PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27126828-4 2016 Several oral agents are used in treating patients with lung cancer driven by mutations of genes coding for anaplastic lymphoma kinase (ALK) and epidermal growth factor receptor (EGFR); currently available agents include the ALK inhibitors certinib and crizotinib and the EGFR inhibitors afatinib, erlotinib, and gefitinib. Erlotinib Hydrochloride 297-306 ALK receptor tyrosine kinase Homo sapiens 224-227 29526950-1 2018 A 63-year-old woman with pulmonary adenocarcinoma (stage IIIB) that was positive for an epidermal growth factor receptor (EGFR) mutation and an anaplastic lymphoma kinase (ALK) rearrangement was treated with erlotinib as the first-line treatment, resulting in a stable disease. Erlotinib Hydrochloride 208-217 ALK receptor tyrosine kinase Homo sapiens 144-170 29526950-1 2018 A 63-year-old woman with pulmonary adenocarcinoma (stage IIIB) that was positive for an epidermal growth factor receptor (EGFR) mutation and an anaplastic lymphoma kinase (ALK) rearrangement was treated with erlotinib as the first-line treatment, resulting in a stable disease. Erlotinib Hydrochloride 208-217 ALK receptor tyrosine kinase Homo sapiens 172-175 27070423-7 2016 RESULTS: HCC827 (Exon19: E746-A750 del) and H3122 (EML4-ALK) cells were inhibited by lower concentrations of erlotinib and crizotinib, respectively than A549, H460, and H1975 (L858R+T790M) cells were. Erlotinib Hydrochloride 109-118 ALK receptor tyrosine kinase Homo sapiens 56-59 25788996-0 2015 Response to erlotinib in a patient with lung adenocarcinoma harbouring the EML4-ALK translocation: A case report. Erlotinib Hydrochloride 12-21 ALK receptor tyrosine kinase Homo sapiens 80-83 26788139-1 2015 Non-small-cell lung cancer (NSCLC) with echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) translocation is resistant to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), including gefitinib and erlotinib, but responds to the ALK-TKI crizotinib. Erlotinib Hydrochloride 256-265 ALK receptor tyrosine kinase Homo sapiens 122-125 25788996-6 2015 The present study reports the case of a patient possessing the EML4-ALK rearrangement that was initially treated with erlotinib and achieved a lasting clinical response. Erlotinib Hydrochloride 118-127 ALK receptor tyrosine kinase Homo sapiens 68-71 24566025-3 2014 In the presence of EGFR mutation or ALK rearrangement, specific inhibitors have shown superior efficacy to chemotherapy in first-line treatment for anti-EGFR (erlotinib and gefitinib) and in second-line treatment for anti-ALK (crizotinib). Erlotinib Hydrochloride 159-168 ALK receptor tyrosine kinase Homo sapiens 36-39 25990337-5 2015 Patients with ALK rearrangements treated with specific ALK inhibitors such as crizotinib or EGFR-activating mutations treated with gefitinib, erlotinib or afatinib have improved progression-free survival and better quality of life than patients treated with chemotherapy. Erlotinib Hydrochloride 142-151 ALK receptor tyrosine kinase Homo sapiens 14-17 25990337-5 2015 Patients with ALK rearrangements treated with specific ALK inhibitors such as crizotinib or EGFR-activating mutations treated with gefitinib, erlotinib or afatinib have improved progression-free survival and better quality of life than patients treated with chemotherapy. Erlotinib Hydrochloride 142-151 ALK receptor tyrosine kinase Homo sapiens 55-58 25407901-2 2014 It has been suggested that EML4-ALK fusion is associated with the resistance in NSCLCs to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs), such as gefitinib and erlotinib. Erlotinib Hydrochloride 185-194 ALK receptor tyrosine kinase Homo sapiens 32-35 24355409-5 2014 Following the development of small molecules (gefitinib/erlotinib and crizotinib) able to reversibly inhibit the epidermal growth factor receptor (EGFR) and signaling pathways mediated by anaplastic lymphoma kinase (ALK), respectively, the MET signaling pathway has also been recognized as a potential target. Erlotinib Hydrochloride 56-65 ALK receptor tyrosine kinase Homo sapiens 188-214 24355409-5 2014 Following the development of small molecules (gefitinib/erlotinib and crizotinib) able to reversibly inhibit the epidermal growth factor receptor (EGFR) and signaling pathways mediated by anaplastic lymphoma kinase (ALK), respectively, the MET signaling pathway has also been recognized as a potential target. Erlotinib Hydrochloride 56-65 ALK receptor tyrosine kinase Homo sapiens 216-219 23714542-7 2013 Patients with EGFR mutations or ALK fusions should be treated with erlotinib or crizotinib, respectively, even in patients with tumor-related poor performance. Erlotinib Hydrochloride 67-76 ALK receptor tyrosine kinase Homo sapiens 32-35 24192124-3 2013 EGFR mutation as well as KRAS and ALK rearrangements are important biomarkers in the field owing to potential targeted therapies involved in clinical practice: erlotinib, geftinib, cetuximab and crizotinib. Erlotinib Hydrochloride 160-169 ALK receptor tyrosine kinase Homo sapiens 34-37 23733083-4 2013 CONCLUSION: EGFR activating mutations (exons 18 to 21) and EML4-ALK rearrangement are clinically important markers able to select NSCLC patients which benefit from EGFR or ALK tyrosine kinase inhibitors (gefitinib, erlotinib, crizotinib). Erlotinib Hydrochloride 215-224 ALK receptor tyrosine kinase Homo sapiens 172-175 22005476-0 2011 Lung adenocarcinoma with concurrent exon 19 EGFR mutation and ALK rearrangement responding to erlotinib. Erlotinib Hydrochloride 94-103 ALK receptor tyrosine kinase Homo sapiens 62-65 22286583-4 2012 At the moment, established personalized treatment approaches include treatment of patients with NSCLC and activating epidermal growth factor receptor (EGFR) mutations with the EGFR-directed tyrosine kinase inhibitors gefitinib or erlotinib, and treatment of NSCLC patients with genetic aberrations in the anaplastic lymphoma kinase (ALK) oncogene with the mesenchymal-epithelial transition factor (MET)/ALK inhibitor crizotinib. Erlotinib Hydrochloride 230-239 ALK receptor tyrosine kinase Homo sapiens 305-331 22286583-4 2012 At the moment, established personalized treatment approaches include treatment of patients with NSCLC and activating epidermal growth factor receptor (EGFR) mutations with the EGFR-directed tyrosine kinase inhibitors gefitinib or erlotinib, and treatment of NSCLC patients with genetic aberrations in the anaplastic lymphoma kinase (ALK) oncogene with the mesenchymal-epithelial transition factor (MET)/ALK inhibitor crizotinib. Erlotinib Hydrochloride 230-239 ALK receptor tyrosine kinase Homo sapiens 333-336 22286583-4 2012 At the moment, established personalized treatment approaches include treatment of patients with NSCLC and activating epidermal growth factor receptor (EGFR) mutations with the EGFR-directed tyrosine kinase inhibitors gefitinib or erlotinib, and treatment of NSCLC patients with genetic aberrations in the anaplastic lymphoma kinase (ALK) oncogene with the mesenchymal-epithelial transition factor (MET)/ALK inhibitor crizotinib. Erlotinib Hydrochloride 230-239 ALK receptor tyrosine kinase Homo sapiens 403-406 23154552-2 2012 This study investigated retrospectively the benefits of local ablative therapy (LAT) to central nervous system (CNS) and/or limited systemic disease progression and continuation of crizotinib or erlotinib in patients with metastatic ALK gene rearrangement (ALK+) or EGFR-mutant (EGFR-MT) NSCLC, respectively. Erlotinib Hydrochloride 195-204 ALK receptor tyrosine kinase Homo sapiens 233-236 21168933-0 2011 EGFR and EML4-ALK gene mutations in NSCLC: a case report of erlotinib-resistant patient with both concomitant mutations. Erlotinib Hydrochloride 60-69 ALK receptor tyrosine kinase Homo sapiens 14-17 21168933-3 2011 Here, we report a case of a patient with a concomitant EGFR mutation and ALK translocation resistant to erlotinib. Erlotinib Hydrochloride 104-113 ALK receptor tyrosine kinase Homo sapiens 73-76 33125153-7 2020 Statistically significant associations were found between HER2 expression and response to treatment with the ALK/IGF-IR/InsR inhibitor ceritinib and fibroblast growth factor receptor (FGFR)1/2/3 inhibitor AZD4547, HER3 and IGF-IR expression and their response to treatment with TKIs targeting HER family members (erlotinib and afatinib), and c-MET and ALK7 expression and their response to treatment with stattic. Erlotinib Hydrochloride 313-322 ALK receptor tyrosine kinase Homo sapiens 109-112