated tumour-promoting effects in ADC, and that the poor antifibrotic response of SCC-TAFs to nintedanib may contribute to the differential clinical benefit observed in both subtypes. Our findings also support that preclinical models based on carcinoma-TAF interactions may help defining the mechanisms of the poor antifibrotic response of SCC-TAFs to nintedanib and testing new combined therapies to further expand the therapeutic effects of this drug in solid tumours. Twit Text FOAVip Nintedanib selectively inhibits the activation and tumour-promoting effects of fibroblasts from lung adenocarcinoma patients ????Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28898237 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28898237 #FOAvip English Wikipedia <ref>{{Cite pmid|28898237 }}</ref> Nintedanib selectively inhibits the activation and tumour-promoting effects of fibroblasts from lung adenocarcinoma patients #MMPMID28898237 Gabasa M ; Ikemori R ; Hilberg F ; Reguart N ; Alcaraz J Br J Cancer 2017[Oct]; 117 (8 ): 1128-1138 PMID28898237 show ga BACKGROUND: Nintedanib is a clinically approved multikinase receptor inhibitor to treat non-small cell lung cancer with adenocarcinoma (ADC) histology in combination with docetaxel, based on the clinical benefits reported on ADC but not on squamous cell carcinoma (SCC), which are the two most common histologic lung cancer subtypes. METHODS: We examined the potential role of tumour-associated fibroblasts (TAFs) in the differential effects of nintedanib in ADC and SCC. Because TAFs are largely quiescent and activated in histologic sections, we focused on the antifibrotic effects of nintedanib on TAFs stimulated with the potent fibroblast activator TGF-?1, which is upregulated in lung cancer. RESULTS: Nintedanib dose-dependently inhibited the TGF-?1-induced expression of a panel of pro-fibrotic activation markers in both ADC-TAFs and control fibroblasts derived from uninvolved lung parenchyma, whereas such inhibition was very modest in SCC-TAFs. Remarkably, nintedanib abrogated the stimulation of growth and invasion in a panel of carcinoma cell lines induced by secreted factors from activated TAFs in ADC but not SCC, thereby supporting that TGF-? signalling and aberrant TAF-carcinoma cross-talk is regulated by different mechanisms in ADC and SCC. CONCLUSIONS: These results reveal that nintedanib is an effective inhibitor of fibrosis and its associated tumour-promoting effects in ADC, and that the poor antifibrotic response of SCC-TAFs to nintedanib may contribute to the differential clinical benefit observed in both subtypes. Our findings also support that preclinical models based on carcinoma-TAF interactions may help defining the mechanisms of the poor antifibrotic response of SCC-TAFs to nintedanib and testing new combined therapies to further expand the therapeutic effects of this drug in solid tumours. |Adenocarcinoma of Lung [MESH] |Adenocarcinoma/drug therapy/*pathology [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Antineoplastic Combined Chemotherapy Protocols/therapeutic use [MESH] |Blotting, Western [MESH] |Carcinoma, Squamous Cell/drug therapy/pathology [MESH] |Cell Line [MESH] |Cell Line, Tumor [MESH] |Docetaxel [MESH] |Fibroblasts/*drug effects [MESH] |Fibrosis/*pathology [MESH] |Humans [MESH] |Indoles/administration & dosage/*pharmacology [MESH] |Lung Neoplasms/drug therapy/*pathology [MESH] |Neoplasm Invasiveness [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Taxoids/administration & dosage [MESH]Nintedanib selectively inhibits the activation and tumour-promoting ef(epmc).pdf DeepDyve Pubget Overpricing