PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34575554-3 2021 Acquired resistance mechanisms to osimertinib in EGFR-driven NSCLC include MET amplification, EGFR C797S mutation, neuroendocrine differentiation, small-cell lung carcinoma histologic transformation, PD-L1 and KRAS amplifications and ESR1-AKAP12 and MKRN1-BRAF translocations, as well as BRAF V600 mutation. osimertinib 34-45 SAFB like transcription modulator Homo sapiens 75-78 34918545-1 2022 MET amplification (METamp), a mechanism of acquired resistance to EGFR tyrosine kinase inhibitors, occurs in up to 30% of patients with non-small-cell lung cancer (NSCLC) progressing on first-line osimertinib. osimertinib 197-208 SAFB like transcription modulator Homo sapiens 0-3 34918545-2 2022 Combining osimertinib with a MET inhibitor, such as tepotinib, an oral, highly selective, potent MET tyrosine kinase inhibitor, may overcome METamp-driven resistance. osimertinib 10-21 SAFB like transcription modulator Homo sapiens 29-32 34918545-2 2022 Combining osimertinib with a MET inhibitor, such as tepotinib, an oral, highly selective, potent MET tyrosine kinase inhibitor, may overcome METamp-driven resistance. osimertinib 10-21 SAFB like transcription modulator Homo sapiens 97-100 34498213-12 2021 After exposure to the osimertinib/bevacizumab combination, the main secondary alterations were MET amplification, STAT3, IGF1R, PTEN, and PDGFR. osimertinib 22-33 SAFB like transcription modulator Homo sapiens 95-98 35412115-8 2022 An important intrinsic resistance mechanism to osimertinib is the EGFR exon 20 insertion mutation, which is sensitive to the newly Food and Drug Administration (FDA)-approved tyrosine kinase inhibitor mobocertinib and the EGFR/MET bispecific antibody amivantamab. osimertinib 47-58 SAFB like transcription modulator Homo sapiens 227-230 34532491-6 2021 Herein, we report the first case of MET D1228N mutation mediating acquired resistance to osimertinib in a MET TKI-naive NSCLC. osimertinib 89-100 SAFB like transcription modulator Homo sapiens 36-39 34532491-6 2021 Herein, we report the first case of MET D1228N mutation mediating acquired resistance to osimertinib in a MET TKI-naive NSCLC. osimertinib 89-100 SAFB like transcription modulator Homo sapiens 106-109 34532491-7 2021 The patient with advanced lung adenocarcinoma harboring EGFR exon 19 deletion initially responded to osimertinib with progression-free survival (PFS) lasting 11 months and then developed resistance with an acquired mutation of MET D1228N. osimertinib 101-112 SAFB like transcription modulator Homo sapiens 227-230 34532491-11 2021 Based on our findings, patient with MET D1228N mutant lung adenocarcinoma clinically benefited from combinatorial therapy of cabozantinib and osimertinib after osimertinib resistance. osimertinib 142-153 SAFB like transcription modulator Homo sapiens 36-39 34532491-11 2021 Based on our findings, patient with MET D1228N mutant lung adenocarcinoma clinically benefited from combinatorial therapy of cabozantinib and osimertinib after osimertinib resistance. osimertinib 160-171 SAFB like transcription modulator Homo sapiens 36-39 34397683-8 2021 LESSONS: Although osimertinib combined with crizotinib therapy showed dramatic tumor shrinkage in both the primary tumor and bone metastasis to an EGFR T790M-mutant NSCLC patient with MET amplification, the progression-free survival (PFS) was only two months. osimertinib 18-29 SAFB like transcription modulator Homo sapiens 184-187 34590012-0 2021 Intracranial Activity of Osimertinib Plus Capmatinib in a Patient With EGFR and MET-Driven Lung Cancer: Case Report. osimertinib 25-36 SAFB like transcription modulator Homo sapiens 80-83 34590012-1 2021 We previously published in the Journal of Thoracic Oncology the case of a patient with EGFR and MET-driven lung cancer and extracranial response to capmatinib and osimertinib. osimertinib 163-174 SAFB like transcription modulator Homo sapiens 96-99 34590012-3 2021 Adding capmatinib to osimertinib seems to be an effective salvage therapy for patients with EGFR-mutant lung cancer and acquired MET amplification. osimertinib 21-32 SAFB like transcription modulator Homo sapiens 129-132 35331964-8 2022 Reduced PFS on later-line osimertinib in 33 patients was associated with MET, APC and ERBB4 alterations. osimertinib 26-37 SAFB like transcription modulator Homo sapiens 73-76 35462930-6 2022 We here report a patient who acquired EGFR T790M, STRN-ALK fusion, and EGFR amplification after gefitinib progression and subsequent MET amplification acquired from osimertinib. osimertinib 165-176 SAFB like transcription modulator Homo sapiens 133-136 34298655-0 2021 Generation and Characterization of a New Preclinical Mouse Model of EGFR-Driven Lung Cancer with MET-Induced Osimertinib Resistance. osimertinib 109-120 SAFB like transcription modulator Homo sapiens 97-100 34298655-2 2021 We generated a new state-of-the-art mouse strain harboring the human EGFRT790M/L858R oncogene and MET overexpression (EGFR/MET strain) that mimics the MET amplification occurring in one out of five patients with EGFR-mutated lung cancer that relapsed after treatment with osimertinib, a third-generation anti-EGFR TKI. osimertinib 272-283 SAFB like transcription modulator Homo sapiens 98-101 34298655-2 2021 We generated a new state-of-the-art mouse strain harboring the human EGFRT790M/L858R oncogene and MET overexpression (EGFR/MET strain) that mimics the MET amplification occurring in one out of five patients with EGFR-mutated lung cancer that relapsed after treatment with osimertinib, a third-generation anti-EGFR TKI. osimertinib 272-283 SAFB like transcription modulator Homo sapiens 123-126 34298655-2 2021 We generated a new state-of-the-art mouse strain harboring the human EGFRT790M/L858R oncogene and MET overexpression (EGFR/MET strain) that mimics the MET amplification occurring in one out of five patients with EGFR-mutated lung cancer that relapsed after treatment with osimertinib, a third-generation anti-EGFR TKI. osimertinib 272-283 SAFB like transcription modulator Homo sapiens 151-154 34298655-4 2021 Moreover, EGFR/MET-driven lung tumors were resistant to osimertinib, recapitulating the phenotype observed in patients. osimertinib 56-67 SAFB like transcription modulator Homo sapiens 15-18 34298655-5 2021 Conversely, as also observed in patients, the crizotinib (anti-MET TKI) and osimertinib combination improved survival and reduced tumor burden in EGFR/MET mice, further validating the model"s value for preclinical studies. osimertinib 76-87 SAFB like transcription modulator Homo sapiens 151-154 34590028-1 2021 Introduction: MET amplification is a frequently observed mechanism of resistance to osimertinib, and coinhibition strategy of MET and EGFR revealed promising results in recent clinical trials. osimertinib 84-95 SAFB like transcription modulator Homo sapiens 14-17 34590028-1 2021 Introduction: MET amplification is a frequently observed mechanism of resistance to osimertinib, and coinhibition strategy of MET and EGFR revealed promising results in recent clinical trials. osimertinib 84-95 SAFB like transcription modulator Homo sapiens 126-129 34590028-6 2021 Results: After progression on osimertinib and savolitinib, whole-exome analysis revealed MET-dependent mechanisms of resistance, such as acquired MET p.D1246H mutation, MET p.Y1230C mutation, and MET copy number gain. osimertinib 30-41 SAFB like transcription modulator Homo sapiens 89-92 35372088-5 2022 Currently, there are ongoing clinical trials which investigate the MET amplification as a therapeutic target in patients with EGFR mutant NSCLC and acquired resistance to osimertinib, which imply that the MET amplification also had a therapeutic significance. osimertinib 171-182 SAFB like transcription modulator Homo sapiens 67-70 35372088-5 2022 Currently, there are ongoing clinical trials which investigate the MET amplification as a therapeutic target in patients with EGFR mutant NSCLC and acquired resistance to osimertinib, which imply that the MET amplification also had a therapeutic significance. osimertinib 171-182 SAFB like transcription modulator Homo sapiens 205-208 33486418-11 2021 CONCLUSIONS: Mechanisms of resistance to osimertinib as 1st-line therapy differ from those which develop in the 2nd-line setting and commonly include MET amplification. osimertinib 41-52 SAFB like transcription modulator Homo sapiens 150-153 35266116-13 2022 A combination of MET TKIs with epidermal growth factor receptor (EGFR) TKIs (osimertinib + savolitinib, tepotinib + gefitinib) may be a potential solution for MET-driven EGFR TKI resistance. osimertinib 77-88 SAFB like transcription modulator Homo sapiens 159-162 33744716-9 2021 CONCLUSIONS: Loss of the T790M mutation was associated with early resistance to osimertinib, and this was exacerbated by MET amplification. osimertinib 80-91 SAFB like transcription modulator Homo sapiens 121-124 33976623-3 2021 This report describes the successful results obtained with the combination of the third-generation TKI osimertinib with the multitargeted TKI and MET inhibitor crizotinib in a patient with EGFR-mutant NSCLC with emerging MET amplification with a tolerable toxicity profile. osimertinib 103-114 SAFB like transcription modulator Homo sapiens 221-224 33438350-3 2021 Crizotinib was administered in combination with osimertinib due to elevated mesenchymal epithelial transition (MET) copy number amplification. osimertinib 48-59 SAFB like transcription modulator Homo sapiens 111-114 33658860-10 2021 Conclusion: EGFR C797S mutation and MET amplification are leading mechanisms for osimertinib resistance in lung cancer. osimertinib 81-92 SAFB like transcription modulator Homo sapiens 36-39 33658860-3 2021 EGFR C797S and MET amplification are common mechanisms of osimertinib. osimertinib 58-69 SAFB like transcription modulator Homo sapiens 15-18 33163272-0 2020 The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of AZD9291 (osimertinib) against AZD9291-resistant NSCLC cells with activated MET. osimertinib 103-110 SAFB like transcription modulator Homo sapiens 10-13 33621951-0 2021 MET inhibitor, capmatinib overcomes osimertinib resistance via suppression of MET/Akt/snail signaling in non-small cell lung cancer and decreased generation of cancer-associated fibroblasts. osimertinib 36-47 SAFB like transcription modulator Homo sapiens 0-3 33621951-11 2021 CONCLUSION: Taken together, our findings suggested that an increased MET/Akt/Snail signaling was induced between the NSCLC cells and their TME (CAFs), resulting in osimertinib resistance. osimertinib 164-175 SAFB like transcription modulator Homo sapiens 69-72 33324104-7 2020 We then present the most frequent tumor escape mechanisms when osimertinib is prescribed in first line: off-target (MET amplification, HER2 amplification, BRAF mutation, gene fusions, histologic transformation) and on-target mechanisms (EGFR mutation). osimertinib 63-74 SAFB like transcription modulator Homo sapiens 116-119 33186133-0 2020 Crizotinib plus erlotinib overcomes osimertinib resistance in a seriously-ill non-small cell lung cancer patient with acquired MET amplification. osimertinib 36-47 SAFB like transcription modulator Homo sapiens 127-130 33163272-0 2020 The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of AZD9291 (osimertinib) against AZD9291-resistant NSCLC cells with activated MET. osimertinib 103-110 SAFB like transcription modulator Homo sapiens 178-181 33163272-0 2020 The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of AZD9291 (osimertinib) against AZD9291-resistant NSCLC cells with activated MET. osimertinib 112-123 SAFB like transcription modulator Homo sapiens 10-13 33163272-0 2020 The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of AZD9291 (osimertinib) against AZD9291-resistant NSCLC cells with activated MET. osimertinib 112-123 SAFB like transcription modulator Homo sapiens 178-181 33163272-0 2020 The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of AZD9291 (osimertinib) against AZD9291-resistant NSCLC cells with activated MET. osimertinib 133-140 SAFB like transcription modulator Homo sapiens 10-13 33163272-5 2020 However, AZD9291-resistant (AR) cell lines with high levels of MET and p-MET responded to HQP8361 single agent and particularly to the combination of HQP8361 and AZD9291. osimertinib 9-16 SAFB like transcription modulator Homo sapiens 63-66 33163272-5 2020 However, AZD9291-resistant (AR) cell lines with high levels of MET and p-MET responded to HQP8361 single agent and particularly to the combination of HQP8361 and AZD9291. osimertinib 9-16 SAFB like transcription modulator Homo sapiens 73-76 33163272-5 2020 However, AZD9291-resistant (AR) cell lines with high levels of MET and p-MET responded to HQP8361 single agent and particularly to the combination of HQP8361 and AZD9291. osimertinib 162-169 SAFB like transcription modulator Homo sapiens 63-66 33163272-5 2020 However, AZD9291-resistant (AR) cell lines with high levels of MET and p-MET responded to HQP8361 single agent and particularly to the combination of HQP8361 and AZD9291. osimertinib 162-169 SAFB like transcription modulator Homo sapiens 73-76 29506987-7 2018 Alterations in parallel or downstream oncogenes such as MET, KRAS, and PIK3CA were also discovered, potentially contributing to the osimertinib-resistance in patients without EGFR secondary mutations.Conclusions: We present comprehensive mutation profiles of a large cohort of osimertinib-resistance lung cancer patients using mainly cfDNA. osimertinib 132-143 SAFB like transcription modulator Homo sapiens 56-59 31122565-0 2019 A Novel CAV1-MET Fusion in SCLC Transformation Responds to Crizotinib and Osimertinib Treatment. osimertinib 74-85 SAFB like transcription modulator Homo sapiens 13-16 30463991-8 2019 Among three MET-amplified cell lines, one cell line was sensitive to a combination of osimertinib and crizotinib. osimertinib 86-97 SAFB like transcription modulator Homo sapiens 12-15 31941753-5 2020 Recent next-generation sequencing (NGS) of lung cancer samples identified several genetically defined resistance mechanisms to osimertinib, such as EGFR C797S or MET amplification. osimertinib 127-138 SAFB like transcription modulator Homo sapiens 162-165 29506987-7 2018 Alterations in parallel or downstream oncogenes such as MET, KRAS, and PIK3CA were also discovered, potentially contributing to the osimertinib-resistance in patients without EGFR secondary mutations.Conclusions: We present comprehensive mutation profiles of a large cohort of osimertinib-resistance lung cancer patients using mainly cfDNA. osimertinib 277-288 SAFB like transcription modulator Homo sapiens 56-59