PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10854139-5 2000 Gemcitabine and to a lesser extent irinotecan inhibited the secretion of the proinflammatory cytokine IL-6 at concentrations of each drug that produced only small decreases in cell viability. gemcitabine 0-11 interleukin 6 Homo sapiens 102-106 10854139-7 2000 Higher doses of gemcitabine and irinotecan caused a surge in IL-6 release and this was not due to release of intracellular stores of IL-6 through lysis of the cells. gemcitabine 16-27 interleukin 6 Homo sapiens 61-65 10854139-8 2000 CONCLUSIONS: These results suggest that irinotecan and gemcitabine are not only more likely to be active against mesothelioma than other new chemotherapy agents but may also produce a palliative effect in nonresponders to these agents by decreasing the secretion of IL-6. gemcitabine 55-66 interleukin 6 Homo sapiens 266-270 34771621-4 2021 In this study, we show that gemcitabine stimulates the expression of pro-inflammatory cytokines, such as IL6 and IL8, under the influence of the CD95/CD95L system and the pharmacological inhibitor, sCD95Fc, substantially reduced the expression in two PDAC cell lines, PancTuI-luc and A818-4. gemcitabine 28-39 interleukin 6 Homo sapiens 105-108 34259987-0 2021 Activation of autophagy reverses gemcitabine-induced immune inhibition of RAW264.7 macrophages by promoting TNF-alpha, IL-6 and MHC-II expression. gemcitabine 33-44 interleukin 6 Homo sapiens 119-123 34259987-10 2021 GEM reduced immune effect of M1-type RAW264.7 macrophages via inhibiting TNF-alpha, IL-6 and MHC-II expression. gemcitabine 0-3 interleukin 6 Homo sapiens 84-88 31853779-1 2020 BACKGROUND/AIM: We previously demonstrated that inflammatory cytokine interleukin-6 (IL-6) was produced during cancer progression, worked together with transforming growth factor-beta 1 (TGF-beta1), and induced the epithelial-mesenchymal transition (EMT) with chemo-resistance against gemcitabine (GR) at the invasion front of biliary tract cancers (BTCs). gemcitabine 285-296 interleukin 6 Homo sapiens 70-83 31853779-1 2020 BACKGROUND/AIM: We previously demonstrated that inflammatory cytokine interleukin-6 (IL-6) was produced during cancer progression, worked together with transforming growth factor-beta 1 (TGF-beta1), and induced the epithelial-mesenchymal transition (EMT) with chemo-resistance against gemcitabine (GR) at the invasion front of biliary tract cancers (BTCs). gemcitabine 285-296 interleukin 6 Homo sapiens 85-89 29693005-0 2018 Suppression of IL-6 Gene by shRNA Augments Gemcitabine Chemosensitization in Pancreatic Adenocarcinoma Cells. gemcitabine 43-54 interleukin 6 Homo sapiens 15-19 29693005-4 2018 Herein, we investigated whether suppression of IL-6 could augment gemcitabine sensitivity in the PANC-1 cells. gemcitabine 66-77 interleukin 6 Homo sapiens 47-51 29693005-7 2018 In addition, suppression of IL-6 remarkably promoted antitumor effect of gemcitabine, indicating that the combination of shRNA targeting IL-6 with gemcitabine may provide a potential clinical approach for pancreatic cancer therapy. gemcitabine 73-84 interleukin 6 Homo sapiens 28-32 29693005-7 2018 In addition, suppression of IL-6 remarkably promoted antitumor effect of gemcitabine, indicating that the combination of shRNA targeting IL-6 with gemcitabine may provide a potential clinical approach for pancreatic cancer therapy. gemcitabine 73-84 interleukin 6 Homo sapiens 137-141 29693005-7 2018 In addition, suppression of IL-6 remarkably promoted antitumor effect of gemcitabine, indicating that the combination of shRNA targeting IL-6 with gemcitabine may provide a potential clinical approach for pancreatic cancer therapy. gemcitabine 147-158 interleukin 6 Homo sapiens 28-32 28007550-9 2017 Transient changes in urothelial ATP and PGE2 release were observed, with significant increase in release of interleukin-6, interleukin-8 and interleukin-1beta from urothelial cells treated with gemcitabine. gemcitabine 194-205 interleukin 6 Homo sapiens 108-121 27655706-9 2016 Blood levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-1beta increased in gemcitabine alone group, however, it was decreased in gemcitabine with GV1001 group. gemcitabine 96-107 interleukin 6 Homo sapiens 51-69 27687804-9 2016 In vitro, monocytes responding to IL-6 by STAT3 phosphorylation were prevented to respond in gemcitabine medium. gemcitabine 93-104 interleukin 6 Homo sapiens 34-38 25609203-7 2015 rhSDF-1alpha protected Panc-1 cells from GEM-induced apoptosis, and the protective effect was significantly reduced by blocking IL-6 using a neutralizing antibody. gemcitabine 41-44 interleukin 6 Homo sapiens 128-132 24953430-11 2014 In vitro, the induction of STAT3 phosphorylation by recombinant human IL-6 promoted pancreatic ductal adenocarcinoma cell survival during gemcitabine treatment. gemcitabine 138-149 interleukin 6 Homo sapiens 70-74 24953430-13 2014 In particular, the inflammation biomarkers C-reactive protein, IL-6, and IL-1alpha could indicate the prognostic benefit of gemcitabine chemotherapy and should now be tested in prospective patient-controlled trials. gemcitabine 124-135 interleukin 6 Homo sapiens 63-67 23591198-0 2013 Serum levels of IL-6 and IL-1beta can predict the efficacy of gemcitabine in patients with advanced pancreatic cancer. gemcitabine 62-73 interleukin 6 Homo sapiens 16-20 23298711-8 2013 Smad4 functioned in this process in a dominant manner, and inhibition by SMAD4 siRNA reduced IL-6 and TGF-beta1 expression, blocked invasion, and reversed EMT and chemoresistance in cells exposed to rh IL-6 and TGF-beta1 and in gemcitabine-resistant cells. gemcitabine 228-239 interleukin 6 Homo sapiens 202-206 22420547-7 2012 A decrease in Il-6 level after application of Cisplatin and Methotrexate and a 5-10 fold increase in the level of Il-6 after application of Etoposide, Carboplatin, Cytarabine, and Gemcitabine were registered in the medium with ganglioneuroblastoma. gemcitabine 180-191 interleukin 6 Homo sapiens 114-118 21408027-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: In the current study we showed, for the first time, that CDF could significantly inhibit the sphere-forming ability (pancreatospheres) of PC cells consistent with increased disintegration of pancreatospheres, which was associated with attenuation of CSC markers (CD44 and EpCAM), especially in gemcitabine-resistant (MIAPaCa-2) PC cells containing high proportion of CSCs consistent with increased miR-21 and decreased miR-200. gemcitabine 326-337 interleukin 6 Homo sapiens 89-92 18430611-3 2008 The growth-inhibitory activity of gemcitabine-loaded liposomes compared to the free drug was assayed in vitro on U266 (autocrine, interleukin-6-independent) and INA-6 (IL-6-dependent) multiple myeloma cell lines. gemcitabine 34-45 interleukin 6 Homo sapiens 130-143 18430611-3 2008 The growth-inhibitory activity of gemcitabine-loaded liposomes compared to the free drug was assayed in vitro on U266 (autocrine, interleukin-6-independent) and INA-6 (IL-6-dependent) multiple myeloma cell lines. gemcitabine 34-45 interleukin 6 Homo sapiens 168-172 12479703-9 2002 The addition of interleukin 6 to MM1.S cells treated with gemcitabine offered no protection against gemcitabine-induced cell death. gemcitabine 58-69 interleukin 6 Homo sapiens 16-29