PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9514089-2 1998 We now report that therapeutic concentrations (approximately 1 microg/mL) of metformin stimulated the tyrosine kinase activity of the intracellular portion of the beta-subunit of the human insulin receptor (IPbetaIRK), the intracellular portion of the epidermal growth factor receptor and pp60-src, but not cAMP-dependent protein kinase. Metformin 77-86 epidermal growth factor receptor Homo sapiens 252-284 34149406-2 2021 Metformin could enhance the anticancer effects of standard antineoplastic agents (traditional chemotherapy drugs, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), or immune checkpoint inhibitors (ICIs)); however, it is unclear whether metformin can be combined with antineoplastic agents in the treatment of lung cancer. Metformin 0-9 epidermal growth factor receptor Homo sapiens 175-179 34149406-8 2021 Compared to standard antineoplastic agents alone (traditional chemotherapy drugs, EGFR-TKIs or ICIs), the antineoplastic agents combined with metformin significantly improved OS (HR 0.73, 95% CI 0.66-0.81, p < 0.00001) and PFS (HR 0.72, 95% CI 0.59-0.88, p = 0.001); a similar association was found in observational evidence. Metformin 142-151 epidermal growth factor receptor Homo sapiens 82-86 35222283-0 2022 Metformin Downregulates the Expression of Epidermal Growth Factor Receptor Independent of Lowering Blood Glucose in Oral Squamous Cell Carcinoma. Metformin 0-9 epidermal growth factor receptor Homo sapiens 42-74 34875861-8 2021 The risk increases with renal impairment; therefore the metformin dose must be adjusted to the eGFR. Metformin 56-65 epidermal growth factor receptor Homo sapiens 95-99 35337178-0 2022 Metformin Enhances TKI-Afatinib Cytotoxic Effect, Causing Downregulation of Glycolysis, Epithelial-Mesenchymal Transition, and EGFR-Signaling Pathway Activation in Lung Cancer Cells. Metformin 0-9 epidermal growth factor receptor Homo sapiens 127-131 35222283-5 2022 The patients were divided into groups according to whether they were taking metformin for the treatment of T2DM, and the expression of EGFR in different groups was compared. Metformin 76-85 epidermal growth factor receptor Homo sapiens 135-139 35222283-9 2022 Results: EGFR expression in T2DM patients with OSCC taking metformin was significantly lower than that in the non-metformin group. Metformin 59-68 epidermal growth factor receptor Homo sapiens 9-13 35222283-11 2022 In patients with recurrent OSCC with normal blood glucose, metformin remarkably reduced the expression of EGFR in recurrent OSCC tissues. Metformin 59-68 epidermal growth factor receptor Homo sapiens 106-110 35222283-12 2022 Conclusion: Metformin may regulate the expression of EGFR in a way that does not rely on lowering blood glucose. Metformin 12-21 epidermal growth factor receptor Homo sapiens 53-57 34012924-0 2021 Imaging Metformin Efficacy as Add-On Therapy in Cells and Mouse Models of Human EGFR Glioblastoma. Metformin 8-17 epidermal growth factor receptor Homo sapiens 80-84 34983210-8 2022 The risk increases with renal impairment; therefore the metformin dose must be adjusted to the eGFR. Metformin 56-65 epidermal growth factor receptor Homo sapiens 95-99 34004027-4 2021 The relationship between metformin clearance and eGFR metrics and gentamicin clearance was found to be linear suggesting that a proportional dose reduction based on GFR in patients with CKD is reasonable. Metformin 25-34 epidermal growth factor receptor Homo sapiens 49-53 33681180-7 2020 Moreover, treatment with metformin can increase sorafenib sensitivity through AMPK activation in EGFR-overexpressed liver cancer cells. Metformin 25-34 epidermal growth factor receptor Homo sapiens 97-101 33889509-0 2021 Concurrent use of metformin enhances the efficacy of EGFR-TKIs in patients with advanced EGFR-mutant non-small cell lung cancer-an option for overcoming EGFR-TKI resistance. Metformin 18-27 epidermal growth factor receptor Homo sapiens 53-57 33889509-0 2021 Concurrent use of metformin enhances the efficacy of EGFR-TKIs in patients with advanced EGFR-mutant non-small cell lung cancer-an option for overcoming EGFR-TKI resistance. Metformin 18-27 epidermal growth factor receptor Homo sapiens 89-93 33889509-7 2021 Metformin can also augment apoptosis effect of these TKI-resistant cells to EGFR-TKIs. Metformin 0-9 epidermal growth factor receptor Homo sapiens 76-80 33889509-11 2021 Further analysis revealed that metformin obviously prolonged the median PFS2 of osimertinib treatment among patients who progressed to prior line EGFR-TKIs due to secondary EGFR T790M mutation (cohort B). Metformin 31-40 epidermal growth factor receptor Homo sapiens 146-150 33889509-11 2021 Further analysis revealed that metformin obviously prolonged the median PFS2 of osimertinib treatment among patients who progressed to prior line EGFR-TKIs due to secondary EGFR T790M mutation (cohort B). Metformin 31-40 epidermal growth factor receptor Homo sapiens 173-177 33889509-12 2021 Conclusions: Our study suggest that concurrent use of metformin could be beneficial to EGFR-mutant NSCLC patients treated with either first-line EGFR-TKIs or second-line osimertinib. Metformin 54-63 epidermal growth factor receptor Homo sapiens 87-91 33889509-12 2021 Conclusions: Our study suggest that concurrent use of metformin could be beneficial to EGFR-mutant NSCLC patients treated with either first-line EGFR-TKIs or second-line osimertinib. Metformin 54-63 epidermal growth factor receptor Homo sapiens 145-149 33394543-5 2021 Metformin effect on eGFR slope was calculated using a mixed model-repeated measures (MMRM) analysis, and the number of lactic acidosis events was tabulated. Metformin 0-9 epidermal growth factor receptor Homo sapiens 20-24 33394543-8 2021 An improvement in eGFR slope was observed with metformin in the CKD stage 3B cohort in SAVOR, but not in other groups. Metformin 47-56 epidermal growth factor receptor Homo sapiens 18-22 33311577-3 2021 Here we found that background treatment with metformin diminished the SGLT2i-induced reductions in eGFR after 3 months of SGLT2i therapy in patients with type 2 diabetes and hypertension (-2.29 +- 0.90 vs -5.85 +- 1.27 mL/min/1.73 m2 for metformin users (n = 126) and nonusers (n = 97), respectively). Metformin 45-54 epidermal growth factor receptor Homo sapiens 99-103 33311577-3 2021 Here we found that background treatment with metformin diminished the SGLT2i-induced reductions in eGFR after 3 months of SGLT2i therapy in patients with type 2 diabetes and hypertension (-2.29 +- 0.90 vs -5.85 +- 1.27 mL/min/1.73 m2 for metformin users (n = 126) and nonusers (n = 97), respectively). Metformin 238-247 epidermal growth factor receptor Homo sapiens 99-103 33311577-6 2021 Next, we evaluated the interaction between metformin and RASis in the eGFR responses to SGLT2is. Metformin 43-52 epidermal growth factor receptor Homo sapiens 70-74 33311577-7 2021 Under no background treatment with RASis, metformin abrogated the eGFR response to SGLT2is, but this response was preserved when RASis had been given along with metformin (decreases of 0.75 +- 1.28 vs. 4.60 +- 1.15 mL/min/1.73 m2 in eGFR, p = 0.028). Metformin 42-51 epidermal growth factor receptor Homo sapiens 66-70 33311577-9 2021 In conclusion, metformin blunts the SGLT2i-induced decrease in eGFR, but coadministration of RASis ameliorates this response. Metformin 15-24 epidermal growth factor receptor Homo sapiens 63-67 33014814-0 2020 Metformin Overcomes Acquired Resistance to EGFR TKIs in EGFR-Mutant Lung Cancer via AMPK/ERK/NF-kappaB Signaling Pathway. Metformin 0-9 epidermal growth factor receptor Homo sapiens 43-47 33212505-0 2021 Does metformin improve the efficacy of standard epidermal growth factor receptor-tyrosine kinase inhibitor treatment for patients with advanced non-small-cell lung cancer? Metformin 5-14 epidermal growth factor receptor Homo sapiens 48-80 33212505-2 2021 The question addressed was whether metformin improved the efficacy of standard epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer. Metformin 35-44 epidermal growth factor receptor Homo sapiens 139-143 33212505-2 2021 The question addressed was whether metformin improved the efficacy of standard epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer. Metformin 35-44 epidermal growth factor receptor Homo sapiens 177-209 33212505-2 2021 The question addressed was whether metformin improved the efficacy of standard epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer. Metformin 35-44 epidermal growth factor receptor Homo sapiens 211-215 33212505-5 2021 We concluded that the addition of metformin to EGFR-TKI might improve the survival of patients with EGFR-mutated non-small-cell lung cancer and diabetes mellitus type 2. Metformin 34-43 epidermal growth factor receptor Homo sapiens 100-104 33212505-6 2021 However, for non-diabetic non-small-cell lung cancer patients with EGFR mutation, the efficiency of additional metformin in EGFR-TKI treatment remains unclear because of the conflicting results of only 2 available studies. Metformin 111-120 epidermal growth factor receptor Homo sapiens 124-128 32777157-0 2020 Metformin andbetter survival in Type 2 Diabetes patients with NSCLC during EGFR-TKI Treatment: implications of miR-146a? Metformin 0-9 epidermal growth factor receptor Homo sapiens 75-79 33014814-0 2020 Metformin Overcomes Acquired Resistance to EGFR TKIs in EGFR-Mutant Lung Cancer via AMPK/ERK/NF-kappaB Signaling Pathway. Metformin 0-9 epidermal growth factor receptor Homo sapiens 56-60 33014814-9 2020 Metformin inhibited proliferation and promoted apoptosis of lung cancer cells, especially those with acquired EGFR TKI resistance. Metformin 0-9 epidermal growth factor receptor Homo sapiens 110-114 33014814-10 2020 Moreover, metformin reversed and delayed acquired resistance to EGFR TKIs as well as suppressed cancer stemness in EGFR-mutant lung cancer. Metformin 10-19 epidermal growth factor receptor Homo sapiens 64-68 33014814-10 2020 Moreover, metformin reversed and delayed acquired resistance to EGFR TKIs as well as suppressed cancer stemness in EGFR-mutant lung cancer. Metformin 10-19 epidermal growth factor receptor Homo sapiens 115-119 33014814-12 2020 Conclusions: Our data provided novel and further molecular rationale and preclinical data to support combination of metformin with EGFR TKIs to treat EGFR-mutant lung cancer patients, especially those with acquired resistance. Metformin 116-125 epidermal growth factor receptor Homo sapiens 150-154 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. Metformin 43-52 epidermal growth factor receptor Homo sapiens 171-175 32806648-6 2020 We, thus, developed a new therapeutic approach to inhibit EGFR and hypoxia by combination treatment with metformin and gefitinib that sensitized TNBC cells to cisplatin and led to the inhibition of both CD44+/CD24- and ALDH+ CSCs. Metformin 105-114 epidermal growth factor receptor Homo sapiens 58-62 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. Metformin 54-57 epidermal growth factor receptor Homo sapiens 171-175 31409137-0 2019 Metformin Prolongs Survival in Type 2 Diabetes Lung Cancer Patients With EGFR-TKIs. Metformin 0-9 epidermal growth factor receptor Homo sapiens 73-77 31413010-1 2019 PURPOSE: Preclinical and retrospective studies suggested a role for metformin in sensitizing diabetic non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor(EGFR) tyrosine kinase inhibitors(TKIs). Metformin 68-77 epidermal growth factor receptor Homo sapiens 182-186 31486833-3 2019 Particularly, evidence is accumulating regarding the synergistic association between metformin and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs). Metformin 85-94 epidermal growth factor receptor Homo sapiens 99-131 31486833-3 2019 Particularly, evidence is accumulating regarding the synergistic association between metformin and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs). Metformin 85-94 epidermal growth factor receptor Homo sapiens 133-137 31486833-14 2019 Conclusions and Relevance: To our knowledge, this is the first study to prospectively show that the addition of metformin to standard EGFR-TKIs therapy in patients with advanced lung adenocarcinoma significantly improves PFS. Metformin 112-121 epidermal growth factor receptor Homo sapiens 134-138 32444490-1 2020 Metastatic colorectal cancer (mCRC) patients have poor overall survival despite using irinotecan- or oxaliplatin-based chemotherapy combined with anti-EGFR (epidermal growth factor receptor) drugs, especially those with the oncogene mutation of KRAS Metformin has been reported as a potentially novel antitumor agent in many experiments, but its therapeutic activity is discrepant and controversial so far. Metformin 250-259 epidermal growth factor receptor Homo sapiens 157-189 31413010-0 2019 Combination of metformin and gefitinib as first-line therapy for non-diabetic advanced NSCLC patients with EGFR mutations: A randomized, double-blind phase 2 trial. Metformin 15-24 epidermal growth factor receptor Homo sapiens 107-111 31413010-1 2019 PURPOSE: Preclinical and retrospective studies suggested a role for metformin in sensitizing diabetic non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor(EGFR) tyrosine kinase inhibitors(TKIs). Metformin 68-77 epidermal growth factor receptor Homo sapiens 149-181 31192264-9 2019 Further multivariable logistic regression analysis demonstrated that metformin was negatively associated with CAC severity (OR [95% CI] = 0.58 [0.34-0.99]; P = 0.048), which was independent of age, BMI, eGFR, gender, cigarette smoking, duration of diabetes, hypertension, statin prescription, and number of nonmetformin antidiabetic agents. Metformin 69-78 epidermal growth factor receptor Homo sapiens 203-207 30218617-13 2019 Cystatin C-based eGFR selects more complicated patients, where lower doses of metformin are possibly advisable. Metformin 78-87 epidermal growth factor receptor Homo sapiens 17-21 30061044-7 2019 The study demonstrates that although there is a relationship between eGFR and metformin levels, there is not a relationship between metformin levels and plasma lactate. Metformin 78-87 epidermal growth factor receptor Homo sapiens 69-73 31409137-6 2019 Conclusions: In conclusion, metformin may potentially enhance the therapeutic effect and increase survival in type 2 DM patients with lung cancer receiving EGFR-TKI therapy. Metformin 28-37 epidermal growth factor receptor Homo sapiens 156-160 30154647-0 2018 Combined treatment with metformin and gefitinib overcomes primary resistance to EGFR-TKIs with EGFR mutation via targeting IGF-1R signaling pathway. Metformin 24-33 epidermal growth factor receptor Homo sapiens 80-84 30307719-0 2018 Metformin synergistically enhances the antitumor activity of the third-generation EGFR-TKI CO-1686 in lung cancer cells through suppressing NF-kappaB signaling. Metformin 0-9 epidermal growth factor receptor Homo sapiens 82-86 30326091-0 2018 Metformin use was linked to hospitalization for acidosis at 6 y only in patients with eGFR < 30 mL/min/1.73 m2. Metformin 0-9 epidermal growth factor receptor Homo sapiens 86-90 30154647-0 2018 Combined treatment with metformin and gefitinib overcomes primary resistance to EGFR-TKIs with EGFR mutation via targeting IGF-1R signaling pathway. Metformin 24-33 epidermal growth factor receptor Homo sapiens 95-99 28977924-8 2017 The proportion of subjects taking metformin declined progressively across age quartiles along with eGFR values, but remained high in oldest subjects (i.e. 54.5 %). Metformin 34-43 epidermal growth factor receptor Homo sapiens 99-103 29212192-0 2017 Vorinostat and metformin sensitize EGFR-TKI resistant NSCLC cells via BIM-dependent apoptosis induction. Metformin 15-24 epidermal growth factor receptor Homo sapiens 35-39 29212192-3 2017 Vorinostat in combination with metformin - a compound that can inhibit anti-apoptotic proteins expression, might cooperate to activate apoptotic signaling and overcome EGFR-TKI resistance. Metformin 31-44 epidermal growth factor receptor Homo sapiens 168-172 29212192-5 2017 The results showed that vorinostat combined with gefitinib augmented BIM expression and increased the sensitivity of EGFR-TKI resistant NSCLC cells to gefitinib, adding metformin simultaneously could obviously inhibit the expression of anti-apoptotic proteins, and further increased expression levels of BIM and BAX, and as a result, further improved the sensitivity of gefitinib both on the NSCLC cells with intrinsic and acquired resistance to EGFR-TKI. Metformin 169-178 epidermal growth factor receptor Homo sapiens 446-450 29212192-7 2017 These results suggested that the combination of vorinostat and metformin might represent a novel strategy to overcome EGFR-TKI resistance associated with BIM-dependent apoptosis in larger heterogeneous populations. Metformin 63-72 epidermal growth factor receptor Homo sapiens 118-122 29312591-4 2017 In this study, we found that metformin (Met), which is widely used for the treatment of type 2 diabetes (T2D), sensitized lung cancer cells bearing wild-type EGFR to Erlo treatment by enriching cancer cells expressing higher levels of EGFR with persistent phosphorylation. Metformin 29-38 epidermal growth factor receptor Homo sapiens 158-162 29312591-4 2017 In this study, we found that metformin (Met), which is widely used for the treatment of type 2 diabetes (T2D), sensitized lung cancer cells bearing wild-type EGFR to Erlo treatment by enriching cancer cells expressing higher levels of EGFR with persistent phosphorylation. Metformin 29-38 epidermal growth factor receptor Homo sapiens 235-239 28977924-10 2017 The percentage of patients with low eGFR (i.e. <30 ml/min/1.73m2) taking either metformin or sulphonilureas/repaglinide was particularly high (i.e. 15.3% and 34.3% respectively). Metformin 83-92 epidermal growth factor receptor Homo sapiens 36-40 28065465-2 2017 The CGMT trial is a multicenter, phase II randomized, double-blinded, and placebo-controlled study, which is designed to evaluate the safety and efficacy of metformin in combination with gefitinib as first-line therapy in patients presenting with stage IIIb-IV non-small-cell lung cancer expressing the epidermal growth factor receptor mutant. Metformin 157-166 epidermal growth factor receptor Homo sapiens 303-335 28440424-8 2017 Additionally, metformin reduced the levels of phosphorylated epidermal growth factor receptor and ROR2 as well as markedly altered miRNA expression in HuTu80 cells. Metformin 14-23 epidermal growth factor receptor Homo sapiens 61-93 28526011-12 2017 Among those with incident AKI, being on metformin at admission was associated with a higher rate of survival at 28 days (HR 0.81, 95% CI 0.69, 0.94, p = 0.006) even after adjustment for age, sex, pre-admission eGFR, HbA1c and diabetes duration. Metformin 40-49 epidermal growth factor receptor Homo sapiens 210-214 28761738-1 2017 PURPOSE: Our previous works demonstrated the ability of metformin to revert resistance to gefitinib, a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, in non-small-cell lung cancer (NSCLC) EGFR/LKB1 wild-type (WT) cell lines. Metformin 56-65 epidermal growth factor receptor Homo sapiens 113-145 28761738-1 2017 PURPOSE: Our previous works demonstrated the ability of metformin to revert resistance to gefitinib, a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, in non-small-cell lung cancer (NSCLC) EGFR/LKB1 wild-type (WT) cell lines. Metformin 56-65 epidermal growth factor receptor Homo sapiens 147-151 28761738-1 2017 PURPOSE: Our previous works demonstrated the ability of metformin to revert resistance to gefitinib, a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, in non-small-cell lung cancer (NSCLC) EGFR/LKB1 wild-type (WT) cell lines. Metformin 56-65 epidermal growth factor receptor Homo sapiens 218-222 28391030-2 2017 In the present study we investigated the influence of the anti-diabetic drug metformin on the cytotoxic effects of EGFR targeted therapy and chemotherapy in 7 non-small cell lung cancer (NSCLC) cell lines and a cohort of lung cancer patients with/without T2D. Metformin 77-86 epidermal growth factor receptor Homo sapiens 115-119 28391030-8 2017 Consequently, the application of metformin for T2D NSCLC patients receiving chemo or EGFR targeted therapy should be considered with caution. Metformin 33-42 epidermal growth factor receptor Homo sapiens 85-89 28391030-4 2017 EGFR downstream signaling evaluation further demonstrated that metformin, at its IC50 value, modified apoptosis caused in erlotinib or chemotherapeutic agent-treated cells via AKT activation and the inhibition of caspase 3 and PARP cleavages. Metformin 63-72 epidermal growth factor receptor Homo sapiens 0-4 19084933-9 2008 We also observed that metformin treatment dramatically reduced epidermal growth factor receptor (EGFR) and phosphorylated mitogen activated protein kinase (P-MAPK) in both a time- and dose-dependent manner in all cell lines tested. Metformin 22-31 epidermal growth factor receptor Homo sapiens 63-95 27376570-7 2016 Baseline eGFR was better in patients under metformin therapy. Metformin 43-52 epidermal growth factor receptor Homo sapiens 9-13 26830074-2 2016 We demonstrate statistically significant differences regionally in use of metformin at lower eGFR and increasing reliance upon insulin with/without other medications at low eGFR. Metformin 74-83 epidermal growth factor receptor Homo sapiens 93-97 26675396-13 2015 Metformin could enhance the EGFR signaling pathway inhibitor AG1478 inhibition of endometrial cancer cells, which may inhibit EGFR expression of phosphorylated proteins to inhibit the phosphorylation of ERK1/2 proteins and then inhibit proliferation of endometrial cancer cells. Metformin 0-9 epidermal growth factor receptor Homo sapiens 28-32 26675396-13 2015 Metformin could enhance the EGFR signaling pathway inhibitor AG1478 inhibition of endometrial cancer cells, which may inhibit EGFR expression of phosphorylated proteins to inhibit the phosphorylation of ERK1/2 proteins and then inhibit proliferation of endometrial cancer cells. Metformin 0-9 epidermal growth factor receptor Homo sapiens 126-130 24876433-6 2014 A substantial eGFR decline (category: 15-<30 ml/min/1.73 m(2)) was significantly associated with a higher likelihood to have insulin initiated (adjusted hazard ratio [HR]: 2.39; 95% CI: 1.09-5.23) in metformin but not in sulfonylurea (HR: 0.45; 95% CI: 0.16-1.30) users. Metformin 203-212 epidermal growth factor receptor Homo sapiens 14-18 24644001-0 2014 Metformin sensitizes EGFR-TKI-resistant human lung cancer cells in vitro and in vivo through inhibition of IL-6 signaling and EMT reversal. Metformin 0-9 epidermal growth factor receptor Homo sapiens 21-25 24644001-4 2014 This study aims to investigate the effect of metformin on sensitizing EGFR-TKI-resistant human lung cancer cells in vitro and in vivo through inhibition of IL-6 signaling and EMT reversal. Metformin 45-54 epidermal growth factor receptor Homo sapiens 70-74 24644001-10 2014 CONCLUSION: Metformin, generally considered nontoxic and remarkably inexpensive, might be used in combination with TKIs in patients with non-small cell lung cancer, harboring EGFR mutations to overcome TKI resistance and prolong survival. Metformin 12-21 epidermal growth factor receptor Homo sapiens 175-179 24322659-8 2014 Molecular analysis indicated that metformin induced downregulation of ErbB2 and EGFR expression and inhibited the phosphorylation of ErbB family members, insulin-like growth factor-1R, AKT, mTOR, and STAT3 in vivo. Metformin 34-43 epidermal growth factor receptor Homo sapiens 80-84 24322659-8 2014 Molecular analysis indicated that metformin induced downregulation of ErbB2 and EGFR expression and inhibited the phosphorylation of ErbB family members, insulin-like growth factor-1R, AKT, mTOR, and STAT3 in vivo. Metformin 34-43 epidermal growth factor receptor Homo sapiens 70-74 21866433-7 2011 Patients with eGFR >= 60 ml/min/1.73 m (2) receiving contrast medium can continue metformin normally. Metformin 85-94 epidermal growth factor receptor Homo sapiens 14-18 19440038-7 2009 At the molecular level, metformin increases P-AMPK, reduces P-EGFR, EGFR, P-MAPK, P-Src, cyclin D1 and cyclin E (but not cyclin A or B, p27 or p21), and induces PARP cleavage in a dose- and time-dependent manner. Metformin 24-33 epidermal growth factor receptor Homo sapiens 62-66 19440038-7 2009 At the molecular level, metformin increases P-AMPK, reduces P-EGFR, EGFR, P-MAPK, P-Src, cyclin D1 and cyclin E (but not cyclin A or B, p27 or p21), and induces PARP cleavage in a dose- and time-dependent manner. Metformin 24-33 epidermal growth factor receptor Homo sapiens 68-72 27981444-7 2017 Metformin has also been reported to reverse resistance to epidermal growth factor receptor (EGFR)-inhibiting tyrosine kinase inhibitors. Metformin 0-9 epidermal growth factor receptor Homo sapiens 58-90 27981444-7 2017 Metformin has also been reported to reverse resistance to epidermal growth factor receptor (EGFR)-inhibiting tyrosine kinase inhibitors. Metformin 0-9 epidermal growth factor receptor Homo sapiens 92-96 28603691-1 2016 AIMS: Recommendations for metformin use are dependent on eGFR category: eGFR >45 ml/min/1.73 m2 - "first-line agent"; eGFR 30-44 - "use with caution"; eGFR<30 - "do not use". Metformin 26-35 epidermal growth factor receptor Homo sapiens 57-61 28603691-1 2016 AIMS: Recommendations for metformin use are dependent on eGFR category: eGFR >45 ml/min/1.73 m2 - "first-line agent"; eGFR 30-44 - "use with caution"; eGFR<30 - "do not use". Metformin 26-35 epidermal growth factor receptor Homo sapiens 72-76 28603691-1 2016 AIMS: Recommendations for metformin use are dependent on eGFR category: eGFR >45 ml/min/1.73 m2 - "first-line agent"; eGFR 30-44 - "use with caution"; eGFR<30 - "do not use". Metformin 26-35 epidermal growth factor receptor Homo sapiens 72-76 28603691-1 2016 AIMS: Recommendations for metformin use are dependent on eGFR category: eGFR >45 ml/min/1.73 m2 - "first-line agent"; eGFR 30-44 - "use with caution"; eGFR<30 - "do not use". Metformin 26-35 epidermal growth factor receptor Homo sapiens 72-76 28603691-4 2016 METHODS: In a consecutive cohort of 550 Veterans with diabetes, metformin use and eligibility were assessed by eGFR category, using eGFRcr and eGFRcys. Metformin 64-73 epidermal growth factor receptor Homo sapiens 111-115 28603691-8 2016 Metformin use decreased with severity of eGFRcr category, from 63% in eGFRcr >60 to 3% in eGFRcr <30. eGFRcys reclassified 20% of Veterans into different eGFR categories. Metformin 0-9 epidermal growth factor receptor Homo sapiens 41-45 26708419-9 2016 In addition, metformin reduced the phosphorylation of epidermal growth factor receptor (EGFR), particularly the phosphorylation of EGFR at Tyr845, and insulin-like growth factor 1 receptor (IGF-1R) in vitro and in vivo. Metformin 13-22 epidermal growth factor receptor Homo sapiens 54-86 26708419-9 2016 In addition, metformin reduced the phosphorylation of epidermal growth factor receptor (EGFR), particularly the phosphorylation of EGFR at Tyr845, and insulin-like growth factor 1 receptor (IGF-1R) in vitro and in vivo. Metformin 13-22 epidermal growth factor receptor Homo sapiens 88-92 26708419-9 2016 In addition, metformin reduced the phosphorylation of epidermal growth factor receptor (EGFR), particularly the phosphorylation of EGFR at Tyr845, and insulin-like growth factor 1 receptor (IGF-1R) in vitro and in vivo. Metformin 13-22 epidermal growth factor receptor Homo sapiens 131-135 26841718-6 2016 Notably, kinases, particularly SGK1 and EGFR were identified as key molecular targets of metformin. Metformin 89-98 epidermal growth factor receptor Homo sapiens 40-44 26341687-2 2015 Studies have shown that the antidiabetic drug metformin could effectively increase the sensitivity of TKI-resistant lung cancer cells to EGFR-TKI. Metformin 46-55 epidermal growth factor receptor Homo sapiens 137-141 26341687-9 2015 Secondary data analysis showed that metformin use significantly prolonged the median PFS in subgroups using either first-line EGFR-TKI or second-line EGFR-TKI. Metformin 36-45 epidermal growth factor receptor Homo sapiens 126-130 26341687-9 2015 Secondary data analysis showed that metformin use significantly prolonged the median PFS in subgroups using either first-line EGFR-TKI or second-line EGFR-TKI. Metformin 36-45 epidermal growth factor receptor Homo sapiens 150-154 26341687-10 2015 CONCLUSIONS: Metformin and EGFR-TKI have a synergistic effect in the treatment of DM2 NSCLC patients harboring EGFR-activating mutations. Metformin 13-22 epidermal growth factor receptor Homo sapiens 111-115 26341687-11 2015 Metformin use is associated with improved survival and delayed onset of acquired resistance to EGFR-TKI. Metformin 0-9 epidermal growth factor receptor Homo sapiens 95-99 25361177-6 2014 Combined metformin and erlotinib led to partial regression of PTEN-null and EGFR-amplified xenografted MDA-MB-468 BBC tumors with evidence of significant apoptosis, reduction of EGFR and AKT signaling, and lack of altered plasma insulin levels. Metformin 9-18 epidermal growth factor receptor Homo sapiens 76-80 25361177-6 2014 Combined metformin and erlotinib led to partial regression of PTEN-null and EGFR-amplified xenografted MDA-MB-468 BBC tumors with evidence of significant apoptosis, reduction of EGFR and AKT signaling, and lack of altered plasma insulin levels. Metformin 9-18 epidermal growth factor receptor Homo sapiens 178-182 23695170-6 2013 The inhibition of EGFR phosphorylation and of downstream signaling by adding gefitinib to metformin treatment abrogated this phenomenon and induced a strong apoptotic effect in vitro and in vivo. Metformin 90-99 epidermal growth factor receptor Homo sapiens 18-22 19084933-9 2008 We also observed that metformin treatment dramatically reduced epidermal growth factor receptor (EGFR) and phosphorylated mitogen activated protein kinase (P-MAPK) in both a time- and dose-dependent manner in all cell lines tested. Metformin 22-31 epidermal growth factor receptor Homo sapiens 97-101