PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22082529-1 2012 Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT. AZD 6244 79-86 epidermal growth factor receptor Homo sapiens 139-143 22082529-3 2012 We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells. AZD 6244 29-36 epidermal growth factor receptor Homo sapiens 130-134 22082529-3 2012 We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells. AZD 6244 29-36 epidermal growth factor receptor Homo sapiens 182-186 22082529-3 2012 We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells. AZD 6244 139-146 epidermal growth factor receptor Homo sapiens 130-134 22082529-5 2012 Treatment with a combination of EGFR inhibitor and AZD6244 inhibited cell proliferation synergistically without activation of AKT in AZD6244-resistant cells. AZD 6244 133-140 epidermal growth factor receptor Homo sapiens 32-36 21118963-0 2011 MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy. AZD 6244 31-38 epidermal growth factor receptor Homo sapiens 122-126 21118963-3 2011 In this study, we investigated the ability of two MEK inhibitors currently in clinical trials, AS703026 and AZD6244, to address the challenge posed by the resistance of K-ras mutated colorectal cancers to EGFR mAb. AZD 6244 108-115 epidermal growth factor receptor Homo sapiens 205-209 33099927-6 2020 Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma. AZD 6244 85-96 epidermal growth factor receptor Homo sapiens 34-38 20103661-17 2010 CONCLUSIONS: AZD6244-associated skin reactions partly overlap with those observed upon epidermal growth factor receptor inhibition. AZD 6244 13-20 epidermal growth factor receptor Homo sapiens 87-119 19755509-7 2009 The results from Western blots and phosphoprotein arrays showed that, in MEK inhibitor resistant cell lines, AKT was activated through the EGFR/HER3/PI3K pathway following AZD6244 (ARRY-142886) treatment. AZD 6244 172-179 epidermal growth factor receptor Homo sapiens 139-143 35617514-0 2022 Osimertinib plus selumetinib in EGFR-mutated, non-small cell lung cancer after progression on EGFR-TKIs: A Phase 1b, open-label, multicenter trial (TATTON Part B). AZD 6244 17-28 epidermal growth factor receptor Homo sapiens 32-36 30172884-6 2018 Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC. AZD 6244 130-137 epidermal growth factor receptor Homo sapiens 182-186 29928418-1 2018 The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells. AZD 6244 223-230 epidermal growth factor receptor Homo sapiens 68-100 29959144-11 2018 In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials. AZD 6244 182-193 epidermal growth factor receptor Homo sapiens 225-229 29928418-1 2018 The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells. AZD 6244 223-230 epidermal growth factor receptor Homo sapiens 102-106 27287717-7 2016 In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells. AZD 6244 69-76 epidermal growth factor receptor Homo sapiens 190-194 29928418-7 2018 Inhibition of EGFR activity using cetuximab partially abrogated the feedback-activation of phosphorylated receptor tyrosine-protein kinase erB-3 (p-HER3) and p-AKT serine/threonine kinase (AKT), as well as prevented reactivation of p-extracellular regulated kinase (ERK) conferred by AZD6244 treatment. AZD 6244 284-291 epidermal growth factor receptor Homo sapiens 14-18 29928418-9 2018 The EGFR inhibitor cetuximab enhanced the antitumor activity of the MEK inhibitor AZD6244 in colorectal cells in vitro and in vivo. AZD 6244 82-89 epidermal growth factor receptor Homo sapiens 4-8 29526823-2 2018 The aim of this work was to test the efficacy of a complete EGFR-inhibition by osimertinib plus the monoclonal antibody cetuximab or the MEK1/2-inhibitor selumetinib in EGFR-mutated NCLC in vivo models. AZD 6244 154-165 epidermal growth factor receptor Homo sapiens 169-173 29526823-7 2018 CONCLUSIONS: We showed that a dual vertical EGFR blockade with osimertinib plus selumetinib/cetuximab is a novel effective therapeutic option in EGFR-mutated NCLC and that hedgehog pathway activation and its interplay with MAPK is involved in resistance to these combination treatments. AZD 6244 80-91 epidermal growth factor receptor Homo sapiens 145-149 28566331-6 2017 We applied our approach to an ongoing phase Ib clinical trial (TATTON) administering AZD9291 and selumetinib to EGFR-mutant lung cancer patients. AZD 6244 97-108 epidermal growth factor receptor Homo sapiens 112-116 27287717-7 2016 In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells. AZD 6244 69-76 epidermal growth factor receptor Homo sapiens 164-168 27287717-7 2016 In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells. AZD 6244 69-76 epidermal growth factor receptor Homo sapiens 190-194 27287717-7 2016 In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells. AZD 6244 69-76 epidermal growth factor receptor Homo sapiens 190-194 26622906-5 2015 It was found that the growth inhibitory effect of combination treatment with gefitinib and AZD6244 was greater than that of gefitinib alone in the EGFR-TKI-resistant A549 cells. AZD 6244 91-98 epidermal growth factor receptor Homo sapiens 147-151 26622906-8 2015 Thus, a preclinical rationale exists for the use of AZD6244 to enhance the efficacy of gefitinib in patients with EGFR-TKI-resistant NSCLC. AZD 6244 52-59 epidermal growth factor receptor Homo sapiens 114-118 25870145-5 2015 Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor. AZD 6244 124-135 epidermal growth factor receptor Homo sapiens 208-212 25870145-5 2015 Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor. AZD 6244 137-144 epidermal growth factor receptor Homo sapiens 208-212 23588995-4 2013 The expression of epidermal growth factor receptor (EGFR) ligands was assessed by ELISA in both Ras wild-type and Ras mutant cells that were exposed to radiation with or without selumetinib. AZD 6244 178-189 epidermal growth factor receptor Homo sapiens 18-50 23588995-4 2013 The expression of epidermal growth factor receptor (EGFR) ligands was assessed by ELISA in both Ras wild-type and Ras mutant cells that were exposed to radiation with or without selumetinib. AZD 6244 178-189 epidermal growth factor receptor Homo sapiens 52-56 23588995-5 2013 The effects of selumetinib on the TGF-alpha/EGFR signaling cascade in response to radiation were examined by western blot analysis, clonogenic assay and by determing the yield of mitotic catastrophe. AZD 6244 15-26 epidermal growth factor receptor Homo sapiens 44-48 23588995-8 2013 The treatment of cells with selumetinib with or without IR inhibited the phosphorylation of EGFR and checkpoint kinase 2 (Chk2), and reduced the expression of survivin. AZD 6244 28-39 epidermal growth factor receptor Homo sapiens 92-96 23588995-9 2013 Supplementation with exogenous TGF-alpha partially rescued the selumetinib-treated cells from IR-induced cell death, restored EGFR and Chk2 phosphorylation and increased survivin expression. AZD 6244 63-74 epidermal growth factor receptor Homo sapiens 126-130 25959272-4 2015 Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells. AZD 6244 29-40 epidermal growth factor receptor Homo sapiens 92-96 25959272-4 2015 Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells. AZD 6244 105-116 epidermal growth factor receptor Homo sapiens 92-96 25959272-4 2015 Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells. AZD 6244 105-116 epidermal growth factor receptor Homo sapiens 92-96 25959272-8 2015 Taken together, our data demonstrated that blockade of the EGFR might efficiently increase the antitumor activity of selumetinib in a subgroup of TNBC and that this phenomenon might be related to the effects of such combination on both ERK1/2 and AKT activation. AZD 6244 117-128 epidermal growth factor receptor Homo sapiens 59-63 24200969-9 2014 We experimentally showed that TNFalpha, EGFR, IFNalpha, and IFNgamma pathway activities were also upregulated in melanoma cell A375 compared with its sub-line DRO, while DRO was much more sensitive to AZD6244 than A375. AZD 6244 201-208 epidermal growth factor receptor Homo sapiens 40-44