PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25092426-12 2014 The cisplatin-induced generation of reactive oxygen species (ROS) and the activation of the Src/epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase (ERK) pathway were also counteracted by pre-treatment with GW9508. Cisplatin 4-13 epidermal growth factor receptor Homo sapiens 96-128 25092426-12 2014 The cisplatin-induced generation of reactive oxygen species (ROS) and the activation of the Src/epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase (ERK) pathway were also counteracted by pre-treatment with GW9508. Cisplatin 4-13 epidermal growth factor receptor Homo sapiens 130-134 25109763-0 2014 FTY720 and cisplatin synergistically induce the death of cisplatin-resistant melanoma cells through the downregulation of the PI3K pathway and the decrease in epidermal growth factor receptor expression. Cisplatin 11-20 epidermal growth factor receptor Homo sapiens 159-191 25109763-0 2014 FTY720 and cisplatin synergistically induce the death of cisplatin-resistant melanoma cells through the downregulation of the PI3K pathway and the decrease in epidermal growth factor receptor expression. Cisplatin 57-66 epidermal growth factor receptor Homo sapiens 159-191 25092426-13 2014 Thus, the activation of GPR40 attenuates cisplatin-induced apoptosis by inhibiting the generation of ROS, the activation of the Src/EGFR/ERK signaling pathway and the nuclear activation of NF-kappaB and pro-apoptotic factors. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 132-136 25109763-8 2014 In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced. Cisplatin 43-52 epidermal growth factor receptor Homo sapiens 214-246 25109763-8 2014 In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced. Cisplatin 43-52 epidermal growth factor receptor Homo sapiens 248-252 25109763-9 2014 These findings suggest that FTY720 and cisplatin synergistically induce cell death through the downregulation of the PI3K/Akt/mTOR pathway and the decrease in EGFR expression in SK-Mel-28 cells. Cisplatin 39-48 epidermal growth factor receptor Homo sapiens 159-163 24096476-2 2014 We hypothesized that phosphorylation of PXN by the EGFR/Src pathway might contribute to cisplatin resistance via increased Bcl-2 expression. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 51-55 24643932-5 2014 RESULTS: The nanoemulsion with particle size <150 nm were stable in plasma and parenteral fluids for 24 h. Ovarian cancer cells in vitro efficiently took up the non-targeted and EGFR-targeted nanoemulsions; improved cytotoxicity was observed for the these nanoemulsions with the latter showing a 50-fold drop in the IC50 in SKOV3 cells as compared to cisplatin alone. Cisplatin 354-363 epidermal growth factor receptor Homo sapiens 181-185 24947928-5 2014 RESULTS: When tumors were stratified into high and low EGFR expression groups (IHC score threshold 200; scale 0-300), a stronger antitumor activity was seen in the high EGFR expression group compared with the low EGFR expression group in both the cetuximab monotherapy and cisplatin plus cetuximab combination therapy settings. Cisplatin 273-282 epidermal growth factor receptor Homo sapiens 55-59 24947928-5 2014 RESULTS: When tumors were stratified into high and low EGFR expression groups (IHC score threshold 200; scale 0-300), a stronger antitumor activity was seen in the high EGFR expression group compared with the low EGFR expression group in both the cetuximab monotherapy and cisplatin plus cetuximab combination therapy settings. Cisplatin 273-282 epidermal growth factor receptor Homo sapiens 169-173 24947928-5 2014 RESULTS: When tumors were stratified into high and low EGFR expression groups (IHC score threshold 200; scale 0-300), a stronger antitumor activity was seen in the high EGFR expression group compared with the low EGFR expression group in both the cetuximab monotherapy and cisplatin plus cetuximab combination therapy settings. Cisplatin 273-282 epidermal growth factor receptor Homo sapiens 169-173 24947928-6 2014 For tumors treated with cisplatin plus cetuximab, the objective response rate was significantly higher in the high EGFR expression group compared with the low EGFR expression group (68% vs. 29%). Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 115-119 24947928-6 2014 For tumors treated with cisplatin plus cetuximab, the objective response rate was significantly higher in the high EGFR expression group compared with the low EGFR expression group (68% vs. 29%). Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 159-163 24748236-0 2014 Inhibition of EGFR-induced glucose metabolism sensitizes chondrosarcoma cells to cisplatin. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 14-18 25216514-0 2014 Epidermal growth factor receptor (EGFR) is an independent adverse prognostic factor in esophageal adenocarcinoma patients treated with cisplatin-based neoadjuvant chemotherapy. Cisplatin 135-144 epidermal growth factor receptor Homo sapiens 0-32 25216514-0 2014 Epidermal growth factor receptor (EGFR) is an independent adverse prognostic factor in esophageal adenocarcinoma patients treated with cisplatin-based neoadjuvant chemotherapy. Cisplatin 135-144 epidermal growth factor receptor Homo sapiens 34-38 25216514-11 2014 Furthermore, EGFR overexpression is involved in resistance to cisplatin-based neoadjuvant chemotherapy. Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 13-17 24748236-4 2014 In addition, overexpression of EGFR contributed to cisplatin resistance. Cisplatin 51-60 epidermal growth factor receptor Homo sapiens 31-35 24748236-6 2014 Interestingly, cisplatin-resistant chondrosarcoma cells showed upregulated glucose metabolism and EGFR signaling pathway. Cisplatin 15-24 epidermal growth factor receptor Homo sapiens 98-102 24748236-7 2014 Finally, we demonstrated that the combination of either EGFR inhibitor or anaerobic glycolysis inhibitor with cisplatin showed synergistically inhibitory effects on cisplatin-resistant chondrosarcoma cells through the inducements of apoptosis and cell cycle arrest. Cisplatin 165-174 epidermal growth factor receptor Homo sapiens 56-60 24772316-0 2014 Erlotinib with pemetrexed/cisplatin for patients with EGFR wild-type lung adenocarcinoma with brain metastases. Cisplatin 26-35 epidermal growth factor receptor Homo sapiens 54-58 24631944-11 2014 Our functional analysis provided the evidence demonstrating that expression of S100A9 and EGFR closely associated chemoresistance, and that inhibition of S100A9 and EGFR may sensitize bladder tumor cells to the cisplatin-based chemotherapy. Cisplatin 211-220 epidermal growth factor receptor Homo sapiens 165-169 24565522-0 2014 Cisplatin-alginate conjugate liposomes for targeted delivery to EGFR-positive ovarian cancer cells. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 64-68 24565522-9 2014 These results suggest that CS-EGF-Lip may offer a promising strategy for CDDP delivery in the treatment of EGFR-positive ovarian carcinoma or similar tumors, with enhanced efficacy and fewer adverse effects. Cisplatin 73-77 epidermal growth factor receptor Homo sapiens 107-111 24662458-7 2014 Patients treated with cisplatin were younger (median age 61 versus 63, p < 0.01) and had less comorbidities (summary comorbidity score > 2, 7.7% versus 12.8%, p = 0.01) and higher eGFR (87 versus 84 mL/min/1.73 m). Cisplatin 22-31 epidermal growth factor receptor Homo sapiens 186-190 24772316-13 2014 Therefore, erlotinib combined with pemetrexed/cisplatin, was found to be effective in the treatment of patients with EGFR wild-type lung adenocarcinoma. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 117-121 23764753-0 2013 Exon 4 deletion variant of epidermal growth factor receptor enhances invasiveness and cisplatin resistance in epithelial ovarian cancer. Cisplatin 86-95 epidermal growth factor receptor Homo sapiens 27-59 25841484-8 2014 The clinical benefits for afatinib over cisplatin-pemetrexed chemotherapy for EGFR mutation-positive advanced non-small cell lung patients seem overwhelming, and are clinically meaningful. Cisplatin 40-49 epidermal growth factor receptor Homo sapiens 78-82 23764753-8 2013 Interestingly, de4 EGFR transfectants displayed significantly lower sensitivity to cisplatin than EGFR transfectants, which could be ascribed to the upregulation of Bcl-2 and downregulation of BAD in the de4 EGFR transfectants. Cisplatin 83-92 epidermal growth factor receptor Homo sapiens 19-23 23764753-9 2013 Collectively, these results demonstrate that de4 EGFR plays an important role in the invasiveness and cisplatin resistance in epithelial ovarian cancer cells and may provide a new potential therapeutic target for epithelial ovarian cancer. Cisplatin 102-111 epidermal growth factor receptor Homo sapiens 49-53 22458639-9 2013 Our findings indicated that the combination of lapatinib and cisplatin is one of the promising treatment strategies for esophageal carcinomas with EGFR and HER2 overexpression. Cisplatin 61-70 epidermal growth factor receptor Homo sapiens 147-151 23816960-0 2013 Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. Cisplatin 31-40 epidermal growth factor receptor Homo sapiens 110-114 23733761-0 2013 Randomized phase II study of the anti-epidermal growth factor receptor monoclonal antibody cetuximab with cisplatin versus cisplatin alone in patients with metastatic triple-negative breast cancer. Cisplatin 106-115 epidermal growth factor receptor Homo sapiens 38-70 24394076-1 2013 We report a case of human epidermal growth factor receptor(HER)2-positive advanced gastric cancer successfully treated with a combination of capecitabine, cisplatin(CDDP), and trastuzumab as first-line chemotherapy. Cisplatin 155-164 epidermal growth factor receptor Homo sapiens 26-58 24394076-1 2013 We report a case of human epidermal growth factor receptor(HER)2-positive advanced gastric cancer successfully treated with a combination of capecitabine, cisplatin(CDDP), and trastuzumab as first-line chemotherapy. Cisplatin 165-169 epidermal growth factor receptor Homo sapiens 26-58 23966292-11 2013 Our findings provide insight into the mechanisms of cisplatin and PARP inhibitor sensitivity of EGFR-mutant cells, yielding potential therapeutic opportunities for further treatment individualization in this genetically defined subset of lung cancer. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 96-100 23891507-1 2013 INTRODUCTION: The sole agents pemetrexed (PEM), docetaxel and anti-EGFR agents are approved second-line therapies for non-small cell lung cancer (NSCLC) after failure with cisplatin-based doublets. Cisplatin 172-181 epidermal growth factor receptor Homo sapiens 67-71 23625205-9 2013 Pretreatment with EGFR inhibitor AG1478 or phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 rescued ADAM17-mediated cisplatin resistance of HCC cells. Cisplatin 123-132 epidermal growth factor receptor Homo sapiens 18-22 23625205-12 2013 Taken together, our results indicated that ADAM17 is upregulated by hypoxia and contributes to hypoxia-induced cisplatin resistance via EGFR/PI3K/Akt pathway. Cisplatin 111-120 epidermal growth factor receptor Homo sapiens 136-140 23460709-4 2013 Adding EGFR inhibition to standard cisplatin-radiotherapy may improve efficacy. Cisplatin 35-44 epidermal growth factor receptor Homo sapiens 7-11 23344263-0 2013 Caspase-independent cell death is involved in the negative effect of EGF receptor inhibitors on cisplatin in non-small cell lung cancer cells. Cisplatin 96-105 epidermal growth factor receptor Homo sapiens 69-81 23300028-3 2013 The phase III FLEX trial demonstrated an increase in survival for cisplatin/vinorelbine plus cetuximab compared to chemotherapy alone in patients with advanced EGFR-expressing NSCLC. Cisplatin 66-75 epidermal growth factor receptor Homo sapiens 160-164 23344263-10 2013 To overcome this, we showed that SAHA and erastin, the inducers of ROS-mediated CID, strongly enhanced the effect of cisplatin in WT EGFR cells. Cisplatin 117-126 epidermal growth factor receptor Homo sapiens 133-137 22271880-1 2012 PURPOSE: Erlotinib, an orally active selective inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase, has synergistic activity with radiation and with cisplatin. Cisplatin 170-179 epidermal growth factor receptor Homo sapiens 98-102 22788833-8 2012 CONCLUSIONS: The combination of low dose cisplatin and low dose UV-C synergistically exerted anti-cancer effect by down-regulating RTK, such as EGFR and HER2. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 144-148 22643066-11 2013 Cisplatin-resistant tumor cells expressed significantly lower levels of EGFR protein (P = 0.04) compared to cisplatin-sensitive cells and tended to have lower levels of phosphorylated Akt (pAkt; P = 0.13) and lower expression levels of amphiregulin (P = 0.18). Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 72-76 21909139-5 2012 The inhibition of EGFR or Stat3 activity repressed Survivin, VEGF and Vimentin expression and the colony-forming potential, viability, motility and migration of the resistant cells, and sensitized them to cisplatin. Cisplatin 205-214 epidermal growth factor receptor Homo sapiens 18-22 21909139-8 2012 Hyperactive EGFR signaling through Stat3 and the Jak-Stat3 activity together promote ovarian cancer progression to cisplatin resistance and therefore represent targets for preventing the development of cisplatin resistance and the recurrent disease during cisplatin therapy in ovarian cancer. Cisplatin 115-124 epidermal growth factor receptor Homo sapiens 12-16 21909139-8 2012 Hyperactive EGFR signaling through Stat3 and the Jak-Stat3 activity together promote ovarian cancer progression to cisplatin resistance and therefore represent targets for preventing the development of cisplatin resistance and the recurrent disease during cisplatin therapy in ovarian cancer. Cisplatin 202-211 epidermal growth factor receptor Homo sapiens 12-16 21909139-8 2012 Hyperactive EGFR signaling through Stat3 and the Jak-Stat3 activity together promote ovarian cancer progression to cisplatin resistance and therefore represent targets for preventing the development of cisplatin resistance and the recurrent disease during cisplatin therapy in ovarian cancer. Cisplatin 202-211 epidermal growth factor receptor Homo sapiens 12-16 22313686-2 2012 In the presence of gefitinib, cisplatin-induced growth inhibition and apoptosis were significantly enhanced in Caov-3 and RMG-1 cells, which express EGFR, and in A2780, which lacks EGFR but expresses HER-2. Cisplatin 30-39 epidermal growth factor receptor Homo sapiens 149-153 22313686-2 2012 In the presence of gefitinib, cisplatin-induced growth inhibition and apoptosis were significantly enhanced in Caov-3 and RMG-1 cells, which express EGFR, and in A2780, which lacks EGFR but expresses HER-2. Cisplatin 30-39 epidermal growth factor receptor Homo sapiens 181-185 22313686-7 2012 These results suggest that combination therapy with cisplatin and gefitinib may increase the therapeutic efficacy of cisplatin by blocking EGFR downstream signaling and/or inhibiting DNA repair in ovarian cancer. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 139-143 22313686-7 2012 These results suggest that combination therapy with cisplatin and gefitinib may increase the therapeutic efficacy of cisplatin by blocking EGFR downstream signaling and/or inhibiting DNA repair in ovarian cancer. Cisplatin 117-126 epidermal growth factor receptor Homo sapiens 139-143 21947696-0 2012 Prognosis of esophageal squamous cell carcinoma in patients positive for human epidermal growth factor receptor family can be improved by initial chemotherapy with docetaxel, fluorouracil, and cisplatin. Cisplatin 193-202 epidermal growth factor receptor Homo sapiens 79-111 22088438-0 2012 L1 cell adhesion molecule and epidermal growth factor receptor activation confer cisplatin resistance in intrahepatic cholangiocarcinoma cells. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 30-62 22088438-3 2012 Here, we report that epidermal growth factor receptor (EGFR) signaling and L1 cell adhesion molecule (L1CAM) conferred cisplatin resistance in SCK(R) cells in an additive fashion. Cisplatin 119-128 epidermal growth factor receptor Homo sapiens 21-53 22088438-3 2012 Here, we report that epidermal growth factor receptor (EGFR) signaling and L1 cell adhesion molecule (L1CAM) conferred cisplatin resistance in SCK(R) cells in an additive fashion. Cisplatin 119-128 epidermal growth factor receptor Homo sapiens 55-59 22088438-5 2012 Inhibition of EGFR activation or L1ACM greatly sensitized the cells to cisplatin. Cisplatin 71-80 epidermal growth factor receptor Homo sapiens 14-18 23581227-4 2012 We found that CDDP could inhibit the growth of U251 cell line and induced activation of the EGFR. Cisplatin 14-18 epidermal growth factor receptor Homo sapiens 92-96 23581227-6 2012 The mechanisms underlying the effect of the combined treatment of LRIG1 and CDDP could be that LRIG1 blocked CDDP-induced EGFR activation and regulated the apoptosis proteins. Cisplatin 76-80 epidermal growth factor receptor Homo sapiens 122-126 23581227-6 2012 The mechanisms underlying the effect of the combined treatment of LRIG1 and CDDP could be that LRIG1 blocked CDDP-induced EGFR activation and regulated the apoptosis proteins. Cisplatin 109-113 epidermal growth factor receptor Homo sapiens 122-126 21809030-0 2011 A monoclonal antibody targeted against epidermal growth factor receptor variant III enhances cisplatin efficiency. Cisplatin 93-102 epidermal growth factor receptor Homo sapiens 39-71 23049743-7 2012 Moreover, CD44(high)/EGFR(low) cells showed a low sensitivity to radiation, cisplatin, cetuximab and gefitinib, and a high sensitivity to dasatinib relative to its CD44(high)/EGFR(high) and CD44(low) counterparts. Cisplatin 76-85 epidermal growth factor receptor Homo sapiens 21-25 22173497-0 2011 EGFR inhibitor enhances cisplatin sensitivity of human glioma cells. Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 0-4 22173497-5 2011 The results showed that CDDP could induce the activation of EGFR and the components in its downstream signaling pathways in a concentration-dependent manner. Cisplatin 24-28 epidermal growth factor receptor Homo sapiens 60-64 22173497-8 2011 It was concluded that the combined treatment of AG1478 and CDDP may exert synergistic inhibitory effects on the growth of glioma cells by suppressing the activities of EGFR, AKT and ERK. Cisplatin 59-63 epidermal growth factor receptor Homo sapiens 168-172 21440325-9 2011 In presence of EGFR mutation negative or unknown status, patients with advanced squamous NSCLC, with good performance status (PS) and without major co-morbidities, chemotherapy with third-generation regimens containing cisplatin is the recommended treatment. Cisplatin 219-228 epidermal growth factor receptor Homo sapiens 15-19 21681119-9 2011 The inhibition rate of cisplatin in tumors with EGFR mutations (group M) was 34.8 +- 15.5%, which was significantly lower (p = 0.0153) than in wild-type tumors (group W; 46.6 +- 14.0%). Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 48-52 21478906-5 2011 The beta1 integrin-silenced cells show a defective activation of the EGFR signaling cascade, leading to decreased in vitro proliferation, enhanced sensitivity to cisplatin and Gefitinib, impaired migration and invasive behavior. Cisplatin 162-171 epidermal growth factor receptor Homo sapiens 69-73 21782507-1 2011 BACKGROUND: Findings from the phase 3 FLEX study showed that the addition of cetuximab to cisplatin and vinorelbine significantly improved overall survival, compared with cisplatin and vinorelbine alone, in the first-line treatment of EGFR-expressing, advanced non-small-cell lung cancer (NSCLC). Cisplatin 90-99 epidermal growth factor receptor Homo sapiens 235-239 21431282-1 2011 One aspect of chemotherapy insensitivity and resistance results from induction of epidermal growth factor receptor (EGFR) internalization and initial DNA damage repair in response to DNA-damaging stimuli, such as cisplatin (CDDP). Cisplatin 213-222 epidermal growth factor receptor Homo sapiens 82-114 21431282-1 2011 One aspect of chemotherapy insensitivity and resistance results from induction of epidermal growth factor receptor (EGFR) internalization and initial DNA damage repair in response to DNA-damaging stimuli, such as cisplatin (CDDP). Cisplatin 213-222 epidermal growth factor receptor Homo sapiens 116-120 21329967-1 2011 BACKGROUND: The purpose of this study was to evaluate the safety and efficacy of cetuximab (C225), an antibody that inhibits epidermal growth factor receptor (EGFR) activity, with cisplatin and to explore associations between EGFR protein expression with patient demographics or clinical outcome. Cisplatin 180-189 epidermal growth factor receptor Homo sapiens 159-163 21431282-1 2011 One aspect of chemotherapy insensitivity and resistance results from induction of epidermal growth factor receptor (EGFR) internalization and initial DNA damage repair in response to DNA-damaging stimuli, such as cisplatin (CDDP). Cisplatin 224-228 epidermal growth factor receptor Homo sapiens 82-114 21431282-1 2011 One aspect of chemotherapy insensitivity and resistance results from induction of epidermal growth factor receptor (EGFR) internalization and initial DNA damage repair in response to DNA-damaging stimuli, such as cisplatin (CDDP). Cisplatin 224-228 epidermal growth factor receptor Homo sapiens 116-120 20705357-6 2011 Patients who had received first-line docetaxel/cisplatin attained an overall survival of 19.2 months when treated with second-line EGFR TKIs, in comparison with 10.7 months when treated with second-line chemotherapy (P = 0.0002). Cisplatin 47-56 epidermal growth factor receptor Homo sapiens 131-135 20864569-5 2011 Promising results were shown in phase II trials in which the anti-epidermal growth factor receptor monoclonal antibody cetuximab was added to induction therapy with TPF, docetaxel/cisplatin, or paclitaxel/carboplatin, and in some of these studies, to subsequent CRT. Cisplatin 180-189 epidermal growth factor receptor Homo sapiens 66-98 20705357-10 2011 Second-line EGFR TKIs improved survival in patients receiving first-line cisplatin-based treatment. Cisplatin 73-82 epidermal growth factor receptor Homo sapiens 12-16 21252285-6 2011 Treatment with cisplatin/TRAIL also inhibited the expression of EGFR, p63, survivin, Bcl-2, and Bcl-xL in TNBC cells. Cisplatin 15-24 epidermal growth factor receptor Homo sapiens 64-68 21258258-7 2011 RESULTS: Of the 15 cell lines tested, combined gefitinib/cisplatin was significantly antagonistic in 10 wild-type and three sensitizing-EGFR mutant cell lines (group mean combination index = 1.184, 95% confidence interval = 1.12-1.24, p = 0.001). Cisplatin 57-66 epidermal growth factor receptor Homo sapiens 136-140 21258258-11 2011 CONCLUSIONS: In most EGFR wild-type or sensitizing-mutant NSCLC cells, the concomitant gefitinib/cisplatin combination showed antagonism, likely because gefitinib interfered with cisplatin entry into the cell. Cisplatin 97-106 epidermal growth factor receptor Homo sapiens 21-25 22715590-0 2011 The effect of acquired cisplatin resistance on sensitivity to EGFR tyrosine kinase inhibitors in EGFR mutant lung cancer cells. Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 62-66 21266349-0 2011 EGFR nuclear translocation modulates DNA repair following cisplatin and ionizing radiation treatment. Cisplatin 58-67 epidermal growth factor receptor Homo sapiens 0-4 21266349-11 2011 In summary, EGFR nuclear localization was required for modulation of cisplatin and IR-induced repair of DNA damage. Cisplatin 69-78 epidermal growth factor receptor Homo sapiens 12-16 21266349-12 2011 EGFR-DNA-PKcs binding was induced by cisplatin or IR but not by EGFR nuclear translocation per se. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 0-4 22715590-0 2011 The effect of acquired cisplatin resistance on sensitivity to EGFR tyrosine kinase inhibitors in EGFR mutant lung cancer cells. Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 97-101 22715590-2 2011 This study was designed to define whether exposure to cisplatin could affect the sensitivity to EGFR TKIs because conflicting results have been presented. Cisplatin 54-63 epidermal growth factor receptor Homo sapiens 96-100 22715590-6 2011 The IC50 value and apoptotic fractions after exposure to EGFR TKIs, such as gefitinib, erlotinib, and BIBW 2992, were almost the same in the cisplatin-resistant sublines compared to that of the parent cells. Cisplatin 141-150 epidermal growth factor receptor Homo sapiens 57-61 20215522-0 2010 Role of epidermal growth factor receptor degradation in cisplatin-induced cytotoxicity in head and neck cancer. Cisplatin 56-65 epidermal growth factor receptor Homo sapiens 8-40 20726858-9 2010 However, gemcitabine, paclitaxel, or cisplatin treatment enhanced the Akt activation, heterodimer formation of EGFR with HER3, and secretion of amphiregulin, indicating that the presence of gemcitabine promoted the activity of targeted molecules including amphiregulin, Akt, and HER3 for pancreatic cancer therapy. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 111-115 20959404-0 2010 cIAP2 upregulated by E6 oncoprotein via epidermal growth factor receptor/phosphatidylinositol 3-kinase/AKT pathway confers resistance to cisplatin in human papillomavirus 16/18-infected lung cancer. Cisplatin 137-146 epidermal growth factor receptor Homo sapiens 40-72 20959404-9 2010 Pretreatment with EGFR or PI3K inhibitor in TL-1 cells diminished the resistance to cisplatin. Cisplatin 84-93 epidermal growth factor receptor Homo sapiens 18-22 20959404-13 2010 CONCLUSIONS: cIAP2 upregulated by E6 via EGFR/PI3K/AKT cascades may contribute to cisplatin resistance, revealing that the EGFR or PI3K inhibitor combined with cisplatin may improve the chemotherapeutic efficacy in HPV-infected lung cancer. Cisplatin 82-91 epidermal growth factor receptor Homo sapiens 41-45 20959404-13 2010 CONCLUSIONS: cIAP2 upregulated by E6 via EGFR/PI3K/AKT cascades may contribute to cisplatin resistance, revealing that the EGFR or PI3K inhibitor combined with cisplatin may improve the chemotherapeutic efficacy in HPV-infected lung cancer. Cisplatin 82-91 epidermal growth factor receptor Homo sapiens 123-127 20959404-13 2010 CONCLUSIONS: cIAP2 upregulated by E6 via EGFR/PI3K/AKT cascades may contribute to cisplatin resistance, revealing that the EGFR or PI3K inhibitor combined with cisplatin may improve the chemotherapeutic efficacy in HPV-infected lung cancer. Cisplatin 160-169 epidermal growth factor receptor Homo sapiens 41-45 20215522-2 2010 In this study, we investigated a possible role of epidermal growth factor (EGF) receptor (EGFR) phosphorylation and degradation in cisplatin-induced cytotoxicity. Cisplatin 131-140 epidermal growth factor receptor Homo sapiens 50-88 20215522-2 2010 In this study, we investigated a possible role of epidermal growth factor (EGF) receptor (EGFR) phosphorylation and degradation in cisplatin-induced cytotoxicity. Cisplatin 131-140 epidermal growth factor receptor Homo sapiens 90-94 20215522-3 2010 Cisplatin treatment led to an increase in initial EGFR phosphorylation at Y1045, the binding site of ubiquitin ligase, Casitas B-lineage lymphoma (c-Cbl), followed by ubiquitination in the relatively cisplatin-sensitive cell lines. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 50-54 20215522-3 2010 Cisplatin treatment led to an increase in initial EGFR phosphorylation at Y1045, the binding site of ubiquitin ligase, Casitas B-lineage lymphoma (c-Cbl), followed by ubiquitination in the relatively cisplatin-sensitive cell lines. Cisplatin 200-209 epidermal growth factor receptor Homo sapiens 50-54 20215522-4 2010 However, cisplatin-resistant cell lines underwent minimal EGFR phosphorylation at the Y1045 site and minimal ubiquitination. Cisplatin 9-18 epidermal growth factor receptor Homo sapiens 58-62 20215522-5 2010 We found that EGFR degradation in response to cisplatin was highly correlated with cytotoxicity in seven head and neck cancer cell lines. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 14-18 20215522-6 2010 Pretreatment with EGF enhanced cisplatin-induced EGFR degradation and cytotoxicity, whereas erlotinib pretreatment blocked EGFR phosphorylation, degradation, and cisplatin-induced cytotoxicity. Cisplatin 31-40 epidermal growth factor receptor Homo sapiens 49-53 20215522-7 2010 Expression of a mutant Y1045F EGFR, which is relatively resistant to c-Cbl-mediated degradation, in Chinese hamster ovary cells and the UMSCC11B human head and neck cancer cell line protected EGFR from cisplatin-induced degradation and enhanced cell survival compared with wild-type (WT) EGFR. Cisplatin 202-211 epidermal growth factor receptor Homo sapiens 192-196 20215522-7 2010 Expression of a mutant Y1045F EGFR, which is relatively resistant to c-Cbl-mediated degradation, in Chinese hamster ovary cells and the UMSCC11B human head and neck cancer cell line protected EGFR from cisplatin-induced degradation and enhanced cell survival compared with wild-type (WT) EGFR. Cisplatin 202-211 epidermal growth factor receptor Homo sapiens 192-196 20215522-9 2010 These results show that cisplatin-induced EGFR phosphorylation and subsequent ubiquitination and degradation is an important determinant of cisplatin sensitivity. Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 42-46 20215522-9 2010 These results show that cisplatin-induced EGFR phosphorylation and subsequent ubiquitination and degradation is an important determinant of cisplatin sensitivity. Cisplatin 140-149 epidermal growth factor receptor Homo sapiens 42-46 20215522-10 2010 Our findings suggest that treatment with an EGFR inhibitor before cisplatin would be antagonistic, as EGFR inhibition would protect EGFR from cisplatin-mediated phosphorylation and subsequent ubiquitination and degradation, which may explain the negative results of several recent clinical trials. Cisplatin 142-151 epidermal growth factor receptor Homo sapiens 44-48 20215522-10 2010 Our findings suggest that treatment with an EGFR inhibitor before cisplatin would be antagonistic, as EGFR inhibition would protect EGFR from cisplatin-mediated phosphorylation and subsequent ubiquitination and degradation, which may explain the negative results of several recent clinical trials. Cisplatin 142-151 epidermal growth factor receptor Homo sapiens 102-106 20215522-10 2010 Our findings suggest that treatment with an EGFR inhibitor before cisplatin would be antagonistic, as EGFR inhibition would protect EGFR from cisplatin-mediated phosphorylation and subsequent ubiquitination and degradation, which may explain the negative results of several recent clinical trials. Cisplatin 142-151 epidermal growth factor receptor Homo sapiens 102-106 20693797-4 2010 Our study was designed to evaluate the impact of EGFR stimulation on cisplatin-induced DNA damage. Cisplatin 69-78 epidermal growth factor receptor Homo sapiens 49-53 20022809-13 2010 INTERPRETATION: Patients with lung cancer who are selected by EGFR mutations have longer progression-free survival if they are treated with gefitinib than if they are treated with cisplatin plus docetaxel. Cisplatin 180-189 epidermal growth factor receptor Homo sapiens 62-66 20693797-7 2010 Twenty-four-hour stimulation of tissue cultures with transforming growth factor alpha (TGF-alpha), a specific EGFR ligand, resulted in a reduction of cisplatin-induced DNA damage by 35% in cases, whereas in controls TGF-alpha had no effect. Cisplatin 150-159 epidermal growth factor receptor Homo sapiens 110-114 20693797-8 2010 This reflects a statistically significant increase in cellular chemoresistance to cisplatin following TGF-alpha stimulation and helps to further understand effects of EGFR antisense therapy in combination with chemotherapy. Cisplatin 82-91 epidermal growth factor receptor Homo sapiens 167-171 19375813-3 2010 We found that treatment with cisplatin further augmented HO-1 expression, which was associated with activation of the epidermal growth factor receptor (EGFR) mediated signaling pathway and subsequent nuclear translocation of NF-kappaB. Cisplatin 29-38 epidermal growth factor receptor Homo sapiens 118-150 19375813-3 2010 We found that treatment with cisplatin further augmented HO-1 expression, which was associated with activation of the epidermal growth factor receptor (EGFR) mediated signaling pathway and subsequent nuclear translocation of NF-kappaB. Cisplatin 29-38 epidermal growth factor receptor Homo sapiens 152-156 19375813-4 2010 In concordance with the findings, treatment with EGFR-selective tyrosine kinase inhibitor (AG1478) or an Akt inhibitor, which interfere with the post-EGFR signaling pathway, suppressed cisplatin induced HO-1 expression. Cisplatin 185-194 epidermal growth factor receptor Homo sapiens 49-53 19375813-4 2010 In concordance with the findings, treatment with EGFR-selective tyrosine kinase inhibitor (AG1478) or an Akt inhibitor, which interfere with the post-EGFR signaling pathway, suppressed cisplatin induced HO-1 expression. Cisplatin 185-194 epidermal growth factor receptor Homo sapiens 150-154 19375813-7 2010 Collectively, the results indicate that resistance to cisplatin in A549 cells is associated with HO-1 through EGFR mediated signaling pathway including activation of the PI3k/Akt and NF-kappaB systems. Cisplatin 54-63 epidermal growth factor receptor Homo sapiens 110-114 19375813-8 2010 Our data also suggest that the chemosensitivity of A549 cells to cisplatin is restored by EGFR-selective tyrosine kinase inhibitor and an Akt inhibitor. Cisplatin 65-74 epidermal growth factor receptor Homo sapiens 90-94 19917871-15 2009 Cetuximab is recommended with cisplatin-vinorelbine for patients with EGFR-positive tumors by immunohistochemistry. Cisplatin 30-39 epidermal growth factor receptor Homo sapiens 70-74 19399750-1 2009 BACKGROUND: This study was to explore whether the efficacy of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor ZD1839 (Z, Iressa, gefitinib) plus chemotherapeutic agents docetaxel (D) and cisplatin (P) may benefit from sequencing of the combination. Cisplatin 209-218 epidermal growth factor receptor Homo sapiens 66-98 19399750-1 2009 BACKGROUND: This study was to explore whether the efficacy of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor ZD1839 (Z, Iressa, gefitinib) plus chemotherapeutic agents docetaxel (D) and cisplatin (P) may benefit from sequencing of the combination. Cisplatin 209-218 epidermal growth factor receptor Homo sapiens 100-104 19785057-4 2009 In a phase III trial, cetuximab combined with cisplatin/ vinorelbine resulted in superior survival compared to chemotherapy alone in patients with advanced EGFR-positive NSCLC. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 156-160 19724896-9 2009 Our results indicate that SNPs in DNA repair genes (XRCC3241 and XPD751) influence the ICS and together with the expression of EGFR, Hsp70, Bax, and Bcl-2, they could predict the cisplatin sensitivity of head and neck cancer cell lines (r=0.614, p<or=0.001). Cisplatin 179-188 epidermal growth factor receptor Homo sapiens 127-131 19414362-2 2009 The aim of this study was to investigate the influence of EGFR stimulation on cisplatin sensitivity in 3 previously well characterized HNSCC cell lines. Cisplatin 78-87 epidermal growth factor receptor Homo sapiens 58-62 19632939-5 2009 Recently, the addition of cetuximab to the regimen of cisplatin and vinorelbine resulted in improved overall survival in patients with advanced NSCLC with EGFR-expressing tumors. Cisplatin 54-63 epidermal growth factor receptor Homo sapiens 155-159 19254954-7 2009 Lapatinib, a clinically active EGFR inhibitor, significantly reversed the epidermal growth factor-induced cisplatin resistance. Cisplatin 106-115 epidermal growth factor receptor Homo sapiens 31-35 19220256-0 2009 Dual epidermal growth factor receptor and vascular endothelial growth factor receptor inhibition with vandetanib sensitizes bladder cancer cells to cisplatin in a dose- and sequence-dependent manner. Cisplatin 148-157 epidermal growth factor receptor Homo sapiens 5-37 19414362-11 2009 Taken together the data suggest that EGFR stimulation in some cases could be an important prerequisite for cisplatin sensitivity. Cisplatin 107-116 epidermal growth factor receptor Homo sapiens 37-41 19259093-0 2009 Biomarker analysis in stage III-IV (M0) gastric cancer patients who received curative surgery followed by adjuvant 5-fluorouracil and cisplatin chemotherapy: epidermal growth factor receptor (EGFR) associated with favourable survival. Cisplatin 134-143 epidermal growth factor receptor Homo sapiens 158-190 19956435-0 2009 Nuclear EGFR is required for cisplatin resistance and DNA repair. Cisplatin 29-38 epidermal growth factor receptor Homo sapiens 8-12 19956435-2 2009 Recently, it has been shown that the DNA damage-inducing agents ionizing radiation (IR) and cisplatin are able to induce EGFR nuclear localization, and this nuclear localization is correlated with increased DNA-PK activity, which plays an essential role in DNA double stranded repair. Cisplatin 92-101 epidermal growth factor receptor Homo sapiens 121-125 19956435-4 2009 We found that mutation in the nuclear localization signal (NLS) of EGFR (mNLS), known to be unable to translocate to the nucleus, released EGFR induced resistance to cisplatin. Cisplatin 166-175 epidermal growth factor receptor Homo sapiens 67-71 19956435-4 2009 We found that mutation in the nuclear localization signal (NLS) of EGFR (mNLS), known to be unable to translocate to the nucleus, released EGFR induced resistance to cisplatin. Cisplatin 166-175 epidermal growth factor receptor Homo sapiens 139-143 19956435-6 2009 In addition, we show that the re-expression of a functional nuclear localization sequence in EGFR (mNLS-R) is not only able to restore its resistance to cisplatin, but also reduced the DNA damage caused by cisplatin, and restored DNA repair activity. Cisplatin 153-162 epidermal growth factor receptor Homo sapiens 93-97 19956435-6 2009 In addition, we show that the re-expression of a functional nuclear localization sequence in EGFR (mNLS-R) is not only able to restore its resistance to cisplatin, but also reduced the DNA damage caused by cisplatin, and restored DNA repair activity. Cisplatin 206-215 epidermal growth factor receptor Homo sapiens 93-97 19956435-7 2009 Thus, we demonstrate here that nuclear EGFR is required for DNA repair and resistance to cisplatin treatment. Cisplatin 89-98 epidermal growth factor receptor Homo sapiens 39-43 18927293-12 2008 CONCLUSIONS: EGFR-targeted cytotoxic reagents such as scFv(14E1)-ETA and TGF-alpha-ETA represent promising candidates for further development as antineuroblastoma agents, especially in combination with cisplatin. Cisplatin 202-211 epidermal growth factor receptor Homo sapiens 13-17 19149612-5 2009 In a phase III trial, cetuximab combined with cisplatin/vinorelbine resulted in superior survival compared to chemotherapy alone in patients with advanced EGFR-positive NSCLC. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 155-159 19027738-0 2008 The anti-EGFR monoclonal antibody blocks cisplatin-induced activation of EGFR signaling mediated by HB-EGF. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 9-13 19027738-0 2008 The anti-EGFR monoclonal antibody blocks cisplatin-induced activation of EGFR signaling mediated by HB-EGF. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 73-77 19027738-2 2008 We now show that cisplatin activates signaling by the epidermal growth factor receptor (EGFR) by inducing cleavage of heparin-binding epidermal growth factor-like growth factor (HB-EGF). Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 54-86 19027738-2 2008 We now show that cisplatin activates signaling by the epidermal growth factor receptor (EGFR) by inducing cleavage of heparin-binding epidermal growth factor-like growth factor (HB-EGF). Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 88-92 19027738-3 2008 Matuzumab, a monoclonal antibody to EGFR, inhibited cisplatin-induced EGFR signaling, likely through competition with the soluble form of HB-EGF for binding to EGFR. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 36-40 19027738-3 2008 Matuzumab, a monoclonal antibody to EGFR, inhibited cisplatin-induced EGFR signaling, likely through competition with the soluble form of HB-EGF for binding to EGFR. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 70-74 18980981-0 2008 Reduced Erlotinib sensitivity of epidermal growth factor receptor-mutant non-small cell lung cancer following cisplatin exposure: a cell culture model of second-line erlotinib treatment. Cisplatin 110-119 epidermal growth factor receptor Homo sapiens 33-65 18980981-7 2008 This lingering effect of cisplatin exposure appears to reflect changes in PTEN tumor suppressor activity and persistent EGFR-independent signaling through the phosphatidylinositol 3-kinase/AKT survival pathway. Cisplatin 25-34 epidermal growth factor receptor Homo sapiens 120-124 18927293-0 2008 Cisplatin-resistant neuroblastoma cells express enhanced levels of epidermal growth factor receptor (EGFR) and are sensitive to treatment with EGFR-specific toxins. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 67-99 18927293-0 2008 Cisplatin-resistant neuroblastoma cells express enhanced levels of epidermal growth factor receptor (EGFR) and are sensitive to treatment with EGFR-specific toxins. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 101-105 18927293-0 2008 Cisplatin-resistant neuroblastoma cells express enhanced levels of epidermal growth factor receptor (EGFR) and are sensitive to treatment with EGFR-specific toxins. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 143-147 18927293-2 2008 Here, EGFR expression and functionality was investigated in parental chemosensitive neuroblastoma cell lines (UKF-NB-3, IMR-32, NLF, SH-SY5Y) and their cisplatin-resistant sublines (UKF-NB-3(r)CDDP(1000), IMR-32(r)CDDP(1000), NLF(r)CDDP(1000), and SH-SY5Y(r)CDDP(500)). Cisplatin 152-161 epidermal growth factor receptor Homo sapiens 6-10 18927293-9 2008 Furthermore, adaptation of chemosensitive neuroblastoma cells to cisplatin increased EGFR expression and sensitivity to both recombinant toxins. Cisplatin 65-74 epidermal growth factor receptor Homo sapiens 85-89 19027738-3 2008 Matuzumab, a monoclonal antibody to EGFR, inhibited cisplatin-induced EGFR signaling, likely through competition with the soluble form of HB-EGF for binding to EGFR. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 70-74 19027738-5 2008 Our findings shed light on the mechanism by which monoclonal antibodies to EGFR might augment the efficacy of cisplatin. Cisplatin 110-119 epidermal growth factor receptor Homo sapiens 75-79 19047094-9 2008 In these cells, STAT5 activation was associated with resistance to cisplatin-mediated apoptosis and growth inhibition induced by the epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib. Cisplatin 67-76 epidermal growth factor receptor Homo sapiens 133-165 18927293-10 2008 Treatment of chemosensitive neuroblastoma cells with cisplatin reversibly increased EGFR expression, whereas cisplatin-resistant cells showed enhanced EGFR expression independent of the presence of cisplatin. Cisplatin 53-62 epidermal growth factor receptor Homo sapiens 84-88 18211286-11 2008 This FASN-triggered HER1/HER2-breast cancer-like phenotype was specifically inhibitable either by FASN inhibitor C75 or by Tyr-kinase inhibitors (TKIs) gefitinib (Iressa) and lapatinib (Tykerb) but not by chemotherapeutic agents such as cisplatin. Cisplatin 237-246 epidermal growth factor receptor Homo sapiens 20-24 18927293-10 2008 Treatment of chemosensitive neuroblastoma cells with cisplatin reversibly increased EGFR expression, whereas cisplatin-resistant cells showed enhanced EGFR expression independent of the presence of cisplatin. Cisplatin 109-118 epidermal growth factor receptor Homo sapiens 151-155 18927293-10 2008 Treatment of chemosensitive neuroblastoma cells with cisplatin reversibly increased EGFR expression, whereas cisplatin-resistant cells showed enhanced EGFR expression independent of the presence of cisplatin. Cisplatin 109-118 epidermal growth factor receptor Homo sapiens 151-155 18347929-0 2008 EGFR inhibitor enhances cisplatin sensitivity of oral squamous cell carcinoma cell lines. Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 0-4 18347929-3 2008 Recently, EGFR and its downstream signaling pathways were identified as being associated with cisplatin sensitivity. Cisplatin 94-103 epidermal growth factor receptor Homo sapiens 10-14 18347929-4 2008 In addition, EGFR inhibitors have shown significant promise for patients who failed cisplatin-based therapy. Cisplatin 84-93 epidermal growth factor receptor Homo sapiens 13-17 18347929-5 2008 In this study, we investigated whether treatment with an EGFR inhibitor improves cisplatin sensitivity in oral squamous cell carcinoma (OSCC) cell lines. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 57-61 18347929-7 2008 Higher expression of EGFR and p-EGFR was found in the two cisplatin-resistant cell lines compared with the corresponding parental cell lines. Cisplatin 58-67 epidermal growth factor receptor Homo sapiens 21-25 18347929-7 2008 Higher expression of EGFR and p-EGFR was found in the two cisplatin-resistant cell lines compared with the corresponding parental cell lines. Cisplatin 58-67 epidermal growth factor receptor Homo sapiens 32-36 18347929-9 2008 These results suggest that the combination of an EGFR inhibitor and cisplatin may be useful as a rational strategy for the treatment of patients with oral cancer with acquired cisplatin resistance. Cisplatin 176-185 epidermal growth factor receptor Homo sapiens 49-53 17942395-0 2008 Epidermal growth factor receptor pathway analysis identifies amphiregulin as a key factor for cisplatin resistance of human breast cancer cells. Cisplatin 94-103 epidermal growth factor receptor Homo sapiens 0-32 17942395-4 2008 The cisplatin-resistant MCF-7 cells are characterized by increased EGFR phosphorylation, high levels of AKT1 kinase activity, and ERK1 phosphorylation. Cisplatin 4-13 epidermal growth factor receptor Homo sapiens 67-71 17942395-3 2008 We generated cisplatin-resistant MCF-7 cells and determined the functional status of epidermal growth factor receptor (EGFR), MAPK, and AKT signaling pathways by phosphoreceptor tyrosine kinase and phospho-MAPK arrays. Cisplatin 13-22 epidermal growth factor receptor Homo sapiens 85-117 17942395-3 2008 We generated cisplatin-resistant MCF-7 cells and determined the functional status of epidermal growth factor receptor (EGFR), MAPK, and AKT signaling pathways by phosphoreceptor tyrosine kinase and phospho-MAPK arrays. Cisplatin 13-22 epidermal growth factor receptor Homo sapiens 119-123 16442503-7 2006 Vector-based shRNA against EGFR caused G1 arrest, induced apoptosis, and subsequently increased the sensitivity to cisplatin, doxorubicin and paclitaxel by about four- to seven-fold in both HLAC lines. Cisplatin 115-124 epidermal growth factor receptor Homo sapiens 27-31 18196976-7 2008 Taken together, the results clearly suggested that NCX-4016 causes significant induction of cell cycle arrest and apoptosis in cisplatin-resistant human ovarian cancer cells via down-regulation of EGFR/PI3K/STAT3 signaling and modulation of Bcl-2 family proteins. Cisplatin 127-136 epidermal growth factor receptor Homo sapiens 197-201 17487368-9 2007 Therefore, EGFR inhibitors can provide partial regulation of cisplatin-mediated apoptosis in OSCC cells by modulating expression of cIAP-1, XIAP, Bcl-2, Bcl-xL, Bax and Bak. Cisplatin 61-70 epidermal growth factor receptor Homo sapiens 11-15 17487368-10 2007 These results suggest that EGFR inhibitors may represent a novel strategy for overcoming resistance to cisplatin-mediated apoptosis via the phosphatidylinositol 3-kinase/Akt pathway. Cisplatin 103-112 epidermal growth factor receptor Homo sapiens 27-31 16731747-2 2006 In this study, we characterized a panel of human EGFR wild-type and mutant NSCLC cells for their sensitivity to gefitinib alone and in combination with cisplatin or Taxol. Cisplatin 152-161 epidermal growth factor receptor Homo sapiens 49-53 17876336-9 2007 EGFR expression was significantly associated with response to cisplatin-based chemotherapy: the response rates were 50 and 22% in patients with EGFR-positive tumours and EGFR-negative tumours, respectively (P<0.05). Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 0-4 17876336-9 2007 EGFR expression was significantly associated with response to cisplatin-based chemotherapy: the response rates were 50 and 22% in patients with EGFR-positive tumours and EGFR-negative tumours, respectively (P<0.05). Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 144-148 17876336-9 2007 EGFR expression was significantly associated with response to cisplatin-based chemotherapy: the response rates were 50 and 22% in patients with EGFR-positive tumours and EGFR-negative tumours, respectively (P<0.05). Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 144-148 17686445-2 2007 Impressive responses are observed in patients with epidermal growth factor receptor (EGFR) tyrosine kinase mutations following treatment with gefitinib and erlotinib; and methylation of the mitotic checkpoint gene 14-3-3sigma in circulating tumour serum DNA predicts response to cisplatin/gemcitabine therapy. Cisplatin 279-288 epidermal growth factor receptor Homo sapiens 85-89 18337622-6 2007 Cisplatin sensitivity in HDRA was also demonstrated to have a significant association with epidermal growth factor receptor (EGFR) expression in which the group with cisplatin resistance tended to have a higher expression level than the sensitive group (p = 0.0385). Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 91-123 18337622-6 2007 Cisplatin sensitivity in HDRA was also demonstrated to have a significant association with epidermal growth factor receptor (EGFR) expression in which the group with cisplatin resistance tended to have a higher expression level than the sensitive group (p = 0.0385). Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 125-129 18337622-6 2007 Cisplatin sensitivity in HDRA was also demonstrated to have a significant association with epidermal growth factor receptor (EGFR) expression in which the group with cisplatin resistance tended to have a higher expression level than the sensitive group (p = 0.0385). Cisplatin 166-175 epidermal growth factor receptor Homo sapiens 91-123 18337622-6 2007 Cisplatin sensitivity in HDRA was also demonstrated to have a significant association with epidermal growth factor receptor (EGFR) expression in which the group with cisplatin resistance tended to have a higher expression level than the sensitive group (p = 0.0385). Cisplatin 166-175 epidermal growth factor receptor Homo sapiens 125-129 16785992-2 2006 In this study, we report that Cisplatin activates PKB/Akt in several cancer cell lines and that this activation is mediated by EGFR, Src and PI3-kinase. Cisplatin 30-39 epidermal growth factor receptor Homo sapiens 127-131 16785992-4 2006 While investigating the EGFR-dependent PKB/Akt activation in MDA-MB-468 cells, we found that the EGFR receptor undergoes a gel mobility shift upon Cisplatin treatment, which is mediated by p38(MAPK). Cisplatin 147-156 epidermal growth factor receptor Homo sapiens 24-28 16785992-4 2006 While investigating the EGFR-dependent PKB/Akt activation in MDA-MB-468 cells, we found that the EGFR receptor undergoes a gel mobility shift upon Cisplatin treatment, which is mediated by p38(MAPK). Cisplatin 147-156 epidermal growth factor receptor Homo sapiens 97-101 16785992-6 2006 We found that Cisplatin induces EGFR internalization, which is mediated by p38(MAPK-)dependent phosphorylation of the receptor on threonine 669. Cisplatin 14-23 epidermal growth factor receptor Homo sapiens 32-36 17062690-8 2006 Of note, epidermal growth factor receptor, one of the new biological targets of chemotherapy for mesothelioma, was down-regulated and HtrA1, a serine protease recently shown to be an endogenous mediator of CDDP cytotoxicity, was up-regulated following piroxicam treatment both in vitro and in vivo. Cisplatin 206-210 epidermal growth factor receptor Homo sapiens 9-41 16984384-0 2006 Small interfering RNA targeting epidermal growth factor receptor enhances chemosensitivity to cisplatin, 5-fluorouracil and docetaxel in head and neck squamous cell carcinoma. Cisplatin 94-103 epidermal growth factor receptor Homo sapiens 32-64 16984384-7 2006 Treatment with EGFR siRNA in combination with cisplatin, 5-FU and docetaxel enhanced chemosensitivity with a significant increase in apoptosis. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 15-19 16984384-8 2006 EGFR siRNA delivered by atelocollagen enhanced the antitumor effect of cisplatin in the HNSCC xenograft model. Cisplatin 71-80 epidermal growth factor receptor Homo sapiens 0-4 16932740-9 2006 Hence, by preventing EGFR-mediated survival signaling, the internalization route we uncovered enhances the cytotoxic effect of drugs like cis-platinum, which may underlie interactions between chemotherapy and EGFR-targeting drugs. Cisplatin 138-150 epidermal growth factor receptor Homo sapiens 21-25 16932740-9 2006 Hence, by preventing EGFR-mediated survival signaling, the internalization route we uncovered enhances the cytotoxic effect of drugs like cis-platinum, which may underlie interactions between chemotherapy and EGFR-targeting drugs. Cisplatin 138-150 epidermal growth factor receptor Homo sapiens 209-213 15999529-9 2005 We conclude that, although siRNA against EGFR has efficacy against the PC-3 line when administered either alone vs untreated controls, with Taxol vs Taxol alone, or with cisplatin vs cisplatin alone, it is not more effective than the better characterized MR2 oligo. Cisplatin 170-179 epidermal growth factor receptor Homo sapiens 41-45 16061661-0 2005 Altered ErbB receptor signaling and gene expression in cisplatin-resistant ovarian cancer. Cisplatin 55-64 epidermal growth factor receptor Homo sapiens 8-12 16061661-2 2005 We have shown that development of resistance to this treatment can modify cell signaling responses in a model system wherein cisplatin treatment has altered cell responsiveness to ligands of the erbB receptor family. Cisplatin 125-134 epidermal growth factor receptor Homo sapiens 195-199 16505093-2 2006 We previously showed that the EGFR inhibitor gefitinib modulated repair of DNA damage following exposure to cisplatin and etoposide involving the DNA-dependent protein kinase (DNA-PK) pathway. Cisplatin 108-117 epidermal growth factor receptor Homo sapiens 30-34 16000298-2 2005 An increase in nuclear EGFR is also observed after treatment with H2O2, heat, or cisplatin. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 23-27 15999529-9 2005 We conclude that, although siRNA against EGFR has efficacy against the PC-3 line when administered either alone vs untreated controls, with Taxol vs Taxol alone, or with cisplatin vs cisplatin alone, it is not more effective than the better characterized MR2 oligo. Cisplatin 183-192 epidermal growth factor receptor Homo sapiens 41-45 15890569-0 2005 Expression of the epidermal growth factor receptor and Her-2 are predictors of favorable outcome and reduced complete response rates, respectively, in patients with muscle-invading bladder cancers treated by concurrent radiation and cisplatin-based chemotherapy: a report from the Radiation Therapy Oncology Group. Cisplatin 233-242 epidermal growth factor receptor Homo sapiens 18-50 12894544-2 2003 In this study we wanted to elucidate whether the described cumulative effect of cisplatin and Anti-EGFR therapy also depends on the EGFR expression. Cisplatin 80-89 epidermal growth factor receptor Homo sapiens 132-136 15987992-6 2005 The EGFR-directed monoclonal antibody (MAb) cetuximab (Erbitux) in combination with chemotherapy has shown some activity in the treatment of recurrent/metastatic disease both as first-line therapy and following cisplatin failure, and preliminary results suggest single-agent activity in platinum-resistant disease. Cisplatin 211-220 epidermal growth factor receptor Homo sapiens 4-8 15182504-10 2004 Based on the value of IC50 obtained by Origin 6.0 software, we concluded that dsRNA-EGFR increased the sensitivity of SPC-A-1 to cisplatin by seven-fold. Cisplatin 129-138 epidermal growth factor receptor Homo sapiens 84-88 15182504-12 2004 The finding from chemosensitivity assay further revealed that dsRNA-EGFR was associated with an addictive or synergistic effect on tumor growth inhibition when combined with cisplatin. Cisplatin 174-183 epidermal growth factor receptor Homo sapiens 68-72 14704124-7 2004 Compared with the control group, dsRNA-EGFR reduced the cell number by 85.0 %, decreased the colonies by 63.3 %, inhibited the migration by 87.2 %, and increased the sensitivity of A549 to cisplatin by four-fold. Cisplatin 189-198 epidermal growth factor receptor Homo sapiens 39-43 14704124-8 2004 CONCLUSION: Sequence specific dsRNA-EGFR were capable of suppressing EGF receptor expression, hence significantly inhibiting cellular proliferation and motility, and enhancing chemosensitivity of A549 cells to cisplatin. Cisplatin 210-219 epidermal growth factor receptor Homo sapiens 36-40 16037687-10 2005 Pretreatment of EGFR inhibitors by 24 h significantly enhanced the cytotoxic effect of doxorubicin, paclitaxel, cisplatin, and 5-fluororuacil in NPC-TW04 cells. Cisplatin 112-121 epidermal growth factor receptor Homo sapiens 16-20 15733386-8 2004 The EGFR sequence-specific siRNA transfected A549 cells were much more sensitive to the cytotoxic effect of cisplatin with a 77.2% decrease in IC(50) compared to the non-sequence-specific iRNA transfected A540 cells. Cisplatin 108-117 epidermal growth factor receptor Homo sapiens 4-8 12888834-3 2003 We have previously demonstrated a synergistic interaction between ZD1839 and cisplatin/5-fluorouracil (5FU) in CAL33, a human head and neck cancer cell line that markedly expresses EGFR. Cisplatin 77-86 epidermal growth factor receptor Homo sapiens 181-185 12894544-6 2003 The combination of antibodies with cisplatinum resulted in an EGFR-independent tumor growth inhibition which was stronger than observed in the case of monotherapy. Cisplatin 35-46 epidermal growth factor receptor Homo sapiens 62-66 11459199-9 2001 As a result, the resistance index of low EGFR-expressing ME180/Pt cells compared with intermediate EGFR-expressing ME180 cells was reduced only from five- to fourfold for cisplatin and from seven- to fourfold for CPT when ME180 cells were exposed to CP358774. Cisplatin 171-180 epidermal growth factor receptor Homo sapiens 41-45 12610866-2 2003 Epidermal growth factor receptor inhibitors have shown promising antitumor activity against cisplatin-resistant non-small cell lung cancer in phase II trials. Cisplatin 92-101 epidermal growth factor receptor Homo sapiens 0-32 12483525-7 2002 CDDP induces the activation of c-Src, and EGFR activation is blocked by Src-family inhibitor PP1, suggesting that Src kinases mediate CDDP-induced EGFR activation. Cisplatin 134-138 epidermal growth factor receptor Homo sapiens 42-46 12483525-7 2002 CDDP induces the activation of c-Src, and EGFR activation is blocked by Src-family inhibitor PP1, suggesting that Src kinases mediate CDDP-induced EGFR activation. Cisplatin 134-138 epidermal growth factor receptor Homo sapiens 147-151 12483525-8 2002 We propose that EGFR activation in response to CDDP is a survival response, since inhibition of EGFR activation enhances CDDP-induced death. Cisplatin 47-51 epidermal growth factor receptor Homo sapiens 16-20 12483525-8 2002 We propose that EGFR activation in response to CDDP is a survival response, since inhibition of EGFR activation enhances CDDP-induced death. Cisplatin 121-125 epidermal growth factor receptor Homo sapiens 16-20 12483525-8 2002 We propose that EGFR activation in response to CDDP is a survival response, since inhibition of EGFR activation enhances CDDP-induced death. Cisplatin 121-125 epidermal growth factor receptor Homo sapiens 96-100 12483525-9 2002 These findings show that signals generated by DNA damage can modulate EGFR activity, and argue that interfering with CDDP-induced EGFR activation in tumor cells might be a useful approach to sensitize these cells to genotoxic agents. Cisplatin 117-121 epidermal growth factor receptor Homo sapiens 70-74 12483525-9 2002 These findings show that signals generated by DNA damage can modulate EGFR activity, and argue that interfering with CDDP-induced EGFR activation in tumor cells might be a useful approach to sensitize these cells to genotoxic agents. Cisplatin 117-121 epidermal growth factor receptor Homo sapiens 130-134 11604556-0 2001 Evidence for epidermal growth factor receptor-enhanced chemosensitivity in combinations of cisplatin and the new irreversible tyrosine kinase inhibitor CI-1033. Cisplatin 91-100 epidermal growth factor receptor Homo sapiens 13-45 11604556-2 2001 This report is the first to show that inhibition of the EGFR tyrosine kinase by an irreversible binder synergizes with cisplatin, at least in EGFR-overexpressing tissue culture cell lines in vitro. Cisplatin 119-128 epidermal growth factor receptor Homo sapiens 56-60 11604556-2 2001 This report is the first to show that inhibition of the EGFR tyrosine kinase by an irreversible binder synergizes with cisplatin, at least in EGFR-overexpressing tissue culture cell lines in vitro. Cisplatin 119-128 epidermal growth factor receptor Homo sapiens 142-146 12483525-0 2002 Cisplatin-induced activation of the EGF receptor. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 36-48 12483525-3 2002 Here we report that CDDP also activates a membrane-integrated protein, the epidermal growth factor receptor (EGFR). Cisplatin 20-24 epidermal growth factor receptor Homo sapiens 75-107 12483525-3 2002 Here we report that CDDP also activates a membrane-integrated protein, the epidermal growth factor receptor (EGFR). Cisplatin 20-24 epidermal growth factor receptor Homo sapiens 109-113 12483525-4 2002 We show that EGFR is activated in response to CDDP in various types of cells that overexpress the receptor, including transformed human glioma cells and human breast tumor cells. Cisplatin 46-50 epidermal growth factor receptor Homo sapiens 13-17 12483525-5 2002 CDDP-induced EGFR activation requires its kinase activity, as it can be blocked by an EGFR kinase inhibitor or by expression of a kinase dead receptor. Cisplatin 0-4 epidermal growth factor receptor Homo sapiens 13-17 12483525-5 2002 CDDP-induced EGFR activation requires its kinase activity, as it can be blocked by an EGFR kinase inhibitor or by expression of a kinase dead receptor. Cisplatin 0-4 epidermal growth factor receptor Homo sapiens 86-90 12483525-6 2002 We also show that CDDP-induced EGFR activation is independent of receptor ligand. Cisplatin 18-22 epidermal growth factor receptor Homo sapiens 31-35 12483525-7 2002 CDDP induces the activation of c-Src, and EGFR activation is blocked by Src-family inhibitor PP1, suggesting that Src kinases mediate CDDP-induced EGFR activation. Cisplatin 0-4 epidermal growth factor receptor Homo sapiens 147-151 11565870-0 2001 Human glioblastoma xenografts overexpressing a tumor-specific mutant epidermal growth factor receptor sensitized to cisplatin by the AG1478 tyrosine kinase inhibitor. Cisplatin 116-125 epidermal growth factor receptor Homo sapiens 69-101 11565870-2 2001 The most common mutant EGFR, (AEGFR, also known as de2-7 EGFR and EGFRvIII) lacks a portion of the extracellular domain, enhances tumorigenicity in vivo, and causes resistance to the chemotherapeutic drug cisplatin (CDDP). Cisplatin 205-214 epidermal growth factor receptor Homo sapiens 23-27 11565870-2 2001 The most common mutant EGFR, (AEGFR, also known as de2-7 EGFR and EGFRvIII) lacks a portion of the extracellular domain, enhances tumorigenicity in vivo, and causes resistance to the chemotherapeutic drug cisplatin (CDDP). Cisplatin 205-214 epidermal growth factor receptor Homo sapiens 31-35 11565870-2 2001 The most common mutant EGFR, (AEGFR, also known as de2-7 EGFR and EGFRvIII) lacks a portion of the extracellular domain, enhances tumorigenicity in vivo, and causes resistance to the chemotherapeutic drug cisplatin (CDDP). Cisplatin 216-220 epidermal growth factor receptor Homo sapiens 23-27 11565870-2 2001 The most common mutant EGFR, (AEGFR, also known as de2-7 EGFR and EGFRvIII) lacks a portion of the extracellular domain, enhances tumorigenicity in vivo, and causes resistance to the chemotherapeutic drug cisplatin (CDDP). Cisplatin 216-220 epidermal growth factor receptor Homo sapiens 31-35 11565870-7 2001 Expression of AEGFR, but not wild-type EGFR, conferred CDDP resistance to the cells in vivo. Cisplatin 55-59 epidermal growth factor receptor Homo sapiens 15-19 11565870-11 2001 The synergistic growth suppression by the CDDP/AG1478 combination was not observed in xenografts overexpressing wild-type EGFR or kinase-deficient AEGFR. Cisplatin 42-46 epidermal growth factor receptor Homo sapiens 122-126 11410862-7 2001 Furthermore, a potentiation in the growth inhibitory effect on GEO cancer cells was observed after treatment with these EGFR antisense MBOs in combination with cytotoxic drugs, including cisplatin, doxorubicin, paclitaxel, or topotecan. Cisplatin 187-196 epidermal growth factor receptor Homo sapiens 120-124 11459199-0 2001 Sensitivity to topoisomerase I inhibitors and cisplatin is associated with epidermal growth factor receptor expression in human cervical squamous carcinoma ME180 sublines. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 75-107 11459199-5 2001 By MTT assay and compared with parental, intermediate-level EGFR-expressing ME180 cells, high EGFR-expressing ME180/TNF cells had a three- to fourfold increased sensitivity to cisplatin, camptothecin (CPT), and topotecan, and low EGFR-expressing ME180/Pt cells had a five- to ninefold reduced sensitivity to the same agents. Cisplatin 176-185 epidermal growth factor receptor Homo sapiens 94-98 11459199-5 2001 By MTT assay and compared with parental, intermediate-level EGFR-expressing ME180 cells, high EGFR-expressing ME180/TNF cells had a three- to fourfold increased sensitivity to cisplatin, camptothecin (CPT), and topotecan, and low EGFR-expressing ME180/Pt cells had a five- to ninefold reduced sensitivity to the same agents. Cisplatin 176-185 epidermal growth factor receptor Homo sapiens 94-98 10761709-2 2000 Overexpressions of epidermal growth factor receptor (EGFR) and HER-2/neu have been reported to affect the sensitivity of certain human cancer cells to cisplatin, presumably by modification of DNA repair activity through interference with NER. Cisplatin 151-160 epidermal growth factor receptor Homo sapiens 19-51 11350885-0 2001 Epidermal growth factor receptor-targeted therapy with C225 and cisplatin in patients with head and neck cancer. Cisplatin 64-73 epidermal growth factor receptor Homo sapiens 0-32 11391854-1 2001 PURPOSE: Activation of the epidermal growth factor (EGF) receptor has previously been shown to increase the sensitivity of cancer cells to DNA-damaging agents, including cisplatin, UV-B, and gamma-radiation. Cisplatin 170-179 epidermal growth factor receptor Homo sapiens 27-65 10761709-2 2000 Overexpressions of epidermal growth factor receptor (EGFR) and HER-2/neu have been reported to affect the sensitivity of certain human cancer cells to cisplatin, presumably by modification of DNA repair activity through interference with NER. Cisplatin 151-160 epidermal growth factor receptor Homo sapiens 53-57 10761709-7 2000 These results suggest that NER activity may play an important role in the cisplatin resistance of NSCLC cells and there may be an association between enhanced NER activity and high levels of p185neu and probably EGFR in NSCLC cells. Cisplatin 74-83 epidermal growth factor receptor Homo sapiens 212-216 10601618-3 2000 Treatment of EGFr positive cell lines, Hep2, KB and MCF-7 but not EGFr negative Fen by EGF prior to exposure to cisplatin inhibited the cells by between 10-15% (p<0.05). Cisplatin 112-121 epidermal growth factor receptor Homo sapiens 13-17 10601618-6 2000 These data indicated that pre-exposure of tumour cells to EGF altered their response to cisplatin and LAK killing and this depended on the degree of EGFr expression. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 149-153 10629487-1 2000 Recent literature by Fan et al (1993) demonstrated that addition of cisplatin and monoclonal antibody to the epidermal growth factor receptor (EGFR MAb) of the human squamous cell carcinoma (SCC), A431, eradicated gross tumors in nude mice. Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 109-141 10629487-1 2000 Recent literature by Fan et al (1993) demonstrated that addition of cisplatin and monoclonal antibody to the epidermal growth factor receptor (EGFR MAb) of the human squamous cell carcinoma (SCC), A431, eradicated gross tumors in nude mice. Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 143-147 10629487-6 2000 SCC-25 cells exhibited a greater decrease in growth with the addition of 16 nmol/L EGFR MAb to cisplatin compared with the cytotoxicity of cisplatin alone (P < 0.001). Cisplatin 95-104 epidermal growth factor receptor Homo sapiens 83-87 10629487-6 2000 SCC-25 cells exhibited a greater decrease in growth with the addition of 16 nmol/L EGFR MAb to cisplatin compared with the cytotoxicity of cisplatin alone (P < 0.001). Cisplatin 139-148 epidermal growth factor receptor Homo sapiens 83-87 10226546-4 1999 NCI-H596 cells, which strongly express EGFR, were more resistant to the growth inhibitory effects of cisplatin, doxorubicin and etoposide than were NCI-H358 cells, which only weakly express EGFR. Cisplatin 101-110 epidermal growth factor receptor Homo sapiens 39-43 10803405-12 2000 Additionally, a cisplatin-resistant cell line, A2780/CP70, which has an increase in AP-1 activity compared with the parental cell line, A2780, was found to have an increase in EGFR level. Cisplatin 16-25 epidermal growth factor receptor Homo sapiens 176-180 10213228-5 1999 Previous studies have suggested the potentiation of the antitumor activity of certain cytotoxic drugs, such as cisplatin and doxorubicin, in human cancer cell lines by treatment with anti-EGFR antibodies. Cisplatin 111-120 epidermal growth factor receptor Homo sapiens 188-192 9588705-7 1998 It is also shown that EGFR mRNA levels in normal oral epithelial cells were elevated after exposure to cisplatin. Cisplatin 103-112 epidermal growth factor receptor Homo sapiens 22-26 9494544-9 1997 Combined treatment with MAb and cisplatin led to a significant decrease in cisplatin IC50 values in 5 cell lines expressing more than 1200 fmol EGFR/mg (dose modification by factor 2.1-4.1). Cisplatin 32-41 epidermal growth factor receptor Homo sapiens 144-148 9494544-10 1997 In conclusion, anti-EGFR MAb exert direct antiproliferative activity in HNSCC lines and show additive effects in combination with cisplatin. Cisplatin 130-139 epidermal growth factor receptor Homo sapiens 20-24 9816301-5 1996 Because LPA is present in high levels in ascitic fluid from ovarian cancer patients, and the EGF receptor is expressed by tumor cells from a significant portion of patients where it correlates with prognosis, growth factor modulation of cis-DDP-induced apoptosis may play a role in the poor prognosis associated with ovarian cancer. Cisplatin 237-244 epidermal growth factor receptor Homo sapiens 93-105 9060958-1 1997 BACKGROUND: Epidermal growth factor receptor (EGF-R) perturbation by receptor ligand(s), e.g., epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), or receptor-specific antibodies accentuates cisplatin-induced toxicity in tumor cells. Cisplatin 219-228 epidermal growth factor receptor Homo sapiens 12-44 9060958-1 1997 BACKGROUND: Epidermal growth factor receptor (EGF-R) perturbation by receptor ligand(s), e.g., epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), or receptor-specific antibodies accentuates cisplatin-induced toxicity in tumor cells. Cisplatin 219-228 epidermal growth factor receptor Homo sapiens 46-51 9060958-3 1997 PURPOSE: Therefore, we have studied the role of EGF-R expression on cisplatin-mediated cytotoxicity. Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 48-53 9060958-9 1997 By use of a colony-forming assay, the 1-hour IC50 (i.e., the concentration of drug required for 1 hour to achieve 50% cell kill) for cisplatin was 2 microM or less for parental and vector-transfected clones (n = 4), whereas it was 25 microM or more for all MDA-468/AS-EGFR clones (n = 3). Cisplatin 133-142 epidermal growth factor receptor Homo sapiens 268-272 9060958-16 1997 CONCLUSIONS: These data indicate that a critical level of EGF-R signaling, which is amplified in some common human cancers, is necessary for cisplatin-mediated apoptosis in tumor cells and suggest an inhibitory effect of this pathway on the repair of cisplatin-damaged DNA. Cisplatin 141-150 epidermal growth factor receptor Homo sapiens 58-63 9060958-16 1997 CONCLUSIONS: These data indicate that a critical level of EGF-R signaling, which is amplified in some common human cancers, is necessary for cisplatin-mediated apoptosis in tumor cells and suggest an inhibitory effect of this pathway on the repair of cisplatin-damaged DNA. Cisplatin 251-260 epidermal growth factor receptor Homo sapiens 58-63 21541503-3 1996 In this report, we show that the growth of well-established xenografts of the human epidermoid carcinoma cell line KB could be significantly inhibited by the combination of cisplatin plus C225, a chimeric anti-EGFR monoclonal antibody, whereas the individual treatments had no effect on tumor growth. Cisplatin 173-182 epidermal growth factor receptor Homo sapiens 210-214 21541503-5 1996 In addition, cisplatin plus C225 inhibited the overall phosphorylation patterns including EGFR activation. Cisplatin 13-22 epidermal growth factor receptor Homo sapiens 90-94 7847819-3 1994 Treatment of OVCAR-3 cells with cisplatin, etoposide or epirubicin for two hours resulted in a marked augmentation of EGF-R expression and growth inhibition, on the other hand, incubation with substances blocking RNA or protein synthesis, actinomycin-D and cycloheximide, resulted in a reduction of both EGF-R expression and growth rate. Cisplatin 32-41 epidermal growth factor receptor Homo sapiens 118-123 8758793-9 1996 Transfection with pDOR-erbB-neo rendered the cells significantly, more sensitive to chemotherapeutic drugs (5-fluorouracil, cisplatinum) than the parental cells. Cisplatin 124-135 epidermal growth factor receptor Homo sapiens 23-27 7847819-3 1994 Treatment of OVCAR-3 cells with cisplatin, etoposide or epirubicin for two hours resulted in a marked augmentation of EGF-R expression and growth inhibition, on the other hand, incubation with substances blocking RNA or protein synthesis, actinomycin-D and cycloheximide, resulted in a reduction of both EGF-R expression and growth rate. Cisplatin 32-41 epidermal growth factor receptor Homo sapiens 304-309 33794187-0 2021 FGFR3 phosphorylates EGFR to promote cisplatin-resistance in ovarian cancer. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 21-25 34547305-0 2022 Coupling EGFR-antagonistic affibody enhanced therapeutic effects of cisplatin liposomes in EGFR-expressing tumor models. Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 9-13 34547305-0 2022 Coupling EGFR-antagonistic affibody enhanced therapeutic effects of cisplatin liposomes in EGFR-expressing tumor models. Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 91-95 34547305-2 2022 In this study, a high-affinity EGFR-antagonistic affibody (ZEGFR) molecule coupled with cisplatin-loaded PEGylated liposomes (LS-DDP) was applied to actively target EGFR+ A431 tumor cells in vitro and in vivo. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 165-169 34359721-0 2021 Neuropilin-1 Expression Associates with Poor Prognosis in HNSCC and Elicits EGFR Activation upon CDDP-Induced Cytotoxic Stress. Cisplatin 97-101 epidermal growth factor receptor Homo sapiens 76-80 34976847-6 2021 Results: Compared with concurrent anti-EGFR agents alone, combining concurrent cisplatin and anti-EGFR agents significantly improved the OS (5-year 94.7% versus 84.3%, P=0.012) and PFS (5-year 82.0% versus 71.7%, P=0.039) of NPC patients with more severe hematologic toxicity and mucositis. Cisplatin 79-88 epidermal growth factor receptor Homo sapiens 39-43 34873481-4 2021 In this work, we present evidence that genetic instability measured by mutation frequency is induced by treatment with the EGFR inhibitor afatinib or cisplatin in head and neck squamous cancer cells. Cisplatin 150-159 epidermal growth factor receptor Homo sapiens 123-127 34410944-0 2021 Induction of Apoptosis and Inhibition of EGFR/NF-kappaB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin. Cisplatin 139-148 epidermal growth factor receptor Homo sapiens 41-45 34410944-5 2021 RESULTS: Cisplatin-induced epidermal growth factor receptor (EGFR)/nuclear factor kappaB (NF-kappaB) signaling was effectively inhibited by regorafenib treatment. Cisplatin 9-18 epidermal growth factor receptor Homo sapiens 27-59 34410944-5 2021 RESULTS: Cisplatin-induced epidermal growth factor receptor (EGFR)/nuclear factor kappaB (NF-kappaB) signaling was effectively inhibited by regorafenib treatment. Cisplatin 9-18 epidermal growth factor receptor Homo sapiens 61-65 34410944-6 2021 Regorafenib, erlotinib (EGFR inhibitor) and QNZ (NF-kappaB inhibitor) may all enhance the cytotoxicity effect of cisplatin. Cisplatin 113-122 epidermal growth factor receptor Homo sapiens 24-28 34410944-9 2021 CONCLUSION: Apoptosis induction and EGFR/NF-kappaB inactivation correlate with regorafenib-enhanced anti-NSCLC efficacy of cisplatin. Cisplatin 123-132 epidermal growth factor receptor Homo sapiens 36-40 34359721-5 2021 In fact, NRP-1 can lead to cisplatin-induced EGFR phosphorylation, an escape mechanism activated by cancer cells upon cytotoxic stress. Cisplatin 27-36 epidermal growth factor receptor Homo sapiens 45-49 34917992-7 2021 Conclusions: EGFR tyrosine inhibitors plus irinotecan plus cisplatin chemotherapy might be a potential treatment option for advanced pulmonary neuroendocrine neoplasms harboring EGFR mutations. Cisplatin 59-68 epidermal growth factor receptor Homo sapiens 13-17 34917992-7 2021 Conclusions: EGFR tyrosine inhibitors plus irinotecan plus cisplatin chemotherapy might be a potential treatment option for advanced pulmonary neuroendocrine neoplasms harboring EGFR mutations. Cisplatin 59-68 epidermal growth factor receptor Homo sapiens 178-182 34294133-0 2021 Optimizing cisplatin delivery to triple-negative breast cancer through novel EGFR aptamer-conjugated polymeric nanovectors. Cisplatin 11-20 epidermal growth factor receptor Homo sapiens 77-81 34294133-5 2021 METHODS: Nanotechnological procedures were applied to entrap cisplatin at high efficacy into polymeric nanoparticles (PNPs) that were conjugated on their surface with the epidermal growth factor receptor (EGFR) selective and cell-internalizing CL4 aptamer to improve targeted therapy. Cisplatin 61-70 epidermal growth factor receptor Homo sapiens 171-203 34294133-5 2021 METHODS: Nanotechnological procedures were applied to entrap cisplatin at high efficacy into polymeric nanoparticles (PNPs) that were conjugated on their surface with the epidermal growth factor receptor (EGFR) selective and cell-internalizing CL4 aptamer to improve targeted therapy. Cisplatin 61-70 epidermal growth factor receptor Homo sapiens 205-209 34061460-1 2021 A 72-year-old man, diagnosed with advanced lung squamous cell carcinoma, was administered of cisplatin plus gemcitabine with necitumumab, a human monoclonal antibody that binds to the epidermal growth factor receptor (EGFR), as a sixth-line treatment. Cisplatin 93-102 epidermal growth factor receptor Homo sapiens 184-216 34061460-1 2021 A 72-year-old man, diagnosed with advanced lung squamous cell carcinoma, was administered of cisplatin plus gemcitabine with necitumumab, a human monoclonal antibody that binds to the epidermal growth factor receptor (EGFR), as a sixth-line treatment. Cisplatin 93-102 epidermal growth factor receptor Homo sapiens 218-222 34068624-0 2021 Targeting SIRT2 Sensitizes Melanoma Cells to Cisplatin via an EGFR-Dependent Mechanism. Cisplatin 45-54 epidermal growth factor receptor Homo sapiens 62-66 34123574-6 2021 Priming of drug sensitive or resistant cells with EGFR BATs followed by retargeting with lower concentrations of 50% inhibitory concentration of gemcitabine or cisplatin showed enhanced cytotoxicity. Cisplatin 160-169 epidermal growth factor receptor Homo sapiens 50-54 34065402-0 2021 KRAS and EGFR Mutations Differentially Alter ABC Drug Transporter Expression in Cisplatin-Resistant Non-Small Cell Lung Cancer. Cisplatin 80-89 epidermal growth factor receptor Homo sapiens 9-13 34065402-4 2021 Cisplatin resistance (CR) was generated in A549 (KRAS) and PC9 (EGFR) cell lines and gene expression was tested. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 64-68 34065402-10 2021 The study confirmed that, in lung AC-s, KRAS and EGFR driver mutations differentially affect both drug transporter expression and the cisplatin-induced WNT signalling microenvironment. Cisplatin 134-143 epidermal growth factor receptor Homo sapiens 49-53 35241559-2 2022 Our study investigated the association between epidermal growth factor receptor (EGFR) status in recurrent/metastatic SGC and the effectiveness of treatment with cisplatin/carboplatin and 5-fluorouracil plus cetuximab (EXTREME). Cisplatin 162-171 epidermal growth factor receptor Homo sapiens 81-85 35238281-0 2022 BEZ235 reduction of cisplatin resistance on wild-type EGFR non-small cell lung cancer cells. Cisplatin 20-29 epidermal growth factor receptor Homo sapiens 54-58 35238281-1 2022 Cisplatin, as a first-line chemotherapy drug for advanced wild-type epidermal growth factor receptor (wtEGFR) non-small cell lung cancer (NSCLC), often loses effectiveness because of acquired drug resistance. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 68-100 35070983-14 2021 Furthermore, quercetin combined with cisplatin downregulated the expression of EGFR, MYC, CCND1, and ERBB2 proteins and upregulated CASP8 expression in HeLa and SiHa cells. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 79-83 33353547-9 2020 Surprisingly, an increase in Ki67 expressing tumor cells were observed in spheroids treated with cisplatin for 3 days, correlating with increased expression of EGFR. Cisplatin 97-106 epidermal growth factor receptor Homo sapiens 160-164 34026617-2 2021 In this review, we first summarize the molecular mechanisms of chemotherapy resistance that occur during the treatment with cisplatin, 5-fluorouracil, and docetaxel/paclitaxel, including DNA/RNA damage repair, drug efflux, apoptosis inhibition, and epidermal growth factor receptor/focal adhesion kinase/nuclear factor-kappaB activation. Cisplatin 124-133 epidermal growth factor receptor Homo sapiens 249-281 33994369-0 2021 Cisplatin Activates the Growth Inhibitory Signaling Pathways by Enhancing the Production of Reactive Oxygen Species in Non-small Cell Lung Cancer Carrying an EGFR Exon 19 Deletion. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 158-162 33613698-3 2021 Methods: Herein, we introduce our phase II study of cisplatin plus vinorelbine combined with atezolizumab as adjuvant therapy for completely resected NSCLC with EGFR mutation. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 161-165 34023418-6 2021 Silencing GABRP induced down-regulation of EGFR signaling, which hindered cell stemness and enhanced sensitivity to chemotherapies, including paclitaxel, doxorubicin, and cisplatin. Cisplatin 171-180 epidermal growth factor receptor Homo sapiens 43-47 33169187-8 2021 However, co-administration of gefitinib and oxaliplatin or cisplatin was frequently antagonistic in cell-based assays in EGFR CNG ESCC, whereas the combination of gefitinib with docetaxel or irinotecan was more efficacious. Cisplatin 59-68 epidermal growth factor receptor Homo sapiens 121-125 33332190-1 2021 PURPOSE: ADJUVANT-CTONG1104 (ClinicalTrials.gov identifier: NCT01405079), a randomized phase III trial, showed that adjuvant gefitinib treatment significantly improved disease-free survival (DFS) versus vinorelbine plus cisplatin (VP) in patients with epidermal growth factor receptor (EGFR) mutation-positive resected stage II-IIIA (N1-N2) non-small-cell lung cancer (NSCLC). Cisplatin 220-229 epidermal growth factor receptor Homo sapiens 252-284 33332190-1 2021 PURPOSE: ADJUVANT-CTONG1104 (ClinicalTrials.gov identifier: NCT01405079), a randomized phase III trial, showed that adjuvant gefitinib treatment significantly improved disease-free survival (DFS) versus vinorelbine plus cisplatin (VP) in patients with epidermal growth factor receptor (EGFR) mutation-positive resected stage II-IIIA (N1-N2) non-small-cell lung cancer (NSCLC). Cisplatin 220-229 epidermal growth factor receptor Homo sapiens 286-290 33111200-7 2021 Protein-protein interaction network obtained from common DEGs in cisplatin and doxorubicin treatments revealed that GSK3beta, NACC1, and EGFR are the principal genes regulating the response of the KO cells. Cisplatin 65-74 epidermal growth factor receptor Homo sapiens 137-141 33015030-8 2020 Valproic acid also induced a dose-dependent downregulation of epidermal growth factor receptor (EGFR) expression and of MAPK and AKT downstream signaling pathways and prevent CDDP- and/or CX-induced EGFR nuclear translocation, a well-known mechanism of resistance to chemotherapy. Cisplatin 175-179 epidermal growth factor receptor Homo sapiens 199-203 32660222-0 2020 EGFR Blockade Reverses Cisplatin Resistance in Human Epithelial Ovarian Cancer Cells. Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 0-4 32660222-4 2020 These studies highlight the role of EGFR as an attractive therapeutic target in cisplatin-resistant EOC cells. Cisplatin 80-89 epidermal growth factor receptor Homo sapiens 36-40 32660222-11 2020 The data suggested that EGFR and cisplatin drives chemoresistance in the EOC cells through MEKK signal transduction as well as through EGFR/MEKK pathways in the cells, respectively. Cisplatin 33-42 epidermal growth factor receptor Homo sapiens 135-139 32641710-11 2020 We conclude that an eGFR is sufficient for assessing kidney function in patients with cancer undergoing cisplatin therapy. Cisplatin 104-113 epidermal growth factor receptor Homo sapiens 20-24 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. Cisplatin 159-168 epidermal growth factor receptor Homo sapiens 58-62 32342201-0 2020 Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells. Cisplatin 27-36 epidermal growth factor receptor Homo sapiens 57-61 32342201-3 2020 As EGFR is the most important pro-survival/proliferation signal receptor in NSCLC cells, we aimed at investigating whether cisplatin resistance is related to EGFR activation and further evaluating the combined effects of cisplatin/gefitinib (EGFR-tyrosine kinase inhibitor, EGFR-TKI) on cisplatin-resistant wtEGFR NSCLC cells. Cisplatin 123-132 epidermal growth factor receptor Homo sapiens 3-7 32342201-3 2020 As EGFR is the most important pro-survival/proliferation signal receptor in NSCLC cells, we aimed at investigating whether cisplatin resistance is related to EGFR activation and further evaluating the combined effects of cisplatin/gefitinib (EGFR-tyrosine kinase inhibitor, EGFR-TKI) on cisplatin-resistant wtEGFR NSCLC cells. Cisplatin 123-132 epidermal growth factor receptor Homo sapiens 158-162 32342201-3 2020 As EGFR is the most important pro-survival/proliferation signal receptor in NSCLC cells, we aimed at investigating whether cisplatin resistance is related to EGFR activation and further evaluating the combined effects of cisplatin/gefitinib (EGFR-tyrosine kinase inhibitor, EGFR-TKI) on cisplatin-resistant wtEGFR NSCLC cells. Cisplatin 123-132 epidermal growth factor receptor Homo sapiens 158-162 32342201-4 2020 MATERIALS AND METHODS: EGFR activation was analysed in parental and cisplatin-resistant wtEGFR NSCLC cell lines (H358 and H358R, A549 and A549R). Cisplatin 68-77 epidermal growth factor receptor Homo sapiens 23-27 32342201-7 2020 RESULTS: EGFR was significantly phosphorylated in cisplatin-resistant wtEGFR NSCLC cells H358R and A549R than their parental cells. Cisplatin 50-59 epidermal growth factor receptor Homo sapiens 9-13 32342201-11 2020 CONCLUSION: Abnormal activation of EGFR may induce wtEGFR NSCLC cell resistance to cisplatin. Cisplatin 83-92 epidermal growth factor receptor Homo sapiens 35-39 32434541-9 2020 In contrast, under the same culture conditions KRAS/EGFR WT or KRAS mutant cancer cells are more sensitive to cisplatin than EGFR mutant cells. Cisplatin 110-119 epidermal growth factor receptor Homo sapiens 52-56 32236608-0 2020 CD44 inhibition attenuates EGFR signaling and enhances cisplatin sensitivity in human EGFR wild-type non-small-cell lung cancer cells. Cisplatin 55-64 epidermal growth factor receptor Homo sapiens 86-90 32236608-2 2020 This study aimed to explore whether CD44 inhibition improves the sensitivity of epidermal growth factor receptor (EGFR) wild-type NSCLC cells to cisplatin and how it affects wild-type EGFR in NSCLC cells. Cisplatin 145-154 epidermal growth factor receptor Homo sapiens 114-118 32236608-6 2020 Furthermore, the CD44 expression level was positively correlated with wild-type EGFR level in human lung adenocarcinoma tissues and CD44 inhibition significantly accelerated the degradation of EGFR, indicating that enhanced sensitivity of H460 cells to cisplatin by downregulation of CD44 might be due to EGFR degradation. Cisplatin 253-262 epidermal growth factor receptor Homo sapiens 193-197 32236608-6 2020 Furthermore, the CD44 expression level was positively correlated with wild-type EGFR level in human lung adenocarcinoma tissues and CD44 inhibition significantly accelerated the degradation of EGFR, indicating that enhanced sensitivity of H460 cells to cisplatin by downregulation of CD44 might be due to EGFR degradation. Cisplatin 253-262 epidermal growth factor receptor Homo sapiens 193-197 32236608-7 2020 This study demonstrated that suppression of CD44 deactivated EGFR signals in NSCLC cells with wild-type EGFR, thereby contributing to the inhibition of cell proliferation and the reinforcement of cisplatin sensitivity. Cisplatin 196-205 epidermal growth factor receptor Homo sapiens 61-65 31856423-7 2020 Western blotting was performed to investigate changes in the expression levels of YAP, TAZ, Bcl-2, and EGFR in U87 and U251 cells treated with BPD, cisplatin, and paclitaxel, both as monotherapies and in combination. Cisplatin 148-157 epidermal growth factor receptor Homo sapiens 103-107 32269724-7 2020 Our study suggests that EGFR/ErbB2 activation is one of the driving pathways in developing cisplatin-resistance in ovarian cancer, and that sanguinarine has the potential to be developed as an effective therapy to overcome this therapeutic resistance. Cisplatin 91-100 epidermal growth factor receptor Homo sapiens 24-28 32389961-4 2020 In the analysis of up to 6 cycles of CDDP administration, the serum Mg levels and eGFR of CDDP-treated patients (n=614)were significantly reduced(p<0.001 and p=0.002, respectively, ANOVA). Cisplatin 37-41 epidermal growth factor receptor Homo sapiens 82-86 32389961-4 2020 In the analysis of up to 6 cycles of CDDP administration, the serum Mg levels and eGFR of CDDP-treated patients (n=614)were significantly reduced(p<0.001 and p=0.002, respectively, ANOVA). Cisplatin 90-94 epidermal growth factor receptor Homo sapiens 82-86 31881486-0 2020 Circular RNA CDR1-AS contributes to pemetrexed and cisplatin chemoresistance through EGFR/PI3K signaling pathway in lung adenocarcinoma. Cisplatin 51-60 epidermal growth factor receptor Homo sapiens 85-89 31881486-8 2020 The activating of EGFR/PI3K pathway mostly restored the effecting of CDR1-AS silence on PTX and CDDP sensitivity in A549/CR cells, CDR1-AS contributed to PTX and CDDP chemoresistance through EGFR/PI3K signaling pathway in LUAD. Cisplatin 96-100 epidermal growth factor receptor Homo sapiens 18-22 31881486-8 2020 The activating of EGFR/PI3K pathway mostly restored the effecting of CDR1-AS silence on PTX and CDDP sensitivity in A549/CR cells, CDR1-AS contributed to PTX and CDDP chemoresistance through EGFR/PI3K signaling pathway in LUAD. Cisplatin 162-166 epidermal growth factor receptor Homo sapiens 18-22 31881486-10 2020 The high-expression of CDR1-AS is related with the PTX and CDDP insensitivity of LUAD patients, CDR1-AS promotes PTX and CDDP chemoresistance through EGFR/PI3K signaling pathway in LUAD. Cisplatin 59-63 epidermal growth factor receptor Homo sapiens 150-154 31881486-10 2020 The high-expression of CDR1-AS is related with the PTX and CDDP insensitivity of LUAD patients, CDR1-AS promotes PTX and CDDP chemoresistance through EGFR/PI3K signaling pathway in LUAD. Cisplatin 121-125 epidermal growth factor receptor Homo sapiens 150-154 31959339-1 2020 BACKGROUND: Palliative chemotherapy of advanced oesophageal squamous cell cancer (ESCC) consists of cisplatin/5-fluorouracil (CF) to target epidermal growth factor receptor (EGFR) with panitumumab (P); chemotherapy enhanced overall survival (OS) in advanced colorectal or squamous cell head and neck cancers. Cisplatin 100-109 epidermal growth factor receptor Homo sapiens 140-172 31959339-1 2020 BACKGROUND: Palliative chemotherapy of advanced oesophageal squamous cell cancer (ESCC) consists of cisplatin/5-fluorouracil (CF) to target epidermal growth factor receptor (EGFR) with panitumumab (P); chemotherapy enhanced overall survival (OS) in advanced colorectal or squamous cell head and neck cancers. Cisplatin 100-109 epidermal growth factor receptor Homo sapiens 174-178 31262325-10 2019 Moreover, BEZ235 synergistically enhanced cisplatin-induced apoptosis in NSCLC cells by enhancing or prolonging DNA damage and BIBW2992-induced apoptosis in EGFR-TKI-resistant NSCLC cells containing a second TKI-resistant EGFR mutant. Cisplatin 42-51 epidermal growth factor receptor Homo sapiens 222-226 30815759-7 2019 Co-treatment of GC1118 and cisplatin or 5-FU inhibited colony formation and migration to a greater extent, even following EGFR ligand stimulation. Cisplatin 27-36 epidermal growth factor receptor Homo sapiens 122-126 31189612-0 2019 Vorinostat Potentiates 5-Fluorouracil/Cisplatin Combination by Inhibiting Chemotherapy-Induced EGFR Nuclear Translocation and Increasing Cisplatin Uptake. Cisplatin 38-47 epidermal growth factor receptor Homo sapiens 95-99 31360122-2 2019 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin 111-120 epidermal growth factor receptor Homo sapiens 35-67 31360122-2 2019 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin 111-120 epidermal growth factor receptor Homo sapiens 69-73 31360122-2 2019 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin 122-126 epidermal growth factor receptor Homo sapiens 35-67 31360122-2 2019 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin 122-126 epidermal growth factor receptor Homo sapiens 69-73 31360122-10 2019 Results: We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production. Cisplatin 113-117 epidermal growth factor receptor Homo sapiens 137-141 31360122-12 2019 Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production. Cisplatin 26-30 epidermal growth factor receptor Homo sapiens 126-130 31360122-13 2019 In contrast, in chemoresistant NSCLC, activated Akt promotes EGFR signaling by the positive feedback loop and suppresses CDDP-induced ROS production and apoptosis. Cisplatin 121-125 epidermal growth factor receptor Homo sapiens 61-65 31319622-8 2019 Furthermore, the combination of WA and chemotherapeutic drugs, including cisplatin and pemetrexed, exerted synergistic effects on the inhibition of epidermal growth factor receptor (EGFR) wild-type lung cancer cell viability. Cisplatin 73-82 epidermal growth factor receptor Homo sapiens 148-180 31319622-8 2019 Furthermore, the combination of WA and chemotherapeutic drugs, including cisplatin and pemetrexed, exerted synergistic effects on the inhibition of epidermal growth factor receptor (EGFR) wild-type lung cancer cell viability. Cisplatin 73-82 epidermal growth factor receptor Homo sapiens 182-186 31814556-8 2020 Conversely, Rh2 was found to repress cisplatin-induced phosphorylation of epidermal growth factor receptor, phosphoinositide 3-kinase, protein kinase B, and autophagy. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 74-106 33197924-10 2020 CONCLUSIONS: Our study demonstrated that adjuvant EGFR-TKI treatment significantly increased the DFS of patients with stage IIIA-N2 NSCLC when compared with cisplatin-based chemotherapy. Cisplatin 157-166 epidermal growth factor receptor Homo sapiens 50-54 31553438-1 2019 BACKGROUND: Primary analysis of the phase III study WJTOG 3405 demonstrated superiority of progression-free survival (PFS) for gefitinib (G) in patients treated with the epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) gefitinib compared with cisplatin plus docetaxel (CD) as the first-line treatment of stage IIIB/IV or postoperative recurrent EGFR mutation-positive non-small-cell lung cancer. Cisplatin 266-275 epidermal growth factor receptor Homo sapiens 204-208 31559456-0 2019 Epidermal growth factor receptor/heme oxygenase-1 axis is involved in chemoresistance to cisplatin and pirarubicin in HepG2 cell lines and hepatoblastoma specimens. Cisplatin 89-98 epidermal growth factor receptor Homo sapiens 0-32 31559456-9 2019 Combination treatment of EGFR inhibitor with CDDP and THP increased the cytotoxic effect in HepG2 cells. Cisplatin 45-49 epidermal growth factor receptor Homo sapiens 25-29 31559456-11 2019 CONCLUSION: The cytotoxic effects of CDDP and THP were both enhanced under HO-1 knockdown conditions as well as under conditions that inhibit the activation pathway of HO-1 by EGFR inhibitors. Cisplatin 37-41 epidermal growth factor receptor Homo sapiens 176-180 31545462-0 2019 Lung carcinoma therapy using epidermal growth factor receptor-targeted lipid polymeric nanoparticles co-loaded with cisplatin and doxorubicin. Cisplatin 116-125 epidermal growth factor receptor Homo sapiens 29-61 31545462-4 2019 In the present study, EGFR-targeted nanoparticles were constructed and co-delivered cisplatin (CDDP) and doxorubicin (DOX) for lung cancer therapy. Cisplatin 84-93 epidermal growth factor receptor Homo sapiens 22-26 31387179-7 2019 In in vitro experiment, WEE1 expression was higher in EGFR-TKIs resistant than EGFR-TKIs sensitive cell lines and was gradually increased following cisplatin or gemcitabine treatment with the enrichment of G2/M cell cycle phase. Cisplatin 148-157 epidermal growth factor receptor Homo sapiens 54-58 31387179-7 2019 In in vitro experiment, WEE1 expression was higher in EGFR-TKIs resistant than EGFR-TKIs sensitive cell lines and was gradually increased following cisplatin or gemcitabine treatment with the enrichment of G2/M cell cycle phase. Cisplatin 148-157 epidermal growth factor receptor Homo sapiens 79-83 31171399-0 2019 Gefitinib with or without Transarterial Infusion Chemotherapy (Cisplatin) for Large Nonsmall Cell Lung Cancer with Epidermal Growth Factor Receptor Mutations. Cisplatin 63-72 epidermal growth factor receptor Homo sapiens 115-147 31289485-0 2019 Positive PD-L1 expression is predictive for patients with advanced EGFR wild-type non-small cell lung cancer treated with gemcitabine and cisplatin. Cisplatin 138-147 epidermal growth factor receptor Homo sapiens 67-71 31289524-10 2019 Furthermore, the radiosensitization effects of curcumin and cisplatin on NSCLC A549 cells, which include inhibition of proliferation, migration and invasion, may be associated with the inhibition of the EGFR-associated signaling pathway. Cisplatin 60-69 epidermal growth factor receptor Homo sapiens 203-207 31138260-0 2019 Third generation EGFR inhibitor osimertinib combined with pemetrexed or cisplatin exerts long-lasting anti-tumor effect in EGFR-mutated pre-clinical models of NSCLC. Cisplatin 72-81 epidermal growth factor receptor Homo sapiens 123-127 31142791-7 2019 Intriguingly, in the EGFR-mutated NCI-H1975 and HCC827 cells, TTF-1 desensitized these cells to cisplatin; concomitantly, TTF-1 conferred an increase in p-AKT. Cisplatin 96-105 epidermal growth factor receptor Homo sapiens 21-25 31138260-13 2019 CONCLUSIONS: Our results identify a combination between osimertinib and pemetrexed or cisplatin potentially useful in the treatment of EGFR-mutated NSCLC patients, which might delay the appearance of osimertinib resistance with long-lasting effects. Cisplatin 86-95 epidermal growth factor receptor Homo sapiens 135-139 31161851-3 2019 In this study, we report an unexpected favorable response to etoposide and cisplatin (EP) from an EGFR-mutant patient who developed SCLC transformation at disease progression after the administration of erlotinib with a progression-free survivalof 7.7 months. Cisplatin 75-84 epidermal growth factor receptor Homo sapiens 98-102 30417422-11 2019 Furthermore, ADAMTS18 suppressed epidermal growth factor receptor/protein kinase B (EGFR/AKT) signaling, which sensitized lung cancer cells to cisplatin. Cisplatin 143-152 epidermal growth factor receptor Homo sapiens 33-65 30417422-11 2019 Furthermore, ADAMTS18 suppressed epidermal growth factor receptor/protein kinase B (EGFR/AKT) signaling, which sensitized lung cancer cells to cisplatin. Cisplatin 143-152 epidermal growth factor receptor Homo sapiens 84-88 30417422-12 2019 Thus, our results demonstrated that the tumor suppressor gene ADAMTS18 was downregulated in lung cancer by promoter CpG methylation, and it promoted sensitivity to cisplatin via EGFR/AKT signaling. Cisplatin 164-173 epidermal growth factor receptor Homo sapiens 178-182 30449625-2 2019 Whether replacement of cisplatin with cetuximab-an antibody against the epidermal growth factor receptor-can preserve high survival and reduce treatment toxicity is unknown. Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 72-104 30229902-0 2019 Pyruvate dehydrogenase kinase 1 contributes to cisplatin resistance of ovarian cancer through EGFR activation. Cisplatin 47-56 epidermal growth factor receptor Homo sapiens 94-98 30664215-0 2019 Cx32 mediates cisplatin resistance in human ovarian cancer cells by affecting drug efflux transporter expression and activating the EGFR-Akt pathway. Cisplatin 14-23 epidermal growth factor receptor Homo sapiens 132-136 30021363-9 2018 CONCLUSION: YAP enhances gastric cancer cell proliferation and attenuates sensitivity to cisplatin potentially through targeting the EGFR signaling, indicating that YAP/EGFR signaling axis may serve as a potential target for treatment of gastric cancer. Cisplatin 89-98 epidermal growth factor receptor Homo sapiens 169-173 30320337-0 2018 Downregulation of microRNA-4295 enhances cisplatin-induced gastric cancer cell apoptosis through the EGFR/PI3K/Akt signaling pathway by targeting LRIG1. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 101-105 30320337-2 2018 The aim of the present study was to investigate the mechanism of microRNA-4295 (miR-4295), which regulates cisplatin (DDP)-induced apoptosis in GC cells through the leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1)-mediated epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Cisplatin 107-116 epidermal growth factor receptor Homo sapiens 237-269 30320337-2 2018 The aim of the present study was to investigate the mechanism of microRNA-4295 (miR-4295), which regulates cisplatin (DDP)-induced apoptosis in GC cells through the leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1)-mediated epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Cisplatin 107-116 epidermal growth factor receptor Homo sapiens 271-275 30413194-2 2018 In vivo studies have linked EGFR subcellular trafficking and chemo-resistance to cisplatin-based chemotherapies. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 28-32 30413194-4 2018 We aimed to investigate the prognostic significance of EGFR expression in patients receiving cisplatin-based adjuvant chemotherapy following radical cystectomy for advanced BC. Cisplatin 93-102 epidermal growth factor receptor Homo sapiens 55-59 30413194-16 2018 Furthermore, in vitro experiments demonstrated that inhibition of EGFR may sensitize cellular responses to cisplatin. Cisplatin 107-116 epidermal growth factor receptor Homo sapiens 66-70 30423706-0 2019 Targeting graphene quantum dots to epidermal growth factor receptor for delivery of cisplatin and cellular imaging. Cisplatin 84-93 epidermal growth factor receptor Homo sapiens 35-67 30423706-7 2019 The targeted CDDP-loaded nanocarriers ((CDDP)GQDs-scFvB10) exhibited significantly higher toxicity on MDA-MB-231 cells compared to non-targeted ones suggesting their efficient uptake through EGFR. Cisplatin 13-17 epidermal growth factor receptor Homo sapiens 191-195 30423706-7 2019 The targeted CDDP-loaded nanocarriers ((CDDP)GQDs-scFvB10) exhibited significantly higher toxicity on MDA-MB-231 cells compared to non-targeted ones suggesting their efficient uptake through EGFR. Cisplatin 40-44 epidermal growth factor receptor Homo sapiens 191-195 30423706-8 2019 In contrast, cells with saturated EGFR showed lower uptake and cytotoxic effect of (CDDP)GQDs-scFvB10, demonstrating selectivity of the nanocarriers towards EGFR-overexpressing cells. Cisplatin 84-88 epidermal growth factor receptor Homo sapiens 34-38 30423706-8 2019 In contrast, cells with saturated EGFR showed lower uptake and cytotoxic effect of (CDDP)GQDs-scFvB10, demonstrating selectivity of the nanocarriers towards EGFR-overexpressing cells. Cisplatin 84-88 epidermal growth factor receptor Homo sapiens 157-161 30347860-4 2018 Actively targeted cisplatin micelles were prepared through surface modification of acetal-poly(ethylene oxide)-poly(alpha-carboxyl-epsilon-caprolactone) (acetal-PEO-PCCL) micelles with epidermal growth factor receptor (EGFR)-targeting peptide, GE11 (YHWYGYTPQNVI). Cisplatin 18-27 epidermal growth factor receptor Homo sapiens 185-217 30347860-4 2018 Actively targeted cisplatin micelles were prepared through surface modification of acetal-poly(ethylene oxide)-poly(alpha-carboxyl-epsilon-caprolactone) (acetal-PEO-PCCL) micelles with epidermal growth factor receptor (EGFR)-targeting peptide, GE11 (YHWYGYTPQNVI). Cisplatin 18-27 epidermal growth factor receptor Homo sapiens 219-223 30347860-6 2018 A significant increase in micellar cisplatin uptake was observed in MDA-MB-231 cells that overexpress EGFR, following surface modification of micelles with GE11. Cisplatin 35-44 epidermal growth factor receptor Homo sapiens 102-106 29101518-0 2018 Phase1 study of cisplatin plus pemetrexed with erlotinib and bevacizumab for chemotherapy-naive advanced non-squamous non-small cell lung cancer with EGFR mutations. Cisplatin 16-25 epidermal growth factor receptor Homo sapiens 150-154 29551903-4 2018 Hence, the aim of this study was to explore the therapeutic efficacy and underlying mechanism of the sensitization to radiation or cisplatin of icotinib hydrochloride (IH), a high-selective EGFR tyrosine kinase inhibitor (TKI), in the Hela S3 human CC cell line. Cisplatin 131-140 epidermal growth factor receptor Homo sapiens 190-194 29982103-5 2018 One of the mechanisms for overcoming cisplatin resistance in these cells is mediated by the inhibition of epidermal growth factor receptor (EGFR), though not all the EGFR inhibitors are equally active. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 106-138 29982103-5 2018 One of the mechanisms for overcoming cisplatin resistance in these cells is mediated by the inhibition of epidermal growth factor receptor (EGFR), though not all the EGFR inhibitors are equally active. Cisplatin 37-46 epidermal growth factor receptor Homo sapiens 140-144 29982103-6 2018 The increased levels of total EGFR and phosphorylated-EGFR (p-EGFR) in the A2780-cis cells were reduced after the combined treatment of cisplatin with EGFR inhibitors. Cisplatin 136-145 epidermal growth factor receptor Homo sapiens 30-34 29982103-6 2018 The increased levels of total EGFR and phosphorylated-EGFR (p-EGFR) in the A2780-cis cells were reduced after the combined treatment of cisplatin with EGFR inhibitors. Cisplatin 136-145 epidermal growth factor receptor Homo sapiens 54-58 29982103-6 2018 The increased levels of total EGFR and phosphorylated-EGFR (p-EGFR) in the A2780-cis cells were reduced after the combined treatment of cisplatin with EGFR inhibitors. Cisplatin 136-145 epidermal growth factor receptor Homo sapiens 54-58 29982103-6 2018 The increased levels of total EGFR and phosphorylated-EGFR (p-EGFR) in the A2780-cis cells were reduced after the combined treatment of cisplatin with EGFR inhibitors. Cisplatin 136-145 epidermal growth factor receptor Homo sapiens 54-58 29982103-7 2018 In addition, a knockdown of EGFR mRNA reduced cisplatin resistance in the A2780-cis cells. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 28-32 29644460-8 2018 CONCLUSION: The combination of cisplatin/pemetrexed/bevacizumab followed by pemetrexed/bevacizumab maintenance therapy exhibited favorable efficacy and manageable toxicity profiles in patients with EGFR-wild type non-squamous NSCLC (UMIN-CTR number: UMIN000003645). Cisplatin 31-40 epidermal growth factor receptor Homo sapiens 198-202 29805654-0 2018 Cisplatin-induced non-canonical endocytosis of EGFR via p38 phosphorylation of the C-terminal region containing Ser-1015 in non-small cell lung cancer cells. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 47-51 29805654-4 2018 In the present study, the role of non-canonical EGFR regulation has been investigated in NSCLC cells treated with cisplatin, a common chemotherapeutic agent. Cisplatin 114-123 epidermal growth factor receptor Homo sapiens 48-52 29805654-5 2018 Cisplatin-induced p38 activation triggered the Ser-1015 phosphorylation of EGFR, with similar kinetics to previously reported Ser-1047 phosphorylation, in a tyrosine kinase-independent manner. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 75-79 29805654-8 2018 The results of the present study provide mechanistic evidence for the cisplatin-induced non-canonical regulation of EGFR. Cisplatin 70-79 epidermal growth factor receptor Homo sapiens 116-120 30093972-0 2018 Positive crosstalk between EGFR and the TF-PAR2 pathway mediates resistance to cisplatin and poor survival in cervical cancer. Cisplatin 79-88 epidermal growth factor receptor Homo sapiens 27-31 30093972-10 2018 PAR2-AP decreased cisplatin-induced apoptosis through an EGFR- and COX2-dependent mechanism. Cisplatin 18-27 epidermal growth factor receptor Homo sapiens 57-61 29644460-1 2018 PURPOSE: This phase II study was performed to evaluate the efficacy and safety of cisplatin/pemetrexed combined with 15 mg/kg of bevacizumab followed by pemetrexed/bevacizumab maintenance therapy as first-line chemotherapy in advanced non-squamous non-small cell lung cancer (NSCLC) limited to epidermal growth factor receptor (EGFR)-wild type. Cisplatin 82-91 epidermal growth factor receptor Homo sapiens 294-326 29644460-1 2018 PURPOSE: This phase II study was performed to evaluate the efficacy and safety of cisplatin/pemetrexed combined with 15 mg/kg of bevacizumab followed by pemetrexed/bevacizumab maintenance therapy as first-line chemotherapy in advanced non-squamous non-small cell lung cancer (NSCLC) limited to epidermal growth factor receptor (EGFR)-wild type. Cisplatin 82-91 epidermal growth factor receptor Homo sapiens 328-332 29662625-9 2018 Consequently, cisplatin strongly induced phosphorylation of ADAM17-downstream mediators, the EGFR and extracellular signal-regulated kinases (ERK). Cisplatin 14-23 epidermal growth factor receptor Homo sapiens 93-97 29328423-1 2018 Cisplatin and cetuximab, an anti-epidermal growth factor receptor (EGFR) monoclonal humanized antibody, have been used for treatment of laryngeal squamous cell carcinoma (LSCC). Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 28-65 29328423-1 2018 Cisplatin and cetuximab, an anti-epidermal growth factor receptor (EGFR) monoclonal humanized antibody, have been used for treatment of laryngeal squamous cell carcinoma (LSCC). Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 67-71 29100507-13 2017 CONCLUSION: Simultaneous inhibition of EGFR and IGF1R in cisplatin-resistant TNBC cell lines was synergistic regarding inhibition of proliferation and induction of apoptosis. Cisplatin 57-66 epidermal growth factor receptor Homo sapiens 39-43 29344640-0 2018 Over-regulation of microRNA-133b inhibits cell proliferation of cisplatin-induced non-small cell lung cancer cells through PI3K/Akt and JAK2/STAT3 signaling pathway by targeting EGFR. Cisplatin 64-73 epidermal growth factor receptor Homo sapiens 178-182 29344640-5 2018 EGFR inhibitor (lapatinib) suppressed EGFR protein expression, inhibited cell proliferation and LDH activity, and induced apoptosis and caspase-3 activity in cisplatin-induced A549 cells by over-regulation of microRNA-133b. Cisplatin 158-167 epidermal growth factor receptor Homo sapiens 0-4 29344640-6 2018 When EGFR protein expression was suppressed, PI3K, p-Akt, p-JAK2 and p-STAT3, decreased cyclin D1 and increased Bax protein expression in cisplatin-induced A549 cells by over-regulation of microRNA-133b. Cisplatin 138-147 epidermal growth factor receptor Homo sapiens 5-9 29344640-7 2018 Altogether, our results indicated that over-regulation of microRNA-133b inhibits cell proliferation of cisplatin-induced NSCLC by PI3K/Akt and JAK2/STAT3 signaling pathway by targeting EGFR. Cisplatin 103-112 epidermal growth factor receptor Homo sapiens 185-189 28635183-2 2017 The specific targeting ability of cetuximab-NDs-cisplatin system on human liver hepatocellular carcinoma (HepG2) cells is evaluated through epidermal growth factor receptor (EGFR) blocking experiments, since EGFR is over-expressed on HepG2 cell membrane. Cisplatin 48-57 epidermal growth factor receptor Homo sapiens 140-172 28635183-2 2017 The specific targeting ability of cetuximab-NDs-cisplatin system on human liver hepatocellular carcinoma (HepG2) cells is evaluated through epidermal growth factor receptor (EGFR) blocking experiments, since EGFR is over-expressed on HepG2 cell membrane. Cisplatin 48-57 epidermal growth factor receptor Homo sapiens 174-178 28635183-2 2017 The specific targeting ability of cetuximab-NDs-cisplatin system on human liver hepatocellular carcinoma (HepG2) cells is evaluated through epidermal growth factor receptor (EGFR) blocking experiments, since EGFR is over-expressed on HepG2 cell membrane. Cisplatin 48-57 epidermal growth factor receptor Homo sapiens 208-212 29434871-3 2018 In addition, CDDP has been identified to cause negative feedback inhibition of activated EGFR in lung cancer cells. Cisplatin 13-17 epidermal growth factor receptor Homo sapiens 89-93 29174310-3 2018 We aimed to compare the efficacy of adjuvant gefitinib versus vinorelbine plus cisplatin in patients with completely resected EGFR-mutant stage II-IIIA (N1-N2) NSCLC. Cisplatin 79-88 epidermal growth factor receptor Homo sapiens 126-130 28828595-0 2017 The EGFR Inhibitor Gefitinib Enhanced the Response of Human Oral Squamous Cell Carcinoma to Cisplatin In Vitro. Cisplatin 92-101 epidermal growth factor receptor Homo sapiens 4-8 28828595-1 2017 INTRODUCTION: The epidermal growth factor receptor (EGFR) is highly expressed in a variety of solid tumors including oral cavity squamous cell carcinoma (OSCC) and has been implicated in the resistance of these tumors to cisplatin. Cisplatin 221-230 epidermal growth factor receptor Homo sapiens 18-50 28828595-1 2017 INTRODUCTION: The epidermal growth factor receptor (EGFR) is highly expressed in a variety of solid tumors including oral cavity squamous cell carcinoma (OSCC) and has been implicated in the resistance of these tumors to cisplatin. Cisplatin 221-230 epidermal growth factor receptor Homo sapiens 52-56 28828595-2 2017 This study was performed to determine if the EGFR tyrosine kinase inhibitor gefitinib could enhance the cytotoxic effect of cisplatin on OSCC cells in vitro. Cisplatin 124-133 epidermal growth factor receptor Homo sapiens 45-49 28828595-10 2017 CONCLUSION: Thus, in OSCC cells in vitro, inhibition of EGFR activity with gefitinib enhances the apoptotic effect of cisplatin. Cisplatin 118-127 epidermal growth factor receptor Homo sapiens 56-60 28828595-11 2017 This has potential implications for enhancement of cisplatin effectiveness in tumors that over-express the EGFR. Cisplatin 51-60 epidermal growth factor receptor Homo sapiens 107-111 28910149-0 2017 Dual Targeting of Epidermal Growth Factor Receptor and HER3 by MEHD7945A as Monotherapy or in Combination with Cisplatin Partially Overcomes Cetuximab Resistance in Head and Neck Squamous Cell Carcinoma Cell Lines. Cisplatin 111-120 epidermal growth factor receptor Homo sapiens 18-50 28522592-2 2017 This work aimed at questioning the effects of cisplatin initial treatment on the EGFR pathway in non-small cell lung cancer and the functional consequences in vitro and in in vivo animal models of patient-derived xenografts (PDX). Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 81-85 28522592-3 2017 We establish here that cisplatin pretreatment specifically sensitizes wild-type EGFR-expressing cells to erlotinib, contrary to what happens in mutant EGFR cells and with a blocking EGFR antibody, both in vitro and in vivo The sensitization entails the activation of the kinase Src upstream of EGFR, thereafter transactivating EGFR through a ligand-independent activation. Cisplatin 23-32 epidermal growth factor receptor Homo sapiens 80-84 28275299-8 2017 Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway and protein-protein interaction analysis demonstrated that the differentially expressed mRNAs were enriched in PI3K-Akt, Notch, MAPK, ErbB, Jak-STAT, NF-kappaB signaling pathways which may be involved in cisplatin resistance. Cisplatin 267-276 epidermal growth factor receptor Homo sapiens 197-201 28340378-9 2017 Some of the drugs developed after cisplatin discovery, have been targeted the epidermal growth factor receptor, anaplastic lymphoma kinase, programmed cell death 1 ligand and vascular endothelial growth factor. Cisplatin 34-43 epidermal growth factor receptor Homo sapiens 78-110 28011380-0 2017 Propofol enhances the cisplatin-induced apoptosis on cervical cancer cells via EGFR/JAK2/STAT3 pathway. Cisplatin 22-31 epidermal growth factor receptor Homo sapiens 79-83 28011380-8 2017 In genetic level, propofol could enhance the anti-tumor effect of cisplatin through EGFR/JAK2/STAT3 pathway. Cisplatin 66-75 epidermal growth factor receptor Homo sapiens 84-88 28011380-9 2017 Further studies indicated that overexpression of EGFR and STAT3 is related to poor prognoses in cervical cancer patients, which contributed to confirm the clinical role of combined application of propofol and cisplatin. Cisplatin 209-218 epidermal growth factor receptor Homo sapiens 49-53 28011380-10 2017 CONCLUSION: Propofol enhances the cisplatin-induced cell apoptosis cervical cancer cells via EGFR/JAK2/STAT3 pathway and may be developed as a potential therapeutic agent to treat cervical cancer. Cisplatin 34-43 epidermal growth factor receptor Homo sapiens 93-97 27535835-0 2016 Silencing of fused toes homolog enhances cisplatin sensitivity in cervical cancer cells by inhibiting epidermal growth factor receptor-mediated repair of DNA damage. Cisplatin 41-50 epidermal growth factor receptor Homo sapiens 102-134 27435393-9 2017 Furthermore, the EGFR/STAT3 pathway contributed to CDDP-induced CEBPD expression in UCUB cells. Cisplatin 51-55 epidermal growth factor receptor Homo sapiens 17-21 27733374-2 2016 In this trial, the epidermal growth-factor receptor (EGFR) pathway was targeted using the IgG2 monoclonal antibody panitumumab in combination with cisplatin chemoradiotherapy (CRT) in high-risk, resected HNSCC. Cisplatin 147-156 epidermal growth factor receptor Homo sapiens 19-51 27733374-2 2016 In this trial, the epidermal growth-factor receptor (EGFR) pathway was targeted using the IgG2 monoclonal antibody panitumumab in combination with cisplatin chemoradiotherapy (CRT) in high-risk, resected HNSCC. Cisplatin 147-156 epidermal growth factor receptor Homo sapiens 53-57 27435393-0 2017 Inhibition of the EGFR/STAT3/CEBPD Axis Reverses Cisplatin Cross-resistance with Paclitaxel in the Urothelial Carcinoma of the Urinary Bladder. Cisplatin 49-58 epidermal growth factor receptor Homo sapiens 18-22 27435393-4 2017 EXPERIMENTAL DESIGN: Loss-of-function assays were performed to elucidate the role of the EGFR and STAT3 in CDDP-induced CCAAT/enhancer-binding protein delta (CEBPD) expression in UCUB cells. Cisplatin 107-111 epidermal growth factor receptor Homo sapiens 89-93 27697601-0 2017 Overcoming cisplatin resistance in non-small cell lung cancer with Mad2 silencing siRNA delivered systemically using EGFR-targeted chitosan nanoparticles. Cisplatin 11-20 epidermal growth factor receptor Homo sapiens 117-121 27884140-6 2016 A reasonable option may be to employ the combination of cisplatin, cetuximab and VPA in recurrent/metastatic SCCHN taking advantage of the possible positive interaction between histone deacetylase inhibitors, cisplatin and/or anti-EGFR. Cisplatin 56-65 epidermal growth factor receptor Homo sapiens 231-235 27535835-2 2016 EGFR is activated by cisplatin, and this may lead to resistance to this drug. Cisplatin 21-30 epidermal growth factor receptor Homo sapiens 0-4 27535835-10 2016 RESULTS: Among the lines tested, ME180 cells showed the highest basal expression of EGFR and increased nuclear phosphorylated EGFR in response to cisplatin. Cisplatin 146-155 epidermal growth factor receptor Homo sapiens 84-88 27535835-10 2016 RESULTS: Among the lines tested, ME180 cells showed the highest basal expression of EGFR and increased nuclear phosphorylated EGFR in response to cisplatin. Cisplatin 146-155 epidermal growth factor receptor Homo sapiens 126-130 27535835-11 2016 In ME180 cells, the activation of EGFR and DNA-PK by cisplatin was attenuated by silencing FTS. Cisplatin 53-62 epidermal growth factor receptor Homo sapiens 34-38 27535835-14 2016 CONCLUSION: FTS is involved in EGFR-mediated repair of DNA damage induced by cisplatin in ME180 cells. Cisplatin 77-86 epidermal growth factor receptor Homo sapiens 31-35 27535835-15 2016 This suggests that FTS can be a target to increase the efficacy of cisplatin in cervical cancer cells that exhibit increased nuclear phosphorylated EGFR in response to cisplatin. Cisplatin 67-76 epidermal growth factor receptor Homo sapiens 148-152 27535835-15 2016 This suggests that FTS can be a target to increase the efficacy of cisplatin in cervical cancer cells that exhibit increased nuclear phosphorylated EGFR in response to cisplatin. Cisplatin 168-177 epidermal growth factor receptor Homo sapiens 148-152 26950292-5 2016 Necitumumab is a new anti-EGFR monoclonal antibody that improves survival when combined to cisplatin/gemcitabine chemotherapy and has been approved in first-line advanced NSCLC. Cisplatin 91-100 epidermal growth factor receptor Homo sapiens 26-30 27669890-2 2016 Our aim was to clarify whether mRNA expression of EGFR-ligands was linked to prognosis and cisplatin resistance, and if so, which ligand was most important and how was the expression regulated. Cisplatin 91-100 epidermal growth factor receptor Homo sapiens 50-54 27602148-6 2016 It was observed that RNAi-mediated downregulation of EGFR or MRP2 increased the sensitivity to 5-FU and cisplatin in OC2 cells. Cisplatin 104-113 epidermal growth factor receptor Homo sapiens 53-57 27602148-9 2016 In contrast, downregulation of MRP2 was demonstrated to significantly enhance the therapeutic effects of cisplatin in EGFR-downregulated OC2 tumors. Cisplatin 105-114 epidermal growth factor receptor Homo sapiens 118-122 27766772-1 2016 This article demonstrates a case of a lung adenocarcinoma patient in stage IV harboring an epidermal growth factor receptor (EGFR) 19 exon deletion mutation treated with 500 mg/m2 pemetrexed and 75 mg/m2 cisplatin on day 1, sequenced with 250 mg gefitinib on prescription on days 4-28 for six cycles as first-line, then by gefitinib combined with pemetrexed as maintenance therapy. Cisplatin 204-213 epidermal growth factor receptor Homo sapiens 91-123 27766772-1 2016 This article demonstrates a case of a lung adenocarcinoma patient in stage IV harboring an epidermal growth factor receptor (EGFR) 19 exon deletion mutation treated with 500 mg/m2 pemetrexed and 75 mg/m2 cisplatin on day 1, sequenced with 250 mg gefitinib on prescription on days 4-28 for six cycles as first-line, then by gefitinib combined with pemetrexed as maintenance therapy. Cisplatin 204-213 epidermal growth factor receptor Homo sapiens 125-129 27073199-11 2016 At any time point after the first cycle of cisplatin, <3% of patients progressed to eGFR<29 ml/min per 1.73 m(2), and none were known to be on dialysis. Cisplatin 43-52 epidermal growth factor receptor Homo sapiens 87-91 27073199-14 2016 The lowest dose categories of cisplatin (<=100 and 101-250 mg/m(2)) are associated with increases in eGFR (P=0.06 and P=0.02, respectively) compared with the highest dose category (>701 mg/m(2)). Cisplatin 30-39 epidermal growth factor receptor Homo sapiens 104-108 26980454-0 2016 Biodistribution and pharmacokinetics of Mad2 siRNA-loaded EGFR-targeted chitosan nanoparticles in cisplatin sensitive and resistant lung cancer models. Cisplatin 98-107 epidermal growth factor receptor Homo sapiens 58-62 26895469-9 2016 Our findings reveal a new mechanism by which EGFR/PI3K/Akt/mTOR signaling promotes head and neck cancer progression and underscores the need for developing a therapeutic strategy for targeting IKK/NF-kappaB either as a single agent or in combination with cisplatin in head and neck cancer. Cisplatin 255-264 epidermal growth factor receptor Homo sapiens 45-49 27301192-2 2016 In the present study, we have developed EGFR-targeted albumin-cisplatin nanoparticles for tumor targeted delivery of cisplatin. Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 40-44 27301192-2 2016 In the present study, we have developed EGFR-targeted albumin-cisplatin nanoparticles for tumor targeted delivery of cisplatin. Cisplatin 117-126 epidermal growth factor receptor Homo sapiens 40-44 27301192-3 2016 The cisplatin NPs were conjugated with EGFR aptamer, which binded to Hela cells specifically, then taken up by tumor cells through receptor mediated endocytosis. Cisplatin 4-13 epidermal growth factor receptor Homo sapiens 39-43 27301192-5 2016 Here we demonstrate that the EGFR aptamer functioned NPs enhanced in vitro antitumor effects and markedly improved its tolerability and in vivo efficacy when compared with free cisplatin and other single treatment. Cisplatin 177-186 epidermal growth factor receptor Homo sapiens 29-33 27029054-0 2016 Exosomes derived from gefitinib-treated EGFR-mutant lung cancer cells alter cisplatin sensitivity via up-regulating autophagy. Cisplatin 76-85 epidermal growth factor receptor Homo sapiens 40-44 26980454-1 2016 BACKGROUND: The present study focuses on biodistribution profile and pharmacokinetic parameters of EGFR-targeted chitosan nanoparticles (TG CS nanoparticles) for siRNA/cisplatin combination therapy of lung cancer. Cisplatin 168-177 epidermal growth factor receptor Homo sapiens 99-103 27186285-0 2016 Effect of the BRCA1-SIRT1-EGFR axis on cisplatin sensitivity in ovarian cancer. Cisplatin 39-48 epidermal growth factor receptor Homo sapiens 26-30 27186285-1 2016 There is accumulating evidence that breast cancer 1 (BRCA1), sirtuin 1 (SIRT1), and epidermal growth factor receptor (EGFR) help to modulate cisplatin cytotoxicity. Cisplatin 141-150 epidermal growth factor receptor Homo sapiens 84-116 27186285-1 2016 There is accumulating evidence that breast cancer 1 (BRCA1), sirtuin 1 (SIRT1), and epidermal growth factor receptor (EGFR) help to modulate cisplatin cytotoxicity. Cisplatin 141-150 epidermal growth factor receptor Homo sapiens 118-122 27186285-2 2016 The role of dynamic crosstalk among BRCA1, SIRT1, and EGFR in cisplatin sensitivity remains largely unknown. Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 54-58 27186285-3 2016 We found that BRCA1, SIRT1, and EGFR levels were increased in cisplatin-resistant ovarian cancers compared with those in cisplatin-sensitive ovarian cancers. Cisplatin 62-71 epidermal growth factor receptor Homo sapiens 32-36 27614872-1 2016 BACKGROUND: In the SQUIRE study, adding the anti-epidermal growth factor receptor (EGFR) IgG1 antibody necitumumab to first-line gemcitabine and cisplatin (GC + N) in advanced squamous non-small-cell lung cancer (sqNSCLC) significantly improved overall survival (OS); the safety profile was acceptable. Cisplatin 145-154 epidermal growth factor receptor Homo sapiens 83-87 27186285-5 2016 Treatment with 5 and 10 mug/ml cisplatin induced a gradual increase in BRCA1 and SIRT1 levels and a gradual decrease in NAD levels and NAD-mediated SIRT1 activity, whereas EGFR levels were increased or decreased by treatment with 5 or 10 mug/ml cisplatin, respectively. Cisplatin 31-40 epidermal growth factor receptor Homo sapiens 172-176 26620316-11 2016 CONCLUSIONS: PAC-1 showed anti-tumor activity in NSCLCs in vitro and a synergistic effect with cisplatin in EGFR(wt)KRAS(wt) H1299 cells. Cisplatin 95-104 epidermal growth factor receptor Homo sapiens 108-112 26782932-0 2016 Co-treatment of wild-type EGFR head and neck cancer cell lines with afatinib and cisplatin. Cisplatin 81-90 epidermal growth factor receptor Homo sapiens 26-30 26654941-8 2016 Hyperthermia and cisplatin synergistically downregulated the EGFR protein level, leading to quenching of signal from EGFR and induction of apoptosis. Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 61-65 26654941-8 2016 Hyperthermia and cisplatin synergistically downregulated the EGFR protein level, leading to quenching of signal from EGFR and induction of apoptosis. Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 117-121 27313893-0 2016 Cetuximab and Cisplatin Show Different Combination Effect in Nasopharyngeal Carcinoma Cells Lines via Inactivation of EGFR/AKT Signaling Pathway. Cisplatin 14-23 epidermal growth factor receptor Homo sapiens 118-122 27313893-9 2016 Our results showed that cisplatin-induced apoptosis was significantly enhanced by cetuximab in the high EGFR-expressing HNE1 cells but not in CNE2 cells. Cisplatin 24-33 epidermal growth factor receptor Homo sapiens 104-108 26568478-2 2015 It is known that cisplatin can activate epidermal growth factor receptor (EGFR), which may provide a survival benefit in cancers. Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 40-72 26534724-3 2015 The mean change of eGFR (100% to baseline) in CDDP-treated patients was -9.2%, which was significantly lower than that in the population with CBP therapy. Cisplatin 46-50 epidermal growth factor receptor Homo sapiens 19-23 26568478-2 2015 It is known that cisplatin can activate epidermal growth factor receptor (EGFR), which may provide a survival benefit in cancers. Cisplatin 17-26 epidermal growth factor receptor Homo sapiens 74-78 26568478-4 2015 In this study, we explore the therapeutic potential of TM on cisplatin-mediated EGFR regulation. Cisplatin 61-70 epidermal growth factor receptor Homo sapiens 80-84 26568478-7 2015 TM suppressed cisplatin-induced activation of EGFR while potentiating activation of p38; the activation of p38 signaling appeared to promote cisplatin-induced EGFR degradation. Cisplatin 14-23 epidermal growth factor receptor Homo sapiens 46-50 26568478-7 2015 TM suppressed cisplatin-induced activation of EGFR while potentiating activation of p38; the activation of p38 signaling appeared to promote cisplatin-induced EGFR degradation. Cisplatin 141-150 epidermal growth factor receptor Homo sapiens 159-163 26351843-8 2015 Acute cisplatin treatment activates the EGFR and downstream signaling pathways, and induces an EGFR mediated increase in DNMT activity. Cisplatin 6-15 epidermal growth factor receptor Homo sapiens 40-44 26300055-13 2015 The inhibition of this pathway at various level (PKC-alpha, EGFR or ERK1/2) increased cisplatin-induced cytotoxicity. Cisplatin 86-95 epidermal growth factor receptor Homo sapiens 60-64 26351843-4 2015 Others have shown that EGFR activation is linked to cisplatin treatment and platinum resistance. Cisplatin 52-61 epidermal growth factor receptor Homo sapiens 23-27 26351843-8 2015 Acute cisplatin treatment activates the EGFR and downstream signaling pathways, and induces an EGFR mediated increase in DNMT activity. Cisplatin 6-15 epidermal growth factor receptor Homo sapiens 95-99 26351843-5 2015 We hypothesized that cisplatin induced activation of the EGFR mediates changes in DNA methylation associated with the development of platinum resistance. Cisplatin 21-30 epidermal growth factor receptor Homo sapiens 57-61 26351843-10 2015 EGFR inhibition during repeated cisplatin treatments generated cells that were more sensitive to cisplatin and did not develop increases in DNA methylation or DNMT activity compared to controls. Cisplatin 32-41 epidermal growth factor receptor Homo sapiens 0-4 26351843-7 2015 We also developed an in vitro model of platinum resistance to examine the effects of EGFR inhibition on acquisition of cisplatin resistance. Cisplatin 119-128 epidermal growth factor receptor Homo sapiens 85-89 26351843-10 2015 EGFR inhibition during repeated cisplatin treatments generated cells that were more sensitive to cisplatin and did not develop increases in DNA methylation or DNMT activity compared to controls. Cisplatin 97-106 epidermal growth factor receptor Homo sapiens 0-4 25979647-0 2015 Autophagy Inhibition Overcomes the Antagonistic Effect Between Gefitinib and Cisplatin in Epidermal Growth Factor Receptor Mutant Non--Small-Cell Lung Cancer Cells. Cisplatin 77-86 epidermal growth factor receptor Homo sapiens 90-122 25843489-3 2015 Patients with EGFR wild type received 4 cycles of bevacizumab, pemetrexed, and cisplatin, followed by maintenance with bevacizumab and pemetrexed until progression. Cisplatin 79-88 epidermal growth factor receptor Homo sapiens 14-18 25979647-2 2015 In the present study, the role of autophagy in the combination of gefitinib and cisplatin on EGFR-TKI-sensitive human lung cancer cell line was investigated. Cisplatin 80-89 epidermal growth factor receptor Homo sapiens 93-97 25979647-15 2015 CONCLUSION: The combination of gefitinib with cisplatin generates antagonistic effects on EGFR-TKI-sensitive cells. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 90-94 25979647-16 2015 However, inhibiting autophagy produces a synergistic effect, suggesting that gefitinib and cisplatin combined with an autophagy inhibitor (especially CQ) might be a beneficial strategy to overcome the antagonistic effects between EGFR-TKIs and chemotherapeutic agents. Cisplatin 91-100 epidermal growth factor receptor Homo sapiens 230-234 25980493-8 2015 Finally, the activation of the HRAS/PI3K/AKT pathway by EGFR-induced SOS1 also inhibits cisplatin-induced apoptosis, suggesting a common apoptosis-evasion mechanism in hepatoma cells. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 56-60 26141950-8 2015 Contrary to our hypothesis, EGFR inhibitors added to cisplatin treatment caused variable effects among cell lines, with attenuation of p-S727-STAT1 and enhancement of cisplatin-induced cell death in some cells and minimal effect in other cells. Cisplatin 167-176 epidermal growth factor receptor Homo sapiens 28-32 26141950-10 2015 Together, these results suggest that cisplatin-induced cell death is associated with STAT1 phosphorylation, and the addition of anti-EGFR therapy to cisplatin has variable effects on STAT1 and cell death in HNSCC. Cisplatin 149-158 epidermal growth factor receptor Homo sapiens 133-137 25908039-0 2015 Transformation to small cell lung cancer as an acquired resistance mechanism in EGFR-mutant lung adenocarcinoma: a case report of complete response to etoposide and cisplatin. Cisplatin 165-174 epidermal growth factor receptor Homo sapiens 80-84 26066081-2 2015 We show that the p38 MAP kinase-dependent, EGFR tyrosine kinase (TK)-independent EGFR internalization induced by ultraviolet light C (UVC) or the cancer therapeutic cisplatin, is followed by diversion from the canonical endocytic pathway. Cisplatin 165-174 epidermal growth factor receptor Homo sapiens 43-47 26066081-2 2015 We show that the p38 MAP kinase-dependent, EGFR tyrosine kinase (TK)-independent EGFR internalization induced by ultraviolet light C (UVC) or the cancer therapeutic cisplatin, is followed by diversion from the canonical endocytic pathway. Cisplatin 165-174 epidermal growth factor receptor Homo sapiens 81-85 26066081-6 2015 In contrast to the internalization-independent EGF-stimulated activation, UVC/cisplatin-triggered EGFR activation depends on EGFR internalization and intracellular retention. Cisplatin 78-87 epidermal growth factor receptor Homo sapiens 98-102 26066081-6 2015 In contrast to the internalization-independent EGF-stimulated activation, UVC/cisplatin-triggered EGFR activation depends on EGFR internalization and intracellular retention. Cisplatin 78-87 epidermal growth factor receptor Homo sapiens 125-129 25701783-0 2015 Role of tyrosine kinase-independent phosphorylation of EGFR with activating mutation in cisplatin-treated lung cancer cells. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 55-59 25695283-4 2015 Previous studies have confirmed that the epidermal growth factor receptor (EGFR) and its signaling pathways are important in the chemoresistance of cancer cells against CDDP-induced cell apoptosis. Cisplatin 169-173 epidermal growth factor receptor Homo sapiens 41-73 25695283-4 2015 Previous studies have confirmed that the epidermal growth factor receptor (EGFR) and its signaling pathways are important in the chemoresistance of cancer cells against CDDP-induced cell apoptosis. Cisplatin 169-173 epidermal growth factor receptor Homo sapiens 75-79 25695283-8 2015 The results showed that CDDP inhibited the growth of the T24 cell line and induced activation of EGFR. Cisplatin 24-28 epidermal growth factor receptor Homo sapiens 97-101 25695283-9 2015 Overexpression of LRIG1 increased the inhibitory effect of CDDP on the T24 cell line, which may be associated with inactivation of the EGFR signaling pathway, followed by the decrease of Bcl-2 expression and a concomitantly induced expression of Bax. Cisplatin 59-63 epidermal growth factor receptor Homo sapiens 135-139 25701783-3 2015 The purpose of this study is to investigate the role of non-canonical EGFR pathway in resistance mechanism against cisplatin treatment. Cisplatin 115-124 epidermal growth factor receptor Homo sapiens 70-74 25701783-5 2015 It is interesting that internalization mechanism of EGFR was switched from tyrosine kinase-dependent to p38-dependent fashions, which is involved in a survival pathway that counteracts cisplatin treatment. Cisplatin 185-194 epidermal growth factor receptor Homo sapiens 52-56 25701783-6 2015 We therefore introduce a potential combinatorial therapy composed of p38 inhibition and cisplatin to block the activation of EGFR, therefore inducing cancer cell death and apoptosis. Cisplatin 88-97 epidermal growth factor receptor Homo sapiens 125-129 25784483-0 2015 Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer. Cisplatin 59-68 epidermal growth factor receptor Homo sapiens 42-46 24985049-10 2015 Erlotinib combined with pemetrexed/cisplatin may be effective in the treatment of LM in EGFR mutation patients after gefitinib failure. Cisplatin 35-44 epidermal growth factor receptor Homo sapiens 88-92 26491668-6 2015 Results demonstrate that combined treatment with cetuximab and cisplatin exerts synergistic anticancer effects on colon cancer cells and also suggest that the ERK pathway plays a critical role in these effects via the suppression of the EGFR signaling pathway, along with the inhibition of COX-2, IL-8, and AP-1 and NF-kappaB. Cisplatin 63-72 epidermal growth factor receptor Homo sapiens 237-241 25748238-0 2015 Erlotinib-cisplatin combination inhibits growth and angiogenesis through c-MYC and HIF-1alpha in EGFR-mutated lung cancer in vitro and in vivo. Cisplatin 10-19 epidermal growth factor receptor Homo sapiens 97-101 25748238-4 2015 In NSCLC cells harboring epidermal growth factor receptor (EGFR) mutations, combination erlotinib-cisplatin treatment led to synergistic cell death, but there was minimal efficacy in NSCLC cells with wild-type EGFR. Cisplatin 98-107 epidermal growth factor receptor Homo sapiens 25-57 25748238-4 2015 In NSCLC cells harboring epidermal growth factor receptor (EGFR) mutations, combination erlotinib-cisplatin treatment led to synergistic cell death, but there was minimal efficacy in NSCLC cells with wild-type EGFR. Cisplatin 98-107 epidermal growth factor receptor Homo sapiens 59-63 25748238-4 2015 In NSCLC cells harboring epidermal growth factor receptor (EGFR) mutations, combination erlotinib-cisplatin treatment led to synergistic cell death, but there was minimal efficacy in NSCLC cells with wild-type EGFR. Cisplatin 98-107 epidermal growth factor receptor Homo sapiens 210-214 25748238-9 2015 These results suggest that low dose erlotinib-cisplatin combination exhibits its anti-tumor activity by targeting angiogenesis through the modulation of the c-MYC/HIF-1alpha/VEGF pathway in NSCLC with EGFR exon 19 deletions. Cisplatin 46-55 epidermal growth factor receptor Homo sapiens 201-205 25370413-6 2015 Cisplatin and paclitaxel significantly increased the expression of EGFR phosphorylation in the HCC827 cell line. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 67-71 25370413-8 2015 Cisplatin/paclitaxel followed by icotinib influenced the expression of p-EGFR and p-AKT, although the expression of p-ERK1/2 remained unchanged. Cisplatin 0-9 epidermal growth factor receptor Homo sapiens 73-77 25369798-12 2014 Additionally, the use of anti-EGFR MoAbs significantly increased the risk of severe infections when used in conjunction with cisplatin (RR 1.48, 95%CI 1.22 to 1.79, P<0.001) or irinotecan (RR 1.53, 95%CI 1.12 to 2.10, P=0.008). Cisplatin 125-134 epidermal growth factor receptor Homo sapiens 30-34