PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33971844-1	2021	BACKGROUND: Osimertinib is a third generation tyrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) in lung cancer.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	95-127
33943009-0	2021	Targeting the EMT transcription factor Snail overcomes resistance to osimertinib in EGFR-mutant non-small cell lung cancer.	osimertinib	69-80	snail family transcriptional repressor 1	Homo sapiens	39-44
33943009-0	2021	Targeting the EMT transcription factor Snail overcomes resistance to osimertinib in EGFR-mutant non-small cell lung cancer.	osimertinib	69-80	epidermal growth factor	Homo sapiens	84-88
33943009-1	2021	BACKGROUND: The resistance mechanism of the third generation of epidermal growth factor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib is complex.	osimertinib	127-138	epidermal growth factor	Homo sapiens	64-87
33943009-1	2021	BACKGROUND: The resistance mechanism of the third generation of epidermal growth factor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib is complex.	osimertinib	127-138	epidermal growth factor	Homo sapiens	89-93
33943009-4	2021	Whether targeting Snail can reverse the resistance of osimertinib by downregulating Snail is unknown.	osimertinib	54-65	snail family transcriptional repressor 1	Homo sapiens	18-23
33943009-4	2021	Whether targeting Snail can reverse the resistance of osimertinib by downregulating Snail is unknown.	osimertinib	54-65	snail family transcriptional repressor 1	Homo sapiens	84-89
33943009-12	2021	The expression of Snail was upregulated in the osimertinib-resistant cell line H1975/OR.	osimertinib	47-58	snail family transcriptional repressor 1	Homo sapiens	18-23
33943009-13	2021	Knockdown of Snail increased the sensitivity of H1975/OR cells to osimertinib.	osimertinib	66-77	snail family transcriptional repressor 1	Homo sapiens	13-18
33943009-15	2021	CDK 4/6 inhibitor palbociclib combined with osimertinib could reverse the resistance of osimertinib in H1975/OR.	osimertinib	88-99	cyclin dependent kinase 4	Homo sapiens	0-7
33943009-16	2021	CONCLUSIONS: Snail plays an important role in the third generation of EGFR-TKI osimertinib resistance, which may be reversed by downregulating Snail.	osimertinib	79-90	snail family transcriptional repressor 1	Homo sapiens	13-18
33943009-16	2021	CONCLUSIONS: Snail plays an important role in the third generation of EGFR-TKI osimertinib resistance, which may be reversed by downregulating Snail.	osimertinib	79-90	snail family transcriptional repressor 1	Homo sapiens	143-148
33812963-0	2021	Polyphyllin I reverses the resistance of osimertinib in non-small cell lung cancer cell through regulation of PI3K/Akt signaling.	osimertinib	41-52	AKT serine/threonine kinase 1	Homo sapiens	115-118
33971844-1	2021	BACKGROUND: Osimertinib is a third generation tyrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) in lung cancer.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	129-133
33813328-1	2021	BACKGROUND: Osimertinib is now a standard treatment for patients with previously untreated EGFR-mutated advanced non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	91-95
33813328-3	2021	PATIENTS AND METHODS: We conducted an open-label randomised phase 2 study to evaluate osimertinib and carboplatin-pemetrexed combination in comparison with osimertinib monotherapy in EGFR mutation-positive NSCLC patients who experienced disease progression associated with the emergence of the T790M resistance mutation of EGFR during first-line EGFR-TKI therapy.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	183-187
33813328-10	2021	CONCLUSION: This is the first randomised study to investigate the efficacy and safety of the combination of osimertinib and cytotoxic chemotherapy for EGFR-mutated NSCLC.	osimertinib	108-119	epidermal growth factor receptor	Homo sapiens	151-155
33809064-2	2021	Third-generation EGFR-TKIs, such as osimertinib and rociletinib (CO-1686), was developed to target such resistance mutations.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	17-21
33819860-0	2021	Cytotoxic chemotherapeutic agents and the EGFR-TKI osimertinib induce calreticulin exposure in non-small cell lung cancer.	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	42-46
33819860-0	2021	Cytotoxic chemotherapeutic agents and the EGFR-TKI osimertinib induce calreticulin exposure in non-small cell lung cancer.	osimertinib	51-62	calreticulin	Homo sapiens	70-82
33819860-3	2021	MATERIALS AND METHODS: We investigated the ability of seven cytotoxic chemotherapeutic agents and the third-generation EGFR-TKI osimertinib to induce translocation of the DAMP calreticulin to the cell surface in multiple NSCLC cell lines.	osimertinib	128-139	epidermal growth factor receptor	Homo sapiens	119-123
33819860-3	2021	MATERIALS AND METHODS: We investigated the ability of seven cytotoxic chemotherapeutic agents and the third-generation EGFR-TKI osimertinib to induce translocation of the DAMP calreticulin to the cell surface in multiple NSCLC cell lines.	osimertinib	128-139	calreticulin	Homo sapiens	176-188
33819860-4	2021	The plasma concentration of soluble CRT in advanced NSCLC patients treated with cytotoxic chemotherapy or osimertinib was measured.	osimertinib	106-117	calreticulin	Homo sapiens	36-39
33819860-8	2021	Osimertinib similarly increased ecto-CRT expression in association with apoptosis induction in five EGFR-mutated NSCLC cell lines.	osimertinib	0-11	tripartite motif containing 33	Homo sapiens	32-36
33819860-8	2021	Osimertinib similarly increased ecto-CRT expression in association with apoptosis induction in five EGFR-mutated NSCLC cell lines.	osimertinib	0-11	calreticulin	Homo sapiens	37-40
33819860-8	2021	Osimertinib similarly increased ecto-CRT expression in association with apoptosis induction in five EGFR-mutated NSCLC cell lines.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	100-104
33819860-9	2021	Furthermore, the plasma concentration of soluble CRT in 16 NSCLC patients treated with single-agent pemetrexed or docetaxel and in nine EGFR-mutated NSCLC patients treated with osimertinib was increased after treatment onset.	osimertinib	177-188	calreticulin	Homo sapiens	49-52
33819860-9	2021	Furthermore, the plasma concentration of soluble CRT in 16 NSCLC patients treated with single-agent pemetrexed or docetaxel and in nine EGFR-mutated NSCLC patients treated with osimertinib was increased after treatment onset.	osimertinib	177-188	epidermal growth factor receptor	Homo sapiens	136-140
33819860-10	2021	CONCLUSION: Our findings indicate that antimetabolites, microtubule inhibitors, and osimertinib are effective inducers both of CRT exposure in NSCLC cell lines and of soluble CRT release in patients with advanced NSCLC, suggesting that these agents might prove effective for promotion of antitumor immunity in combination immunotherapy.	osimertinib	84-95	calreticulin	Homo sapiens	127-130
33819860-10	2021	CONCLUSION: Our findings indicate that antimetabolites, microtubule inhibitors, and osimertinib are effective inducers both of CRT exposure in NSCLC cell lines and of soluble CRT release in patients with advanced NSCLC, suggesting that these agents might prove effective for promotion of antitumor immunity in combination immunotherapy.	osimertinib	84-95	calreticulin	Homo sapiens	175-178
33816581-1	2021	Cardiac arrest occurred in an 85-year-old female administered osimertinib for advanced lung cancer expressing epidermal growth factor receptor (EGFR) mutations.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	110-142
33816581-1	2021	Cardiac arrest occurred in an 85-year-old female administered osimertinib for advanced lung cancer expressing epidermal growth factor receptor (EGFR) mutations.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	144-148
32798009-0	2020	Osimertinib for the Treatment of EGFR Mutation-Positive Lung Adenocarcinoma Complicated With Dermatomyositis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	33-37
33796513-9	2021	In this case, the need for intense daily radiation treatment with its associated toxicities was negated, and as such we propose that osimertinib may be a promising treatment for choroidal metastasis secondary to EGFR-mutated lung adenocarcinoma.	osimertinib	133-144	epidermal growth factor receptor	Homo sapiens	212-216
33589348-2	2021	AIMS: Multiple studies have shown conflicting results on the correlation between the EGFR T790M quantitative level and survival outcomes in osimertinib-treated patients.	osimertinib	140-151	epidermal growth factor receptor	Homo sapiens	85-89
32796633-3	2020	We report a case of an 80-year-old Japanese woman with lung adenocarcinoma harboring an EGFR-sensitizing mutation who was treated with osimertinib as the first-line treatment.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	88-92
33034420-0	2020	Lung adenocarcinoma in a patient with a cis EGFR L858R-K860I doublet mutation identified using NGS-based profiling test: Negative diagnosis on initial companion test and successful treatment with osimertinib.	osimertinib	196-207	epidermal growth factor receptor	Homo sapiens	44-48
33034420-8	2020	The patient was then successfully treated with a third-generation EGFR-tyrosine kinase inhibitor, osimertinib.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	66-70
33034420-8	2020	The patient was then successfully treated with a third-generation EGFR-tyrosine kinase inhibitor, osimertinib.	osimertinib	98-109	TXK tyrosine kinase	Homo sapiens	71-86
33034420-13	2020	WHAT THIS STUDY ADDS: Osimertinib was effective in an NSCLC patient with EGFR L858R and K860I mutations.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	73-77
32890631-0	2020	Osimertinib in CNS progressive EGFR-mutant lung cancer: Do we need to detect T790M?	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	31-35
34323489-1	2022	The pyrimidine core-containing compound Osimertinib is the only epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) from the third generation that has been approved by the U.S. Food and Drug Administration to target threonine 790 methionine (T790M) resistance while sparing the wild-type epidermal growth factor receptor (WT EGFR).	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	124-128
34839016-1	2022	BACKGROUND: While osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) is the standard treatment in patients with advanced non-small cell lung cancer (NSCLC) with sensitising EGFR and acquired T790M mutations, progression inevitably occurs.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	50-82
34839016-1	2022	BACKGROUND: While osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) is the standard treatment in patients with advanced non-small cell lung cancer (NSCLC) with sensitising EGFR and acquired T790M mutations, progression inevitably occurs.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	84-88
34839016-1	2022	BACKGROUND: While osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) is the standard treatment in patients with advanced non-small cell lung cancer (NSCLC) with sensitising EGFR and acquired T790M mutations, progression inevitably occurs.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	226-230
34839016-3	2022	PATIENTS AND METHODS: BOOSTER is an open-label randomised phase II trial investigating the efficacy and safety of combined osimertinib 80 mg daily and bevacizumab 15 mg/kg every 3 weeks, versus osimertinib alone, in patients with EGFR-mutant advanced NSCLC and acquired T790M mutations after failure on previous EGFR TKI therapy.	osimertinib	123-134	epidermal growth factor receptor	Homo sapiens	230-234
34648945-11	2022	Kinase activity of the BRAF protein isolated from X12CL was inhibited by treatment with the EGFR TKIs gefitinib and osimertinib, and expression of BRAFG469V in non-EGFR-expressing NR6 cells promoted growth in low serum, which was also sensitive to EGFR TKIs.	osimertinib	116-127	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-27
34648945-11	2022	Kinase activity of the BRAF protein isolated from X12CL was inhibited by treatment with the EGFR TKIs gefitinib and osimertinib, and expression of BRAFG469V in non-EGFR-expressing NR6 cells promoted growth in low serum, which was also sensitive to EGFR TKIs.	osimertinib	116-127	epidermal growth factor receptor	Homo sapiens	92-96
34958168-1	2022	BACKGROUND: Osimertinib is the standard first-line treatment for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	114-146
34958168-1	2022	BACKGROUND: Osimertinib is the standard first-line treatment for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	148-152
34962076-0	2022	Combined targeting of EGFR and BRAF triggers regression of osimertinib resistance by using osimertinib and vemurafenib concurrently in a patient with heterogeneity between different lesions.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	22-26
34962076-0	2022	Combined targeting of EGFR and BRAF triggers regression of osimertinib resistance by using osimertinib and vemurafenib concurrently in a patient with heterogeneity between different lesions.	osimertinib	59-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
34918542-8	2022	In one of the studies (called the FLAURA study), the third-generation EGFR TKI osimertinib improved overall survival (the length of time that patients survived, from first dose of treatment to death) when compared to first-generation EGFR TKIs.	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	70-74
34962076-7	2022	This case highlights the consideration of heterogeneity between different lesions and provides a successful example of the concurrent therapy with vemurafenib and osimertinib for triggering regression of osimertinb resistance induced by BRAF mutation.	osimertinib	163-174	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	237-241
34323489-1	2022	The pyrimidine core-containing compound Osimertinib is the only epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) from the third generation that has been approved by the U.S. Food and Drug Administration to target threonine 790 methionine (T790M) resistance while sparing the wild-type epidermal growth factor receptor (WT EGFR).	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	306-338
34323489-1	2022	The pyrimidine core-containing compound Osimertinib is the only epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) from the third generation that has been approved by the U.S. Food and Drug Administration to target threonine 790 methionine (T790M) resistance while sparing the wild-type epidermal growth factor receptor (WT EGFR).	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	343-347
34323489-3	2022	A tertiary cystein 797 to serine 797 (C797S) mutation in the EGFR kinase domain has hampered Osimertinib treatment in patients with advanced EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	61-65
34323489-3	2022	A tertiary cystein 797 to serine 797 (C797S) mutation in the EGFR kinase domain has hampered Osimertinib treatment in patients with advanced EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	141-145
34861243-6	2022	Notably, Dic was shown to synergistically improve the chemo-sensitivity of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI)-resistant lung cancer cells to gefitinib and osimertinib.	osimertinib	190-201	epidermal growth factor receptor	Homo sapiens	135-139
34794818-3	2022	The third-generation EGFR tyrosine kinase inhibitors (TKIs) Rociletinib and Osimertinib (AZD9291) achieved remarkable clinical efficacy.	osimertinib	89-96	epidermal growth factor receptor	Homo sapiens	21-25
34599981-0	2022	PAR2 blockade reverses osimertinib resistance in non-small-cell lung cancer cells via attenuating ERK-mediated EMT and PD-L1 expression.	osimertinib	23-34	F2R like trypsin receptor 1	Homo sapiens	0-4
34599981-0	2022	PAR2 blockade reverses osimertinib resistance in non-small-cell lung cancer cells via attenuating ERK-mediated EMT and PD-L1 expression.	osimertinib	23-34	mitogen-activated protein kinase 1	Homo sapiens	98-101
34599981-0	2022	PAR2 blockade reverses osimertinib resistance in non-small-cell lung cancer cells via attenuating ERK-mediated EMT and PD-L1 expression.	osimertinib	23-34	IL2 inducible T cell kinase	Homo sapiens	111-114
34599981-0	2022	PAR2 blockade reverses osimertinib resistance in non-small-cell lung cancer cells via attenuating ERK-mediated EMT and PD-L1 expression.	osimertinib	23-34	CD274 molecule	Homo sapiens	119-124
34599981-1	2022	Osimertinib, as the third-generation EGFR tyrosine kinase inhibitors (EGFR-TKIs), is a first-line molecularly targeted drug for non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	70-74
34599981-5	2022	This study firstly discovered that PAR2 expression was notably enhanced when NSCLC cells became resistant to osimertinib.	osimertinib	109-120	F2R like trypsin receptor 1	Homo sapiens	35-39
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	29-40	F2R like trypsin receptor 1	Homo sapiens	2-6
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	54-58
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	29-40	IL2 inducible T cell kinase	Homo sapiens	97-100
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	29-40	CD274 molecule	Homo sapiens	105-110
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	147-158	F2R like trypsin receptor 1	Homo sapiens	2-6
34548332-7	2022	We further developed a preclinical strategy to enhance the efficacy of HER3-DXd through osimertinib pre-treatment, which increased membrane expression of HER3 and led to enhanced internalization and efficacy of HER3-DXd.	osimertinib	88-99	erb-b2 receptor tyrosine kinase 3	Homo sapiens	71-75
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	147-158	mitogen-activated protein kinase 1	Homo sapiens	76-79
34599981-6	2022	A PAR2 inhibitor facilitated osimertinib to attenuate EGFR transactivation, ERK phosphorylation, EMT and PD-L1 expression which were associated to osimertinib resistance.	osimertinib	147-158	IL2 inducible T cell kinase	Homo sapiens	97-100
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	F2R like trypsin receptor 1	Homo sapiens	37-41
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	mitogen-activated protein kinase 1	Homo sapiens	78-81
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	IL2 inducible T cell kinase	Homo sapiens	91-94
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	CD274 molecule	Homo sapiens	99-104
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	mitogen-activated protein kinase 1	Homo sapiens	143-146
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	IL2 inducible T cell kinase	Homo sapiens	216-219
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	193-204	CD274 molecule	Homo sapiens	221-226
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	264-275	F2R like trypsin receptor 1	Homo sapiens	37-41
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	264-275	mitogen-activated protein kinase 1	Homo sapiens	78-81
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	264-275	CD274 molecule	Homo sapiens	99-104
34599981-8	2022	Importantly, this reversal effect of PAR2 blockade was uncovered to depend on ERK-mediated EMT and PD-L1, since inhibition of beta-arrestin or ERK, which could be modulated by PAR2, sensitized osimertinib to prevent EMT, PD-L1 expression and consequently overcame osimertinib resistance.	osimertinib	264-275	F2R like trypsin receptor 1	Homo sapiens	176-180
34599981-9	2022	Thus, this study demonstrated that PAR2 antagonism could limit ERK-mediated EMT and immune checkpoints, consequently attenuating EGFR transactivation and reactivate osimertinib.	osimertinib	165-176	F2R like trypsin receptor 1	Homo sapiens	35-39
34599981-9	2022	Thus, this study demonstrated that PAR2 antagonism could limit ERK-mediated EMT and immune checkpoints, consequently attenuating EGFR transactivation and reactivate osimertinib.	osimertinib	165-176	mitogen-activated protein kinase 1	Homo sapiens	63-66
34599981-10	2022	It suggested that PAR2 may be a novel drug target for osimertinib resistance, and PAR2 inhibition may be a promising strategy candidate for reversing EGFR-TKI resistance in NSCLC.	osimertinib	54-65	F2R like trypsin receptor 1	Homo sapiens	18-22
34706132-1	2022	Osimertinib is a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) for lung adenocarcinoma (LUAD) harboring activating mutations, but patients ultimately develop acquired resistance.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	94-98
34548332-7	2022	We further developed a preclinical strategy to enhance the efficacy of HER3-DXd through osimertinib pre-treatment, which increased membrane expression of HER3 and led to enhanced internalization and efficacy of HER3-DXd.	osimertinib	88-99	erb-b2 receptor tyrosine kinase 3	Homo sapiens	154-158
34548332-7	2022	We further developed a preclinical strategy to enhance the efficacy of HER3-DXd through osimertinib pre-treatment, which increased membrane expression of HER3 and led to enhanced internalization and efficacy of HER3-DXd.	osimertinib	88-99	erb-b2 receptor tyrosine kinase 3	Homo sapiens	211-215
34865963-5	2022	The introduction of the 3G EGFR-TKI, osimertinib, provides an opportunity to overcome T790M-mediated resistance to 1G, and 2G EGFR-TKIs.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	27-31
34544302-7	2022	RESULTS: Of the 782 patients who received first-line (1L) therapy with first-/second-generation EGFR TKIs in the cohort A, erlotinib was the most common (58%), and osimertinib was the most widely prescribed second-line (2L) therapy (52%).	osimertinib	164-175	epidermal growth factor receptor	Homo sapiens	96-100
34865963-5	2022	The introduction of the 3G EGFR-TKI, osimertinib, provides an opportunity to overcome T790M-mediated resistance to 1G, and 2G EGFR-TKIs.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	126-130
34865963-6	2022	Additionally, with the use of osimertinib, fewer T790M mutations are being detected as T790M is not a reported resistance mechanism to 3G EGFR-TKIs.	osimertinib	30-41	epidermal growth factor receptor	Homo sapiens	138-142
34758637-0	2022	First-line osimertinib in EGFR mutation-positive non-small cell lung cancer patients with poor performance status.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	26-30
34844838-7	2022	In addition, MEOX2/GLI1 was shown to be involved in the increased proliferation of tumour cells and resistance capacity to cisplatin, EGFR-TKIs (erlotinib and AZD9291 "osimertinib"), AZD8542-SMO, and AZD6244-MEKK1/2.	osimertinib	159-166	mesenchyme homeobox 2	Homo sapiens	13-18
34844838-7	2022	In addition, MEOX2/GLI1 was shown to be involved in the increased proliferation of tumour cells and resistance capacity to cisplatin, EGFR-TKIs (erlotinib and AZD9291 "osimertinib"), AZD8542-SMO, and AZD6244-MEKK1/2.	osimertinib	159-166	GLI family zinc finger 1	Homo sapiens	19-23
34844838-7	2022	In addition, MEOX2/GLI1 was shown to be involved in the increased proliferation of tumour cells and resistance capacity to cisplatin, EGFR-TKIs (erlotinib and AZD9291 "osimertinib"), AZD8542-SMO, and AZD6244-MEKK1/2.	osimertinib	168-179	mesenchyme homeobox 2	Homo sapiens	13-18
34844838-7	2022	In addition, MEOX2/GLI1 was shown to be involved in the increased proliferation of tumour cells and resistance capacity to cisplatin, EGFR-TKIs (erlotinib and AZD9291 "osimertinib"), AZD8542-SMO, and AZD6244-MEKK1/2.	osimertinib	168-179	GLI family zinc finger 1	Homo sapiens	19-23
34844838-7	2022	In addition, MEOX2/GLI1 was shown to be involved in the increased proliferation of tumour cells and resistance capacity to cisplatin, EGFR-TKIs (erlotinib and AZD9291 "osimertinib"), AZD8542-SMO, and AZD6244-MEKK1/2.	osimertinib	168-179	epidermal growth factor receptor	Homo sapiens	134-138
34969538-1	2022	INTRODUCTION: The third-generation tyrosine kinase inhibitor (TKI) osimertinib is recommended as a first-line treatment in advanced non-small cell lung cancer harboring an activating mutation of Epidermal Growth Factor Receptor (EGFR).	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	195-227
34643820-0	2022	Osimertinib in poor performance status patients with T790M-positive advanced non-small-cell lung cancer after progression of first- and second-generation EGFR-TKI treatments (NEJ032B).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	154-158
34643820-1	2022	BACKGROUND: Osimertinib is effective in patients with T790M mutation-positive advanced non-small-cell lung cancer (NSCLC) resistant to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	135-167
34643820-1	2022	BACKGROUND: Osimertinib is effective in patients with T790M mutation-positive advanced non-small-cell lung cancer (NSCLC) resistant to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	169-173
34643820-11	2022	Patients negative for activating EGFR mutations after osimertinib administration had longer median PFS than those positive for these mutations.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	33-37
34643820-12	2022	CONCLUSION: Osimertinib was sufficiently effective in EGFR-TKI-resistant, poor PS patients with T790M mutation-positive advanced NSCLC.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	54-58
34826601-0	2022	The natural product berberine synergizes with osimertinib preferentially against MET-amplified osimertinib-resistant lung cancer via direct MET inhibition.	osimertinib	46-57	met proto-oncogene	Mus musculus	81-84
34826601-0	2022	The natural product berberine synergizes with osimertinib preferentially against MET-amplified osimertinib-resistant lung cancer via direct MET inhibition.	osimertinib	46-57	met proto-oncogene	Mus musculus	140-143
34826601-2	2022	Osimertinib is the first third-generation EGFR-tyrosine kinase inhibitor (TKI) approved for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and those resistant to earlier generation EGFR-TKIs due to a T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Mus musculus	42-46
34826601-2	2022	Osimertinib is the first third-generation EGFR-tyrosine kinase inhibitor (TKI) approved for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and those resistant to earlier generation EGFR-TKIs due to a T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Mus musculus	160-164
34826601-2	2022	Osimertinib is the first third-generation EGFR-tyrosine kinase inhibitor (TKI) approved for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and those resistant to earlier generation EGFR-TKIs due to a T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Mus musculus	217-221
34826601-4	2022	One known mechanism of acquired resistance to osimertinib and other EGFR-TKIs is MET (c-MET) gene amplification.	osimertinib	46-57	met proto-oncogene	Mus musculus	81-84
34826601-4	2022	One known mechanism of acquired resistance to osimertinib and other EGFR-TKIs is MET (c-MET) gene amplification.	osimertinib	46-57	met proto-oncogene	Mus musculus	86-91
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	51-62	met proto-oncogene	Mus musculus	130-133
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	51-62	epidermal growth factor receptor	Mus musculus	166-170
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	51-62	BCL2-like 11 (apoptosis facilitator)	Mus musculus	247-250
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	51-62	myeloid cell leukemia sequence 1	Mus musculus	265-270
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	144-155	met proto-oncogene	Mus musculus	130-133
34826601-5	2022	Here, we report that berberine, when combined with osimertinib, synergistically and selectively decreased the survival of several MET-amplified osimertinib-resistant EGFR mutant NSCLC cell lines with enhanced induction of apoptosis likely through Bim elevation and Mcl-1 reduction.	osimertinib	144-155	epidermal growth factor receptor	Mus musculus	166-170
34826601-6	2022	Importantly, this combination effectively enhanced suppressive effect on the growth of MET-amplified osimertinib-resistant xenografts in nude mice and was well tolerated.	osimertinib	101-112	met proto-oncogene	Mus musculus	87-90
34826601-9	2022	These findings collectively suggest that berberine can act as a naturally-existing MET inhibitor to synergize with osimertinib in overcoming osimertinib acquired resistance caused by MET amplification.	osimertinib	115-126	met proto-oncogene	Mus musculus	83-86
34826601-9	2022	These findings collectively suggest that berberine can act as a naturally-existing MET inhibitor to synergize with osimertinib in overcoming osimertinib acquired resistance caused by MET amplification.	osimertinib	115-126	met proto-oncogene	Mus musculus	183-186
34826601-9	2022	These findings collectively suggest that berberine can act as a naturally-existing MET inhibitor to synergize with osimertinib in overcoming osimertinib acquired resistance caused by MET amplification.	osimertinib	141-152	met proto-oncogene	Mus musculus	83-86
34969538-1	2022	INTRODUCTION: The third-generation tyrosine kinase inhibitor (TKI) osimertinib is recommended as a first-line treatment in advanced non-small cell lung cancer harboring an activating mutation of Epidermal Growth Factor Receptor (EGFR).	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	229-233
34826601-9	2022	These findings collectively suggest that berberine can act as a naturally-existing MET inhibitor to synergize with osimertinib in overcoming osimertinib acquired resistance caused by MET amplification.	osimertinib	141-152	met proto-oncogene	Mus musculus	183-186
34974477-1	2022	Osimertinib is the most reliable epidermal growth factor receptor-tyrosine kinase (EGFR-TKI) and is recommended as the first-line EGFR-TKI.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	83-87
34894319-0	2022	Representativeness of Phase III Trial for Osimertinib in Pretreated Advanced EGFR-Mutated Non-small-cell Lung Cancer Patients and Treatment Outcomes in Clinical Practice.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	77-81
34974477-1	2022	Osimertinib is the most reliable epidermal growth factor receptor-tyrosine kinase (EGFR-TKI) and is recommended as the first-line EGFR-TKI.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	130-134
34964276-0	2022	Effectiveness of alectinib and osimertinib in a brain metastasized lung adenocarcinoma patient with concurrent EGFR mutations and DCTN1-ALK fusion.	osimertinib	31-42	ALK receptor tyrosine kinase	Homo sapiens	136-139
34979367-4	2022	In quest for finding newer moieties, we have developed a pharmacophore model utilizing drugs like lazertinib, osimertinib, nazartinib, avitinib, afatininb, and talazoparib that are known to inhibit EGFR along with their downstream signaling.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	198-202
34987382-1	2021	Osimertinib shows strong clinical activity in first- and second-line treatment of nonsmall-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations, especially EGFR T790M.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	130-162
34987382-1	2021	Osimertinib shows strong clinical activity in first- and second-line treatment of nonsmall-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations, especially EGFR T790M.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	164-168
34987382-1	2021	Osimertinib shows strong clinical activity in first- and second-line treatment of nonsmall-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations, especially EGFR T790M.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	192-196
34301748-1	2021	On December 18, 2020, the U.S. Food and Drug Administration (FDA) approved osimertinib as adjuvant therapy in patients with non-small cell lung cancer (NSCLC) whose tumors have epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21 (L858R) mutations, as detected by an FDA-approved test.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	177-209
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
34944068-6	2021	Cells driven by EGFR-D770>GY were insensitive to erlotinib and osimertinib, displayed sensitivity to poziotinib and dacomitinib and were uniquely sensitive to afatinib and dacomitinib in comparison with other more typical EGFR exon 20 insertion mutations using proliferation and biochemical assays.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	16-20
34921211-6	2021	Moreover, only osimertinib/trametinib combination treatment, but not monotherapy with either of these drugs, leads to robust tumor shrinkage in EGFR-driven xenograft models harboring BRAFV600E mutations.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	144-148
34911336-1	2022	Third-generation EGFR tyrosine kinase inhibitors (TKIs), such as osimertinib, have demonstrated efficacy in patients with EGFR-mutant non-small cell lung cancer; however, almost all patients will eventually relapse.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	17-21
34911336-1	2022	Third-generation EGFR tyrosine kinase inhibitors (TKIs), such as osimertinib, have demonstrated efficacy in patients with EGFR-mutant non-small cell lung cancer; however, almost all patients will eventually relapse.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	122-126
34534838-1	2021	To resolve the problem of drug resistance caused by epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancer, we used the principle of collocation to design and synthesize a series of aminopyrimidine derivatives with 4,5,6,7-tetrahydrothieno (3,2-c)pyridine side chains (according to the binding mode of AZD9291 to EGFRT790M) for use as EGFRL858R/T790M kinase inhibitors.	osimertinib	327-334	epidermal growth factor receptor	Homo sapiens	52-84
34301748-1	2021	On December 18, 2020, the U.S. Food and Drug Administration (FDA) approved osimertinib as adjuvant therapy in patients with non-small cell lung cancer (NSCLC) whose tumors have epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21 (L858R) mutations, as detected by an FDA-approved test.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	211-215
34907286-6	2021	The integrative analysis confirmed that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with osimertinib sensitivity.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	66-70
34808132-0	2021	Targeting ROR1 in combination with osimertinib in EGFR mutant lung cancer cells.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	50-54
34808132-1	2021	Lung cancer that exhibits epidermal growth factor receptor (EGFR) gene mutation is sensitive to EGFR-tyrosine kinase inhibitors (TKIs), such as osimertinib.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	26-58
34808132-1	2021	Lung cancer that exhibits epidermal growth factor receptor (EGFR) gene mutation is sensitive to EGFR-tyrosine kinase inhibitors (TKIs), such as osimertinib.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	60-64
34808132-1	2021	Lung cancer that exhibits epidermal growth factor receptor (EGFR) gene mutation is sensitive to EGFR-tyrosine kinase inhibitors (TKIs), such as osimertinib.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	96-100
34808132-7	2021	In conclusion, targeting ROR1 in combination with osimertinib in EGFR mutant lung cancer may be a novel therapeutic option.	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	65-69
34907286-6	2021	The integrative analysis confirmed that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with osimertinib sensitivity.	osimertinib	134-145	epiregulin	Homo sapiens	86-90
34907286-6	2021	The integrative analysis confirmed that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with osimertinib sensitivity.	osimertinib	134-145	heparin binding EGF like growth factor	Homo sapiens	92-97
34907286-6	2021	The integrative analysis confirmed that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with osimertinib sensitivity.	osimertinib	134-145	transforming growth factor alpha	Homo sapiens	99-103
34907286-6	2021	The integrative analysis confirmed that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with osimertinib sensitivity.	osimertinib	134-145	epithelial mitogen	Homo sapiens	109-113
34846235-0	2021	Cost-effectiveness of osimertinib in the treatment of advanced EGFR-mutated non-small cell lung cancer: a systematic review.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	63-67
34846235-2	2021	Although targeted tyrosine kinase inhibitors (TKIs) have reconstructed the care of these patients, the resistance of TKIs to the secondary EGFR-T790M mutation in advanced or metastatic NSCLC, led to the introduction of the third generation of them, like osimertinib.	osimertinib	254-265	epidermal growth factor receptor	Homo sapiens	139-143
34846235-10	2021	Therefore, further studies in those countries are needed to evaluate the cost-effectiveness of osimertinib for sensitizing EGFR mutation without T790M and required T790M in advanced or metastatic NSCLC.	osimertinib	95-106	epidermal growth factor receptor	Homo sapiens	123-127
34950579-10	2021	In EGFR-mutant patients, osimertinib showed the greatest benefit in iPFS (HR=0.32, 95%CI 0.15-0.69) compared to conventional chemotherapy, while gefitinib + chemotherapy showed the greatest overall PFS benefit (HR=0.26, 95%CI 0.10-0.70).	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	3-7
34920242-1	2021	INTRODUCTION: After the development of acquired resistance to osimertinib, the standard-of-care treatment for advanced EGFR-mutated NSCLC is chemotherapy.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	119-123
34865626-1	2021	BACKGROUND: The study aimed to compare the efficacy of osimertinib plus cranial radiotherapy (RT) with osimertinib alone in advanced non-small-cell lung cancer (NSCLC) patients harboring epidermal growth factor receptor (EGFR) mutations and brain metastases (BMs).	osimertinib	103-114	epidermal growth factor receptor	Homo sapiens	187-219
34865626-1	2021	BACKGROUND: The study aimed to compare the efficacy of osimertinib plus cranial radiotherapy (RT) with osimertinib alone in advanced non-small-cell lung cancer (NSCLC) patients harboring epidermal growth factor receptor (EGFR) mutations and brain metastases (BMs).	osimertinib	103-114	epidermal growth factor receptor	Homo sapiens	221-225
34464874-1	2021	The emergence of the C797S mutation in EGFR is a frequent mechanism of resistance to osimertinib in the treatment of non-small cell lung cancer (NSCLC).	osimertinib	85-96	epidermal growth factor receptor	Mus musculus	39-43
34464874-5	2021	When tested in Ba/F3 cells expressing EGFRL858R/T790M/C797S, compound 11 resulted significantly more potent than osimertinib at inhibiting both EGFR autophosphorylation and proliferation, even if the inhibition of EGFR autophosphorylation by compound 11 in Ba/F3 cells was not long lasting.	osimertinib	113-124	epidermal growth factor receptor	Mus musculus	144-148
34486915-0	2021	Intracranial effect of osimertinib in relapsed EGFR-mutated T790M-positive and -negative non-small cell lung cancer patients: results from a phase II study.	osimertinib	23-34	epidermal growth factor receptor	Homo sapiens	47-51
34926262-3	2021	Here, we report a case of acquired EGFR L858R/L718Q mutation with advanced NSCLC that resistant to osimertinib, which was successfully overcome using dacomitinib.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	35-39
34926262-13	2021	The acquired EGFR L718Q mutation in subsequent resistance to osimertinib could be overcome using dacomitinib, indicating a promising treatment option in the clinic.	osimertinib	61-72	epidermal growth factor receptor	Homo sapiens	13-17
34855271-1	2022	With the widely clinical use of third-generation EGFR inhibitor osimertinib for the treatment of EGFR-mutated NSCLC, acquired resistance caused by EGFR C797S tertiary mutation has become a concerned problem.	osimertinib	64-75	epidermal growth factor receptor	Mus musculus	49-53
34855271-1	2022	With the widely clinical use of third-generation EGFR inhibitor osimertinib for the treatment of EGFR-mutated NSCLC, acquired resistance caused by EGFR C797S tertiary mutation has become a concerned problem.	osimertinib	64-75	epidermal growth factor receptor	Mus musculus	97-101
34855271-1	2022	With the widely clinical use of third-generation EGFR inhibitor osimertinib for the treatment of EGFR-mutated NSCLC, acquired resistance caused by EGFR C797S tertiary mutation has become a concerned problem.	osimertinib	64-75	epidermal growth factor receptor	Mus musculus	147-151
34855271-5	2022	Meanwhile, LS-106 exhibited comparable kinase inhibitory effect to osimertinib on EGFRL858R/T790M and wild-type EGFR.	osimertinib	67-78	epidermal growth factor receptor	Mus musculus	112-116
34635007-3	2021	AZD3759 and osimertinib are both BBB-penetrating EGFR inhibitors.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	49-53
34363425-2	2021	This assay can be combined with our method for osimertinib, allowing quantification of the most used ALK- and EGFR- tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer with a single-assay setup.	osimertinib	47-58	ALK receptor tyrosine kinase	Homo sapiens	101-104
34612594-0	2021	Possibility of brigatinib-based therapy, or chemotherapy plus anti-angiogenic treatment after resistance of osimertinib harboring EGFR T790M-cis-C797S mutations in lung adenocarcinoma patients.	osimertinib	108-119	epidermal growth factor receptor	Homo sapiens	130-134
34612594-1	2021	BACKGROUND: There was no standard treatment for patients who acquired resistance to osimertinib mediated by epidermal growth factor receptor (EGFR) T790M-cis-C797S.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	108-140
34612594-1	2021	BACKGROUND: There was no standard treatment for patients who acquired resistance to osimertinib mediated by epidermal growth factor receptor (EGFR) T790M-cis-C797S.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	142-146
34634633-0	2021	Treating disease progression with osimertinib in EGFR-mutated non-small-cell lung cancer: novel targeted agents and combination strategies.	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	49-53
34723634-11	2021	To date, the study has shown that osimertinib could be beneficial for patients with resectable EGFR-mutated NSCLC.	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	95-99
34749119-0	2021	Osimertinib as first-line treatment for advanced epidermal growth factor receptor mutation-positive non-small-cell lung cancer in a real-world setting (OSI-FACT).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	49-81
34749119-1	2021	BACKGROUND: Osimertinib is the standard of care in the initial treatment for advanced epidermal growth factor receptor (EGFR) mutation-positive lung cancer.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	86-118
34749119-1	2021	BACKGROUND: Osimertinib is the standard of care in the initial treatment for advanced epidermal growth factor receptor (EGFR) mutation-positive lung cancer.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	120-124
34749119-3	2021	METHODS: We performed a retrospective multicentre cohort study for 538 EGFR mutation-positive patients, who received osimertinib as the initial treatment between August 2018 and December 2019.	osimertinib	117-128	epidermal growth factor receptor	Homo sapiens	71-75
34749119-11	2021	CONCLUSION: During initial treatment with osimertinib, PD-L1 expression is significantly related to PFS.	osimertinib	42-53	CD274 molecule	Homo sapiens	55-60
34763195-1	2021	AIM OF THE STUDY: The AZENT (NCT02841579) study aimed to assess the efficacy and safety of first-line osimertinib in patients with epidermal growth factor receptor(EGFR)mutation-positive advanced non-small-cell lung cancer (NSCLC) and with a coexisting low allelic fraction of Thr790Met.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	131-163
34763195-1	2021	AIM OF THE STUDY: The AZENT (NCT02841579) study aimed to assess the efficacy and safety of first-line osimertinib in patients with epidermal growth factor receptor(EGFR)mutation-positive advanced non-small-cell lung cancer (NSCLC) and with a coexisting low allelic fraction of Thr790Met.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	164-168
34763195-16	2021	CONCLUSION: Despite early study termination, osimertinib first-line therapy yields an overall PFS of 23.1 months in EGFR-mutant patients harbouring a coexisting low allelic fraction of EGFR Thr790Met mutation.	osimertinib	45-56	epidermal growth factor receptor	Homo sapiens	116-120
34763195-16	2021	CONCLUSION: Despite early study termination, osimertinib first-line therapy yields an overall PFS of 23.1 months in EGFR-mutant patients harbouring a coexisting low allelic fraction of EGFR Thr790Met mutation.	osimertinib	45-56	epidermal growth factor receptor	Homo sapiens	185-189
34723634-15	2021	Based on the results from ADAURA, osimertinib has been approved for the treatment of resectable EGFR-mutated NSCLC after tumor removal.	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	96-100
34215931-1	2021	OBJECTIVES: The study was designed to investigate the safety of ramucirumab administered in combination with erlotinib or osimertinib for patients with untreated EGFR-mutated non-small cell lung cancer (NSCLC) and asymptomatic brain metastases, a patient subgroup in which these regimens have remained untested.	osimertinib	122-133	epidermal growth factor receptor	Homo sapiens	162-166
34525256-0	2021	Clinical Outcomes of Patients Taking First-generation EGFR-TKIs May Predict the Benefits Afforded by Osimertinib in EGFR T790M-mutant NSCLC Patients.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	54-58
34525256-0	2021	Clinical Outcomes of Patients Taking First-generation EGFR-TKIs May Predict the Benefits Afforded by Osimertinib in EGFR T790M-mutant NSCLC Patients.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	116-120
34525256-2	2021	The association between the clinical outcomes of patients on first-line EGFR-TKIs and the efficacy of osimertinib as second-line treatment has not been previously assessed.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	72-76
34525256-4	2021	PATIENTS AND METHODS: We retrospectively analyzed 67 patients with EGFR mutations on osimertinib after treatment with first-generation EGFR-TKIs.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	67-71
34525256-4	2021	PATIENTS AND METHODS: We retrospectively analyzed 67 patients with EGFR mutations on osimertinib after treatment with first-generation EGFR-TKIs.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	135-139
34525256-7	2021	Correlation analysis showed that the female sex and isolated (not multiple) progression on first-line EGFR-TKIs were correlated with a superior response to osimertinib.	osimertinib	156-167	epidermal growth factor receptor	Homo sapiens	102-106
34525256-9	2021	Univariate analysis indicated that the treatment response, PFS, and progression when on first-line EGFR-TKIs affected the PFS on osimertinib.	osimertinib	129-140	epidermal growth factor receptor	Homo sapiens	99-103
34525256-10	2021	Multivariate analysis showed that progression when on first-line EGFR-TKIs was independently prognostic of a response to osimertinib.	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	65-69
34525256-12	2021	A low frequency of the EGFR T790M allele in plasma tended to predict an inferior efficacy of osimertinib and shorter PFS.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	23-27
34525256-13	2021	CONCLUSION: We found that patients who benefited from first-line EGFR-TKIs may experience prolonged PFS and a higher response rate when subsequently given osimertinib.	osimertinib	155-166	epidermal growth factor receptor	Homo sapiens	65-69
34525256-14	2021	A low plasma frequency of the EGFR T790M allele may predict poor osimertinib efficacy and shorter PFS.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	30-34
34419684-1	2021	BACKGROUND: Osimertinib has been reported to be effective against central nervous system (CNS) metastasis from activating epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	122-154
34419684-1	2021	BACKGROUND: Osimertinib has been reported to be effective against central nervous system (CNS) metastasis from activating epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	156-160
34419684-3	2021	PURPOSE: This study aimed to evaluate the efficacy of osimertinib against radiotherapy-naive CNS metastasis from sensitizing EGFR mutation-positive NSCLC.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	125-129
34419684-19	2021	The primary endpoint was met, and the results demonstrated the efficacy of osimertinib in patients with CNS metastasis harboring EGFR T790M mutations especially for EGFR-sensitizing mutation of exon 19 deletion.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	129-133
34419684-19	2021	The primary endpoint was met, and the results demonstrated the efficacy of osimertinib in patients with CNS metastasis harboring EGFR T790M mutations especially for EGFR-sensitizing mutation of exon 19 deletion.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	165-169
34739853-3	2021	However, the phase 3 ADAURA trial has recently shown that the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, reduces the risk of disease recurrence by 80% versus placebo in the adjuvant setting for patients with stage IB-IIIA EGFR mutation-positive NSCLC following complete tumor resection with or without adjuvant chemotherapy, according to physician and patient choice.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	62-94
34649106-18	2021	CONCLUSION: Sequential afatinib and osimertinib demonstrated encouraging activity in patients with EGFR mutation-positive NSCLC and acquired T790M.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	99-103
34739853-3	2021	However, the phase 3 ADAURA trial has recently shown that the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, reduces the risk of disease recurrence by 80% versus placebo in the adjuvant setting for patients with stage IB-IIIA EGFR mutation-positive NSCLC following complete tumor resection with or without adjuvant chemotherapy, according to physician and patient choice.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	96-100
34739853-3	2021	However, the phase 3 ADAURA trial has recently shown that the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, reduces the risk of disease recurrence by 80% versus placebo in the adjuvant setting for patients with stage IB-IIIA EGFR mutation-positive NSCLC following complete tumor resection with or without adjuvant chemotherapy, according to physician and patient choice.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	265-269
34723634-0	2021	A plain language summary of results from the ADAURA study: osimertinib after surgery for patients who have early-stage EGFR-mutated non-small cell lung cancer.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	119-123
34808485-0	2021	A phase I/II study of osimertinib in EGFR exon 20 insertion mutation-positive non-small cell lung cancer.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	37-41
34723634-2	2021	Osimertinib (TAGRISSO ) is a medication used to treat a type of NSCLC with a change (mutation) in the EGFR gene, known as EGFR-mutated NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	102-106
34723634-2	2021	Osimertinib (TAGRISSO ) is a medication used to treat a type of NSCLC with a change (mutation) in the EGFR gene, known as EGFR-mutated NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	122-126
34723634-2	2021	Osimertinib (TAGRISSO ) is a medication used to treat a type of NSCLC with a change (mutation) in the EGFR gene, known as EGFR-mutated NSCLC.	osimertinib	13-21	epidermal growth factor receptor	Homo sapiens	102-106
34723634-2	2021	Osimertinib (TAGRISSO ) is a medication used to treat a type of NSCLC with a change (mutation) in the EGFR gene, known as EGFR-mutated NSCLC.	osimertinib	13-21	epidermal growth factor receptor	Homo sapiens	122-126
34808485-1	2021	OBJECTIVES: Several preclinical data proposed a potential efficacy of osimertinib, a third-generation EGFR tyrosine kinase inhibitor, for EGFR exon 20 insertion (EGFR ex20ins)-positive non-small cell lung cancer (NSCLC).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	138-142
34808485-1	2021	OBJECTIVES: Several preclinical data proposed a potential efficacy of osimertinib, a third-generation EGFR tyrosine kinase inhibitor, for EGFR exon 20 insertion (EGFR ex20ins)-positive non-small cell lung cancer (NSCLC).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	162-166
34808485-4	2021	In this study, we performed a prospective, single-arm, multi-center, open-label, non-randomized phase I/II study to evaluate efficacy of osimertinib for EGFR ex20ins-positive NSCLC.	osimertinib	137-148	epidermal growth factor receptor	Homo sapiens	153-157
34635799-4	2021	Osimertinib facilitated degradation of the mature form of SREBP1 (mSREBP1) in a GSK3/FBXW7-dependent manner and reduced protein levels of its regulated genes in EGFR-mutant NSCLC cells/tumors accompanied with suppression of lipogenesis.	osimertinib	0-11	F-box and WD repeat domain containing 7	Homo sapiens	85-90
34808485-10	2021	Interestingly, the exploratory study demonstrated statistically significant positive correlation between plasma osimertinib concentration/in vitro IC50 ratio and PFS (R = 0.9912, P = 0.0001), highlighting the mutation type-specific concentration-dependent efficacy of osimertinib for EGFR ex20ins-positive NSCLC.	osimertinib	268-279	epidermal growth factor receptor	Homo sapiens	284-288
34635799-4	2021	Osimertinib facilitated degradation of the mature form of SREBP1 (mSREBP1) in a GSK3/FBXW7-dependent manner and reduced protein levels of its regulated genes in EGFR-mutant NSCLC cells/tumors accompanied with suppression of lipogenesis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	161-165
34635799-6	2021	Both genetic and pharmacological inhibition of SREBP1 sensitized osimertinib-resistant cells and tumors to osimertinib primarily through enhancing Bim-dependent induction of apoptosis, whereas enforced expression of ectopic SREBP1 in sensitive EGFR-mutant NSCLC cells compromised osimertinib"s cell-killing effects.	osimertinib	65-76	sterol regulatory element binding transcription factor 1	Homo sapiens	47-53
34635799-6	2021	Both genetic and pharmacological inhibition of SREBP1 sensitized osimertinib-resistant cells and tumors to osimertinib primarily through enhancing Bim-dependent induction of apoptosis, whereas enforced expression of ectopic SREBP1 in sensitive EGFR-mutant NSCLC cells compromised osimertinib"s cell-killing effects.	osimertinib	107-118	sterol regulatory element binding transcription factor 1	Homo sapiens	47-53
34635799-6	2021	Both genetic and pharmacological inhibition of SREBP1 sensitized osimertinib-resistant cells and tumors to osimertinib primarily through enhancing Bim-dependent induction of apoptosis, whereas enforced expression of ectopic SREBP1 in sensitive EGFR-mutant NSCLC cells compromised osimertinib"s cell-killing effects.	osimertinib	107-118	BCL2 like 11	Homo sapiens	147-150
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	62-73	sterol regulatory element binding transcription factor 1	Homo sapiens	78-84
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	131-135
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	276-280
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	158-169	sterol regulatory element binding transcription factor 1	Homo sapiens	78-84
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	158-169	epidermal growth factor receptor	Homo sapiens	131-135
34635799-7	2021	Collectively, we have demonstrated a novel connection between osimertinib and SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osimertinib and suggested an effective strategy for overcoming acquired resistance to osimertinib, and possibly other EGFR inhibitors, via targeting SREBP1.	osimertinib	244-255	sterol regulatory element binding transcription factor 1	Homo sapiens	78-84
34727807-0	2021	Carcinomatosis under control by osimertinib in EGFR and TP53 mutated lung adenocarcinoma.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	47-51
34704378-3	2021	In total, 76 patients with EGFR T790M mutation who received osimertinib after re-biopsy or liquid biopsy were enrolled for the analysis.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	27-31
34704378-5	2021	A significant difference was observed in the disease control rate between those who received osimertinib treatment after chemotherapy (group A) and those who received osimertinib immediately following EGFR-TKI therapy (group B) (34 (94.4%) vs. 31 (77.5%), p = 0.036).	osimertinib	167-178	epidermal growth factor receptor	Homo sapiens	201-205
34704378-8	2021	Osimertinib treatment following first/second generation EGFR-TKI treatment or chemotherapy resulted in improved survival benefit.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	56-60
34727807-0	2021	Carcinomatosis under control by osimertinib in EGFR and TP53 mutated lung adenocarcinoma.	osimertinib	32-43	tumor protein p53	Homo sapiens	56-60
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	fibroblast activation protein alpha	Homo sapiens	188-217
34848786-1	2021	Osimertinib is a standard of care therapy for previously untreated epidermal growth factor receptor mutation-positive non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	67-99
34885115-0	2021	The MEK/ERK/miR-21 Signaling Is Critical in Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	44-55	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
34885115-0	2021	The MEK/ERK/miR-21 Signaling Is Critical in Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	44-55	mitogen-activated protein kinase 1	Homo sapiens	8-11
34885115-0	2021	The MEK/ERK/miR-21 Signaling Is Critical in Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	44-55	microRNA 21	Homo sapiens	12-18
34885115-0	2021	The MEK/ERK/miR-21 Signaling Is Critical in Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	70-74
34885115-1	2021	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR) inhibitor, Osimertinib, is used to treat non-small cell lung cancer (NSCLC) patients with tyrosine kinase inhibitor (TKI) resistance caused by acquired EGFR T790M mutation.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	33-65
34885115-1	2021	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR) inhibitor, Osimertinib, is used to treat non-small cell lung cancer (NSCLC) patients with tyrosine kinase inhibitor (TKI) resistance caused by acquired EGFR T790M mutation.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	67-71
34885115-1	2021	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR) inhibitor, Osimertinib, is used to treat non-small cell lung cancer (NSCLC) patients with tyrosine kinase inhibitor (TKI) resistance caused by acquired EGFR T790M mutation.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	225-229
34885115-6	2021	In this report, we reveal the possible regulatory mechanism and inhibitory effect of the MEK inhibitor trametinib applied to MEK/ERK/miR-21 axis and PDCD4 in Osimertinib resistance.	osimertinib	158-169	mitogen-activated protein kinase kinase 7	Homo sapiens	89-92
34885115-6	2021	In this report, we reveal the possible regulatory mechanism and inhibitory effect of the MEK inhibitor trametinib applied to MEK/ERK/miR-21 axis and PDCD4 in Osimertinib resistance.	osimertinib	158-169	mitogen-activated protein kinase kinase 7	Homo sapiens	125-128
34885115-6	2021	In this report, we reveal the possible regulatory mechanism and inhibitory effect of the MEK inhibitor trametinib applied to MEK/ERK/miR-21 axis and PDCD4 in Osimertinib resistance.	osimertinib	158-169	mitogen-activated protein kinase 1	Homo sapiens	129-132
34885115-6	2021	In this report, we reveal the possible regulatory mechanism and inhibitory effect of the MEK inhibitor trametinib applied to MEK/ERK/miR-21 axis and PDCD4 in Osimertinib resistance.	osimertinib	158-169	microRNA 21	Homo sapiens	133-139
34885115-6	2021	In this report, we reveal the possible regulatory mechanism and inhibitory effect of the MEK inhibitor trametinib applied to MEK/ERK/miR-21 axis and PDCD4 in Osimertinib resistance.	osimertinib	158-169	programmed cell death 4	Homo sapiens	149-154
34885115-14	2021	RESULT: ERK2 expression correlated with EGFR expression and higher ERK2 level was associated with worse prognosis of patients and Osimertinib resistance.	osimertinib	130-141	mitogen-activated protein kinase 1	Homo sapiens	8-12
34885115-14	2021	RESULT: ERK2 expression correlated with EGFR expression and higher ERK2 level was associated with worse prognosis of patients and Osimertinib resistance.	osimertinib	130-141	epidermal growth factor receptor	Homo sapiens	40-44
34885115-14	2021	RESULT: ERK2 expression correlated with EGFR expression and higher ERK2 level was associated with worse prognosis of patients and Osimertinib resistance.	osimertinib	130-141	mitogen-activated protein kinase 1	Homo sapiens	67-71
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	interleukin 6	Homo sapiens	60-64
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	C-X-C motif chemokine ligand 8	Homo sapiens	66-70
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	hepatocyte growth factor	Homo sapiens	76-100
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	hepatocyte growth factor	Homo sapiens	102-105
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	actin alpha 1, skeletal muscle	Homo sapiens	176-185
34635799-0	2021	Induction of SREBP1 degradation coupled with suppression of SREBP1-mediated lipogenesis impacts the response of EGFR mutant NSCLC cells to osimertinib.	osimertinib	139-150	sterol regulatory element binding transcription factor 1	Homo sapiens	13-19
34635799-0	2021	Induction of SREBP1 degradation coupled with suppression of SREBP1-mediated lipogenesis impacts the response of EGFR mutant NSCLC cells to osimertinib.	osimertinib	139-150	sterol regulatory element binding transcription factor 1	Homo sapiens	60-66
34635799-0	2021	Induction of SREBP1 degradation coupled with suppression of SREBP1-mediated lipogenesis impacts the response of EGFR mutant NSCLC cells to osimertinib.	osimertinib	139-150	epidermal growth factor receptor	Homo sapiens	112-116
34635799-1	2021	Emergence of acquired resistance to osimertinib (AZD9291), the first-approved third-generation EGFR inhibitor that selectively and irreversibly inhibits the activating EGFR mutations and the resistant T790M mutation, is a giant and urgent clinical challenge.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	95-99
34635799-1	2021	Emergence of acquired resistance to osimertinib (AZD9291), the first-approved third-generation EGFR inhibitor that selectively and irreversibly inhibits the activating EGFR mutations and the resistant T790M mutation, is a giant and urgent clinical challenge.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	168-172
34635799-1	2021	Emergence of acquired resistance to osimertinib (AZD9291), the first-approved third-generation EGFR inhibitor that selectively and irreversibly inhibits the activating EGFR mutations and the resistant T790M mutation, is a giant and urgent clinical challenge.	osimertinib	49-56	epidermal growth factor receptor	Homo sapiens	95-99
34635799-1	2021	Emergence of acquired resistance to osimertinib (AZD9291), the first-approved third-generation EGFR inhibitor that selectively and irreversibly inhibits the activating EGFR mutations and the resistant T790M mutation, is a giant and urgent clinical challenge.	osimertinib	49-56	epidermal growth factor receptor	Homo sapiens	168-172
34635799-2	2021	Fully understanding the biology underlying the response of EGFR mutant non-small cell lung cancer (NSCLC) to osimertinib is the foundation for development of mechanism-driven strategies to overcome acquired resistance to osimertinib or other third-generation EGFR inhibitors.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	59-63
34635799-2	2021	Fully understanding the biology underlying the response of EGFR mutant non-small cell lung cancer (NSCLC) to osimertinib is the foundation for development of mechanism-driven strategies to overcome acquired resistance to osimertinib or other third-generation EGFR inhibitors.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	259-263
34635799-3	2021	This study focused on tackling this important issue by elucidating the critical role of sterol regulatory element-binding protein 1 (SREBP1) degradation in conferring the response of EGFR mutant NSCLC cells to osimertinib and by validating the strategy via directly targeting SREBP1 for overcoming osimertinib acquired resistance.	osimertinib	210-221	sterol regulatory element binding transcription factor 1	Homo sapiens	88-131
34635799-3	2021	This study focused on tackling this important issue by elucidating the critical role of sterol regulatory element-binding protein 1 (SREBP1) degradation in conferring the response of EGFR mutant NSCLC cells to osimertinib and by validating the strategy via directly targeting SREBP1 for overcoming osimertinib acquired resistance.	osimertinib	210-221	sterol regulatory element binding transcription factor 1	Homo sapiens	133-139
34635799-3	2021	This study focused on tackling this important issue by elucidating the critical role of sterol regulatory element-binding protein 1 (SREBP1) degradation in conferring the response of EGFR mutant NSCLC cells to osimertinib and by validating the strategy via directly targeting SREBP1 for overcoming osimertinib acquired resistance.	osimertinib	210-221	epidermal growth factor receptor	Homo sapiens	183-187
34635799-3	2021	This study focused on tackling this important issue by elucidating the critical role of sterol regulatory element-binding protein 1 (SREBP1) degradation in conferring the response of EGFR mutant NSCLC cells to osimertinib and by validating the strategy via directly targeting SREBP1 for overcoming osimertinib acquired resistance.	osimertinib	298-309	sterol regulatory element binding transcription factor 1	Homo sapiens	276-282
34635799-4	2021	Osimertinib facilitated degradation of the mature form of SREBP1 (mSREBP1) in a GSK3/FBXW7-dependent manner and reduced protein levels of its regulated genes in EGFR-mutant NSCLC cells/tumors accompanied with suppression of lipogenesis.	osimertinib	0-11	sterol regulatory element binding transcription factor 1	Homo sapiens	58-64
34635799-4	2021	Osimertinib facilitated degradation of the mature form of SREBP1 (mSREBP1) in a GSK3/FBXW7-dependent manner and reduced protein levels of its regulated genes in EGFR-mutant NSCLC cells/tumors accompanied with suppression of lipogenesis.	osimertinib	0-11	sterol regulatory element binding transcription factor 1	Mus musculus	66-73
34807331-0	2022	First-line osimertinib for poor performance status patients with EGFR mutation-positive non-small cell lung cancer: A prospective observational study.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	65-69
34807331-1	2022	OBJECTIVE: The clinical outcomes of poor performance status (PS) patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) who are treated with osimertinib as a first-line treatment have not been sufficiently evaluated.	osimertinib	183-194	epidermal growth factor receptor	Homo sapiens	79-111
34807331-1	2022	OBJECTIVE: The clinical outcomes of poor performance status (PS) patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) who are treated with osimertinib as a first-line treatment have not been sufficiently evaluated.	osimertinib	183-194	epidermal growth factor receptor	Homo sapiens	113-117
34807331-2	2022	This study aimed to assess the efficacy and safety of osimertinib in chemotherapy-naive and poor PS (2 or more) patients with NSCLC harboring sensitive EGFR mutations.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	152-156
34807331-3	2022	MATERIALS AND METHODS: We assessed the clinical effects of osimertinib as a first-line treatment for patients with poor PS NSCLC with an exon 19 deletion or exon 21 L858R mutation in EGFR.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	183-187
34807331-10	2022	CONCLUSION: Considering the findings of this study, osimertinib appears to be an effective and safe treatment option for patients with poor PS and advanced NSCLC harboring sensitive EGFR mutations.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	182-186
34849025-0	2021	A Prospective Observational Study of Osimertinib for Chemo-Naive Elderly Patients with EGFR Mutation-Positive Non-Small Cell Lung Cancer.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	87-91
34849025-1	2021	Background: The clinical outcomes of elderly patients with EGFR-mutated non-small cell lung cancer (NSCLC) who are treated with osimertinib have not been sufficiently evaluated.	osimertinib	128-139	epidermal growth factor receptor	Homo sapiens	59-63
34849025-2	2021	This study aimed to assess the efficacy and safety of osimertinib in elderly chemotherapy-naive patients with NSCLC harboring sensitive EGFR mutations.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	136-140
34849025-3	2021	Patients and Methods: We assessed the clinical effects of osimertinib as a first-line treatment for elderly NSCLC patients (>=75 years of age) with an exon 19 deletion or exon 21 L858R mutation in EGFR.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	197-201
34849025-11	2021	Conclusion: Considering the findings of this study and despite an observed discordance between PFS and TTF, osimertinib appears to be an effective and safe treatment option in elderly patients with advanced NSCLC harboring sensitive EGFR mutations.	osimertinib	108-119	epidermal growth factor receptor	Homo sapiens	233-237
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	fibroblast activation protein alpha	Homo sapiens	219-222
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	platelet derived growth factor receptor beta	Homo sapiens	229-268
34885115-15	2021	CAFs derived from Osimertinib-resistant cells secreted more IL-6, IL-8, and hepatocyte growth factor (HGF), expressed stronger CAF markers including alpha-smooth muscle actin (alpha-SMA), fibroblast activation protein (FAP) plus platelet-derived growth factor receptor (PDGFR), and enhanced stemness and Osimertinib resistance in NSCLC cells.	osimertinib	18-29	platelet derived growth factor receptor beta	Homo sapiens	270-275
34885115-19	2021	CONCLUSIONS: Our results suggested that MEK/ERK/miR-21 signaling is critical in Osimertinib resistance and CAF transformation of NSCLC cells, and MEK inhibitor Trametinib significantly suppressed Osimertinib-resistant NSCLC tumor growth by abolishing both processes.	osimertinib	80-91	mitogen-activated protein kinase kinase 7	Homo sapiens	40-43
34885115-19	2021	CONCLUSIONS: Our results suggested that MEK/ERK/miR-21 signaling is critical in Osimertinib resistance and CAF transformation of NSCLC cells, and MEK inhibitor Trametinib significantly suppressed Osimertinib-resistant NSCLC tumor growth by abolishing both processes.	osimertinib	80-91	mitogen-activated protein kinase 1	Homo sapiens	44-47
34885115-19	2021	CONCLUSIONS: Our results suggested that MEK/ERK/miR-21 signaling is critical in Osimertinib resistance and CAF transformation of NSCLC cells, and MEK inhibitor Trametinib significantly suppressed Osimertinib-resistant NSCLC tumor growth by abolishing both processes.	osimertinib	80-91	microRNA 21	Homo sapiens	48-54
34830377-4	2021	Several EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including erlotinib, gefitinib, and osimertinib, are effective therapeutic agents in EGFR-mutated NSCLC.	osimertinib	89-100	epidermal growth factor receptor	Rattus norvegicus	8-12
34798865-11	2021	Multivariate logistic regression analysis at 3 months from the start of EGFR-TKI treatment revealed that oligo-residual disease (P < 0.001), the lack of residual central nervous system metastases (P = 0.032), and initial treatment with osimertinib (P = 0.028) were independent predictors of PD limited to residual disease sites.	osimertinib	236-247	epidermal growth factor receptor	Homo sapiens	72-76
34802213-0	2021	(Osimertinib Re-challenge for EGFR-mutant NSCLC after  : Osimertinib-induced Interstitial Lung Disease: A Case Report).	osimertinib	1-12	epidermal growth factor receptor	Homo sapiens	30-34
34802213-2	2021	We report a case of a 64-year-old male with stage IV adeno-non-small cell lung cancer (NSCLC) harboring an exon 19 deletion in the epidermal growth factor receptor (EGFR) treated with osimertinib 80 mg/d for first-line targeted therapy.	osimertinib	184-195	epidermal growth factor receptor	Homo sapiens	131-163
34802213-2	2021	We report a case of a 64-year-old male with stage IV adeno-non-small cell lung cancer (NSCLC) harboring an exon 19 deletion in the epidermal growth factor receptor (EGFR) treated with osimertinib 80 mg/d for first-line targeted therapy.	osimertinib	184-195	epidermal growth factor receptor	Homo sapiens	165-169
34830377-4	2021	Several EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including erlotinib, gefitinib, and osimertinib, are effective therapeutic agents in EGFR-mutated NSCLC.	osimertinib	89-100	epidermal growth factor receptor	Rattus norvegicus	41-45
34830377-4	2021	Several EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including erlotinib, gefitinib, and osimertinib, are effective therapeutic agents in EGFR-mutated NSCLC.	osimertinib	89-100	epidermal growth factor receptor	Rattus norvegicus	138-142
34806395-7	2021	In Japan, osimertinib treatment after failure of EGFR-TKI treatments requires the T790M mutation in the tumor, blood or body fluid, so BE treatment was started as second-line treatment.	osimertinib	10-21	epidermal growth factor receptor	Homo sapiens	49-53
34831415-6	2021	After the role of EGFR T790M mutation in acquired drug resistance was reported, osimertinib, a third-generation irreversible EGFR-TKI, was designed to overcome the resistance conferred by T790M mutation.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	125-129
34831415-6	2021	After the role of EGFR T790M mutation in acquired drug resistance was reported, osimertinib, a third-generation irreversible EGFR-TKI, was designed to overcome the resistance conferred by T790M mutation.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	18-22
34871271-2	2021	Osimertinib is a promising option for NSCLC with LM harboring epidermal growth factor receptor (EGFR) mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	96-100
34816394-1	2021	Osimertinib (OB) is a third-generation irreversible tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR), overexpressed in non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	92-124
34816394-1	2021	Osimertinib (OB) is a third-generation irreversible tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR), overexpressed in non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	126-130
34455456-5	2021	AZD9291 was also shown to overcome acquired resistance to gefitinib in PC-9-Br in MTT assays (0.23 +- 0.031 microM at 48 h and 0.03 +- 0.008 microM at 72 h).	osimertinib	0-7	proprotein convertase subtilisin/kexin type 9	Mus musculus	71-75
34278827-0	2021	Neoadjuvant osimertinib with/without chemotherapy versus chemotherapy alone for EGFR-mutated resectable non-small-cell lung cancer: NeoADAURA.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	80-84
34389237-0	2021	Biomarker-Directed Phase II Platform Study in Patients With EGFR Sensitizing Mutation-Positive Advanced/Metastatic Non-Small Cell Lung Cancer Whose Disease Has Progressed on First-Line Osimertinib Therapy (ORCHARD).	osimertinib	185-196	epidermal growth factor receptor	Homo sapiens	60-64
34389237-1	2021	INTRODUCTION: Osimertinib, a third-generation, irreversible, epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), selectively inhibits both EGFR-TKI sensitizing (EGFRm) and EGFR T790M resistance mutations and has demonstrated efficacy in non-small cell lung cancer (NSCLC) CNS metastases.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	121-125
34389237-1	2021	INTRODUCTION: Osimertinib, a third-generation, irreversible, epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), selectively inhibits both EGFR-TKI sensitizing (EGFRm) and EGFR T790M resistance mutations and has demonstrated efficacy in non-small cell lung cancer (NSCLC) CNS metastases.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	191-195
34278827-1	2021	Osimertinib is a third-generation, irreversible oral EGFR-tyrosine kinase inhibitor), that potently inhibits EGFR-tyrosine kinase inhibitor-sensitizing mutations and T790M resistance mutations together with efficacy in CNS metastases in patients with non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	53-57
34278827-1	2021	Osimertinib is a third-generation, irreversible oral EGFR-tyrosine kinase inhibitor), that potently inhibits EGFR-tyrosine kinase inhibitor-sensitizing mutations and T790M resistance mutations together with efficacy in CNS metastases in patients with non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	109-113
34242789-9	2021	Osimertinib in combination with mTOR inhibitors abrogated acquired resistance to osimertinib.	osimertinib	0-11	mechanistic target of rapamycin kinase	Homo sapiens	32-36
34558640-3	2021	Osimertinib is a representative of the 3rd-generation EGFR-TKIs that target T790M mutation, and has satisfactory efficacy in the treatment of T790M-positive NSCLC with disease progression following use of 1st- or 2nd-generation EGFR-TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	54-58
34558640-3	2021	Osimertinib is a representative of the 3rd-generation EGFR-TKIs that target T790M mutation, and has satisfactory efficacy in the treatment of T790M-positive NSCLC with disease progression following use of 1st- or 2nd-generation EGFR-TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	228-232
34242789-8	2021	The MTORL1433S mutation was oncogenic in Ba/F3 models and showed resistance to osimertinib through AKT signaling activation in NCI-H1975 cells harboring the MTORL1433S mutation edited by CRISPR/Cas9 (IC50, 800 +- 67 nM).	osimertinib	79-90	AKT serine/threonine kinase 1	Homo sapiens	99-102
34849493-1	2021	Introduction: With the approval of first-line osimertinib treatment in stage IV EGFR-mutated NSCLC, detection of resistance mechanisms will become increasingly important-and complex.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	80-84
34242789-9	2021	Osimertinib in combination with mTOR inhibitors abrogated acquired resistance to osimertinib.	osimertinib	81-92	mechanistic target of rapamycin kinase	Homo sapiens	32-36
34994592-0	2021	Patient With Stage IV NSCLC and CNS Metastasis With EGFR Exon 18-25 Kinase Domain Duplication With Response to Osimertinib as a First-Line Therapy.	osimertinib	111-122	epidermal growth factor receptor	Homo sapiens	52-56
34994624-0	2021	Divergent RET- and BRAF-Mediated Resistance to Osimertinib in EGFR-Mutant NSCLC: A Case Report.	osimertinib	47-58	ret proto-oncogene	Homo sapiens	10-13
34994604-0	2021	Standard-Dose Osimertinib in EGFR-Mutated Non-Small-Cell Lung Adenocarcinoma With Leptomeningeal Disease.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	29-33
34994604-3	2021	This study reports on outcomes of patients with EGFR-mutated non-small-cell lung cancer who developed LMD and were subsequently treated with osimertinib.	osimertinib	141-152	epidermal growth factor receptor	Homo sapiens	48-52
34994624-0	2021	Divergent RET- and BRAF-Mediated Resistance to Osimertinib in EGFR-Mutant NSCLC: A Case Report.	osimertinib	47-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
34994624-0	2021	Divergent RET- and BRAF-Mediated Resistance to Osimertinib in EGFR-Mutant NSCLC: A Case Report.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	62-66
34694530-0	2021	Correction to: Osimertinib: A Review in Previously Untreated, EGFR Mutation-Positive, Advanced NSCLC.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	62-66
34887192-1	2022	INTRODUCTION: Osimertinib is a standard first-line treatment for non-small cell lung cancer (NSCLC) harboring mutations of the epidermal growth factor receptor gene (EGFR).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	127-159
34245854-0	2021	Inhibition of MEK5/ERK5 signaling overcomes acquired resistance to the third generation EGFR inhibitor, osimertinib, via enhancing Bim-dependent apoptosis.	osimertinib	104-115	mitogen-activated protein kinase kinase 5	Homo sapiens	14-18
34245854-0	2021	Inhibition of MEK5/ERK5 signaling overcomes acquired resistance to the third generation EGFR inhibitor, osimertinib, via enhancing Bim-dependent apoptosis.	osimertinib	104-115	mitogen-activated protein kinase 7	Homo sapiens	19-23
34245854-0	2021	Inhibition of MEK5/ERK5 signaling overcomes acquired resistance to the third generation EGFR inhibitor, osimertinib, via enhancing Bim-dependent apoptosis.	osimertinib	104-115	epidermal growth factor receptor	Homo sapiens	88-92
34245854-0	2021	Inhibition of MEK5/ERK5 signaling overcomes acquired resistance to the third generation EGFR inhibitor, osimertinib, via enhancing Bim-dependent apoptosis.	osimertinib	104-115	BCL2 like 11	Homo sapiens	131-134
34245854-1	2021	The promising therapeutic efficacy of the third generation EGFR inhibitor, osimertinib (AZD9291), for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC) has been demonstrated in the clinic both as first-line and second line therapy.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	59-63
34245854-1	2021	The promising therapeutic efficacy of the third generation EGFR inhibitor, osimertinib (AZD9291), for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC) has been demonstrated in the clinic both as first-line and second line therapy.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	133-137
34245854-1	2021	The promising therapeutic efficacy of the third generation EGFR inhibitor, osimertinib (AZD9291), for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC) has been demonstrated in the clinic both as first-line and second line therapy.	osimertinib	88-95	epidermal growth factor receptor	Homo sapiens	59-63
34245854-1	2021	The promising therapeutic efficacy of the third generation EGFR inhibitor, osimertinib (AZD9291), for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC) has been demonstrated in the clinic both as first-line and second line therapy.	osimertinib	88-95	epidermal growth factor receptor	Homo sapiens	133-137
34245854-5	2021	Osimertinib combined with either ERK5 or MEK5 inhibitors synergistically decreased the survival of osimertinib-resistant cell lines with enhanced induction of apoptosis primarily via augmenting Bim expression.	osimertinib	99-110	mitogen-activated protein kinase 7	Homo sapiens	33-37
34245854-5	2021	Osimertinib combined with either ERK5 or MEK5 inhibitors synergistically decreased the survival of osimertinib-resistant cell lines with enhanced induction of apoptosis primarily via augmenting Bim expression.	osimertinib	99-110	mitogen-activated protein kinase kinase 5	Homo sapiens	41-45
34245854-7	2021	Together, these findings suggest the potential role of MEK5-ERK5 signaling in modulating development of acquired resistance to osimertinib and value of targeting this signaling as a potential strategy in overcoming acquired resistance to osimertinib and possibly other third generation EGFR inhibitors.	osimertinib	127-138	mitogen-activated protein kinase kinase 5	Homo sapiens	55-59
34245854-7	2021	Together, these findings suggest the potential role of MEK5-ERK5 signaling in modulating development of acquired resistance to osimertinib and value of targeting this signaling as a potential strategy in overcoming acquired resistance to osimertinib and possibly other third generation EGFR inhibitors.	osimertinib	127-138	mitogen-activated protein kinase 7	Homo sapiens	60-64
34245854-7	2021	Together, these findings suggest the potential role of MEK5-ERK5 signaling in modulating development of acquired resistance to osimertinib and value of targeting this signaling as a potential strategy in overcoming acquired resistance to osimertinib and possibly other third generation EGFR inhibitors.	osimertinib	238-249	mitogen-activated protein kinase kinase 5	Homo sapiens	55-59
34702733-1	2021	According to a preclinical report, the investigational tyrosine kinase inhibitor BDTX-1535 may mitigate resistance to osimertinib, the standard of care for EGFR-mutant non-small cell lung cancer.	osimertinib	118-129	epidermal growth factor receptor	Homo sapiens	156-160
34770832-2	2021	The similarity search of icotinib, almonertinib, and olmutinib against a database of 154 EGFR ligands revealed the highest similarity scores with erlotinib (0.9333), osimertinib (0.9487), and WZ4003 (0.8421), respectively.	osimertinib	166-177	epidermal growth factor receptor	Homo sapiens	89-93
34771484-7	2021	Our findings revealed that PC9 and PC9-GR3 models cultured on PCL-ES scaffolds showed higher resistance to osimertinib, upregulation of ABCB1, Vimentin, Snail, Twist, Sox2, Oct-4, and CD166, downregulation of E-cadherin and CD133, and the activation of Hedgehog pathway.	osimertinib	107-118	proprotein convertase subtilisin/kexin type 9	Homo sapiens	27-30
34771484-7	2021	Our findings revealed that PC9 and PC9-GR3 models cultured on PCL-ES scaffolds showed higher resistance to osimertinib, upregulation of ABCB1, Vimentin, Snail, Twist, Sox2, Oct-4, and CD166, downregulation of E-cadherin and CD133, and the activation of Hedgehog pathway.	osimertinib	107-118	proprotein convertase subtilisin/kexin type 9	Homo sapiens	35-38
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	67-78	tumor protein p53	Homo sapiens	10-13
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	67-78	tumor protein p53	Homo sapiens	201-204
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	186-197	tumor protein p53	Homo sapiens	10-13
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	186-197	tumor protein p53	Homo sapiens	201-204
34790799-0	2021	AZD9291-resistant non-small cell lung cancer cell-derived exosomal lnc-MZT2A-5:1 induces the activation of fibroblasts.	osimertinib	0-7	mitotic spindle organizing protein 2A	Homo sapiens	71-76
34740861-0	2022	Postoperative Chemotherapy Use and Outcomes From ADAURA: Osimertinib as Adjuvant Therapy for Resected EGFR-Mutated NSCLC.	osimertinib	57-68	aurora kinase A	Homo sapiens	49-55
34740861-0	2022	Postoperative Chemotherapy Use and Outcomes From ADAURA: Osimertinib as Adjuvant Therapy for Resected EGFR-Mutated NSCLC.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	102-106
34740861-2	2022	In the phase III, ADAURA study (NCT02511106), osimertinib demonstrated a highly statistically significant improvement in disease-free survival (DFS) in patients with resected stage IB IIIA EGFRm NSCLC.	osimertinib	46-57	aurora kinase A	Homo sapiens	18-24
34656143-10	2021	Pharmacologic inhibition of EZH1/2 in combination with osimertinib prevented relapse with squamous-features in an EGFR-mutant patient-derived xenograft model, and inhibition of EZH1/2 or PI3K/AKT signaling re-sensitized resistant squamous-like tumors to osimertinib.	osimertinib	55-66	epidermal growth factor receptor	Homo sapiens	114-118
34734065-2	2021	AZD9291 has been developed as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) with activity against T790M mutation.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	49-81
34734065-2	2021	AZD9291 has been developed as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) with activity against T790M mutation.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	83-87
34602008-1	2021	AIM: To evaluate the cost-effectiveness of first-line treatments such as erlotinib, gefitinib, afatinib, dacomitinib, and osimertinib, for patients diagnosed with stage IIIB/IV NSCLC harbouring EGFR mutations.	osimertinib	122-133	epidermal growth factor receptor	Homo sapiens	194-198
34638461-5	2021	Herein, we employed stable isotope labeling by amino acids in cell culture (SILAC) quantitative mass spectrometry-based proteomics to investigate potential immune escape molecular mechanisms in osimertinib resistant EGFR mutant lung adenocarcinoma by interrogating the alterations in the human leukocyte antigen (HLA) Class I-presented immunopeptidome, Class I-interactome, and the whole cell proteome between isogenic osimertinib-sensitive and -resistant human lung adenocarcinoma cells.	osimertinib	194-205	epidermal growth factor receptor	Homo sapiens	216-220
34605320-1	2022	INTRODUCTION: Osimertinib is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	74-106
34605320-3	2022	CASE REPORT: We report a previously healthy 56-year-old woman who developed elevated serum creatine kinase levels during osimertinib monotherapy for epidermal growth factor receptor mutation-positive lung adenocarcinoma.	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	149-181
34593465-3	2021	PATIENTS AND METHODS: We retrospectively investigated the survival time of patients diagnosed with EGFR-mutated advanced or recurrent NSCLC who had received afatinib, a second-generation EGFR-TKI, or osimertinib, a third-generation EGFR-TKI, as the first-line treatment.	osimertinib	200-211	epidermal growth factor receptor	Homo sapiens	232-236
34364740-1	2021	Osimertinib is used as a first-line treatment for metastatic non-small cell lung cancer with positive epidermal growth factor receptor mutations based on the results of the FLAURA trial.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	102-134
34364740-2	2021	However, as with any other epidermal growth factor receptor tyrosine kinase inhibitor, resistance also develops for osimertinib.	osimertinib	116-127	epidermal growth factor receptor	Homo sapiens	27-59
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	126-137	CD274 molecule	Homo sapiens	0-5
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	57-89
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	91-95
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	155-159
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	138-145	CD274 molecule	Homo sapiens	0-5
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	138-145	epidermal growth factor receptor	Homo sapiens	57-89
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	138-145	epidermal growth factor receptor	Homo sapiens	91-95
34887192-1	2022	INTRODUCTION: Osimertinib is a standard first-line treatment for non-small cell lung cancer (NSCLC) harboring mutations of the epidermal growth factor receptor gene (EGFR).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	166-170
34183449-2	2021	PD-L1 expression may also impact therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR mutant non-small cell lung cancers (NSCLCs) and can even be altered during the treatment albeit with largely undefined mechanisms.	osimertinib	138-145	epidermal growth factor receptor	Homo sapiens	155-159
34183449-3	2021	This study primarily focuses on elucidating the mechanism by which osimertinib induces PD-L1 degradation in addition to validating osimertinib"s effect on decreasing PD-L1 expression in EGFR mutant NSCLC cells and tumors.	osimertinib	67-78	CD274 molecule	Homo sapiens	87-92
34183449-3	2021	This study primarily focuses on elucidating the mechanism by which osimertinib induces PD-L1 degradation in addition to validating osimertinib"s effect on decreasing PD-L1 expression in EGFR mutant NSCLC cells and tumors.	osimertinib	131-142	CD274 molecule	Homo sapiens	166-171
34638411-4	2021	In the case of first-line treatment by first (erlotinib, gefitinib)- or second-generation (afatinib) TKIs, osimertinib is approved in second-line treatment for patients with T790M EGFR mutation.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	180-184
34183449-3	2021	This study primarily focuses on elucidating the mechanism by which osimertinib induces PD-L1 degradation in addition to validating osimertinib"s effect on decreasing PD-L1 expression in EGFR mutant NSCLC cells and tumors.	osimertinib	131-142	epidermal growth factor receptor	Homo sapiens	186-190
34183449-10	2021	Collectively, these results strongly suggest that MARCH8 is a previously undiscovered E3 ubiquitin ligase responsible for PD-L1 degradation including osimertinib-induced PD-L1 degradation, establishing a novel connection between MARCH8 and PD-L1 regulation.	osimertinib	150-161	CD274 molecule	Homo sapiens	170-175
34858779-10	2021	The response of Osimertinib in 74 EGFR p.T790M-positive patients detected by dPCR, including 26 determined as negative by ARMS-PCR, were evaluated to have an ORR of 44.59% and a DCR of 90.54%.	osimertinib	16-27	epidermal growth factor receptor	Homo sapiens	34-38
34858779-11	2021	Conclusions: dPCR is a sensitive and accurate tool for ctDNA-based EGFR p.T790M detection due to its significantly improved sensitivity without compromising specificity, and dPCR is equivalent to ARMS-PCR as a companion diagnostic tool while benefiting more patients under Osimertinib treatment.	osimertinib	273-284	epidermal growth factor receptor	Homo sapiens	67-71
34621884-0	2021	Non-small-cell lung cancer with epidermal growth factor receptor L861Q-L833F compound mutation benefits from both afatinib and osimertinib: A case report.	osimertinib	127-138	epidermal growth factor receptor	Homo sapiens	32-64
34660285-0	2021	Machine Learning-Based CT Radiomics Analysis for Prognostic Prediction in Metastatic Non-Small Cell Lung Cancer Patients With EGFR-T790M Mutation Receiving Third-Generation EGFR-TKI Osimertinib Treatment.	osimertinib	182-193	epidermal growth factor receptor	Homo sapiens	126-130
34660285-0	2021	Machine Learning-Based CT Radiomics Analysis for Prognostic Prediction in Metastatic Non-Small Cell Lung Cancer Patients With EGFR-T790M Mutation Receiving Third-Generation EGFR-TKI Osimertinib Treatment.	osimertinib	182-193	epidermal growth factor receptor	Homo sapiens	173-177
34660285-1	2021	Background and Purpose: As a third-generation EGFR tyrosine kinase inhibitor (TKI), osimertinib is approved for treating advanced non-small cell lung cancer (NSCLC) patients with EGFR-T790M mutation after progression on first- or second-generation EGFR-TKIs such as gefitinib, erlotinib and afatinib.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	179-183
34660285-1	2021	Background and Purpose: As a third-generation EGFR tyrosine kinase inhibitor (TKI), osimertinib is approved for treating advanced non-small cell lung cancer (NSCLC) patients with EGFR-T790M mutation after progression on first- or second-generation EGFR-TKIs such as gefitinib, erlotinib and afatinib.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	248-252
34660285-2	2021	We aim at exploring the feasibility and effectiveness of using radiomic features from chest CT scan to predict the prognosis of metastatic non-small cell lung cancer (NSCLC) patients with EGFR-T790M mutation receiving second-line osimertinib therapy.	osimertinib	230-241	epidermal growth factor receptor	Homo sapiens	188-192
34585625-0	2021	Transient asymptomatic pulmonary opacities and interstitial lung disease in EGFR-mutated non-small cell lung cancer treated with osimertinib.	osimertinib	129-140	epidermal growth factor receptor	Homo sapiens	76-80
34585625-1	2021	INTRODUCTION: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	48-80
34585625-1	2021	INTRODUCTION: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	82-86
34585625-1	2021	INTRODUCTION: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	164-168
34585625-3	2021	METHODS: In this multicentric study, we retrospectively analyzed 92 patients with EGFR-mutated NSCLC treated with osimertinib.	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	82-86
34621884-9	2021	CONCLUSION: Our case revealed that both afatinib and the osimertinib + bevacizumab combination demonstrated clinical efficacy in NSCLC harboring an EGFR L833F-L861Q compound mutation.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	148-152
34303194-0	2021	IGFBP7 overexpression promotes acquired resistance to AZD9291 in non-small cell lung cancer.	osimertinib	54-61	insulin like growth factor binding protein 7	Homo sapiens	0-6
34303194-1	2021	AZD9291 (osimertinib) is the third-generation EGFR-TKI treat for EGFR mutated NSCLC patients.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	65-69
34303194-5	2021	We found that insulin-like growth factor binding protein 7 (IGFBP7) expression was markedly increased in HCC827/AZDR cells and AZD9291-resistant patients by RNA sequencing and immunohistochemical analysis, respectively.	osimertinib	127-134	insulin like growth factor binding protein 7	Homo sapiens	14-58
34303194-5	2021	We found that insulin-like growth factor binding protein 7 (IGFBP7) expression was markedly increased in HCC827/AZDR cells and AZD9291-resistant patients by RNA sequencing and immunohistochemical analysis, respectively.	osimertinib	127-134	insulin like growth factor binding protein 7	Homo sapiens	60-66
34303194-6	2021	Reduced IGFBP7 in HCC827/AZDR cells by si-RNA interference recovered the sensitivity to AZD9291 partially and increased AZD9291-induced cell apoptosis.	osimertinib	88-95	insulin like growth factor binding protein 7	Homo sapiens	8-14
34303194-6	2021	Reduced IGFBP7 in HCC827/AZDR cells by si-RNA interference recovered the sensitivity to AZD9291 partially and increased AZD9291-induced cell apoptosis.	osimertinib	120-127	insulin like growth factor binding protein 7	Homo sapiens	8-14
34303194-7	2021	Enhancing IGFBP7 expression in EGFR-mutated non-small cell lung cancer (NSCLC) cells using lentiviruses infection reduced their sensitivity to AZD9291.	osimertinib	143-150	insulin like growth factor binding protein 7	Homo sapiens	10-16
34303194-7	2021	Enhancing IGFBP7 expression in EGFR-mutated non-small cell lung cancer (NSCLC) cells using lentiviruses infection reduced their sensitivity to AZD9291.	osimertinib	143-150	epidermal growth factor receptor	Homo sapiens	31-35
34303194-8	2021	This study is the first to discover that high IGFBP7 expression could occur following treatment with AZD9291.	osimertinib	101-108	insulin like growth factor binding protein 7	Homo sapiens	46-52
34303194-1	2021	AZD9291 (osimertinib) is the third-generation EGFR-TKI treat for EGFR mutated NSCLC patients.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	46-50
34491761-1	2021	The epidermal growth factor receptor (EGFR) harboring activating mutations is a clinically validated target in non-small-cell lung cancer, and a number of inhibitors of the EGFR tyrosine kinase domain, including osimertinib, have been approved for clinical use.	osimertinib	212-223	epidermal growth factor receptor	Mus musculus	38-42
34303194-1	2021	AZD9291 (osimertinib) is the third-generation EGFR-TKI treat for EGFR mutated NSCLC patients.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	65-69
34491761-1	2021	The epidermal growth factor receptor (EGFR) harboring activating mutations is a clinically validated target in non-small-cell lung cancer, and a number of inhibitors of the EGFR tyrosine kinase domain, including osimertinib, have been approved for clinical use.	osimertinib	212-223	epidermal growth factor receptor	Mus musculus	173-177
34303194-1	2021	AZD9291 (osimertinib) is the third-generation EGFR-TKI treat for EGFR mutated NSCLC patients.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	46-50
34536138-0	2021	A comprehensive prognostic analysis of osimertinib treatment in advanced non-small cell lung cancer patients with acquired EGFR-T790M mutation: a real-world study.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	123-127
34536138-1	2021	PURPOSE: Osimertinib is the standard treatment for advanced non-small cell lung cancer (NSCLC) patients with T790M mutation after the failure of first-/second-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI).	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	231-235
34536138-7	2021	Notably, the PFS of the prior EGFR-TKI was independently related to ORR (OR, 95% CI 0.98, 0.96-1.00, p = 0.030), PFS (HR, 95% CI 0.98, 0.97-1.00, p = 0.009) and OS (HR, 95% CI 0.96, 0.93-0.98, p < 0.001) of osimertinib treatment.	osimertinib	207-218	epidermal growth factor receptor	Homo sapiens	30-34
34536138-11	2021	CONCLUSION: PFS of the prior EGFR-TKI treatment, performance status score and bone metastasis were independent prognosticators of the osimertinib treatment.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	29-33
34145929-0	2021	MUSASHI-2 confers resistance to third-generation EGFR-tyrosine kinase inhibitor osimertinib in lung adenocarcinoma.	osimertinib	80-91	musashi RNA binding protein 2	Homo sapiens	0-9
34720947-3	2021	Our case involves a 63-year-old nonsmoking male who was initially diagnosed with EGFR mutation-positive metastatic nonsquamous, non-small cell lung adenocarcinoma, who subsequently developed HCC and squamous cell carcinoma of the femur despite first-line treatment with EGFR-blocking osimertinib.	osimertinib	284-295	epidermal growth factor receptor	Homo sapiens	81-85
34720947-3	2021	Our case involves a 63-year-old nonsmoking male who was initially diagnosed with EGFR mutation-positive metastatic nonsquamous, non-small cell lung adenocarcinoma, who subsequently developed HCC and squamous cell carcinoma of the femur despite first-line treatment with EGFR-blocking osimertinib.	osimertinib	284-295	epidermal growth factor receptor	Homo sapiens	270-274
34247147-7	2021	In vitro and in vivo experiments demonstrated that CD74 upregulation confers resistance to the EGFR-TKI osimertinib and blocks apoptosis, enabling tumor regrowth.	osimertinib	104-115	CD74 molecule	Homo sapiens	51-55
34289988-0	2021	Targeting c-Myc to overcome acquired resistance of EGFR mutant NSCLC cells to the third generation EGFR tyrosine kinase inhibitor, osimertinib.	osimertinib	131-142	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	10-15
34289988-0	2021	Targeting c-Myc to overcome acquired resistance of EGFR mutant NSCLC cells to the third generation EGFR tyrosine kinase inhibitor, osimertinib.	osimertinib	131-142	epidermal growth factor receptor	Homo sapiens	51-55
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	81-113
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	115-119
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	234-238
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	81-113
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	115-119
34289988-1	2021	Osimertinib (AZD9291 or TAGRISSOTM) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	234-238
34289988-4	2021	Consequently, we have identified a novel connection between osimertinib or other EGFR TKI and c-Myc.	osimertinib	60-71	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	94-99
34289988-5	2021	Osimertinib rapidly and sustainably decreased c-Myc levels primarily via enhancing protein degradation in EGFR-mutant (EGFRm) NSCLC cell lines and xenograft tumors.	osimertinib	0-11	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	46-51
34289988-5	2021	Osimertinib rapidly and sustainably decreased c-Myc levels primarily via enhancing protein degradation in EGFR-mutant (EGFRm) NSCLC cell lines and xenograft tumors.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	106-110
34289988-6	2021	c-Myc levels were substantially elevated in different EGFRm NSCLC cell lines with acquired resistance to osimertinib in comparison with their corresponding parental cell lines and could not be reduced any further by osimertinib.	osimertinib	216-227	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-5
34289988-8	2021	Suppression of c-Myc through knockdown or pharmacological targeting with BET inhibitors restored the response of resistant cell lines to osimertinib.	osimertinib	137-148	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	15-20
34289988-8	2021	Suppression of c-Myc through knockdown or pharmacological targeting with BET inhibitors restored the response of resistant cell lines to osimertinib.	osimertinib	137-148	delta/notch like EGF repeat containing	Homo sapiens	73-76
34289988-9	2021	These findings indicate that c-Myc modulation mediates the therapeutic efficacy of osimertinib and the development of osimertinib-acquired resistance.	osimertinib	83-94	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	29-34
34289988-9	2021	These findings indicate that c-Myc modulation mediates the therapeutic efficacy of osimertinib and the development of osimertinib-acquired resistance.	osimertinib	118-129	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	29-34
34217707-3	2021	Consequently, mutant selective third-generation EGFR TKIs represented by AZD9291 (Osimertinib) have been developed to offer more effective therapeutic treatment, but the clinical application is limited by the acquired resistance and the high costs.	osimertinib	73-80	epidermal growth factor receptor	Homo sapiens	48-52
34217707-3	2021	Consequently, mutant selective third-generation EGFR TKIs represented by AZD9291 (Osimertinib) have been developed to offer more effective therapeutic treatment, but the clinical application is limited by the acquired resistance and the high costs.	osimertinib	82-93	epidermal growth factor receptor	Homo sapiens	48-52
34575554-1	2021	Osimertinib has become a standard of care in the first-line treatment of advanced-stage non-small-cell lung cancer (NSCLC) harboring exon 19 and 21 activating mutations in the EGFR gene.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	176-180
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	epidermal growth factor receptor	Homo sapiens	49-53
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
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	epidermal growth factor receptor	Homo sapiens	94-98
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	CD274 molecule	Homo sapiens	200-205
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	KRAS proto-oncogene, GTPase	Homo sapiens	210-214
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	estrogen receptor 1	Homo sapiens	234-238
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	A-kinase anchoring protein 12	Homo sapiens	239-245
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	makorin ring finger protein 1	Homo sapiens	250-255
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	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	256-260
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	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	288-292
34575554-5	2021	In this review, we discuss the rationale for EGFR/BRAF/MEK co-inhibition in the light of a clinical case of EGFR-mutant NSCLC developing a BRAF V600 mutation as an acquired resistance mechanism to osimertinib and responding to the association of osimertinib plus dabrafenib and trametinib.	osimertinib	197-208	epidermal growth factor receptor	Homo sapiens	45-49
34575554-5	2021	In this review, we discuss the rationale for EGFR/BRAF/MEK co-inhibition in the light of a clinical case of EGFR-mutant NSCLC developing a BRAF V600 mutation as an acquired resistance mechanism to osimertinib and responding to the association of osimertinib plus dabrafenib and trametinib.	osimertinib	197-208	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
34575554-5	2021	In this review, we discuss the rationale for EGFR/BRAF/MEK co-inhibition in the light of a clinical case of EGFR-mutant NSCLC developing a BRAF V600 mutation as an acquired resistance mechanism to osimertinib and responding to the association of osimertinib plus dabrafenib and trametinib.	osimertinib	197-208	mitogen-activated protein kinase kinase 7	Homo sapiens	55-58
34575554-5	2021	In this review, we discuss the rationale for EGFR/BRAF/MEK co-inhibition in the light of a clinical case of EGFR-mutant NSCLC developing a BRAF V600 mutation as an acquired resistance mechanism to osimertinib and responding to the association of osimertinib plus dabrafenib and trametinib.	osimertinib	197-208	epidermal growth factor receptor	Homo sapiens	108-112
34575554-5	2021	In this review, we discuss the rationale for EGFR/BRAF/MEK co-inhibition in the light of a clinical case of EGFR-mutant NSCLC developing a BRAF V600 mutation as an acquired resistance mechanism to osimertinib and responding to the association of osimertinib plus dabrafenib and trametinib.	osimertinib	197-208	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	139-143
34703647-0	2021	HIF1A-AS2 induces osimertinib resistance in lung adenocarcinoma patients by regulating the miR-146b-5p/IL-6/STAT3 axis.	osimertinib	18-29	HIF1A antisense RNA 2	Homo sapiens	0-9
34703647-0	2021	HIF1A-AS2 induces osimertinib resistance in lung adenocarcinoma patients by regulating the miR-146b-5p/IL-6/STAT3 axis.	osimertinib	18-29	interleukin 6	Homo sapiens	103-107
34703647-0	2021	HIF1A-AS2 induces osimertinib resistance in lung adenocarcinoma patients by regulating the miR-146b-5p/IL-6/STAT3 axis.	osimertinib	18-29	signal transducer and activator of transcription 3	Homo sapiens	108-113
34703647-4	2021	We examined the function of HIF1A-AS2 in modifying tumor aggravation and osimertinib resistance in lung adenocarcinoma.	osimertinib	73-84	HIF1A antisense RNA 2	Homo sapiens	28-37
34703647-6	2021	HIF1A-AS2 silencing inhibited the proliferation, migration, and tumorigenesis of LUAD cells and therapeutic efficacy of osimertinib against tumor cells in vitro and in vivo.	osimertinib	120-131	HIF1A antisense RNA 2	Homo sapiens	0-9
34388376-5	2021	Importantly, osimertinib resistance caused by epithelial-mesenchymal transition (EMT) activates the ATR-CHK1-Aurora B signaling cascade and thereby engenders hypersensitivity to respective kinase inhibitors by activating BIM-mediated mitotic catastrophe.	osimertinib	13-24	ATR serine/threonine kinase	Homo sapiens	100-103
34388376-5	2021	Importantly, osimertinib resistance caused by epithelial-mesenchymal transition (EMT) activates the ATR-CHK1-Aurora B signaling cascade and thereby engenders hypersensitivity to respective kinase inhibitors by activating BIM-mediated mitotic catastrophe.	osimertinib	13-24	checkpoint kinase 1	Homo sapiens	104-108
34388376-5	2021	Importantly, osimertinib resistance caused by epithelial-mesenchymal transition (EMT) activates the ATR-CHK1-Aurora B signaling cascade and thereby engenders hypersensitivity to respective kinase inhibitors by activating BIM-mediated mitotic catastrophe.	osimertinib	13-24	aurora kinase B	Homo sapiens	109-117
34568058-0	2021	A Phase I Trial of Dasatinib and Osimertinib in TKI Naive Patients With Advanced EGFR-Mutant Non-Small-Cell Lung Cancer.	osimertinib	33-44	epidermal growth factor receptor	Homo sapiens	81-85
34568058-1	2021	Background: Osimertinib is an effective first-line therapy option for EGFR-mutant NSCLC, but virtually all patients develop resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	70-74
34568058-4	2021	Method: This is a single-arm phase I/II trial of osimertinib and dasatinib in TKI-naive advanced EGFR-mutant NSCLC (NCT02954523).	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	97-101
34491978-1	2021	BACKGROUND Osimertinib is an oral third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced non-small cell lung cancer (NSCLC) with positive EGFR mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	51-83
34491978-1	2021	BACKGROUND Osimertinib is an oral third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced non-small cell lung cancer (NSCLC) with positive EGFR mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	85-89
34491978-1	2021	BACKGROUND Osimertinib is an oral third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) approved as first-line therapy for advanced non-small cell lung cancer (NSCLC) with positive EGFR mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	216-220
34161878-5	2021	Both pyrimidine analogues 4a and 4b displayed outstanding inhibitory activity against EGFRWT and its two mutated isoforms EGFRL858R and EGFRT790M in comparing to erlotinib and osimertinib as reference drugs.	osimertinib	176-187	epidermal growth factor receptor	Homo sapiens	86-92
34161879-2	2021	Among the derivatives synthesized, 10c (IC50 = 5.192 nM), 10j (IC50 = 10.35 nM), and 10o (IC50 = 0.3524 nM) exhibited higher potencies against EGFRT790/M/L858R compared to the known EGFR inhibitor AZD-9291 (IC50 = 20.80 nM).	osimertinib	197-205	Rho GTPase activating protein 9	Homo sapiens	35-38
34161879-2	2021	Among the derivatives synthesized, 10c (IC50 = 5.192 nM), 10j (IC50 = 10.35 nM), and 10o (IC50 = 0.3524 nM) exhibited higher potencies against EGFRT790/M/L858R compared to the known EGFR inhibitor AZD-9291 (IC50 = 20.80 nM).	osimertinib	197-205	epidermal growth factor receptor	Homo sapiens	182-186
34365179-1	2021	OBJECTIVES: The ADAURA demonstrated the efficacy of osimertinib as adjuvant therapy in patients with resected stage IB-IIIA adenocarcinoma harboring epidermal growth factor receptor (EGFR) mutations.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	149-181
34365179-1	2021	OBJECTIVES: The ADAURA demonstrated the efficacy of osimertinib as adjuvant therapy in patients with resected stage IB-IIIA adenocarcinoma harboring epidermal growth factor receptor (EGFR) mutations.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	183-187
34258882-2	2021	This study aimed to evaluate the efficacy of sequential afatinib and osimertinib treatment in patients with NSCLC harboring EGFR mutations.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	124-128
34145929-0	2021	MUSASHI-2 confers resistance to third-generation EGFR-tyrosine kinase inhibitor osimertinib in lung adenocarcinoma.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	49-53
34145929-2	2021	However, due to acquired resistance to EGFR-TKIs, even patients on third-generation osimertinib, have a poor prognosis.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	39-43
34145929-5	2021	We found that after a long-term exposure to gefitinib, the first-generation EGFR-TKI, lung cancer cells harboring the EGFR-TKI-sensitive mutations became resistant to both gefitinib and osimertinib.	osimertinib	186-197	epidermal growth factor receptor	Homo sapiens	76-80
34145929-9	2021	We demonstrated that the knockdown of MSI2 restored sensitivity to osimertinib or gefitinib in EGFR-TKI-resistant cells to levels similar to those of parental cells in vitro.	osimertinib	67-78	musashi RNA binding protein 2	Homo sapiens	38-42
34145929-11	2021	Moreover, overexpression of MSI2 or Nanog conferred resistance to osimertinib or gefitinib in parental cells.	osimertinib	66-77	musashi RNA binding protein 2	Homo sapiens	28-32
34145929-11	2021	Moreover, overexpression of MSI2 or Nanog conferred resistance to osimertinib or gefitinib in parental cells.	osimertinib	66-77	Nanog homeobox	Homo sapiens	36-41
34117553-1	2021	BACKGROUND: We here applied cancer personalized profiling by deep sequencing (CAPP-seq) to analysis of circulating tumor DNA (ctDNA) to identify resistance mechanisms in osimertinib-treated patients with EGFR T790M-positive non-small cell lung cancer (NSCLC).	osimertinib	170-181	epidermal growth factor receptor	Homo sapiens	204-208
34107727-1	2021	The GioTag study assessed how drugs called afatinib and osimertinib affected people with non-small cell lung cancer (NSCLC) who had mutations in the epidermal growth factor receptor (EGFR) gene.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	149-181
34107727-1	2021	The GioTag study assessed how drugs called afatinib and osimertinib affected people with non-small cell lung cancer (NSCLC) who had mutations in the epidermal growth factor receptor (EGFR) gene.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	183-187
34107727-9	2021	This study showed that afatinib followed by osimertinib treatment was effective in patients with NSCLC with EGFR mutations developing T790M resistance mutations on initial afatinib treatment.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	108-112
34410991-0	2021	Acquired EGFR C797G Mutation Detected by Liquid Biopsy as Resistance Mechanism After Treatment With Osimertinib: A Case Report.	osimertinib	100-111	epidermal growth factor receptor	Homo sapiens	9-13
34410991-1	2021	BACKGROUND: Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor approved for the treatment of T790M-positive non-small-cell lung cancer.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-50
34410991-7	2021	CONCLUSION: Our case report revealed a rare EGFR-dependent acquired resistance mutation to osimertinib in circulating tumor DNA.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	44-48
34117553-8	2021	In addition, one patient who underwent a repeat biopsy was found to harbor the C797S mutation of EGFR after disease progression during osimertinib rechallenge, with this mutation not having been detected at the time of initial progression on osimertinib.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	97-101
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
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	signal transducer and activator of transcription 3	Homo sapiens	114-119
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	insulin like growth factor 1 receptor	Homo sapiens	121-126
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	phosphatase and tensin homolog	Homo sapiens	128-132
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	platelet derived growth factor receptor beta	Homo sapiens	138-143
34498213-15	2021	The pattern of resistance after exposure to osimertinib/bevacizumab includes known mechanisms in the regulation of EGFR, findings that contribute to the understanding and targeting in a stepwise rational this pathway.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	115-119
34436667-2	2021	PATIENTS AND METHODS: 417 patients had stage III-IV NSCLC harboring EGFR mutation and 154 out of 417 patients receiving osimertinib as >= second-line EGFR-TKI were identified.	osimertinib	120-131	epidermal growth factor receptor	Homo sapiens	150-154
34386061-4	2021	The results demonstrated that osimertinib significantly inhibited tumor growth in both the conventional and large models; however, maximum tumor regression was attenuated in the large model in which hypoxia-inducible factor-1alpha (HIF-1alpha) and transforming growth factor-alpha (TGF-alpha) expression levels increased.	osimertinib	30-41	hypoxia inducible factor 1 subunit alpha	Homo sapiens	199-230
34386061-4	2021	The results demonstrated that osimertinib significantly inhibited tumor growth in both the conventional and large models; however, maximum tumor regression was attenuated in the large model in which hypoxia-inducible factor-1alpha (HIF-1alpha) and transforming growth factor-alpha (TGF-alpha) expression levels increased.	osimertinib	30-41	hypoxia inducible factor 1 subunit alpha	Homo sapiens	232-242
34386061-4	2021	The results demonstrated that osimertinib significantly inhibited tumor growth in both the conventional and large models; however, maximum tumor regression was attenuated in the large model in which hypoxia-inducible factor-1alpha (HIF-1alpha) and transforming growth factor-alpha (TGF-alpha) expression levels increased.	osimertinib	30-41	tumor necrosis factor	Homo sapiens	248-280
34386061-4	2021	The results demonstrated that osimertinib significantly inhibited tumor growth in both the conventional and large models; however, maximum tumor regression was attenuated in the large model in which hypoxia-inducible factor-1alpha (HIF-1alpha) and transforming growth factor-alpha (TGF-alpha) expression levels increased.	osimertinib	30-41	transforming growth factor alpha	Homo sapiens	282-291
34386061-6	2021	TGF-alpha attenuated sensitivity to osimertinib in vitro; however, this negative effect was counteracted by the combination of osimertinib and cetuximab, but not osimertinib and bevacizumab.	osimertinib	36-47	transforming growth factor alpha	Homo sapiens	0-9
34145929-12	2021	Finally, MSI2 knockdown greatly increased the sensitivity to osimertinib in vivo.	osimertinib	61-72	musashi RNA binding protein 2	Homo sapiens	9-13
34145930-0	2021	Trametinib overcomes KRAS-G12V-induced osimertinib resistance in a leptomeningeal carcinomatosis model of EGFR-mutant lung cancer.	osimertinib	39-50	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	21-25
34145930-4	2021	We induced osimertinib resistance in a mouse model of LMC using an EGFR-mutant NSCLC cell line (PC9) via continuous oral osimertinib treatment and administration of established resistant cells and examined the resistance mechanism using next-generation sequencing.	osimertinib	11-22	epidermal growth factor receptor	Mus musculus	67-71
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-26
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-64
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-135
34145930-7	2021	Co-treatment with trametinib (a MEK inhibitor) and osimertinib re-sensitized the cells to osimertinib.	osimertinib	90-101	midkine	Mus musculus	32-35
34145930-9	2021	These findings suggest a potential novel therapy against KRAS-G12V-harboring osimertinib-resistant LMC in EGFR-mutant NSCLC.	osimertinib	77-88	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	57-61
34145930-9	2021	These findings suggest a potential novel therapy against KRAS-G12V-harboring osimertinib-resistant LMC in EGFR-mutant NSCLC.	osimertinib	77-88	epidermal growth factor receptor	Mus musculus	106-110
34462521-0	2021	Publisher Correction: The impact of different first-line EGFR-TKIs on the clinical outcome of sequential osimertinib treatment in advanced NSCLC with secondary T790M.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	57-61
34471361-0	2021	Osimertinib in EGFR-Mutated Lung Cancer: A Review of the Existing and Emerging Clinical Data.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
34471361-1	2021	The use of epidermal growth factor receptor (EGFR) inhibitors such as osimertinib has improved outcomes and quality of life for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	11-43
34471361-1	2021	The use of epidermal growth factor receptor (EGFR) inhibitors such as osimertinib has improved outcomes and quality of life for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	45-49
34471361-1	2021	The use of epidermal growth factor receptor (EGFR) inhibitors such as osimertinib has improved outcomes and quality of life for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	142-146
34471361-3	2021	More recently osimertinib has also shown to be beneficial in patients with resectable NSCLC harboring EGFR mutations irrespective of whether they received adjuvant chemotherapy or not.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	102-106
34471361-6	2021	The aim of this review is to provide a comprehensive review of the data with osimertinib in EGFR mutation positive NSCLC, potential resistance mechanisms and an overview of key ongoing clinical trials.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	92-96
34436667-7	2021	A higher risk of treatment failure for osimertinib was found in males, patients with first-line TKI duration <= 12 months, BMI drop > 10%, and PD-L1 expression >= 50% (All p < 0.05).	osimertinib	39-50	CD274 molecule	Homo sapiens	143-148
34436667-9	2021	CONCLUSIONS: This study demonstrates that osimertinib as second line or subsequent TKI in EGFR-TKI-treated patients without identification of T790M revealed lower risk of death compared to first-line first/second generation TKI without subsequent osimertinib, in real-world practice.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	90-94
34436667-10	2021	Additionally, EGFR-mutant patients with PD-L1 expression >= 50% had a higher risk of treatment failure for osimertinib and worse overall survival than those with PD-L1 expression < 50%.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	14-18
34436667-10	2021	Additionally, EGFR-mutant patients with PD-L1 expression >= 50% had a higher risk of treatment failure for osimertinib and worse overall survival than those with PD-L1 expression < 50%.	osimertinib	107-118	CD274 molecule	Homo sapiens	40-45
34436667-11	2021	These results suggest that osimertinib as second line or subsequent TKI may be a potential alternative option for the treatment of patients without identification of T790M and PD-L1 expression >= 50% is associated with a significantly poor outcome in patients receiving osimertinib.	osimertinib	27-38	CD274 molecule	Homo sapiens	176-181
34436667-11	2021	These results suggest that osimertinib as second line or subsequent TKI may be a potential alternative option for the treatment of patients without identification of T790M and PD-L1 expression >= 50% is associated with a significantly poor outcome in patients receiving osimertinib.	osimertinib	270-281	CD274 molecule	Homo sapiens	176-181
34490108-2	2021	Erlotinib, afatinib, and osimertinib interacted with GZ17-6.02 to kill NSCLC cells expressing mutant EGFR proteins.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	101-105
34424565-0	2021	First-Line Osimertinib in Patients with EGFR-Mutant Advanced Non-Small Cell Lung Cancer: Outcome and Safety in the Real World: FLOWER Study.	osimertinib	11-22	calcium channel flower domain containing 1	Homo sapiens	127-133
34424565-1	2021	LESSONS LEARNED: Osimertinib has confirmed effectiveness in this real-world population of patients with EGFR-mutant advanced non-small cell lung cancer population.	osimertinib	17-28	epidermal growth factor receptor	Homo sapiens	104-108
34424565-4	2021	BACKGROUND: Osimertinib became the standard treatment for patients with untreated EGFR-mutant advanced non-small-cell lung cancer (aNSCLC) following results reported in the phase III randomized FLAURA trial.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	82-86
34457028-5	2021	Forty-four osimertinib-treated patients had an improved mOS of 13.15 (95% CI: 5.74-20.57) and a median progression-free survival (PFS) of 9.50 months (95% CI: 6.77-12.23) when compared with patients treated with first- or second-generation EGFR-TKI (mOS = 3.00 months (95% CI: 1.32-4.68) and median PFS = 1.50 months (95% CI: 0.00-3.14)).	osimertinib	11-22	Moloney sarcoma oncogene	Mus musculus	56-59
34457028-6	2021	In the osimertinib group, mOS values for CSF with and without T790M mutation were 22.15 months (95% CI: 9.44-34.87) and 13.39 months (95% CI: 7.01-19.76), respectively, with no statistical differences.	osimertinib	7-18	Moloney sarcoma oncogene	Mus musculus	26-29
34391435-1	2021	BACKGROUND: Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations will inevitably develop drug resistance after being treated with the third-generation EGFR-tyrosine kinase inhibitor (TKI), osimertinib.	osimertinib	235-246	epidermal growth factor receptor	Homo sapiens	61-93
34439260-2	2021	In this study, we focused on the association of ANXA1 and chemosensitivity with a third generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), Osimertinib, in lung cancer cells with EGFR mutations.	osimertinib	170-181	annexin A1	Mus musculus	48-53
34439260-2	2021	In this study, we focused on the association of ANXA1 and chemosensitivity with a third generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), Osimertinib, in lung cancer cells with EGFR mutations.	osimertinib	170-181	epidermal growth factor receptor	Mus musculus	159-163
34439260-5	2021	In lung cancer cells with EGFR mutations, the knockdown of ANXA1 increased the chemosensitivity to Osimertinib, and decreased the tumorigenesis, invasion and migration of lung cancer cells.	osimertinib	99-110	annexin A1	Mus musculus	59-64
34439260-6	2021	Further study showed that the knockdown of ANXA1 inhibited the phosphorylation of EGFR and down-stream Akt pathways and promoted apoptosis in lung cancer cells treated with Osimertinib.	osimertinib	173-184	annexin A1	Mus musculus	43-48
34439260-6	2021	Further study showed that the knockdown of ANXA1 inhibited the phosphorylation of EGFR and down-stream Akt pathways and promoted apoptosis in lung cancer cells treated with Osimertinib.	osimertinib	173-184	epidermal growth factor receptor	Mus musculus	82-86
34439260-6	2021	Further study showed that the knockdown of ANXA1 inhibited the phosphorylation of EGFR and down-stream Akt pathways and promoted apoptosis in lung cancer cells treated with Osimertinib.	osimertinib	173-184	thymoma viral proto-oncogene 1	Mus musculus	103-106
34439260-7	2021	A mice xenograft lung cancer model was established in our study and showed that ANXA1 siRNA enhanced the effects of Osimertinib in vivo.	osimertinib	116-127	annexin A1	Mus musculus	80-85
34391435-1	2021	BACKGROUND: Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations will inevitably develop drug resistance after being treated with the third-generation EGFR-tyrosine kinase inhibitor (TKI), osimertinib.	osimertinib	235-246	epidermal growth factor receptor	Homo sapiens	95-99
34391435-1	2021	BACKGROUND: Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations will inevitably develop drug resistance after being treated with the third-generation EGFR-tyrosine kinase inhibitor (TKI), osimertinib.	osimertinib	235-246	epidermal growth factor receptor	Homo sapiens	197-201
34391435-8	2021	Exosome-derived miR-184 and miR-3913-5p expression levels increased significantly after the onset of osimertinib resistance.	osimertinib	101-112	microRNA 184	Homo sapiens	16-23
34391435-10	2021	In patients with EGFR exon 21 L858R mutation, the increased expression levels of miR-184 and miR-3913-5p derived from serum exosomes indicated osimertinib resistance.	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	17-21
34391435-10	2021	In patients with EGFR exon 21 L858R mutation, the increased expression levels of miR-184 and miR-3913-5p derived from serum exosomes indicated osimertinib resistance.	osimertinib	143-154	microRNA 184	Homo sapiens	81-88
34391435-12	2021	CONCLUSIONS: The expression levels of miR-184 and miR-3913-5p derived from exosomes in the peripheral blood of NSCLC patients could be used as biomarkers to indicate osimertinib resistance.	osimertinib	166-177	microRNA 184	Homo sapiens	38-45
34445227-9	2021	Osimertinib can exert significant growth inhibitory effects in EGFR-mutated NSCLC patients with a high EphB4 status.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	63-67
34413682-1	2021	Purpose: Although patients with primary and acquired epidermal growth factor receptor (EGFR) T790M positive non-small-cell lung cancer (NSCLC) respond to osimertinib treatment, the optimal treatment strategy differs for these two groups of patients.	osimertinib	154-165	epidermal growth factor receptor	Homo sapiens	53-85
34413682-1	2021	Purpose: Although patients with primary and acquired epidermal growth factor receptor (EGFR) T790M positive non-small-cell lung cancer (NSCLC) respond to osimertinib treatment, the optimal treatment strategy differs for these two groups of patients.	osimertinib	154-165	epidermal growth factor receptor	Homo sapiens	87-91
34445227-9	2021	Osimertinib can exert significant growth inhibitory effects in EGFR-mutated NSCLC patients with a high EphB4 status.	osimertinib	0-11	EPH receptor B4	Homo sapiens	103-108
34344199-0	2022	Combination EGFR and RET Inhibition in Acquired Resistance to Osimertinib in EGFR-Mutant NSCLC.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	12-16
34564820-2	2021	Osimertinib (Tagrisso ) is an orally administered, third-generation EGFR tyrosine kinase inhibitor (EGFR-TKI) that is widely approved for the first-line treatment of advanced NSCLC with activating EGFR mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	197-201
34564820-2	2021	Osimertinib (Tagrisso ) is an orally administered, third-generation EGFR tyrosine kinase inhibitor (EGFR-TKI) that is widely approved for the first-line treatment of advanced NSCLC with activating EGFR mutations.	osimertinib	13-21	epidermal growth factor receptor	Homo sapiens	197-201
34564820-3	2021	In the pivotal phase III FLAURA trial, osimertinib significantly prolonged progression-free survival (PFS) and overall survival (OS) relative to first-generation EGFR-TKIs in patients with previously untreated, EGFR mutation-positive, advanced NSCLC.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	211-215
34344199-0	2022	Combination EGFR and RET Inhibition in Acquired Resistance to Osimertinib in EGFR-Mutant NSCLC.	osimertinib	62-73	ret proto-oncogene	Homo sapiens	21-24
34344199-0	2022	Combination EGFR and RET Inhibition in Acquired Resistance to Osimertinib in EGFR-Mutant NSCLC.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	77-81
34532491-1	2021	Osimertinib has efficacy superior to that of standard epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) for the first-line treatment of patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	174-178
34359807-6	2021	Furthermore, the CDK9 inhibitors could markedly reduce the viability of Osimertinib-resistant PC9 and AMG510-resistant H23 and H358 cells with comparable efficacy as the parental cells.	osimertinib	72-83	cyclin dependent kinase 9	Homo sapiens	17-21
34359807-6	2021	Furthermore, the CDK9 inhibitors could markedly reduce the viability of Osimertinib-resistant PC9 and AMG510-resistant H23 and H358 cells with comparable efficacy as the parental cells.	osimertinib	72-83	proprotein convertase subtilisin/kexin type 9	Homo sapiens	94-97
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	epidermal growth factor receptor	Homo sapiens	56-60
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
34097913-1	2021	Third-generation inhibitors of the epidermal growth factor receptor (EGFR), best exemplified by osimertinib, have been developed to selectively target variants of EGFR bearing activating mutations and the mutation of gatekeeper T790 in patients with EGFR-mutated forms of Non-Small Cell Lung Cancer (NSCLC).	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	69-73
34077739-7	2021	Compared to osimertinib-resistant cells, sensitive cells had less ERBB2 Y1248 phosphorylation.	osimertinib	12-23	erb-b2 receptor tyrosine kinase 2	Homo sapiens	66-71
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	AKT serine/threonine kinase 1	Homo sapiens	92-95
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	mechanistic target of rapamycin kinase	Homo sapiens	97-101
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	signal transducer and activator of transcription 3	Homo sapiens	103-108
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	signal transducer and activator of transcription 5A	Homo sapiens	110-115
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	mitogen-activated protein kinase 3	Homo sapiens	117-123
34077739-8	2021	In osimertinib resistant H1975 cells, the drug combination was less capable of inactivating AKT, mTOR, STAT3, STAT5, ERK1/2 whereas it gained the ability to inactivate ERBB3.	osimertinib	3-14	erb-b2 receptor tyrosine kinase 3	Homo sapiens	168-173
34097913-1	2021	Third-generation inhibitors of the epidermal growth factor receptor (EGFR), best exemplified by osimertinib, have been developed to selectively target variants of EGFR bearing activating mutations and the mutation of gatekeeper T790 in patients with EGFR-mutated forms of Non-Small Cell Lung Cancer (NSCLC).	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	163-167
34097913-1	2021	Third-generation inhibitors of the epidermal growth factor receptor (EGFR), best exemplified by osimertinib, have been developed to selectively target variants of EGFR bearing activating mutations and the mutation of gatekeeper T790 in patients with EGFR-mutated forms of Non-Small Cell Lung Cancer (NSCLC).	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	250-254
34233230-9	2021	Osimertinib combined with MET inhibition synergistically induces apoptosis in the MET-amplified EGFR mutant NSCLC cells accompanied with augmented DR4 reduction both in vitro and in vivo.	osimertinib	0-11	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
34157597-1	2021	The C797S mutation encoded by EGFR exon 20 is classically observed as a tertiary event in EGFR-mutant non-small-cell lung carcinoma (NSCLC) primarily treated by first generation tyrosine kinase inhibitors (TKI) and secondarily treated by third-generation TKI, such as osimertinib, if the EGFR-T790M resistance mutation is detected.	osimertinib	268-279	epidermal growth factor receptor	Homo sapiens	30-34
34157597-4	2021	We report the case of a 65 year-old female treated by first-line osimertinib for a multimetastatic exon 19-EGFR-mutant NSCLC.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	107-111
34214933-1	2021	OBJECTIVES: Osimertinib is the main treatment choice for pretreated patients with advanced non-small cell lung cancer (NSCLC) harbouring epidermal growth factor receptor (EGFR) T790M mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	137-169
34214933-1	2021	OBJECTIVES: Osimertinib is the main treatment choice for pretreated patients with advanced non-small cell lung cancer (NSCLC) harbouring epidermal growth factor receptor (EGFR) T790M mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	171-175
34233230-9	2021	Osimertinib combined with MET inhibition synergistically induces apoptosis in the MET-amplified EGFR mutant NSCLC cells accompanied with augmented DR4 reduction both in vitro and in vivo.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	96-100
34233230-9	2021	Osimertinib combined with MET inhibition synergistically induces apoptosis in the MET-amplified EGFR mutant NSCLC cells accompanied with augmented DR4 reduction both in vitro and in vivo.	osimertinib	0-11	TNF receptor superfamily member 10a	Homo sapiens	147-150
34087353-2	2021	However, acquired resistance to mutant EGFR (T790M) can evolve following osimertinib treatment.	osimertinib	73-84	epidermal growth factor receptor	Mus musculus	39-43
34087353-4	2021	Here, we found that heme levels were increased in osimertinib resistant EGFR-mutant NSCLC cell lines and plasma heme levels were also elevated in osimertinib-treated EGFR-mutant NSCLC patients.	osimertinib	50-61	epidermal growth factor receptor	Mus musculus	72-76
34087353-4	2021	Here, we found that heme levels were increased in osimertinib resistant EGFR-mutant NSCLC cell lines and plasma heme levels were also elevated in osimertinib-treated EGFR-mutant NSCLC patients.	osimertinib	146-157	epidermal growth factor receptor	Mus musculus	166-170
34087353-6	2021	DHA downregulated the expression of heme oxygenase 1 and inhibited cell proliferation in osimertinib-resistant EGFR-mutant NSCLC cells (PC9-GR4-AZD1), which was further enhanced by addition of 5-aminolevulinic acid, protoporphyrin IX and hemin.	osimertinib	89-100	epidermal growth factor receptor	Mus musculus	111-115
34087353-6	2021	DHA downregulated the expression of heme oxygenase 1 and inhibited cell proliferation in osimertinib-resistant EGFR-mutant NSCLC cells (PC9-GR4-AZD1), which was further enhanced by addition of 5-aminolevulinic acid, protoporphyrin IX and hemin.	osimertinib	89-100	proprotein convertase subtilisin/kexin type 9	Mus musculus	136-139
34087353-8	2021	Combination treatment with osimertinib and DHA also increased the levels of ROS, downregulated the phosphorylation or protein levels of several RTKs that often are overexpressed in osimertinib-resistant EGFR-mutant NSCLC cells, and inhibited tumor growth without toxicity in a PC9-GR4-AZD1 xenograft mouse model.	osimertinib	27-38	epidermal growth factor receptor	Mus musculus	203-207
34087353-8	2021	Combination treatment with osimertinib and DHA also increased the levels of ROS, downregulated the phosphorylation or protein levels of several RTKs that often are overexpressed in osimertinib-resistant EGFR-mutant NSCLC cells, and inhibited tumor growth without toxicity in a PC9-GR4-AZD1 xenograft mouse model.	osimertinib	27-38	proprotein convertase subtilisin/kexin type 9	Mus musculus	277-280
34087353-8	2021	Combination treatment with osimertinib and DHA also increased the levels of ROS, downregulated the phosphorylation or protein levels of several RTKs that often are overexpressed in osimertinib-resistant EGFR-mutant NSCLC cells, and inhibited tumor growth without toxicity in a PC9-GR4-AZD1 xenograft mouse model.	osimertinib	181-192	epidermal growth factor receptor	Mus musculus	203-207
34087353-9	2021	The results suggest that DHA is able to reverse the resistance to osimertinib in EGFR-mutant NSCLC by elevating ROS level and impair heme metabolism.	osimertinib	66-77	epidermal growth factor receptor	Mus musculus	81-85
34584858-0	2021	Impact of tumor programmed death ligand-1 expression on osimertinib efficacy in untreated EGFR-mutated advanced non-small cell lung cancer: a prospective observational study.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	90-94
34240806-3	2021	Here, we report the case of a 45-year-old Japanese woman with NSCLC positive for EGFR-KDD (duplication of exons 18-25) who developed carcinomatous meningitis and showed a marked response to the EGFR-TKIs erlotinib and osimertinib.	osimertinib	218-229	epidermal growth factor receptor	Homo sapiens	194-198
34445227-0	2021	EphB4 as a Novel Target for the EGFR-Independent Suppressive Effects of Osimertinib on Cell Cycle Progression in Non-Small Cell Lung Cancer.	osimertinib	72-83	EPH receptor B4	Homo sapiens	0-5
34445227-0	2021	EphB4 as a Novel Target for the EGFR-Independent Suppressive Effects of Osimertinib on Cell Cycle Progression in Non-Small Cell Lung Cancer.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	32-36
34445227-1	2021	Osimertinib is the latest generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor used for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	37-69
34445227-1	2021	Osimertinib is the latest generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor used for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	71-75
34445227-1	2021	Osimertinib is the latest generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor used for patients with EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	126-130
34445227-2	2021	We aimed to explore the novel mechanisms of osimertinib by particularly focusing on EGFR-independent effects, which have not been well characterized.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	84-88
34445227-3	2021	We explored the EGFR-independent effects of osimertinib on cell proliferation using NSCLC cell lines, an antibody array analysis, and the association between the action of osimertinib and the ephrin receptor B4 (EphB4).	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	16-20
34584858-1	2021	Background: Osimertinib monotherapy is currently the standard of care as a first-line treatment for patients harboring epidermal growth factor receptor (EGFR) mutations; however, some EGFR-mutated non-small cell lung cancer (NSCLC) patients exhibit primary resistance and an insufficient response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	119-151
34445227-3	2021	We explored the EGFR-independent effects of osimertinib on cell proliferation using NSCLC cell lines, an antibody array analysis, and the association between the action of osimertinib and the ephrin receptor B4 (EphB4).	osimertinib	172-183	EPH receptor B4	Homo sapiens	192-210
34073111-0	2021	Detection of EGFR Mutations in Plasma cfDNA and Paired CTCs of NSCLC Patients before and after Osimertinib Therapy Using Crystal Digital PCR.	osimertinib	95-106	epidermal growth factor receptor	Homo sapiens	13-17
34445227-5	2021	Osimertinib exerted significant inhibitory effects on cell growth and cell cycle progression by promoting the phosphorylation of p53 and p21 and decreasing cyclin D1 expression independently of EGFR.	osimertinib	0-11	tumor protein p53	Homo sapiens	129-132
34445227-5	2021	Osimertinib exerted significant inhibitory effects on cell growth and cell cycle progression by promoting the phosphorylation of p53 and p21 and decreasing cyclin D1 expression independently of EGFR.	osimertinib	0-11	cyclin dependent kinase inhibitor 1A	Homo sapiens	137-140
34445227-5	2021	Osimertinib exerted significant inhibitory effects on cell growth and cell cycle progression by promoting the phosphorylation of p53 and p21 and decreasing cyclin D1 expression independently of EGFR.	osimertinib	0-11	cyclin D1	Homo sapiens	156-165
34445227-6	2021	EphB4 was significantly suppressed by osimertinib and promoted cell growth and sensitivity to osimertinib.	osimertinib	38-49	EPH receptor B4	Homo sapiens	0-5
34445227-6	2021	EphB4 was significantly suppressed by osimertinib and promoted cell growth and sensitivity to osimertinib.	osimertinib	94-105	EPH receptor B4	Homo sapiens	0-5
34445227-8	2021	EphB4 is associated with the EGFR-independent suppressive effects of osimertinib on cell cycle and with a poor clinical outcome.	osimertinib	69-80	EPH receptor B4	Homo sapiens	0-5
34445227-8	2021	EphB4 is associated with the EGFR-independent suppressive effects of osimertinib on cell cycle and with a poor clinical outcome.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	29-33
34331582-1	2022	INTRODUCTION: Osimertinib, an irreversible third-generation EGFR-TKI, is the standard of care for second-line treatment of T790M-mutant advanced NSCLC patients whose disease progressed after first-line EGFR-TKI therapy.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	202-206
34330231-0	2021	Efficacy of osimertinib for preventing leptomeningeal metastasis derived from advanced EGFR-mutated non-small cell lung cancer: a propensity-matched retrospective study.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	87-91
34330231-2	2021	This retrospective study aimed to investigate the potential use of osimertinib for preventing LM in patients with advanced epidermal growth factor receptor (EGFR)-mutated NSCLC.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	123-155
34330231-2	2021	This retrospective study aimed to investigate the potential use of osimertinib for preventing LM in patients with advanced epidermal growth factor receptor (EGFR)-mutated NSCLC.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	157-161
34330231-13	2021	CONCLUSION: Real-world data demonstrate that osimertinib can significantly reduce the incidence of LM in patients with advanced NSCLC harboring common EGFR mutations.	osimertinib	45-56	epidermal growth factor receptor	Homo sapiens	151-155
34397683-0	2021	Dramatic response to osimertinib combined with crizotinib in EGFR T790 M mutation only in blood and Met amplification only in tumor tissue expressive non-small cell lung cancer: A case report.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	61-65
34397683-3	2021	PATIENT CONCERNS: A non-smoking 53-year-old male patient with lung adenocarcinoma underwent gefitinib, afatinib, and osimertinib combined with crizotinib treatment and developed different EGFR resistance mutations.	osimertinib	117-128	epidermal growth factor receptor	Homo sapiens	188-192
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	epidermal growth factor receptor	Homo sapiens	147-151
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
34315851-8	2021	Meanwhile, the second-generation BTK inhibitor Acalabrutinib effectively suppressed SOX2, STAT3/JAK2/Akt axis and potentiated the anti-proliferative effect of Gefitinib and Osimertinib in NSCLC cells, including the T790M H1975 cells.	osimertinib	173-184	Bruton tyrosine kinase	Homo sapiens	33-36
34315851-10	2021	Our findings suggested that BTK mediates stemness and EMT properties, and inhibition of BTK potentiates the effect of Gefitinib and Osimertinib in NSCLC cells resistant to TKI.	osimertinib	132-143	Bruton tyrosine kinase	Homo sapiens	28-31
34315851-10	2021	Our findings suggested that BTK mediates stemness and EMT properties, and inhibition of BTK potentiates the effect of Gefitinib and Osimertinib in NSCLC cells resistant to TKI.	osimertinib	132-143	Bruton tyrosine kinase	Homo sapiens	88-91
34309914-7	2022	RESULTS AND DISCUSSION: Osimertinib was confirmed to have a several-fold higher CNS permeability than other EGFR-TKIs and was recommended as the preferred choice for patients with EGFR-positive LM whether or not they harboured the T790M mutation.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	180-184
34366844-0	2021	Effect of Osimertinib in Combination With Chemotherapy and Bevacizumab for Untreated Epidermal Growth Factor Receptor-Mutated Advanced Non-Small-Cell Lung Cancer: Case Report.	osimertinib	10-21	epidermal growth factor receptor	Homo sapiens	85-117
34366844-1	2021	Introduction: Osimertinib is an oral, third-generation, irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	170-174
34366844-1	2021	Introduction: Osimertinib is an oral, third-generation, irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	195-199
34321891-3	2021	Here, we report that a lung adenocarcinoma patient with EGFR L858R mutation who was treated with second-line osimertinib therapy acquired multiple resistance to osimertinib by the non-invasive circulating tumor DNA (ctDNA) genotyping.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	56-60
34321891-3	2021	Here, we report that a lung adenocarcinoma patient with EGFR L858R mutation who was treated with second-line osimertinib therapy acquired multiple resistance to osimertinib by the non-invasive circulating tumor DNA (ctDNA) genotyping.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	56-60
34327032-13	2021	Because the tumor tissue was found to be positive for the EGFR T790M resistance mutation by bronchoscopy, the EGFR-TKI treatment was changed to osimertinib, decreasing the size of the lung cancer lesions.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	110-114
34267282-3	2021	Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models.	osimertinib	168-179	fibroblast growth factor receptor 1	Homo sapiens	61-96
34267282-3	2021	Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models.	osimertinib	168-179	fibroblast growth factor receptor 1	Homo sapiens	98-103
34267282-3	2021	Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models.	osimertinib	168-179	AKT serine/threonine kinase 1	Homo sapiens	120-123
34267282-3	2021	Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models.	osimertinib	168-179	epidermal growth factor receptor	Homo sapiens	180-184
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	epidermal growth factor receptor	Mus musculus	68-72
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	epidermal growth factor receptor	Homo sapiens	118-122
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
34298655-2	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	epidermal growth factor receptor	Homo sapiens	212-216
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	epidermal growth factor receptor	Homo sapiens	309-313
34298655-4	2021	Moreover, EGFR/MET-driven lung tumors were resistant to osimertinib, recapitulating the phenotype observed in patients.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	10-14
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	epidermal growth factor receptor	Homo sapiens	146-150
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
34326746-0	2021	Response to a Combination of Full-Dose Osimertinib and Ceritinib in a Non-Small Cell Lung Cancer Patient with EML4-ALK Rearrangement and Epidermal Growth Factor Receptor Co-Mutation.	osimertinib	39-50	EMAP like 4	Homo sapiens	110-114
34326746-0	2021	Response to a Combination of Full-Dose Osimertinib and Ceritinib in a Non-Small Cell Lung Cancer Patient with EML4-ALK Rearrangement and Epidermal Growth Factor Receptor Co-Mutation.	osimertinib	39-50	ALK receptor tyrosine kinase	Homo sapiens	115-118
34326746-0	2021	Response to a Combination of Full-Dose Osimertinib and Ceritinib in a Non-Small Cell Lung Cancer Patient with EML4-ALK Rearrangement and Epidermal Growth Factor Receptor Co-Mutation.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	137-169
34326746-5	2021	Here, we report a patient with concomitant ALK rearrangement and EGFR mutation treated with a combination of TKIs: osimertinib and ceritinib.	osimertinib	115-126	ALK receptor tyrosine kinase	Homo sapiens	43-46
34326746-5	2021	Here, we report a patient with concomitant ALK rearrangement and EGFR mutation treated with a combination of TKIs: osimertinib and ceritinib.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	65-69
34240438-2	2022	We report a case of fingerprint loss secondary to combination therapy using osimertinib (an EGFR TKI that targets mutated EGFR kinases) and anlotinib (a TKI that acts on multiple targets including mutated VEGFR kinases).	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	92-96
34240438-2	2022	We report a case of fingerprint loss secondary to combination therapy using osimertinib (an EGFR TKI that targets mutated EGFR kinases) and anlotinib (a TKI that acts on multiple targets including mutated VEGFR kinases).	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	122-126
34263613-0	2022	Nasogastric administration of osimertinib suspension for an epidermal growth factor receptor-mutated lung cancer causing an esophageal stricture: case report.	osimertinib	30-41	epidermal growth factor receptor	Homo sapiens	60-92
34263613-4	2022	Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor that is efficacious against EGFR-sensitizing mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-38
34263613-4	2022	Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor that is efficacious against EGFR-sensitizing mutations.	osimertinib	0-11	TXK tyrosine kinase	Homo sapiens	39-54
34263613-4	2022	Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor that is efficacious against EGFR-sensitizing mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	93-97
34217295-11	2021	CONCLUSIONS: Our data revealed that SHP2 inhibition enhances the anti-cancer effect of Osimertinib in EGFR T790M mutant LUAD by blocking CXCL8-CXCR1/2 loop mediated stemness, which may help provide an alternative therapeutic option to enhance the clinical efficacy of osimertinib in EGFR T790M mutant LUAD patients.	osimertinib	268-279	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	36-40
34306781-4	2021	However, there is a small percentage of primarily resistant cases to osimertinib, mainly due to histologic transformation, acquired EGFR mutations and off-target genetic resistances that lead to a scenery of poor clinical prognosis in which radiotherapy may have a higher relevance for the management of brain metastases.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	132-136
34430591-7	2021	One patient, with EGFR exon 19 deletion (Ex19del), accepted first-line gefitinib treatment and then received osimertinib treatment due to acquisition of an EGFR-T790M mutation.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	156-160
34430591-8	2021	A novel ETV1 mutation (p.P159S) was detected in the SCLC tissue after osimertinib resistance when not coexisting with T790M.	osimertinib	70-81	ETS variant transcription factor 1	Homo sapiens	8-12
34430591-12	2021	ETV1 p.E462Q and p.P159S mutations were also resistant to gefitinib and osimertinib after introduction into H358 cells.	osimertinib	72-83	ETS variant transcription factor 1	Homo sapiens	0-4
34764521-0	2021	Refinement of Covalent EGFR Inhibitor AZD9291 to Eliminate Off-target Activity.	osimertinib	38-45	epidermal growth factor receptor	Homo sapiens	23-27
34764521-2	2021	Tyrosine kinase inhibitors (TKIs) that target EGFR have been used for the treatment of NSCLC, but often develop drug resistance, and the covalent inhibitor AZD9291 has been developed to tackle the problem of drug resistance mediated by the T790M EGFR mutation; however, there is a side effect of hyperglycemia that may be due to off-target activity.	osimertinib	156-163	epidermal growth factor receptor	Homo sapiens	246-250
34764521-3	2021	This study examines analogues of AZD9291 by chemical proteomics, identifying analogues that maintain T790M-EGFR engagement while showing reduced cross-reactivity with off-targets.	osimertinib	33-40	epidermal growth factor receptor	Homo sapiens	107-111
34584858-1	2021	Background: Osimertinib monotherapy is currently the standard of care as a first-line treatment for patients harboring epidermal growth factor receptor (EGFR) mutations; however, some EGFR-mutated non-small cell lung cancer (NSCLC) patients exhibit primary resistance and an insufficient response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	153-157
34584858-1	2021	Background: Osimertinib monotherapy is currently the standard of care as a first-line treatment for patients harboring epidermal growth factor receptor (EGFR) mutations; however, some EGFR-mutated non-small cell lung cancer (NSCLC) patients exhibit primary resistance and an insufficient response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	184-188
34584858-1	2021	Background: Osimertinib monotherapy is currently the standard of care as a first-line treatment for patients harboring epidermal growth factor receptor (EGFR) mutations; however, some EGFR-mutated non-small cell lung cancer (NSCLC) patients exhibit primary resistance and an insufficient response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	300-304
34584858-1	2021	Background: Osimertinib monotherapy is currently the standard of care as a first-line treatment for patients harboring epidermal growth factor receptor (EGFR) mutations; however, some EGFR-mutated non-small cell lung cancer (NSCLC) patients exhibit primary resistance and an insufficient response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	333-337
34584858-3	2021	Methods: We prospectively assessed advanced NSCLC patients with EGFR mutations who were treated with osimertinib at 14 institutions in Japan between September 2019 and December 2020.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	64-68
34584858-6	2021	Multivariate analysis identified tumor PD-L1 expression as an independent predictor for progression-free survival (PFS) with osimertinib treatment (P=0.029).	osimertinib	125-136	CD274 molecule	Homo sapiens	39-44
34584858-7	2021	The objective-response and disease-control rates for osimertinib treatment were significantly lower in patients demonstrating elevated PD-L1 levels relative to those with low or negative PD-L1 level (P=0.043 and P=0.007, respectively).	osimertinib	53-64	CD274 molecule	Homo sapiens	135-140
34584858-8	2021	Furthermore, among patients treated with osimertinib, those with high PD-L1 levels exhibited shorter PFS relative to those with low plus negative PD-L1 level (median PFS: 5.0 vs. 17.4 months; P<0.001).	osimertinib	41-52	CD274 molecule	Homo sapiens	70-75
34584858-8	2021	Furthermore, among patients treated with osimertinib, those with high PD-L1 levels exhibited shorter PFS relative to those with low plus negative PD-L1 level (median PFS: 5.0 vs. 17.4 months; P<0.001).	osimertinib	41-52	CD274 molecule	Homo sapiens	146-151
34584858-9	2021	Conclusions: Elevated tumor PD-L1 expression is associated with poor outcomes of osimertinib monotherapy in previously untreated advanced NSCLC patients with EGFR mutation.	osimertinib	81-92	CD274 molecule	Homo sapiens	28-33
34584858-9	2021	Conclusions: Elevated tumor PD-L1 expression is associated with poor outcomes of osimertinib monotherapy in previously untreated advanced NSCLC patients with EGFR mutation.	osimertinib	81-92	epidermal growth factor receptor	Homo sapiens	158-162
34584858-10	2021	Further clinical trials are warranted to accumulate evidence demonstrating the effectiveness of combination therapy with osimertinib for EGFR-mutated advanced NSCLC patients with elevated tumor PD-L1 expression.	osimertinib	121-132	CD274 molecule	Homo sapiens	194-199
34140482-0	2021	Identification of optimal dosing schedules of dacomitinib and osimertinib for a phase I/II trial in advanced EGFR-mutant non-small cell lung cancer.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	109-113
34140482-1	2021	Despite the clinical success of the third-generation EGFR inhibitor osimertinib as a first-line treatment of EGFR-mutant non-small cell lung cancer (NSCLC), resistance arises due to the acquisition of EGFR second-site mutations and other mechanisms, which necessitates alternative therapies.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	53-57
34140482-1	2021	Despite the clinical success of the third-generation EGFR inhibitor osimertinib as a first-line treatment of EGFR-mutant non-small cell lung cancer (NSCLC), resistance arises due to the acquisition of EGFR second-site mutations and other mechanisms, which necessitates alternative therapies.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	109-113
34140482-1	2021	Despite the clinical success of the third-generation EGFR inhibitor osimertinib as a first-line treatment of EGFR-mutant non-small cell lung cancer (NSCLC), resistance arises due to the acquisition of EGFR second-site mutations and other mechanisms, which necessitates alternative therapies.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	201-205
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	9-33
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	35-38
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	epidermal growth factor receptor	Homo sapiens	118-122
34178120-1	2021	Osimertinib is a third-generation tyrosine kinase inhibitor that became the preferred first-line treatment option for metastatic non-small cell lung cancer with sensitizing epidermal growth factor receptor mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	173-205
34103652-0	2021	The impact of different first-line EGFR-TKIs on the clinical outcome of sequential osimertinib treatment in advanced NSCLC with secondary T790M.	osimertinib	83-94	epidermal growth factor receptor	Homo sapiens	35-39
34103652-1	2021	The impact of different first-line epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)s to the clinical efficacy of osimertinib in EGFR-mutant non-small-cell lung cancer (NSCLC) patients with acquired T790M was still unclear.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	35-67
34103652-1	2021	The impact of different first-line epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)s to the clinical efficacy of osimertinib in EGFR-mutant non-small-cell lung cancer (NSCLC) patients with acquired T790M was still unclear.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	69-73
34103652-1	2021	The impact of different first-line epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)s to the clinical efficacy of osimertinib in EGFR-mutant non-small-cell lung cancer (NSCLC) patients with acquired T790M was still unclear.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	151-155
34103652-5	2021	Among them, the median progression-free survival (PFS) of first-line EGFR-TKI (PFS1) was 14.0 months, and the median PFS of osimertinib (PFS2) was 10.1 months.	osimertinib	124-135	GINS complex subunit 2	Homo sapiens	137-141
34350252-0	2021	Osimertinib for the treatment of epidermal growth factor receptor-mutated non-small cell lung cancer patients with leptomeningeal metastases and different T790M status.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	33-65
34350265-2	2021	Osimertinib is one of the third-generation EGFR-TKIs and is currently the most advanced in clinical development.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	43-47
34073111-4	2021	In the present study we detected EGFR mutations in ctDNA and paired CTCs under osimertinib therapy at two time points using crystal dPCR and the naica  system (Stilla Technologies).	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	33-37
34164239-0	2021	A Rare Case of Small Cell Lung Cancer With an Epidermal Growth Factor Receptor Mutation and Its Response to Osimertinib.	osimertinib	108-119	epidermal growth factor receptor	Homo sapiens	46-78
34113560-10	2021	Moreover, the use of PD-1/PD-L1 blockade prior to or concurrent with osimertinib has been reported to increase the risk of pulmonary toxicity.	osimertinib	69-80	programmed cell death 1	Homo sapiens	21-25
34164239-5	2021	We report a case of EGFR-positive metastatic SCLC in a 63-year-old female who was treated with the third-generation TKI, osimertinib.	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	20-24
34590035-0	2021	EGFR Thr790Leu as a Potential Resistance Mechanism to First-Generation EGFR Tyrosine Kinase Inhibitor May Respond to Osimertinib in Patients With Lung Adenocarcinoma.	osimertinib	117-128	epidermal growth factor receptor	Homo sapiens	0-4
34590033-3	2021	BRAF V600E, as a bypass mechanism on disease progression while receiving osimertinib therapy, has been reported in 3% of EGFR-mutated patients.	osimertinib	73-84	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
34590033-3	2021	BRAF V600E, as a bypass mechanism on disease progression while receiving osimertinib therapy, has been reported in 3% of EGFR-mutated patients.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	121-125
34590035-12	2021	We also report the first clinical evidence of efficacy generated by osimertinib in patients with lung adenocarcinoma harboring primary or acquired EGFR T790L, shedding light on treatment options for this subset of patients.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	147-151
34070173-4	2021	It was revealed that osimertinib, an ATP-competitive covalent EGFR inhibitor, remarkably enhanced the affinity of a recently developed allosteric inhibitor JBJ-04-125-02 for EGFRL858R/T790M.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	62-66
34070173-5	2021	Here, we utilized extensive large-scale molecular dynamics simulations and the reversed allosteric communication to untangle the detailed molecular underpinning, in which occupation of osimertinib at the orthosteric site altered the overall conformational ensemble of EGFR mutant and reshaped the allosteric site via long-distance signaling.	osimertinib	185-196	epidermal growth factor receptor	Homo sapiens	268-272
34590027-2	2021	However, despite its high initial response rates, multiple EGFR-independent mechanisms of resistance have been reported in patients receiving osimertinib.	osimertinib	142-153	epidermal growth factor receptor	Homo sapiens	59-63
34150410-5	2021	This likely represents a synergistic relationship between an epidermal growth factor receptor inhibitor, osimertinib, and a vascular endothelial growth factor receptor inhibitor, ramucirumab.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	61-93
34590037-1	2021	Introduction: Although treatment with osimertinib confers survival benefits in patients with lung cancer with the EGFR T790M mutation, the mechanism of acquired resistance to osimertinib remains poorly understood.	osimertinib	38-49	epidermal growth factor receptor	Homo sapiens	114-118
34068720-2	2021	Osimertinib is a tyrosine kinase approved and effective in treating lung adenocarcinomas that have one of several common activating mutations in epidermal growth factor receptor.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	145-177
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
34590028-1	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	epidermal growth factor receptor	Homo sapiens	134-138
34590028-4	2021	Methods: Whole-exome sequencing was performed in EGFR-mutant, MET-amplified patients who received osimertinib and savolitinib using tissues obtained both before and after therapy.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	49-53
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
34590028-8	2021	Patient 2 harbored an acquired PIK3CA p.H1047R mutation in which resistance could be overcome with combination of PI3K inhibitor and osimertinib in the patient-derived xenograft model.	osimertinib	133-144	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	31-37
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	146-157	epidermal growth factor receptor	Homo sapiens	46-50
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	146-157	EMAP like 4	Homo sapiens	99-103
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	146-157	ALK receptor tyrosine kinase	Homo sapiens	104-107
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	204-215	epidermal growth factor receptor	Homo sapiens	46-50
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	204-215	EMAP like 4	Homo sapiens	99-103
34590027-5	2021	In our case report, we present a patient with EGFR-mutant advanced NSCLC who developed an acquired EML4-ALK rearrangement mediating resistance to osimertinib, which was overcome by using a combination of osimertinib with the ALK tyrosine kinase inhibitor alectinib.	osimertinib	204-215	ALK receptor tyrosine kinase	Homo sapiens	104-107
34250398-1	2021	Patients with EGFR-mutant lung cancer have no approved targeted therapies after disease progression on first-line osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	146-178
34590012-0	2021	Intracranial Activity of Osimertinib Plus Capmatinib in a Patient With EGFR and MET-Driven Lung Cancer: Case Report.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	71-75
34250398-1	2021	Patients with EGFR-mutant lung cancer have no approved targeted therapies after disease progression on first-line osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	180-184
34250398-2	2021	Preclinical studies suggest that tumors with both EGFR-sensitizing alteration and acquired second-site EGFR resistance alterations after treatment with osimertinib retain sensitivity to second-generation EGFR TKIs.	osimertinib	152-163	epidermal growth factor receptor	Homo sapiens	103-107
34250398-2	2021	Preclinical studies suggest that tumors with both EGFR-sensitizing alteration and acquired second-site EGFR resistance alterations after treatment with osimertinib retain sensitivity to second-generation EGFR TKIs.	osimertinib	152-163	epidermal growth factor receptor	Homo sapiens	204-208
34557754-4	2021	The first-generation TKIs include erlotinib, gefitinib, lapatinib, and icotinib; the second-generation ErbB family blockers include afatinib, neratinib, and dacomitinib; whereas osimertinib, approved by the FDA on 2015, is a third-generation TKI targeting EGFR harboring specific mutations.	osimertinib	178-189	epidermal growth factor receptor	Homo sapiens	256-260
34095710-0	2021	Exceptional Response of a Large and Symptomatic EGFR-Mutant Brain Metastasis to Osimertinib: Case Report and Review of the Literature.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	48-52
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	epidermal growth factor receptor	Homo sapiens	87-91
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
34601320-6	2021	NCI-H1975 cells which have an EGFR T790M mutation and an EGFR L858R mutation, were sensitive to osimertinib when propagated as spheroids but not when grown in monolayer.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	30-34
34601320-6	2021	NCI-H1975 cells which have an EGFR T790M mutation and an EGFR L858R mutation, were sensitive to osimertinib when propagated as spheroids but not when grown in monolayer.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	57-61
34589970-2	2021	Osimertinib is the standard of care for patients with NSCLC with acquired EGFR T790M mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	74-78
34589970-13	2021	Conclusions: In patients with EGFR-mutated advanced NSCLC, persistent EGFR T790M or increasing activating mutation AF as detected in ctDNA 4 weeks after the start of osimertinib treatment may predict disease progression within 16 weeks.	osimertinib	166-177	epidermal growth factor receptor	Homo sapiens	30-34
35473448-2	2022	This is relevant in the context of the recently approved introduction of adjuvant EGFR-targeting therapy, specifically osimertinib in resected stage II-III EGFR-mutated NSCLC.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	82-86
35447433-1	2022	The C797S mutation in EGFR is a leading mechanism of clinically acquired resistance against osimertinib for non-small cell lung cancer (NSCLC).	osimertinib	92-103	epidermal growth factor receptor	Mus musculus	22-26
35551303-8	2022	Studies using epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKIs) drugs gefitinib and osimertinib showed clinically relevant responses.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	14-46
35551303-8	2022	Studies using epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKIs) drugs gefitinib and osimertinib showed clinically relevant responses.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	48-52
35045945-11	2022	Moreover, EGFR C797S mutation was detected in 1 patient after resistant to osimertinib treatment.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	10-14
35045945-12	2022	CONCLUSION: Presence of EGFR T854A mutation was rare in NSCLC patients and our retrospective study provides clinical evidence that osimertinib may be an effective treatment to improve survival outcomes in patients with EGFR T854A.	osimertinib	131-142	epidermal growth factor receptor	Homo sapiens	24-28
35045945-12	2022	CONCLUSION: Presence of EGFR T854A mutation was rare in NSCLC patients and our retrospective study provides clinical evidence that osimertinib may be an effective treatment to improve survival outcomes in patients with EGFR T854A.	osimertinib	131-142	epidermal growth factor receptor	Homo sapiens	219-223
35378738-5	2022	Likewise, tyrosine kinase inhibitor drugs such as osimertinib used in lung cancer patients with epidermal growth factor receptor (EGFR) mutation are associated with heart failure or prolongation of the QT interval.	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	96-128
35378738-5	2022	Likewise, tyrosine kinase inhibitor drugs such as osimertinib used in lung cancer patients with epidermal growth factor receptor (EGFR) mutation are associated with heart failure or prolongation of the QT interval.	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	130-134
35378738-6	2022	CASE REPORT: 62-year-old woman diagnosed in September 2019 of lung adenocarcinoma stage IV with bilateral lung and lymph node involvement, carrier of an EGFR mutation (Ex19Del) on treatment with osimertinib.	osimertinib	195-206	epidermal growth factor receptor	Homo sapiens	153-157
35037771-1	2022	INTRODUCTION: Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR) used for the treatment of non-small cell lung cancer (NSCLC) presenting an EGFR mutation.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	83-115
34589970-0	2021	Serial Plasma Cell-Free Circulating Tumor DNA Tests Identify Genomic Alterations for Early Prediction of Osimertinib Treatment Outcome in EGFR T790M-Positive NSCLC.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	138-142
35037771-1	2022	INTRODUCTION: Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR) used for the treatment of non-small cell lung cancer (NSCLC) presenting an EGFR mutation.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	117-121
35294773-4	2022	These results led to osimertinib"s fast track approval by the US Food and Drug Administration, with this drug thus becoming the first EGFR-TKI approved for the treatment of early-stage disease.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	134-138
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
35331964-8	2022	Reduced PFS on later-line osimertinib in 33 patients was associated with MET, APC and ERBB4 alterations.	osimertinib	26-37	erb-b2 receptor tyrosine kinase 4	Homo sapiens	86-91
35530643-11	2022	CONCLUSION: EGFR-mutant NSCLC patients with negative tumor PD-L1 expression showed a higher rate of acquisition of the T790M mutation and implementation rate of osimertinib therapy, leading to a longer time on treatment with EGFR-TKI.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	225-229
35633141-7	2022	Multivariate analysis confirmed that both EGFR-TKI treatment (osimertinib hazard ratio (HR) 0.06, 95% confidence interval (CI) 0.01-0.30; afatinib HR 0.09, 95% CI 0.02-0.39) and a low T790M ratio (HR 0.29, 95% CI 0.12-0.69) were independently favorable prognostic factors for patients with de novo T790M+ NSCLC.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	42-46
35633141-9	2022	In addition, patients treated with first-generation (1G)/second-generation (2G) EGFR-TKIs followed by osimertinib (n = 8) demonstrated the best OS compared with patients treated with frontline osimertinib (n = 5) or 1G/2G EGFR-TKIs without osimertinib (n = 28, p < 0.01).	osimertinib	102-113	olfactory receptor family 1 subfamily G member 1	Homo sapiens	213-220
35633141-9	2022	In addition, patients treated with first-generation (1G)/second-generation (2G) EGFR-TKIs followed by osimertinib (n = 8) demonstrated the best OS compared with patients treated with frontline osimertinib (n = 5) or 1G/2G EGFR-TKIs without osimertinib (n = 28, p < 0.01).	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	222-226
35633141-9	2022	In addition, patients treated with first-generation (1G)/second-generation (2G) EGFR-TKIs followed by osimertinib (n = 8) demonstrated the best OS compared with patients treated with frontline osimertinib (n = 5) or 1G/2G EGFR-TKIs without osimertinib (n = 28, p < 0.01).	osimertinib	240-251	epidermal growth factor receptor	Homo sapiens	80-84
35617514-1	2022	BACKGROUND: MEK/ERK inhibition can overcome acquired resistance to osimertinib in preclinical models.	osimertinib	67-78	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
35617514-1	2022	BACKGROUND: MEK/ERK inhibition can overcome acquired resistance to osimertinib in preclinical models.	osimertinib	67-78	mitogen-activated protein kinase 1	Homo sapiens	16-19
35596880-7	2022	Finally, for epidermal growth factor receptor (EGFR) mutant NSCLC, a phase III trial of osimertinib compared with SOC revealed an improvement in DFS.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	13-45
35596880-7	2022	Finally, for epidermal growth factor receptor (EGFR) mutant NSCLC, a phase III trial of osimertinib compared with SOC revealed an improvement in DFS.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	47-51
35626421-6	2022	Osimertinib given as a second-line treatment eliminated the EGFR-T790M population and simultaneously consolidated the proliferation of the TP53 + RB1 clone that eventually led to the histologic transformation to small-cell lung cancer (SCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	60-64
35626421-6	2022	Osimertinib given as a second-line treatment eliminated the EGFR-T790M population and simultaneously consolidated the proliferation of the TP53 + RB1 clone that eventually led to the histologic transformation to small-cell lung cancer (SCLC).	osimertinib	0-11	tumor protein p53	Homo sapiens	139-143
35626421-6	2022	Osimertinib given as a second-line treatment eliminated the EGFR-T790M population and simultaneously consolidated the proliferation of the TP53 + RB1 clone that eventually led to the histologic transformation to small-cell lung cancer (SCLC).	osimertinib	0-11	RB transcriptional corepressor 1	Homo sapiens	146-149
35621675-11	2022	Due to EGFR gene mutation, the woman was administered osimertinib, however, the treatment did not succeed, and other therapeutic solutions were undertaken.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	7-11
35621675-13	2022	Patients with advanced ADC harboring EGFR mutation can receive osimertinib, a third-generation tyrosine kinase inhibitor (TKI), however, the use of TKIs in SCC remains controversial.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	37-41
35527328-0	2022	Osimertinib, Surgery, and Radiation Therapy in Treating Patients with Stage IIIB or IV Non-Small Cell Lung Cancer with EGFR Mutations (NORTHSTAR).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	119-123
35534623-4	2022	Both "on-target" mechanisms (largely mediated by acquired resistance mutations in the kinase domains of EGFR or ALK) and "off-target" mechanisms of resistance (mediated by non-target kinase alterations such as bypass signalling activation or phenotypic transformation) have been identified in patients with disease progression on osimertinib or lorlatinib.	osimertinib	330-341	epidermal growth factor receptor	Homo sapiens	104-108
35534623-4	2022	Both "on-target" mechanisms (largely mediated by acquired resistance mutations in the kinase domains of EGFR or ALK) and "off-target" mechanisms of resistance (mediated by non-target kinase alterations such as bypass signalling activation or phenotypic transformation) have been identified in patients with disease progression on osimertinib or lorlatinib.	osimertinib	330-341	ALK receptor tyrosine kinase	Homo sapiens	112-115
35510318-8	2022	Changes in response against Gefitinib and Osimertinib were observed with the change of amino acids at the tyrosine kinase domain of EGFRWILD and its mutants (EGFRL858R, EGFRT790M, EGFRT790M+C797S).	osimertinib	42-53	TXK tyrosine kinase	Homo sapiens	106-121
35530643-11	2022	CONCLUSION: EGFR-mutant NSCLC patients with negative tumor PD-L1 expression showed a higher rate of acquisition of the T790M mutation and implementation rate of osimertinib therapy, leading to a longer time on treatment with EGFR-TKI.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	12-16
35530643-11	2022	CONCLUSION: EGFR-mutant NSCLC patients with negative tumor PD-L1 expression showed a higher rate of acquisition of the T790M mutation and implementation rate of osimertinib therapy, leading to a longer time on treatment with EGFR-TKI.	osimertinib	161-172	CD274 molecule	Homo sapiens	59-64
35499406-0	2022	HJM-561, a potent, selective and orally bioavailable EGFR PROTAC that overcomes osimertinib-resistant EGFR triple mutations.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	102-106
35499406-1	2022	The epidermal growth factor receptor (EGFR) C797S mutation is the most common on-target resistance mechanism to osimertinib in patients with advanced non-small-cell lung cancer (NSCLC).	osimertinib	112-123	epidermal growth factor receptor	Homo sapiens	4-36
35499406-1	2022	The epidermal growth factor receptor (EGFR) C797S mutation is the most common on-target resistance mechanism to osimertinib in patients with advanced non-small-cell lung cancer (NSCLC).	osimertinib	112-123	epidermal growth factor receptor	Homo sapiens	38-42
35511414-8	2022	CONCLUSION: Concomitant use of bevacizumab and osimertinib in NSCLC patients with EGFR T790M mutation may have potential therapeutic effect than osimertinib alone.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	82-86
35037771-1	2022	INTRODUCTION: Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR) used for the treatment of non-small cell lung cancer (NSCLC) presenting an EGFR mutation.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	198-202
35037771-2	2022	Although Osimertinib has a better safety profile compared to older EGFR-TKIs and although adverse events (AEs) are described in literature, recently the relationship between Osimertinib therapy and cardiotoxicity is gaining attention.	osimertinib	174-185	epidermal growth factor receptor	Homo sapiens	67-71
35489768-1	2022	BACKGROUND/AIM: Real-world data on the clinical outcomes of first-line osimertinib treatment for non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations is lacking.	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	137-169
35489768-1	2022	BACKGROUND/AIM: Real-world data on the clinical outcomes of first-line osimertinib treatment for non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations is lacking.	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	171-175
35489768-3	2022	PATIENTS AND METHODS: We retrospectively evaluated clinical outcomes of patients with EGFR-mutated NSCLC treated with osimertinib as first-line therapy across 12 institutions in Japan between August 2018 and March 2020.	osimertinib	118-129	epidermal growth factor receptor	Homo sapiens	86-90
35489768-6	2022	Univariate and multivariate analyses demonstrated that high PD-L1 expression was the only independent adverse prognostic factor of osimertinib outcome related to PFS (hazard ratio=2.71; 95%CI=1.26-5.84; p=0.01).	osimertinib	131-142	CD274 molecule	Homo sapiens	60-65
35489768-9	2022	CONCLUSION: Although PD-L1 expression was not associated with either the ORR or frequency of de novo resistance, high PD-L1 expression could be an independent adverse prognostic factor related to PFS in osimertinib treatment.	osimertinib	203-214	CD274 molecule	Homo sapiens	118-123
35023208-1	2022	WHAT IS KNOWN AND OBJECTIVE: Although osimertinib achieved convincing efficacy for patients with EGFR T790M-positive non-small-cell lung cancer (NSCLC) as second-line treatment in the AURA3 clinical trials, patients developed drug resistance ultimately.	osimertinib	38-49	epidermal growth factor receptor	Homo sapiens	97-101
35468939-7	2022	Gefitinib and Osimertinib medications were capable of upregulating KLHDC3 expression to promote p14ARF degradation in the NSCLC cell lines.	osimertinib	14-25	kelch domain containing 3	Homo sapiens	67-73
35468939-7	2022	Gefitinib and Osimertinib medications were capable of upregulating KLHDC3 expression to promote p14ARF degradation in the NSCLC cell lines.	osimertinib	14-25	cyclin dependent kinase inhibitor 2A	Homo sapiens	96-102
35468939-8	2022	KLHDC3 shortage significantly increased the sensitivity of lung cancer cells to epidermal growth factor receptor (EGFR)-targeted drugs, providing an alternative explanation for the development of Gefitinib and Osimertinib resistance in NSCLC therapy.	osimertinib	210-221	kelch domain containing 3	Homo sapiens	0-6
35468939-8	2022	KLHDC3 shortage significantly increased the sensitivity of lung cancer cells to epidermal growth factor receptor (EGFR)-targeted drugs, providing an alternative explanation for the development of Gefitinib and Osimertinib resistance in NSCLC therapy.	osimertinib	210-221	epidermal growth factor receptor	Homo sapiens	80-112
35468939-8	2022	KLHDC3 shortage significantly increased the sensitivity of lung cancer cells to epidermal growth factor receptor (EGFR)-targeted drugs, providing an alternative explanation for the development of Gefitinib and Osimertinib resistance in NSCLC therapy.	osimertinib	210-221	epidermal growth factor receptor	Homo sapiens	114-118
35348294-2	2022	Pigmentary changes caused by EGFR-TKIs are unusual, and to the best of my knowledge, hyperpigmentation with osimertinib has rarely been reported as a skin-related adverse event.	osimertinib	108-119	epidermal growth factor receptor	Homo sapiens	29-33
35571073-3	2022	Materials and methods: Patients with resectable NSCLC with epidermal growth factor receptor (EGFR) mutation who received osimertinib as neoadjuvant therapy followed by surgery at our center were included.	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	59-91
35571073-3	2022	Materials and methods: Patients with resectable NSCLC with epidermal growth factor receptor (EGFR) mutation who received osimertinib as neoadjuvant therapy followed by surgery at our center were included.	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	93-97
35571073-15	2022	Conclusion: Neoadjuvant osimertinib therapy seemed to be safe and feasible for resectable EGFR-mutated NSCLC.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	90-94
35506019-3	2022	The ADAURA trial is a randomized placebo-controlled Phase III trial that demonstrated statistically significant improved disease-free survival (DFS) with the use of 3-years of adjuvant osimertinib in resected stage IB-IIIA NSCLC harboring epidermal growth factor receptor (EGFR) del 19 or L858R mutations.	osimertinib	185-196	epidermal growth factor receptor	Homo sapiens	239-271
35574304-14	2022	Moderate activity was seen against osimertinib resistance EGFR mutations.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	58-62
35445633-1	2022	Osimertinib, almonertinib and furmonertinib are third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) approved for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	126-130
35445633-1	2022	Osimertinib, almonertinib and furmonertinib are third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) approved for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	199-203
35506019-3	2022	The ADAURA trial is a randomized placebo-controlled Phase III trial that demonstrated statistically significant improved disease-free survival (DFS) with the use of 3-years of adjuvant osimertinib in resected stage IB-IIIA NSCLC harboring epidermal growth factor receptor (EGFR) del 19 or L858R mutations.	osimertinib	185-196	epidermal growth factor receptor	Homo sapiens	273-277
35461372-12	2022	Targeting Hsa-miR-22-3p and Hsa-miR-184 desensitized EGFR-mutated (T790M, L578R) NSCLC cells to Osimertinib.	osimertinib	96-107	microRNA 22	Homo sapiens	10-20
35467492-0	2022	Osimertinib and chemotherapy combination to treat brain metastasis flare and osimertinib resistance by EGFR C797S.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	103-107
35467492-3	2022	In this case, we describe a young woman who has extracranial progressive disease due to EGFR C797S resistance mutation while being treated with osimertinib, with a rapid neurological deterioration after osimertinib withdrawal due to flare-phenomenon progression in the brain, and a prompt intracranial response with osimertinib reintroduction in addition to chemotherapy to achieve extracranial diseases control.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	88-92
35467492-3	2022	In this case, we describe a young woman who has extracranial progressive disease due to EGFR C797S resistance mutation while being treated with osimertinib, with a rapid neurological deterioration after osimertinib withdrawal due to flare-phenomenon progression in the brain, and a prompt intracranial response with osimertinib reintroduction in addition to chemotherapy to achieve extracranial diseases control.	osimertinib	316-327	epidermal growth factor receptor	Homo sapiens	88-92
35461372-12	2022	Targeting Hsa-miR-22-3p and Hsa-miR-184 desensitized EGFR-mutated (T790M, L578R) NSCLC cells to Osimertinib.	osimertinib	96-107	microRNA 184	Homo sapiens	28-39
35461372-12	2022	Targeting Hsa-miR-22-3p and Hsa-miR-184 desensitized EGFR-mutated (T790M, L578R) NSCLC cells to Osimertinib.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	53-57
35446957-2	2022	In the FLAURA study, osimertinib, third-generation EGFR-TKI, resulted in significantly longer progression-free survival and overall survival (OS) than first-generation EGFR-TKIs (gefitinib or erlotinib) in patients with previously untreated advanced NSCLC with an EGFR activating mutation.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	51-55
35446957-2	2022	In the FLAURA study, osimertinib, third-generation EGFR-TKI, resulted in significantly longer progression-free survival and overall survival (OS) than first-generation EGFR-TKIs (gefitinib or erlotinib) in patients with previously untreated advanced NSCLC with an EGFR activating mutation.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	264-268
35449204-8	2022	When combined with the third generation EGFR inhibitor, osimertinib (AZD9291), synergistic effects on decreasing the survival of different osimertinib-resistant cell lines were observed with enhanced induction of apoptosis.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	40-44
35449204-8	2022	When combined with the third generation EGFR inhibitor, osimertinib (AZD9291), synergistic effects on decreasing the survival of different osimertinib-resistant cell lines were observed with enhanced induction of apoptosis.	osimertinib	69-76	epidermal growth factor receptor	Homo sapiens	40-44
35449204-8	2022	When combined with the third generation EGFR inhibitor, osimertinib (AZD9291), synergistic effects on decreasing the survival of different osimertinib-resistant cell lines were observed with enhanced induction of apoptosis.	osimertinib	139-150	epidermal growth factor receptor	Homo sapiens	40-44
35530305-1	2022	The efficacy of osimertinib is severely limited by the emergence of EGFR C797S, which is detected in either the cis or trans position with T790M when osimertinib is used as a second-line treatment, and which is largely identified in combination with an EGFR 19 deletion.	osimertinib	16-27	epidermal growth factor receptor	Homo sapiens	68-72
35530305-1	2022	The efficacy of osimertinib is severely limited by the emergence of EGFR C797S, which is detected in either the cis or trans position with T790M when osimertinib is used as a second-line treatment, and which is largely identified in combination with an EGFR 19 deletion.	osimertinib	150-161	epidermal growth factor receptor	Homo sapiens	68-72
35530305-2	2022	The EGFR T790M-cis-G796S mutation, which also occurs in exon 20 as C797S, participates in osimertinib resistance.	osimertinib	90-101	epidermal growth factor receptor	Homo sapiens	4-8
35530305-4	2022	Here, we report data for an advanced NSCLC patient who developed EGFR L858R-T790M-cis-G796S and EGFR L718Q resistance co-mutations following progression with osimertinib.	osimertinib	158-169	epidermal growth factor receptor	Homo sapiens	65-69
35530305-4	2022	Here, we report data for an advanced NSCLC patient who developed EGFR L858R-T790M-cis-G796S and EGFR L718Q resistance co-mutations following progression with osimertinib.	osimertinib	158-169	epidermal growth factor receptor	Homo sapiens	96-100
35530305-8	2022	Our finding provides clinical evidence that the combined target therapy of brigatinib and cetuximab may potentially be an effective treatment strategy for patients with an acquired EGFR T790M-cis-G796S resistance mutation following osimertinib treatment.	osimertinib	232-243	epidermal growth factor receptor	Homo sapiens	181-185
35494030-2	2022	For those patients with EGFR mutations, osimertinib, a third-generation tyrosine kinase inhibitor (TKI), is the first choice of treatment.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	24-28
35452875-0	2022	A dual action small molecule enhances azoles and overcomes resistance through co-targeting Pdr5 and Vma1: Osimertinib targets Pdr5 and Vma1.	osimertinib	106-117	ATPase H+ transporting V1 subunit A	Homo sapiens	100-104
35452875-0	2022	A dual action small molecule enhances azoles and overcomes resistance through co-targeting Pdr5 and Vma1: Osimertinib targets Pdr5 and Vma1.	osimertinib	106-117	ATPase H+ transporting V1 subunit A	Homo sapiens	135-139
35404406-5	2022	In this study, we identify that loss of an epigenetic factor, lysine methyltransferase 5C (KMT5C), drives resistance of NSCLC to multiple EGFRis, including erlotinib, gefitinib, afatinib, and osimertinib.	osimertinib	192-203	lysine methyltransferase 5C	Homo sapiens	62-89
35404406-5	2022	In this study, we identify that loss of an epigenetic factor, lysine methyltransferase 5C (KMT5C), drives resistance of NSCLC to multiple EGFRis, including erlotinib, gefitinib, afatinib, and osimertinib.	osimertinib	192-203	lysine methyltransferase 5C	Homo sapiens	91-96
35422085-8	2022	We revealed that c-FLIP promoted the resistance of NSCLC cells to thiostrepton and osimertinib by upregulating FoxM1.	osimertinib	83-94	CASP8 and FADD-like apoptosis regulator	Mus musculus	17-23
35422085-8	2022	We revealed that c-FLIP promoted the resistance of NSCLC cells to thiostrepton and osimertinib by upregulating FoxM1.	osimertinib	83-94	forkhead box M1	Mus musculus	111-116
35422085-9	2022	Taken together, these results reveal a new mechanism by which c-FLIP regulates FoxM1 and the function of this interaction in the development of thiostrepton and osimertinib resistance.	osimertinib	161-172	CASP8 and FADD-like apoptosis regulator	Mus musculus	62-68
35422085-9	2022	Taken together, these results reveal a new mechanism by which c-FLIP regulates FoxM1 and the function of this interaction in the development of thiostrepton and osimertinib resistance.	osimertinib	161-172	forkhead box M1	Mus musculus	79-84
35494030-5	2022	This 55-year-old male patient was found to have a pL858R mutation on EGFR exon 21 combined with TP53 and ERBB2 mutations after developing drug resistance to osimertinib treatment.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	69-73
35494059-0	2022	Osimertinib-Centered Therapy Against Uncommon Epidermal Growth Factor Receptor-Mutated Non-Small-Cell Lung Cancer- A Mini Review.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	46-78
35494059-1	2022	Osimertinib is a third-generation, irreversible mutant epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is approved by the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	55-87
35494059-1	2022	Osimertinib is a third-generation, irreversible mutant epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is approved by the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	89-93
35494059-2	2022	Osimertinib is currently the first line drug recommended by National Comprehensive Cancer Network (NCCN) guidelines against lung cancer harboring the EGFR TKI-sensitive mutation and acquired EGFR T790M resistance mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	150-154
35494059-2	2022	Osimertinib is currently the first line drug recommended by National Comprehensive Cancer Network (NCCN) guidelines against lung cancer harboring the EGFR TKI-sensitive mutation and acquired EGFR T790M resistance mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	191-195
35494059-3	2022	Osimertinib demonstrated some efficacy in clinical trials and case reports in patients bearing certain uncommon EGFR mutations, but it is not active in patients with other mutations such as C797S.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	112-116
35494059-4	2022	This mini-review presents the mechanisms underlying the variations in patient responses, discusses the use of osimertinib against non-small-cell lung carcinomas with uncommon EGFR mutations, and addresses the future prospects of osimertinib-centered therapy.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	175-179
35463360-2	2022	Third-generation (3rd G) EGFR-TKIs, including osimertinib, offer an effective treatment option for patients with NSCLC resistant 1st and 2nd EGFR-TKIs.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	25-29
35431558-1	2022	Background: Osimertinib is an irreversible tyrosine kinase inhibitor approved for the treatment of metastatic epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	110-142
35431558-1	2022	Background: Osimertinib is an irreversible tyrosine kinase inhibitor approved for the treatment of metastatic epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	144-148
35431558-3	2022	Case Presentation: Herein, we describe the case of a 69-year-old man who received first-line osimertinib for metastatic EGFR-mutated NSCLC.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	120-124
35431558-7	2022	Conclusion: In the current case, first-line treatment with osimertinib at 80 mg daily in a patient with EGFR-mutated NSCLC resulted in severe pancytopenia and a rapid treatment response.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	104-108
35463360-11	2022	This review provides an overview of preclinical studies developed to investigate the mechanisms of acquired resistance to 3rd G EGFR-TKIs, including osimertinib and rociletinib, across all lines of therapy.	osimertinib	149-160	epidermal growth factor receptor	Homo sapiens	128-132
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	epidermal growth factor receptor	Homo sapiens	38-42
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	epidermal growth factor receptor	Homo sapiens	71-75
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
35462930-7	2022	The other patient acquired EGFR T790M and MET amplification post-dacomitinib and acquired CCDC6-RET fusion after osimertinib treatment.	osimertinib	113-124	coiled-coil domain containing 6	Homo sapiens	90-95
35462930-7	2022	The other patient acquired EGFR T790M and MET amplification post-dacomitinib and acquired CCDC6-RET fusion after osimertinib treatment.	osimertinib	113-124	ret proto-oncogene	Homo sapiens	96-99
35479327-4	2022	Case presentation: A 59-year-old female, diagnosed with relapsed stage IV (cT4N2M1c) NSCLC with T790M mutation of the EGFR gene, received osimertinib treatment.	osimertinib	138-149	epidermal growth factor receptor	Homo sapiens	118-122
35386002-1	2022	PURPOSE: Osimertinib is still essential for the treatment of epidermal growth factor receptor (EGFR)-T790M-positive non-small-cell lung cancer (NSCLC) even in a relapsed setting, which suggests the importance of rebiopsy.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	61-93
35386002-1	2022	PURPOSE: Osimertinib is still essential for the treatment of epidermal growth factor receptor (EGFR)-T790M-positive non-small-cell lung cancer (NSCLC) even in a relapsed setting, which suggests the importance of rebiopsy.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	95-99
35379563-4	2022	The AURA3 trial (NCT02151981) was a randomized controlled trial comparing osimertinib with platinum-based doublet chemotherapy (standard care) in patients with locally advanced or metastatic epidermal growth factor receptor mutant- and T790M-positive nonsmall cell lung cancer whose disease has progressed with previous epidermal growth factor receptor tyrosine kinase inhibitor therapy.	osimertinib	74-85	epidermal growth factor receptor	Homo sapiens	191-223
35066105-11	2022	CONCLUSIONS: Distinct molecular driver alterations at osimertinib resistance co-exist with initial EGFR mutations in single cancer cells.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	99-103
35347039-2	2022	Osimertinib can overcome the treatment resistance-associated EGFR T790M mutation, and the sequence of afatinib followed by osimertinib is an effective therapeutic strategy for NSCLC patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	61-65
35066105-1	2022	BACKGROUND: The development of targeted agents, such as osimertinib for EGFR-mutated NSCLC, has drastically improved patient outcome, but tumor resistance eventually always occurs.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	72-76
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	fibroblast growth factor receptor 3	Homo sapiens	135-140
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	transforming acidic coiled-coil containing protein 3	Homo sapiens	141-146
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	ret proto-oncogene	Homo sapiens	160-163
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	ALK receptor tyrosine kinase	Homo sapiens	176-179
35347039-15	2022	T790M mutation detection and osimertinib availability are important for prolonging survival in patients with NSCLC harboring EGFR mutations.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	125-129
35078784-1	2022	The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib has significantly prolonged progression-free survival (PFS) in EGFR-mutant lung cancer patients, including those with brain metastases.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	4-36
35219044-1	2022	AZD9291, with excellent pharmaceutical properties, has been reported to have certain LSD1 inhibitory activity.	osimertinib	0-7	lysine demethylase 1A	Homo sapiens	85-89
35219044-2	2022	Therefore, we carried out structural optimization based on the AZD9291 skeleton to increase the LSD1 inhibitory potential of the compound.	osimertinib	63-70	lysine demethylase 1A	Homo sapiens	96-100
35412115-4	2022	The advent of third-generation EGFR inhibitors (e.g., osimertinib) successfully overcame the T790M resistance mechanism, and osimertinib subsequently became the first-line therapy for EGFR mutant NSCLC.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	31-35
35462930-3	2022	For patients with secondary T790M-positive after early generation EGFR-TKIs, osimertinib is the standard second-line therapy.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	66-70
35412115-4	2022	The advent of third-generation EGFR inhibitors (e.g., osimertinib) successfully overcame the T790M resistance mechanism, and osimertinib subsequently became the first-line therapy for EGFR mutant NSCLC.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	31-35
35412115-4	2022	The advent of third-generation EGFR inhibitors (e.g., osimertinib) successfully overcame the T790M resistance mechanism, and osimertinib subsequently became the first-line therapy for EGFR mutant NSCLC.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	184-188
35412115-5	2022	Currently, research in EGFR mutant NSCLC is primarily focused on targeting resistance mechanisms to osimertinib.	osimertinib	100-111	epidermal growth factor receptor	Homo sapiens	23-27
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	epidermal growth factor receptor	Homo sapiens	66-70
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	epidermal growth factor receptor	Homo sapiens	222-226
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
35431966-2	2022	Although third-generation EGFR-TKI osimertinib is demonstrated with superior efficacy compared with first-generation EGFR-TKIs, acquired resistance to EGFR-TKIs remains the bottleneck.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	26-30
35257278-0	2022	Correction to: Osimertinib in poor performance status patients with T790M-positive advanced non-small-cell lung cancer after progression of first- and second-generation EGFR-TKI treatments (NEJ032B).	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	169-173
35078784-1	2022	The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib has significantly prolonged progression-free survival (PFS) in EGFR-mutant lung cancer patients, including those with brain metastases.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	38-42
35078784-1	2022	The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib has significantly prolonged progression-free survival (PFS) in EGFR-mutant lung cancer patients, including those with brain metastases.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	151-155
35078784-4	2022	Using metastatic models of EGFR-mutant lung cancer, we show that cancer cells expressing high intracellular S100A9 escape osimertinib and initiate brain relapses.	osimertinib	122-133	epidermal growth factor receptor	Homo sapiens	27-31
35078784-4	2022	Using metastatic models of EGFR-mutant lung cancer, we show that cancer cells expressing high intracellular S100A9 escape osimertinib and initiate brain relapses.	osimertinib	122-133	S100 calcium binding protein A9	Homo sapiens	108-114
35078784-7	2022	Importantly, S100A9 expression in cancer cells correlates with poor PFS in osimertinib-treated patients.	osimertinib	75-86	S100 calcium binding protein A9	Homo sapiens	13-19
35088212-1	2022	BACKGROUND AND OBJECTIVE: Osimertinib as first-line treatment for patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor (EGFR) mutations remains controversial.	osimertinib	26-37	epidermal growth factor	Homo sapiens	125-148
35293747-6	2022	Using this strategy, we demonstrated the heterogeneity of TK activity in different non-small cell lung cancer (NSCLC) cell lines and assessed the response of TK activities to the EGFR inhibitor AZD9291 in NSCLC cells.	osimertinib	194-201	epidermal growth factor receptor	Homo sapiens	179-183
35088212-1	2022	BACKGROUND AND OBJECTIVE: Osimertinib as first-line treatment for patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor (EGFR) mutations remains controversial.	osimertinib	26-37	epidermal growth factor	Homo sapiens	150-154
35293747-7	2022	We found that the acquired resistance of H1975 cells to AZD9291 requires SRC activity, and inhibition of SRC plays potential roles in overcoming this resistance.	osimertinib	56-63	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-76
35572898-0	2022	Tracking and tackling the tumor dynamics clonal evolution: osimertinib rechallenge after interval therapy might be an effective treatment approach in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC).	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	184-188
35293747-7	2022	We found that the acquired resistance of H1975 cells to AZD9291 requires SRC activity, and inhibition of SRC plays potential roles in overcoming this resistance.	osimertinib	56-63	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	105-108
35347108-5	2022	Osimertinib led to apoptosis of tumors but simultaneously, it triggered inositol-requiring-enzyme (IRE1alpha)-dependent HER3 upregulation, increased macrophage infiltration, and activated cGAS in cancer cells to produce cGAMP (detected by a lentivirally transduced STING activity biosensor), transactivating STING in macrophages.	osimertinib	0-11	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	99-108
35146920-1	2022	Osimertinib is the most efficient first-line drug, with least adverse effects, for metastatic non-small-cell lung carcinoma (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations with exon 19 deletion or exon 21 L858R mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	142-174
35146920-1	2022	Osimertinib is the most efficient first-line drug, with least adverse effects, for metastatic non-small-cell lung carcinoma (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations with exon 19 deletion or exon 21 L858R mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	176-180
35344648-0	2022	Osimertinib Combined with Systemic Chemotherapy for EGFR Mutant, T790M-Negative, Non-Small Cell Lung Cancer Patients Who Develop Leptomeningeal Metastases with Extracranial Progression to Prior EGFR TKI.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	52-56
35344648-0	2022	Osimertinib Combined with Systemic Chemotherapy for EGFR Mutant, T790M-Negative, Non-Small Cell Lung Cancer Patients Who Develop Leptomeningeal Metastases with Extracranial Progression to Prior EGFR TKI.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	194-198
35344648-3	2022	Osimertinib is a third-generation, irreversible, CNS penetrant, oral EGFR TKI that demonstrates promising efficacy in CNS metastases regardless of T790M.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	69-73
35344648-4	2022	Herein, we report four cases of T790M-negative EGFRm NSCLC patients treated with osimertinib combined with systemic chemotherapy, who progressed on prior EGFR TKI and developed LM with extracranial lesions.	osimertinib	81-92	epidermal growth factor receptor	Homo sapiens	154-158
35245845-0	2022	EGFR-RAD51 fusion in lung adenocarcinoma with systemic and intracranial response to osimertinib: A case report and review of the literature.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	0-4
35245845-0	2022	EGFR-RAD51 fusion in lung adenocarcinoma with systemic and intracranial response to osimertinib: A case report and review of the literature.	osimertinib	84-95	RAD51 recombinase	Homo sapiens	5-10
35245845-3	2022	We report a widely metastatic non-small cell lung cancer in a never-smoker young male patient with sustained near-complete systemic and intracranial response to osimertinib, a third-generation EGFR tyrosine-kinase inhibitor (TKI).	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	193-197
35529794-0	2022	Osimertinib as induction therapy for oligometastatic non-small cell lung cancer with EGFR mutation: a case report.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	85-89
35347108-5	2022	Osimertinib led to apoptosis of tumors but simultaneously, it triggered inositol-requiring-enzyme (IRE1alpha)-dependent HER3 upregulation, increased macrophage infiltration, and activated cGAS in cancer cells to produce cGAMP (detected by a lentivirally transduced STING activity biosensor), transactivating STING in macrophages.	osimertinib	0-11	erb-b2 receptor tyrosine kinase 3	Homo sapiens	120-124
35347108-6	2022	We sought to target osimertinib-induced HER3 upregulation with monoclonal antibodies, which engaged Fc receptor-dependent tumor elimination by macrophages, and STING agonists enhanced macrophage-mediated tumor elimination further.	osimertinib	20-31	erb-b2 receptor tyrosine kinase 3	Homo sapiens	40-44
35347108-7	2022	Thus, by engaging a tumor non-autonomous mechanism involving cGAS-STING and innate immunity, the combination of osimertinib and anti-HER3 antibodies could improve the limited therapeutic and stratification options for advanced stage lung cancer patients with mutant EGFR.	osimertinib	112-123	epidermal growth factor receptor	Homo sapiens	266-270
35287683-3	2022	This study aimed to compare the efficacy of osimertinib plus bevacizumab with osimertinib in EGFR-mutant NSCLC patients with LM.	osimertinib	78-89	epidermal growth factor receptor	Homo sapiens	93-97
35402377-4	2022	In the present research, we found that EGFR-TKIs (such as gefitinib and osimertinib) can induce autophagy in NSCLC cell lines.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	39-43
35402377-6	2022	The use of an autophagy inhibitor could enhance the toxicity of gefitinib and osimertinib, which indicates that the enhancement of protective autophagy might be one of the mechanisms of EGFR-TKI resistance in NSCLC.	osimertinib	78-89	epidermal growth factor receptor	Homo sapiens	186-190
35402377-9	2022	We revealed that the increase in autophagy caused by the reduction of EZH2 was reversed in vitro and in vivo when combining gefitinib or osimertinib with suberoylanilide hydroxamic acid (SAHA), a broad-spectrum histone deacetylase inhibitor (HDACi).	osimertinib	137-148	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	70-74
35323965-1	2022	Osimertinib is active against T790M-positive epidermal growth factor receptor mutant non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	45-77
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
35303882-11	2022	Lovastatin, a drug used to decrease cholesterol level, and XCT790, an inverse agonist of ERRalpha, overcome gefitinib and osimertinib resistance both in vitro and in vivo.	osimertinib	122-133	estrogen related receptor alpha	Homo sapiens	89-97
35359868-1	2022	The aim of this study was to 1) investigate the effects of 27 CYP3A4 variants on the metabolism of osimertinib and 2) study the interactions between osimertinib and others as well as the underlying mechanism.	osimertinib	99-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
35359868-1	2022	The aim of this study was to 1) investigate the effects of 27 CYP3A4 variants on the metabolism of osimertinib and 2) study the interactions between osimertinib and others as well as the underlying mechanism.	osimertinib	149-160	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
35359868-4	2022	The results demonstrated that the relative clearance rates of CYP3A4.19, 10, 18, 5, 16, 14, 11, 2, 13, 12, 7, 8, and 17 in catalyzing osimertinib were significantly reduced to a minimum of 25.68% compared to CYP3A4.1, while those of CYP3A4.29, 32, 33, 28, 15, 34, and 3 were obviously enhanced, ranging from 114.14% to 284.52%.	osimertinib	134-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
35359868-4	2022	The results demonstrated that the relative clearance rates of CYP3A4.19, 10, 18, 5, 16, 14, 11, 2, 13, 12, 7, 8, and 17 in catalyzing osimertinib were significantly reduced to a minimum of 25.68% compared to CYP3A4.1, while those of CYP3A4.29, 32, 33, 28, 15, 34, and 3 were obviously enhanced, ranging from 114.14% to 284.52%.	osimertinib	134-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	233-239
35359868-10	2022	Taken together, our data demonstrate that the genetic polymorphism and proton pump inhibitors remarkably influence the disposition of osimertinib, thereby providing basic data for the precise application of osimertinib.	osimertinib	134-145	ATPase H+/K+ transporting non-gastric alpha2 subunit	Rattus norvegicus	71-82
35287683-10	2022	In the LM xenograft model with H1975 cells, the combined treatment significantly increased the effective intracranial concentration of osimertinib, modulated the level of E-cadherin and downregulated the levels of EGFR and downstream signaling pathways including p-AKT and reduced tumor microvessel density (TMD), indicated that combined osimertinib with bevacizumab may exhibit a synergistic effect in EGFR-mutant LM model possibly by modulating the level of E-cadherin.	osimertinib	135-146	AKT serine/threonine kinase 1	Homo sapiens	265-268
35287683-10	2022	In the LM xenograft model with H1975 cells, the combined treatment significantly increased the effective intracranial concentration of osimertinib, modulated the level of E-cadherin and downregulated the levels of EGFR and downstream signaling pathways including p-AKT and reduced tumor microvessel density (TMD), indicated that combined osimertinib with bevacizumab may exhibit a synergistic effect in EGFR-mutant LM model possibly by modulating the level of E-cadherin.	osimertinib	135-146	epidermal growth factor receptor	Homo sapiens	403-407
35287683-10	2022	In the LM xenograft model with H1975 cells, the combined treatment significantly increased the effective intracranial concentration of osimertinib, modulated the level of E-cadherin and downregulated the levels of EGFR and downstream signaling pathways including p-AKT and reduced tumor microvessel density (TMD), indicated that combined osimertinib with bevacizumab may exhibit a synergistic effect in EGFR-mutant LM model possibly by modulating the level of E-cadherin.	osimertinib	135-146	cadherin 1	Homo sapiens	460-470
35365043-1	2022	Osimertinib, as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI), targeting EGFR exon 19 deletions, L858R, and T790M, has shown robust clinical efficacy and promising survival advantages in a subset of non-small cell lung cancer (NSCLC) patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	69-73
35265776-0	2022	Successful response to first-line treatment with osimertinib for choroidal metastasis from EGFR-mutated non-small-cell lung cancer.	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	91-95
35265776-1	2022	Purpose: Describe the use of osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, as the first-line treatment in a patient with choroidal and central nervous system metastases from EGFR-mutated non-small cell lung cancer.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	61-93
35265776-1	2022	Purpose: Describe the use of osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, as the first-line treatment in a patient with choroidal and central nervous system metastases from EGFR-mutated non-small cell lung cancer.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	95-99
35265776-1	2022	Purpose: Describe the use of osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, as the first-line treatment in a patient with choroidal and central nervous system metastases from EGFR-mutated non-small cell lung cancer.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	227-231
35365043-1	2022	Osimertinib, as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI), targeting EGFR exon 19 deletions, L858R, and T790M, has shown robust clinical efficacy and promising survival advantages in a subset of non-small cell lung cancer (NSCLC) patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	118-122
35365043-3	2022	Besides EGFR C797S mutation and EGFR amplification, a rare EGFR mutation, L718V, has been reported to confer osimertinib resistance in the literature, which is developed in about 8.0% of osimertinib-resistant NSCLC patients.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	59-63
35365042-0	2022	A non-small cell lung cancer (NSCLC) patient harboring a rare epidermal growth factor receptor (EGFR) L858R/V843I mutation complex benefited from osimertinib: a case report.	osimertinib	146-157	epidermal growth factor receptor	Homo sapiens	62-94
35365043-6	2022	Herein, we report that a lung adenocarcinoma patient with acquired EGFR L718V mutation-mediated resistance towards osimertinib derived durable response to the second-generation EGFR-TKI afatinib with a progression-free survival of 18 months and counting.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	67-71
35365042-0	2022	A non-small cell lung cancer (NSCLC) patient harboring a rare epidermal growth factor receptor (EGFR) L858R/V843I mutation complex benefited from osimertinib: a case report.	osimertinib	146-157	epidermal growth factor receptor	Homo sapiens	96-100
35365042-2	2022	The third-generation EGFR-TKI osimertinib, an irreversible TKI, is approved as a therapy for advanced NSCLC with EGFR sensitive mutations.	osimertinib	30-41	epidermal growth factor receptor	Homo sapiens	21-25
35365042-2	2022	The third-generation EGFR-TKI osimertinib, an irreversible TKI, is approved as a therapy for advanced NSCLC with EGFR sensitive mutations.	osimertinib	30-41	epidermal growth factor receptor	Homo sapiens	113-117
35365043-6	2022	Herein, we report that a lung adenocarcinoma patient with acquired EGFR L718V mutation-mediated resistance towards osimertinib derived durable response to the second-generation EGFR-TKI afatinib with a progression-free survival of 18 months and counting.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	177-181
35365042-4	2022	Herein, we present a patient diagnosed with stage IV NSCLC with an EGFR L858R/V843I mutation complex who benefited remarkably from osimertinib therapy.	osimertinib	131-142	epidermal growth factor receptor	Homo sapiens	67-71
35081725-11	2022	Osimertinib has certain efficacy in EGFR p.T790M negative NSCLC patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	36-40
35365042-13	2022	To the best of our knowledge, we report here the first known case of an NSCLC patient with a somatic EGFR L858R/V843I mutation complex who responded well to osimertinib.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	101-105
35365043-0	2022	Durable clinical benefit from afatinib in a lung adenocarcinoma patient with acquired EGFR L718V mutation-mediated resistance towards osimertinib: a case report and literature review.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	86-90
35365043-1	2022	Osimertinib, as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI), targeting EGFR exon 19 deletions, L858R, and T790M, has shown robust clinical efficacy and promising survival advantages in a subset of non-small cell lung cancer (NSCLC) patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	35-67
35343187-0	2022	Safety of osimertinib in adult patients with metastatic epidermal growth factor receptor T790M mutation-positive non-small cell lung cancer: Results from a Phase IV study in India.	osimertinib	10-21	epidermal growth factor receptor	Homo sapiens	56-88
35343187-1	2022	Background: A Phase IV, single-arm study was conducted to assess the safety of osimertinib in Indian patients with epidermal growth factor receptor (EGFR) T790M mutation-positive stage IV non-small cell lung cancer (NSCLC).	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	115-147
35343187-1	2022	Background: A Phase IV, single-arm study was conducted to assess the safety of osimertinib in Indian patients with epidermal growth factor receptor (EGFR) T790M mutation-positive stage IV non-small cell lung cancer (NSCLC).	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	149-153
35105467-2	2022	The Food and Drug Administration and European Medicines Agency have approved several inhibitors for the treatment of non-small cell lung cancer : five tyrosine kinase inhibitors targeting EGFR (erlotinib, gefitinib, afatinib, osimertinib and dacomitinib) and six tyrosine kinase inhibitors targeting ALK (crizotinib, ceritinib, alectinib, brigatinib, lorlatinib and entrectinib).	osimertinib	226-237	epidermal growth factor receptor	Homo sapiens	188-192
35399244-0	2022	Potential treatment strategy for the rare osimertinib resistant EGFR L718Q mutation.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	64-68
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	epidermal growth factor receptor	Homo sapiens	31-63
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	epidermal growth factor receptor	Homo sapiens	65-69
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
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	epidermal growth factor receptor	Homo sapiens	170-174
35189835-8	2022	CONCLUSION: First-line EGFR-TKIs seemed to be less effective in controlling and preventing brain metastasis in patients with uncommon EGFR mutations and Osimertinib was associated with promising efficacy in patients with de novo T790M mutation, which warranted further validation.	osimertinib	153-164	epidermal growth factor receptor	Homo sapiens	23-27
35076999-0	2022	First-line osimertinib treatment in a patient with lung adenocarcinoma with coexisting epidermal growth factor receptor G719S and de novo T790M mutations.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	87-119
35076999-1	2022	Osimertinib is the standard treatment for non-small cell lung cancer (NSCLC) with an active epidermal growth factor receptor (EGFR) mutation and a T790M mutation-present in cases of acquired resistance.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	92-124
35076999-1	2022	Osimertinib is the standard treatment for non-small cell lung cancer (NSCLC) with an active epidermal growth factor receptor (EGFR) mutation and a T790M mutation-present in cases of acquired resistance.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	126-130
35076999-2	2022	However, there have been no reports on the efficacy of osimertinib in patients with EGFR G719S and de novo T790M mutations.	osimertinib	55-66	epidermal growth factor receptor	Homo sapiens	84-88
35088537-2	2022	We report a case of epidermal growth factor receptor (EGFR) mutation-positive C-SCLC in an 84-year-old patient with metastatic brain lesions who developed intrinsic resistance to osimertinib, a tyrosine kinase inhibitor (TKI).	osimertinib	179-190	epidermal growth factor receptor	Homo sapiens	20-52
35088537-2	2022	We report a case of epidermal growth factor receptor (EGFR) mutation-positive C-SCLC in an 84-year-old patient with metastatic brain lesions who developed intrinsic resistance to osimertinib, a tyrosine kinase inhibitor (TKI).	osimertinib	179-190	epidermal growth factor receptor	Homo sapiens	54-58
35119858-2	2022	NSP-037 (18), an irreversible inhibitor of the L858R/T790M double-mutant EGFR (EGFRDM) using alpha-chlorofluoroacetamide (CFA) as a novel warhead, has seven times the inhibition selectivity for EGFRDM over the wild type (EGFRWT), as compared to clinically approved osimertinib (7).	osimertinib	265-276	epidermal growth factor receptor	Homo sapiens	73-77
35119858-2	2022	NSP-037 (18), an irreversible inhibitor of the L858R/T790M double-mutant EGFR (EGFRDM) using alpha-chlorofluoroacetamide (CFA) as a novel warhead, has seven times the inhibition selectivity for EGFRDM over the wild type (EGFRWT), as compared to clinically approved osimertinib (7).	osimertinib	265-276	epidermal growth factor receptor	Homo sapiens	79-85
35251316-1	2022	Introduction: Osimertinib is a third-generation EGFR tyrosine kinase inhibitor (TKI) that is approved for the use of EGFR-mutant non-small cell lung cancer (NSCLC) patients.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	117-121
35251316-11	2022	Among Osimertinib-resistant cell lines and patient-derived models, we noted acquired mutations which were potentially targetable such as NRAS p.Q61K, in which resistance could be overcome with combination of osimertinib and trametinib.	osimertinib	6-17	NRAS proto-oncogene, GTPase	Homo sapiens	137-141
35251316-11	2022	Among Osimertinib-resistant cell lines and patient-derived models, we noted acquired mutations which were potentially targetable such as NRAS p.Q61K, in which resistance could be overcome with combination of osimertinib and trametinib.	osimertinib	208-219	NRAS proto-oncogene, GTPase	Homo sapiens	137-141
35251316-12	2022	A patient-derived xenograft established from osimertinib-resistant patient revealed KRAS p.G12D mutation which could be overcome with combination of osimertinib, trametinib, and buparlisib.	osimertinib	45-56	KRAS proto-oncogene, GTPase	Homo sapiens	84-88
35251316-12	2022	A patient-derived xenograft established from osimertinib-resistant patient revealed KRAS p.G12D mutation which could be overcome with combination of osimertinib, trametinib, and buparlisib.	osimertinib	149-160	KRAS proto-oncogene, GTPase	Homo sapiens	84-88
35197546-0	2022	Ibrutinib reverses IL-6-induced osimertinib resistance through inhibition of Laminin alpha5/FAK signaling.	osimertinib	32-43	interleukin 6	Homo sapiens	19-23
35197546-0	2022	Ibrutinib reverses IL-6-induced osimertinib resistance through inhibition of Laminin alpha5/FAK signaling.	osimertinib	32-43	protein tyrosine kinase 2	Homo sapiens	77-95
35197546-1	2022	Osimertinib, a 3rd generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is the first-line standard-of-care for EGFR-mutant non-small cell lung cancer (NSCLC) patients, while acquired drug resistance will inevitably occur.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	90-94
35197546-3	2022	Here we show that clinically, plasma IL-6 level predicts osimertinib efficacy in EGFR mutant NSCLC patients.	osimertinib	57-68	interleukin 6	Homo sapiens	37-41
35197546-3	2022	Here we show that clinically, plasma IL-6 level predicts osimertinib efficacy in EGFR mutant NSCLC patients.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	81-85
35197546-4	2022	Highly increased IL-6 levels are found in patients with acquired resistance to osimertinib.	osimertinib	79-90	interleukin 6	Homo sapiens	17-21
35197546-5	2022	Addition of IL-6 or exogenous overexpression of IL-6 directly induces osimertinib resistance.	osimertinib	70-81	interleukin 6	Homo sapiens	12-16
35197546-5	2022	Addition of IL-6 or exogenous overexpression of IL-6 directly induces osimertinib resistance.	osimertinib	70-81	interleukin 6	Homo sapiens	48-52
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	137-148	laminin subunit alpha 5	Homo sapiens	19-24
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	137-148	protein tyrosine kinase 2	Homo sapiens	46-77
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	137-148	protein tyrosine kinase 2	Homo sapiens	91-112
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	137-148	protein tyrosine kinase 2	Homo sapiens	114-117
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	226-237	laminin subunit alpha 5	Homo sapiens	19-24
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	226-237	protein tyrosine kinase 2	Homo sapiens	46-77
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	226-237	protein tyrosine kinase 2	Homo sapiens	91-112
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	226-237	protein tyrosine kinase 2	Homo sapiens	114-117
35197546-6	2022	Proteomics reveals LAMA5 (Laminin alpha5) and PTK2, protein tyrosine kinase 2, also called focal adhesion kinase (FAK), are activated in osimertinib-resistant cells, and siRNA knockdown of LAMA5 or PTK2 reverses IL-6-mediated osimertinib resistance.	osimertinib	226-237	laminin subunit alpha 5	Homo sapiens	189-194
35197546-7	2022	Next, using a large-scale compound screening, we identify ibrutinib as a potent inhibitor of IL-6 and Laminin alpha5/FAK signaling, which shows synergy with osimertinib in osimertinib-resistant cells with high IL-6 levels, but not in those with low IL-6 levels.	osimertinib	157-168	interleukin 6	Homo sapiens	93-97
35197546-7	2022	Next, using a large-scale compound screening, we identify ibrutinib as a potent inhibitor of IL-6 and Laminin alpha5/FAK signaling, which shows synergy with osimertinib in osimertinib-resistant cells with high IL-6 levels, but not in those with low IL-6 levels.	osimertinib	157-168	protein tyrosine kinase 2	Homo sapiens	102-120
35197546-7	2022	Next, using a large-scale compound screening, we identify ibrutinib as a potent inhibitor of IL-6 and Laminin alpha5/FAK signaling, which shows synergy with osimertinib in osimertinib-resistant cells with high IL-6 levels, but not in those with low IL-6 levels.	osimertinib	157-168	interleukin 6	Homo sapiens	210-214
35197546-7	2022	Next, using a large-scale compound screening, we identify ibrutinib as a potent inhibitor of IL-6 and Laminin alpha5/FAK signaling, which shows synergy with osimertinib in osimertinib-resistant cells with high IL-6 levels, but not in those with low IL-6 levels.	osimertinib	157-168	interleukin 6	Homo sapiens	249-253
35197546-7	2022	Next, using a large-scale compound screening, we identify ibrutinib as a potent inhibitor of IL-6 and Laminin alpha5/FAK signaling, which shows synergy with osimertinib in osimertinib-resistant cells with high IL-6 levels, but not in those with low IL-6 levels.	osimertinib	172-183	protein tyrosine kinase 2	Homo sapiens	102-120
35197546-9	2022	Taken together, we conclude that Laminin alpha5/FAK signaling is responsible for IL-6-induced osimertinib resistance, which could be reversed by combination of ibrutinib and osimertinib.	osimertinib	94-105	protein tyrosine kinase 2	Homo sapiens	33-51
35197546-9	2022	Taken together, we conclude that Laminin alpha5/FAK signaling is responsible for IL-6-induced osimertinib resistance, which could be reversed by combination of ibrutinib and osimertinib.	osimertinib	94-105	interleukin 6	Homo sapiens	81-85
34985966-4	2022	Adjuvant osimertinib for patients with EGFR-mutant tumors, preoperative chemoimmunotherapy, and adjuvant immunotherapy could improve outcomes for selected patients with resectable lung cancer, and ongoing or planned studies leveraging biomarkers, immunotherapy, and targeted therapy may further improve survival.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	39-43
35102249-1	2022	Treatment of EGFR-mutant non-small cell lung cancer (NSCLC) with mutation-selective third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs) such as osimertinib has achieved remarkable success in the clinic.	osimertinib	153-164	epidermal growth factor receptor	Homo sapiens	13-17
35102249-1	2022	Treatment of EGFR-mutant non-small cell lung cancer (NSCLC) with mutation-selective third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs) such as osimertinib has achieved remarkable success in the clinic.	osimertinib	153-164	epidermal growth factor receptor	Homo sapiens	101-105
35102249-1	2022	Treatment of EGFR-mutant non-small cell lung cancer (NSCLC) with mutation-selective third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs) such as osimertinib has achieved remarkable success in the clinic.	osimertinib	153-164	epidermal growth factor receptor	Homo sapiens	134-138
35102249-3	2022	This study suggests a novel strategy to overcome acquired resistance to osimertinib and other third-generation EGFR-TKIs through directly targeting the intrinsic apoptotic pathway.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	111-115
35102249-4	2022	We found that osimertinib, when combined with Mcl-1 inhibition or Bax activation, synergistically decreased the survival of different osimertinib-resistant cell lines, enhanced the induction of intrinsic apoptosis, and inhibited the growth of osimertinib-resistant tumor in vivo.	osimertinib	14-25	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	46-51
35102249-4	2022	We found that osimertinib, when combined with Mcl-1 inhibition or Bax activation, synergistically decreased the survival of different osimertinib-resistant cell lines, enhanced the induction of intrinsic apoptosis, and inhibited the growth of osimertinib-resistant tumor in vivo.	osimertinib	14-25	BCL2 associated X, apoptosis regulator	Homo sapiens	66-69
35102249-5	2022	Interestingly, the triple-combination of osimertinib with Mcl-1 inhibition and Bax activation exhibited the most potent activity in decreasing the survival and inducing apoptosis of osimertinib-resistant cells and in suppressing the growth of osimertinib-resistant tumors.	osimertinib	41-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	58-63
35102249-5	2022	Interestingly, the triple-combination of osimertinib with Mcl-1 inhibition and Bax activation exhibited the most potent activity in decreasing the survival and inducing apoptosis of osimertinib-resistant cells and in suppressing the growth of osimertinib-resistant tumors.	osimertinib	41-52	BCL2 associated X, apoptosis regulator	Homo sapiens	79-82
35102249-5	2022	Interestingly, the triple-combination of osimertinib with Mcl-1 inhibition and Bax activation exhibited the most potent activity in decreasing the survival and inducing apoptosis of osimertinib-resistant cells and in suppressing the growth of osimertinib-resistant tumors.	osimertinib	182-193	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	58-63
35102249-5	2022	Interestingly, the triple-combination of osimertinib with Mcl-1 inhibition and Bax activation exhibited the most potent activity in decreasing the survival and inducing apoptosis of osimertinib-resistant cells and in suppressing the growth of osimertinib-resistant tumors.	osimertinib	182-193	BCL2 associated X, apoptosis regulator	Homo sapiens	79-82
35102249-7	2022	Hence, this study convincingly demonstrates a novel strategy for overcoming acquired resistance to osimertinib and other 3rd generation EGFR-TKIs by targeting activation of the intrinsic apoptotic pathway through Mcl-1 inhibition, Bax activation or both, warranting further clinical validation of this strategy.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	136-140
35102249-7	2022	Hence, this study convincingly demonstrates a novel strategy for overcoming acquired resistance to osimertinib and other 3rd generation EGFR-TKIs by targeting activation of the intrinsic apoptotic pathway through Mcl-1 inhibition, Bax activation or both, warranting further clinical validation of this strategy.	osimertinib	99-110	BCL2 associated X, apoptosis regulator	Homo sapiens	231-234
35399574-9	2022	This is, to our knowledge, the first report describing response to the 3rd EGFR TKI osimertinib.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	75-79
35197546-9	2022	Taken together, we conclude that Laminin alpha5/FAK signaling is responsible for IL-6-induced osimertinib resistance, which could be reversed by combination of ibrutinib and osimertinib.	osimertinib	174-185	protein tyrosine kinase 2	Homo sapiens	33-51
35197546-9	2022	Taken together, we conclude that Laminin alpha5/FAK signaling is responsible for IL-6-induced osimertinib resistance, which could be reversed by combination of ibrutinib and osimertinib.	osimertinib	174-185	interleukin 6	Homo sapiens	81-85
35144338-8	2022	Twenty-four patients developed disease progression on the first-and second EGFR-TKIs treatments, followed by treatment with the third-generation EGFR-TKIs (Osimertinib) in 12 cases, chemotherapy or anti-angiogenesis therapy in 4 cases, and the optimal supportive treatment in 8 cases.	osimertinib	156-167	epidermal growth factor receptor	Homo sapiens	145-149
35168607-0	2022	Exosomes derived from M2 type tumor-associated macrophages promote osimertinib resistance in non-small cell lung cancer through MSTRG.292666.16-miR-6836-5p-MAPK8IP3 axis.	osimertinib	67-78	microRNA 6836	Homo sapiens	144-152
35168607-0	2022	Exosomes derived from M2 type tumor-associated macrophages promote osimertinib resistance in non-small cell lung cancer through MSTRG.292666.16-miR-6836-5p-MAPK8IP3 axis.	osimertinib	67-78	mitogen-activated protein kinase 8 interacting protein 3	Homo sapiens	156-164
35168607-1	2022	BACKGROUND: Osimertinib resistance limits the treatment of epidermal growth factor receptor-(EGFR)-mutated non-small-cell lung carcinoma (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	59-91
35168607-1	2022	BACKGROUND: Osimertinib resistance limits the treatment of epidermal growth factor receptor-(EGFR)-mutated non-small-cell lung carcinoma (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	93-97
35208635-2	2022	Only a few studies have reported the occurrence of heart failure following the administration of osimertinib, a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor for EGFR mutation-positive advanced non-small cell lung cancer.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	129-161
35208635-2	2022	Only a few studies have reported the occurrence of heart failure following the administration of osimertinib, a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor for EGFR mutation-positive advanced non-small cell lung cancer.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	163-167
35208635-2	2022	Only a few studies have reported the occurrence of heart failure following the administration of osimertinib, a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor for EGFR mutation-positive advanced non-small cell lung cancer.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	199-203
35144642-11	2022	Knock-down of METTL7B by siRNA re-sensitized LUAD cells to gefitinib and osimertinib both in vitro and in vivo.	osimertinib	73-84	methyltransferase like 7B	Mus musculus	14-21
35044639-0	2022	Next-Generation Sequencing Liquid Biopsy-Guided Osimertinib Rechallenge in EGFR-Mutated Advanced Non-Small-Cell Lung Cancer Patients.	osimertinib	48-59	epidermal growth factor receptor	Homo sapiens	75-79
35159036-7	2022	The expert panel analysis concluded: (1) osimertinib 80 mg/day is recommended as a first-line treatment for older patients with the EGFR mutation; (2) full-dose first generation TKI, such as erlotinib or gefitinib, is feasible; (3) ALK and ROS1 rearrangement studies including older patients were too scarce to conclude on any definitive recommendations; and (4) given the actual data, TKI should be prescribed as monotherapy.	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	132-136
35159036-7	2022	The expert panel analysis concluded: (1) osimertinib 80 mg/day is recommended as a first-line treatment for older patients with the EGFR mutation; (2) full-dose first generation TKI, such as erlotinib or gefitinib, is feasible; (3) ALK and ROS1 rearrangement studies including older patients were too scarce to conclude on any definitive recommendations; and (4) given the actual data, TKI should be prescribed as monotherapy.	osimertinib	41-52	ALK receptor tyrosine kinase	Homo sapiens	232-235
35159036-7	2022	The expert panel analysis concluded: (1) osimertinib 80 mg/day is recommended as a first-line treatment for older patients with the EGFR mutation; (2) full-dose first generation TKI, such as erlotinib or gefitinib, is feasible; (3) ALK and ROS1 rearrangement studies including older patients were too scarce to conclude on any definitive recommendations; and (4) given the actual data, TKI should be prescribed as monotherapy.	osimertinib	41-52	ROS proto-oncogene 1, receptor tyrosine kinase	Homo sapiens	240-244
35093869-7	2022	Expression of the anti-apoptotic gene PLK1 was down-regulated in PC-9 and H1975 exposed to osimertinib+ pemetrexed, whereas it was up-regulated in resistant cells.	osimertinib	91-102	polo like kinase 1	Homo sapiens	38-42
35093869-9	2022	CONCLUSION: Blocking PLK1 contributes to mediating the synergistic anti-proliferative effect of osimertinib+pemetrexed.	osimertinib	96-107	polo like kinase 1	Homo sapiens	21-25
35093869-10	2022	PLK1 over-expression may be a critical mechanism for acquired resistance to osimertinib+pemetrexed.	osimertinib	76-87	polo like kinase 1	Homo sapiens	0-4
35044639-1	2022	BACKGROUND AND OBJECTIVES: Osimertinib is considered the treatment of choice for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC) who progressed on EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	95-127
35044639-1	2022	BACKGROUND AND OBJECTIVES: Osimertinib is considered the treatment of choice for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC) who progressed on EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	129-133
35044639-1	2022	BACKGROUND AND OBJECTIVES: Osimertinib is considered the treatment of choice for patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC) who progressed on EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	205-209
35127465-5	2021	Patients who received osimertinib after developing LM (n = 35) had a significantly higher rate of LM disease control (p = 0.008) and significantly longer overall survival (15.0 versus 6.0 months; hazard ratio (HR), 2.4292; 95% CI, 1.234-4.779; p = 0.045) than those who received previous generations of EGFR tyrosine kinase inhibitors (TKIs) or other localized therapies (n = 6).	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	303-307
35194503-0	2022	Treatment of Choroidal Metastasis from Epidermal Growth Factor Mutant Non-Small Cell Lung Cancer with First-line Osimertinib Therapy.	osimertinib	113-124	epidermal growth factor	Homo sapiens	39-62
35194503-1	2022	Purpose: To illustrate the regression of a metastatic lesion through ophthalmic imaging and correlating findings with standard chest imaging and treatment with osimertinib, an oral chemotherapy agent specific to Epidermal Growth Factor Receptor + Non-small Cell Lung Cancer (EGFR+ NSCLC).	osimertinib	160-171	epidermal growth factor receptor	Homo sapiens	212-244
35194503-1	2022	Purpose: To illustrate the regression of a metastatic lesion through ophthalmic imaging and correlating findings with standard chest imaging and treatment with osimertinib, an oral chemotherapy agent specific to Epidermal Growth Factor Receptor + Non-small Cell Lung Cancer (EGFR+ NSCLC).	osimertinib	160-171	epidermal growth factor receptor	Homo sapiens	275-279
35194503-6	2022	Conclusion: After the initiation of osimertinib, ophthalmic and computed tomography imaging highlighted the regression of the ocular metastatic disease and primary malignancy, respectively.Osimertinib is an effective first-line treatment of EGFR+ NSCLC and corresponding metastatic sites.	osimertinib	189-200	epidermal growth factor receptor	Homo sapiens	241-245
35112017-10	2022	Osimertinib can be beneficial for patients with EGFR-positive lung cancer for both ocular and systemic control.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	48-52
35127465-7	2021	Conclusions: Our study provides real-world clinical evidence that patients with EGFR-mutated NSCLC diagnosed with LM who developed LM had better clinical outcomes with osimertinib therapy.	osimertinib	168-179	epidermal growth factor receptor	Homo sapiens	80-84
35038824-1	2022	Purpose: This study was to evaluate anti-tumor efficacy of osimertinib in patients positive for acquired epidermal growth factor receptor (EGFR) T790M mutation in liquid biopsy using plasma, bronchoalveolar lavage fluid (BALF) or bronchial washing fluid (BWF), and pleural effusion.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	105-137
35038824-1	2022	Purpose: This study was to evaluate anti-tumor efficacy of osimertinib in patients positive for acquired epidermal growth factor receptor (EGFR) T790M mutation in liquid biopsy using plasma, bronchoalveolar lavage fluid (BALF) or bronchial washing fluid (BWF), and pleural effusion.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	139-143
35038824-11	2022	Conclusion: Osimertinib showed favorable efficacy in lung cancer patients with acquired resistance to prior EGFR-TKI therapies, who screened positive for harboring T790M mutation detected from cell free DNA extracted from plasma, BALF/BWF, and pleural effusion.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	108-112
35049698-5	2022	Preclinical and clinical data, excluding de novoEGFR exon 20 p.T790M compound mutations, show good responses with EGFR tyrosine kinase inhibitors (TKIs) (combined common mutations: response rate (RR) >= 75% with either first- or second-generation TKIs; combined common plus uncommon: RR 40-80% and 100% with first-generation TKIs and afatinib, respectively; combined uncommon: RR 20-70%, ~80% and ~75% with first-generation TKIs, afatinib and osimertinib, respectively).	osimertinib	443-454	epidermal growth factor receptor	Homo sapiens	114-118
35173881-1	2022	OBJECTIVE: To explore the efficacy and mechanism of osimertinib combined with bevacizumab in treating postoperative epidermal growth factor receptor (EGFR) positive stage II-IIIA lung adenocarcinoma.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	116-148
35173881-1	2022	OBJECTIVE: To explore the efficacy and mechanism of osimertinib combined with bevacizumab in treating postoperative epidermal growth factor receptor (EGFR) positive stage II-IIIA lung adenocarcinoma.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	150-154
35013118-9	2022	The sensitivity of lung cancer cells to gefitinib/osimertinib is highly increased in the presence of the selective NK1R antagonist aprepitant.	osimertinib	50-61	tachykinin receptor 1	Mus musculus	115-119
35106279-0	2022	Effective treatment of pulmonary adenocarcinoma harboring triple EGFR mutations of L858R, T790M, cis-G796s/cis-C797s by osimertinib, brigatinib, and bevacizumab combination therapy: A case report.	osimertinib	120-131	epidermal growth factor receptor	Homo sapiens	65-69
35106279-3	2022	Osimertinib, a 3rd EGFR-TKI, commonly was used in patients who were resistant to early-generation EGFR-TKIs carrying T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	19-23
34983748-1	2022	INTRODUCTION: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is widely used as the first-line treatment for EGFR mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	46-78
35106279-3	2022	Osimertinib, a 3rd EGFR-TKI, commonly was used in patients who were resistant to early-generation EGFR-TKIs carrying T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	98-102
35106279-5	2022	Herein, we report an effective treatment for a case of advanced pulmonary adenocarcinoma patient with triple EGFR mutations of L858R/T790M/cis-C797S and L858R/T790M/cis-G796S by the combination therapy of osimertinib, brigatinib, and bevacizumab after the combination of brigatinib and cetuximab failed.	osimertinib	205-216	epidermal growth factor receptor	Homo sapiens	109-113
35070958-7	2021	With the help of the readers of NKAP and HNRNPA2B1, the cluster mediated m6A formation on pri-Let-7b processing increased the mature Let-7b, the key player in suppressing Notch signaling and re-captivating Osimertinib treatment.	osimertinib	206-217	NFKB activating protein	Homo sapiens	32-36
35070958-7	2021	With the help of the readers of NKAP and HNRNPA2B1, the cluster mediated m6A formation on pri-Let-7b processing increased the mature Let-7b, the key player in suppressing Notch signaling and re-captivating Osimertinib treatment.	osimertinib	206-217	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	41-50
35070958-7	2021	With the help of the readers of NKAP and HNRNPA2B1, the cluster mediated m6A formation on pri-Let-7b processing increased the mature Let-7b, the key player in suppressing Notch signaling and re-captivating Osimertinib treatment.	osimertinib	206-217	microRNA let-7b	Homo sapiens	94-100
35070958-7	2021	With the help of the readers of NKAP and HNRNPA2B1, the cluster mediated m6A formation on pri-Let-7b processing increased the mature Let-7b, the key player in suppressing Notch signaling and re-captivating Osimertinib treatment.	osimertinib	206-217	microRNA let-7b	Homo sapiens	133-139
34983748-1	2022	INTRODUCTION: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is widely used as the first-line treatment for EGFR mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	80-84
34983748-1	2022	INTRODUCTION: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is widely used as the first-line treatment for EGFR mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	166-170
34459459-1	2022	Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor used to treat non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-66
34261918-0	2022	Osimertinib is an effective epidermal growth factor receptor-tyrosine kinase inhibitor choice for lung cancer with epidermal growth factor receptor exon 18-25 kinase domain duplication: report of two cases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	28-60
34261918-8	2022	Here, we describe osimertinib as an effective therapy for EGFR-KDD positive lung adenocarcinoma and thereby provide a new alternative for further treatment following resistance to first- and second-generation EGFR-TKIs.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	58-62
34261918-8	2022	Here, we describe osimertinib as an effective therapy for EGFR-KDD positive lung adenocarcinoma and thereby provide a new alternative for further treatment following resistance to first- and second-generation EGFR-TKIs.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	209-213
34486539-0	2022	Complete remission in leptomeningeal metastasis of NSCLC with rare EGFR-SEPT14 fusion treated with osimertinib combined with intrathecal chemotherapy with pemetrexed.	osimertinib	99-110	septin 14	Homo sapiens	72-78
34459459-1	2022	Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor used to treat non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	68-72
34486539-0	2022	Complete remission in leptomeningeal metastasis of NSCLC with rare EGFR-SEPT14 fusion treated with osimertinib combined with intrathecal chemotherapy with pemetrexed.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	67-71
35242623-0	2022	TP53 co-mutations as an independent prognostic factor in 2nd and further line therapy-EGFR mutated non-small cell lung cancer IV patients treated with osimertinib.	osimertinib	151-162	tumor protein p53	Homo sapiens	0-4
34486539-10	2022	This study presented the first case of NSCLC-LM harboring particular EGFR-SEPT14 fusions, who showed a durable response to osimertinib and intrathecal pemetrexed, providing a potential therapeutic option for NSCLC-LM patients with this particular mutation.	osimertinib	123-134	epidermal growth factor receptor	Homo sapiens	69-73
34486539-10	2022	This study presented the first case of NSCLC-LM harboring particular EGFR-SEPT14 fusions, who showed a durable response to osimertinib and intrathecal pemetrexed, providing a potential therapeutic option for NSCLC-LM patients with this particular mutation.	osimertinib	123-134	septin 14	Homo sapiens	74-80
34520433-2	2022	Third-generation EGFR-TKIs, represented by osimertinib, have been approved to overcome the EGFR T790M mutation in patients who are resistant to first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	17-21
34520433-2	2022	Third-generation EGFR-TKIs, represented by osimertinib, have been approved to overcome the EGFR T790M mutation in patients who are resistant to first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	91-95
34074804-7	2022	Recently developed third-generation irreversible EGFR TKIs (osimertinib and lazertinib) are selective toward driving mutations and the T790M mutation, while sparing wildtype EGFR activity.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	174-178
35261905-3	2022	Here, we describe a case to report the efficacy of afatinib in an EGFR-mutated NSCLC patient with early progression to first-line osimertinib treatment.	osimertinib	130-141	epidermal growth factor receptor	Homo sapiens	66-70
35261905-10	2022	NGS revealed no specific gene mutations causing resistance to osimertinib except for the EGFR L858R mutation; however, his tumor had a relatively high tumor mutational burden.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	89-93
35201951-1	2022	OBJECTIVES: Osimertinib has exhibited promising central nervous system (CNS) efficacy in Epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC) patients.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	89-121
35201951-1	2022	OBJECTIVES: Osimertinib has exhibited promising central nervous system (CNS) efficacy in Epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC) patients.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	123-127
35201951-11	2022	CONCLUSION: For EGFR-mutated NSCLC patients with only intracranial progressions after previous TKI treatments, osimertinib is a promising treatment option regardless of T790M mutational status from plasma genotyping.	osimertinib	111-122	epidermal growth factor receptor	Homo sapiens	16-20
34669648-2	2022	RECENT FINDINGS: Osimertinib has shown favorable efficacy on second-line and first-line treatments in EGFR-mutant advanced nonsmall cell lung cancer (NSCLC).	osimertinib	17-28	epidermal growth factor receptor	Homo sapiens	102-106
35156036-1	2022	Background: Osimertinib is selective for both epidermal growth factor receptor (EGFR)-tyrosine-kinase inhibitor (TKI) sensitizing and Thr790Met mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-78
35156036-1	2022	Background: Osimertinib is selective for both epidermal growth factor receptor (EGFR)-tyrosine-kinase inhibitor (TKI) sensitizing and Thr790Met mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	80-84
35005653-1	2022	Osimertinib is the standard of care for the first-line treatment of EGFR-mutated NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	68-72
35005653-4	2022	Care should be taken in administering osimertinib concurrently with other medications metabolized by the CYP3A4 system, and ongoing work to identify patients at risk for severe reactions is necessary.	osimertinib	38-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-111
35005656-3	2022	Here, we present a case of spontaneous transformation from EGFR-mutant LUAD with loss of p53 and RB to EGFR expression-positive SCLC and neuroendocrine-differentiated LUAD, which was successfully treated with osimertinib.	osimertinib	209-220	epidermal growth factor receptor	Homo sapiens	59-63
35005656-3	2022	Here, we present a case of spontaneous transformation from EGFR-mutant LUAD with loss of p53 and RB to EGFR expression-positive SCLC and neuroendocrine-differentiated LUAD, which was successfully treated with osimertinib.	osimertinib	209-220	tumor protein p53	Homo sapiens	89-92
35005656-3	2022	Here, we present a case of spontaneous transformation from EGFR-mutant LUAD with loss of p53 and RB to EGFR expression-positive SCLC and neuroendocrine-differentiated LUAD, which was successfully treated with osimertinib.	osimertinib	209-220	epidermal growth factor receptor	Homo sapiens	103-107
35242623-12	2022	Conclusions: TP53 mt+ have a negative impact on PFS and OS in a group of patients carrying a sensitizing EGFR mt+ and a T790M resistance mutation treated with Osimertinib.	osimertinib	159-170	tumor protein p53	Homo sapiens	13-17
35242623-12	2022	Conclusions: TP53 mt+ have a negative impact on PFS and OS in a group of patients carrying a sensitizing EGFR mt+ and a T790M resistance mutation treated with Osimertinib.	osimertinib	159-170	epidermal growth factor receptor	Homo sapiens	105-109
34053372-3	2021	Most recently, the FDA granted approval for the adjuvant treatment of patients with early stage mutated EGFR NSCLC after tumor resection.Areas CoveredThis drug discovery case history focuses on the key studies that led to the preclinical discovery and development of osimertinib.	osimertinib	267-278	epidermal growth factor receptor	Homo sapiens	104-108
33710523-12	2021	Only a third receive osimertinib upon progression on 1G/2G EGFR-TKIs.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	59-63
33855865-4	2021	However, while the third-generation EGFR TKI, osimertinib, confers significant overall survival benefit over erlotinib/gefitinib in non-Asians, this is not apparent in Asians, particularly in countries like Japan with well-resourced healthcare.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	36-40
33939301-0	2021	Exosome-derived miR-210 involved in resistance to osimertinib and epithelial-mesenchymal transition in EGFR mutant non-small cell lung cancer cells.	osimertinib	50-61	microRNA 210	Homo sapiens	16-23
33939301-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) approved for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	106-110
33939301-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) approved for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	160-164
33939301-5	2021	We evaluated the profiles of exosomal miRNA associated with resistance to osimertinib in EGFR-mutant NSCLC cells.	osimertinib	74-85	epidermal growth factor receptor	Homo sapiens	89-93
33939301-10	2021	CONCLUSIONS: Exosomal miR-210-3p may play a crucial role in resistance to osimertinib in the tumor microenvironment of EGFR-mutant NSCLC.	osimertinib	74-85	epidermal growth factor receptor	Homo sapiens	119-123
31935159-0	2021	Osimertinib in patients with advanced/metastatic epidermal growth factor receptor T790M mutation-positive non-small cell lung cancer - the Belgian ASTRIS data.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	49-81
31935159-1	2021	Objectives: The aim of ASTRIS, a real-world study, was to assess the safety and efficacy of osimertinib in patients with locally advanced or metastatic (stage IIIB-IV) epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC) who had received prior EGFR-tyrosine kinase inhibitor (TKI) therapy.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	168-200
31935159-1	2021	Objectives: The aim of ASTRIS, a real-world study, was to assess the safety and efficacy of osimertinib in patients with locally advanced or metastatic (stage IIIB-IV) epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC) who had received prior EGFR-tyrosine kinase inhibitor (TKI) therapy.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	202-206
34053372-4	2021	The authors focus on published preclinical studies by scientists from AstraZeneca and highlight key events in the clinical development.Expert opinionAlthough eventually compromised by the cellular plasticity of the tumor and the inevitable acquisition of drug resistance through the use of osimertinib, its key role in the treatment of NSCLC with specific EGFR mutations will be maintained in the near future.	osimertinib	290-301	epidermal growth factor receptor	Homo sapiens	356-360
34058255-0	2021	Clinical value of upfront cranial radiotherapy in osimertinib-treated EGFR-mutant non-small-cell lung cancer with brain metastases.	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	70-74
33829270-0	2021	A novel osimertinib-resistant human lung adenocarcinoma cell line harbouring mutant EGFR and activated IGF1R.	osimertinib	8-19	epidermal growth factor receptor	Homo sapiens	84-88
33829270-0	2021	A novel osimertinib-resistant human lung adenocarcinoma cell line harbouring mutant EGFR and activated IGF1R.	osimertinib	8-19	insulin like growth factor 1 receptor	Homo sapiens	103-108
33829270-1	2021	OBJECTIVE: A third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is the standard treatment for patients with non-small cell lung cancer harbouring mutant EGFR.	osimertinib	103-114	epidermal growth factor receptor	Homo sapiens	30-62
33829270-1	2021	OBJECTIVE: A third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is the standard treatment for patients with non-small cell lung cancer harbouring mutant EGFR.	osimertinib	103-114	epidermal growth factor receptor	Homo sapiens	64-68
33829270-1	2021	OBJECTIVE: A third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is the standard treatment for patients with non-small cell lung cancer harbouring mutant EGFR.	osimertinib	103-114	epidermal growth factor receptor	Homo sapiens	205-209
33829270-2	2021	Unfortunately, these patients inevitably acquire resistance to EGFR-TKI therapies, including osimertinib.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	63-67
33829270-10	2021	ABC-31 cells were resistant to EGFR-TKIs, including osimertinib.	osimertinib	52-63	ATP binding cassette subfamily C member 3	Homo sapiens	0-6
33829270-13	2021	She was re-administered osimertinib since EGFR-TKIs and IGF1R inhibitor combination therapy was impossible in clinical practice.	osimertinib	24-35	insulin like growth factor 1 receptor	Homo sapiens	56-61
34058255-1	2021	BACKGROUND: As a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib has a powerful ability to penetrate the blood-brain barrier and a high potency for controlling brain metastases (BMs) from EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	34-66
34058255-1	2021	BACKGROUND: As a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib has a powerful ability to penetrate the blood-brain barrier and a high potency for controlling brain metastases (BMs) from EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	68-72
34058255-1	2021	BACKGROUND: As a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib has a powerful ability to penetrate the blood-brain barrier and a high potency for controlling brain metastases (BMs) from EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	242-246
34048974-1	2021	Osimertinib (OSI) is the first FDA-approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	61-93
34048974-1	2021	Osimertinib (OSI) is the first FDA-approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	95-99
34048974-12	2021	STATEMENT OF SIGNIFICANCE: : Osimertinib (OSI) is the first FDA-approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	90-122
34048974-12	2021	STATEMENT OF SIGNIFICANCE: : Osimertinib (OSI) is the first FDA-approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	124-128
34044055-0	2021	In vitro inhibition of human UDP-glucuronosyltransferase (UGT) 1A1 by osimertinib, and prediction of in vivo drug-drug interactions.	osimertinib	70-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-66
34059353-7	2021	A high ratio of Her1 heterodimers to homodimers was associated with poor progression-free survival in NSCLC patients treated with osimertinib.	osimertinib	130-141	epidermal growth factor receptor	Homo sapiens	16-20
34044055-1	2021	Osimertinib is the only third-generation epidermal growth factor receptor tyrosine-kinase inhibitor (EGFR-TKI) approved by Food and Drug Administration (FDA).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	101-105
34044055-2	2021	This study aimed to know the inhibitory effect of osimertinib on human UDP-glucosyltransferases (UGTs) and human liver microsomes (HLMs), as well as to identify its potential to cause drug-drug interaction (DDI) arising from the modulation of UGT activity.	osimertinib	50-61	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	97-100
34044055-3	2021	High inhibitory effect of osimertinib was shown towards UGT1A1, 1A3, 1A6, 1A7, 1A8, 1A10, 2B7 and 2B15.	osimertinib	26-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
34044055-4	2021	Especially, osimertinib exhibited competitive inhibition against UGT1A1 with a Ki,u of 0.87 +- 0.12 muM.	osimertinib	12-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
34044055-6	2021	Results from quantitative prediction study indicated that osimertinib administered at 80 mg/day may result in a 4.83% increase in the AUC of drugs mainly metabolized by UGT1A1, implying low risk of DDI via liver metabolism.	osimertinib	58-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
34044055-8	2021	The effects of osimertinib on intestinal UGT should be paid more attention on to avoid unnecessary clinical DDI risks.	osimertinib	15-26	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	41-44
33992097-0	2021	ID1 mediates resistance to osimertinib in EGFR T790M-positive non-small cell lung cancer through epithelial-mesenchymal transition.	osimertinib	27-38	inhibitor of DNA binding 1, HLH protein	Homo sapiens	0-3
34001994-8	2021	Osimertinib stimulated dynamic, yet wide-ranging interferon (IFN) program regulation in EGFR mutant cell lines.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	88-92
33992097-0	2021	ID1 mediates resistance to osimertinib in EGFR T790M-positive non-small cell lung cancer through epithelial-mesenchymal transition.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	42-46
33992097-2	2021	However, the effect of ID1 expression on osimertinib resistance in EGFR T790M-positive NSCLC is not clear.	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	67-71
33992097-11	2021	ID1 expression levels was closely related to E-cadherin and vimentin in both osimertinib-sensitive and resistant cells.	osimertinib	77-88	inhibitor of DNA binding 1, HLH protein	Homo sapiens	0-3
33992097-11	2021	ID1 expression levels was closely related to E-cadherin and vimentin in both osimertinib-sensitive and resistant cells.	osimertinib	77-88	cadherin 1	Homo sapiens	45-55
33992097-11	2021	ID1 expression levels was closely related to E-cadherin and vimentin in both osimertinib-sensitive and resistant cells.	osimertinib	77-88	vimentin	Homo sapiens	60-68
33992097-14	2021	Our study suggests that ID1 may induce EMT in EGFR T790M-positive NSCLC, which mediates drug resistance of osimertinib.	osimertinib	107-118	inhibitor of DNA binding 1, HLH protein	Homo sapiens	24-27
33992097-14	2021	Our study suggests that ID1 may induce EMT in EGFR T790M-positive NSCLC, which mediates drug resistance of osimertinib.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	46-50
33992097-15	2021	CONCLUSIONS: Our study revealed the mechanism of ID1 mediated resistance to osimertinib in EGFR T790M-positive NSCLC through EMT, which may provide new ideas and methods for the treatment of EGFR mutated NSCLC after osimertinib resistance.	osimertinib	76-87	inhibitor of DNA binding 1, HLH protein	Homo sapiens	49-52
33992097-15	2021	CONCLUSIONS: Our study revealed the mechanism of ID1 mediated resistance to osimertinib in EGFR T790M-positive NSCLC through EMT, which may provide new ideas and methods for the treatment of EGFR mutated NSCLC after osimertinib resistance.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	91-95
33992097-15	2021	CONCLUSIONS: Our study revealed the mechanism of ID1 mediated resistance to osimertinib in EGFR T790M-positive NSCLC through EMT, which may provide new ideas and methods for the treatment of EGFR mutated NSCLC after osimertinib resistance.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	191-195
33992097-15	2021	CONCLUSIONS: Our study revealed the mechanism of ID1 mediated resistance to osimertinib in EGFR T790M-positive NSCLC through EMT, which may provide new ideas and methods for the treatment of EGFR mutated NSCLC after osimertinib resistance.	osimertinib	216-227	inhibitor of DNA binding 1, HLH protein	Homo sapiens	49-52
33992097-15	2021	CONCLUSIONS: Our study revealed the mechanism of ID1 mediated resistance to osimertinib in EGFR T790M-positive NSCLC through EMT, which may provide new ideas and methods for the treatment of EGFR mutated NSCLC after osimertinib resistance.	osimertinib	216-227	epidermal growth factor receptor	Homo sapiens	91-95
33988036-0	2021	Real-world data on treatment outcomes in EGFR-mutant non-small-cell lung cancer patients receiving osimertinib in second or further lines.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	41-45
33988036-1	2021	Aims: This study describes real-world outcomes of pretreated EGFR T790M-positive (T790M+) advanced non-small-cell lung cancer patients progressing after first- or second-generation tyrosine kinase inhibitors and receiving osimertinib, compared with T790M-negative (T790M-) patients.	osimertinib	222-233	epidermal growth factor receptor	Homo sapiens	61-65
33993094-0	2021	Weekly osimertinib dosing prevents EGFR mutant tumor cells destined to home mouse lungs.	osimertinib	7-18	epidermal growth factor receptor	Mus musculus	35-39
33982444-2	2021	METHODS: Patients with NSCLC who progressed after treatment with EGFR-TKI, and with EGFR T790 M detected by an approved companion diagnostic test (cobas  ), were treated with osimertinib.	osimertinib	175-186	epidermal growth factor receptor	Homo sapiens	84-88
33982444-12	2021	CONCLUSIONS: NGS of ctDNA could be a promising method for predicting osimertinib efficacy in patients with advanced NSCLC harboring EGFR T790 M.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	132-136
33975616-0	2021	Osimertinib alone as second-line treatment for brain metastases (BM) control may be more limited than for non-BM in advanced NSCLC patients with an acquired EGFR T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	157-161
33975616-1	2021	BACKGROUND: This study was designed to investigate the difference between brain metastases (BM) and non-brain metastases (non-BM) treated by osimertinib in advanced patients with an acquired EGFR T790M mutation after obtaining first-generation EGFR-TKI resistance.	osimertinib	141-152	epidermal growth factor receptor	Homo sapiens	191-195
33975616-1	2021	BACKGROUND: This study was designed to investigate the difference between brain metastases (BM) and non-brain metastases (non-BM) treated by osimertinib in advanced patients with an acquired EGFR T790M mutation after obtaining first-generation EGFR-TKI resistance.	osimertinib	141-152	epidermal growth factor receptor	Homo sapiens	244-248
33975616-14	2021	CONCLUSIONS: In advanced patients with an acquired EGFR T790M mutation after obtaining first-generation EGFR-TKI resistance, osimertinib may be more limited in its control in BM than in non-BM.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	51-55
33975616-14	2021	CONCLUSIONS: In advanced patients with an acquired EGFR T790M mutation after obtaining first-generation EGFR-TKI resistance, osimertinib may be more limited in its control in BM than in non-BM.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	104-108
33977730-0	2021	A non-small cell lung cancer (NSCLC) patient with leptomeningeal metastasis harboring rare epidermal growth factor receptor (EGFR) mutations G719S and L861Q benefited from doubling dosage of osimertinib: a case report.	osimertinib	191-202	epidermal growth factor receptor	Homo sapiens	91-123
33977730-0	2021	A non-small cell lung cancer (NSCLC) patient with leptomeningeal metastasis harboring rare epidermal growth factor receptor (EGFR) mutations G719S and L861Q benefited from doubling dosage of osimertinib: a case report.	osimertinib	191-202	epidermal growth factor receptor	Homo sapiens	125-129
33977730-2	2021	Osimertinib, an irreversible tyrosine kinase inhibitor, is approved as a therapy for advanced NSCLC with epidermal growth factor receptor (EGFR) mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	105-137
33977730-2	2021	Osimertinib, an irreversible tyrosine kinase inhibitor, is approved as a therapy for advanced NSCLC with epidermal growth factor receptor (EGFR) mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	139-143
33977730-3	2021	However, the efficacy and optimal dosage of osimertinib in the treatment of NSCLC patients with LM who harbor uncommon EGFR mutations have yet to be fully investigated.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	119-123
33977730-4	2021	Herein, we report a case of an advanced NSCLC patient with LM carrying EGFR G719S and L861Q, who was successfully treated by osimertinib at 160 mg.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	71-75
33977730-12	2021	To our knowledge, this study provides the first clinical evidence that the administration of osimertinib at 160 mg once daily can achieve an encouraging, durable response in an NSCLC patient with LM carrying EGFR G719S and L861Q.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	208-212
33953280-0	2021	The ratio of T790M to EGFR-activating mutation predicts response of osimertinib in 1st or 2nd generation EGFR-TKI-refractory NSCLC.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	22-26
34026599-0	2021	Resistance Profile of Osimertinib in Pre-treated Patients With EGFR T790M-Mutated Non-small Cell Lung Cancer.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	63-67
34026599-1	2021	Background: Osimertinib efficacy in pre-treated patients with epidermal growth factor receptor (EGFR) T790M-mutated non-small cell lung cancer (NSCLC) has been demonstrated in clinical trials, but real-world data, particularly regarding resistance profile, remains limited.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	62-94
34026599-1	2021	Background: Osimertinib efficacy in pre-treated patients with epidermal growth factor receptor (EGFR) T790M-mutated non-small cell lung cancer (NSCLC) has been demonstrated in clinical trials, but real-world data, particularly regarding resistance profile, remains limited.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	96-100
34026823-1	2021	Currently, there are limited treatment options for patients who developed resistance to osimertinib, a third-generation epidermal growth factor receptor (EGFR) inhibitor.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	120-152
34026823-1	2021	Currently, there are limited treatment options for patients who developed resistance to osimertinib, a third-generation epidermal growth factor receptor (EGFR) inhibitor.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	154-158
34026823-3	2021	This multicenter, retrospective study aimed to evaluate the efficacy of the combination treatment with apatinib and osimertinib in 39 patients with EGFR-mutant non-small cell lung carcinoma (NSCLC) who developed osimertinib resistance.	osimertinib	116-127	epidermal growth factor receptor	Homo sapiens	148-152
34026823-3	2021	This multicenter, retrospective study aimed to evaluate the efficacy of the combination treatment with apatinib and osimertinib in 39 patients with EGFR-mutant non-small cell lung carcinoma (NSCLC) who developed osimertinib resistance.	osimertinib	212-223	epidermal growth factor receptor	Homo sapiens	148-152
34026823-12	2021	The spectrum of resistance to osimertinib mechanisms included c-mesenchymal-epithelial transition factor (c-Met) amplification, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) gain-of-function mutation, phosphatase and tensin homolog (PTEN) loss-of-function mutation, Erb-B2 receptor tyrosine kinase 2 (ERBB2) amplification, and insulin-like growth factor 1 receptor (IGF1R) mutation.	osimertinib	30-41	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-104
34026823-14	2021	The combination of apatinib and osimertinib improved the ORR and the DCR of patients with osimertinib-refractory EGFR-positive NSCLC, thus making it a reasonable treatment choice after the development of osimertinib resistance.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	113-117
34026823-14	2021	The combination of apatinib and osimertinib improved the ORR and the DCR of patients with osimertinib-refractory EGFR-positive NSCLC, thus making it a reasonable treatment choice after the development of osimertinib resistance.	osimertinib	90-101	epidermal growth factor receptor	Homo sapiens	113-117
34026823-14	2021	The combination of apatinib and osimertinib improved the ORR and the DCR of patients with osimertinib-refractory EGFR-positive NSCLC, thus making it a reasonable treatment choice after the development of osimertinib resistance.	osimertinib	90-101	epidermal growth factor receptor	Homo sapiens	113-117
33953280-0	2021	The ratio of T790M to EGFR-activating mutation predicts response of osimertinib in 1st or 2nd generation EGFR-TKI-refractory NSCLC.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	105-109
33976888-4	2021	We treated two elderly patients with de novo EGFR T790M mutations with osimertinib as the first-line therapy.	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	45-49
33976888-0	2021	Long-term response to osimertinib in elderly patients with lung adenocarcinoma harbouring de novo EGFR T790M: a case report and literature review.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	98-102
33976888-1	2021	Osimertinib is a potent and irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that selectively acts on both EGFR-sensitive and EGFR T790M-resistant mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	41-73
33976888-1	2021	Osimertinib is a potent and irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that selectively acts on both EGFR-sensitive and EGFR T790M-resistant mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	75-79
33976888-1	2021	Osimertinib is a potent and irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that selectively acts on both EGFR-sensitive and EGFR T790M-resistant mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	143-147
33976888-1	2021	Osimertinib is a potent and irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that selectively acts on both EGFR-sensitive and EGFR T790M-resistant mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	143-147
33976888-2	2021	Patients with pre-treatment EGFR T790M mutations (de novo EGFR T790M) respond poorly to existing EGFR-TKIs, whereas osimertinib has positive effects.	osimertinib	116-127	epidermal growth factor receptor	Homo sapiens	28-32
33730350-8	2021	While further research, including clinical trial data, is needed, real-world data have also demonstrated the feasibility of sequential afatinib followed by the third-generation TKI osimertinib in T790M-positive EGFR mutation-positive patients, which showed longer overall survival.	osimertinib	181-192	epidermal growth factor receptor	Homo sapiens	211-215
33544933-2	2021	The C797S mutation in the epidermal growth factor receptor (EGFR) confers resistance to osimertinib, a third-generation EGFR-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	26-58
33544933-2	2021	The C797S mutation in the epidermal growth factor receptor (EGFR) confers resistance to osimertinib, a third-generation EGFR-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	60-64
33544933-2	2021	The C797S mutation in the epidermal growth factor receptor (EGFR) confers resistance to osimertinib, a third-generation EGFR-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	120-124
33544933-2	2021	The C797S mutation in the epidermal growth factor receptor (EGFR) confers resistance to osimertinib, a third-generation EGFR-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	88-99	TXK tyrosine kinase	Homo sapiens	125-140
33544933-2	2021	The C797S mutation in the epidermal growth factor receptor (EGFR) confers resistance to osimertinib, a third-generation EGFR-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	120-124
33744716-1	2021	INTRODUCTION: Although osimertinib overcomes the T790M mutation acquired after traditional epidermal growth factor receptor (EGFR) gene tyrosine kinase inhibitor (TKI) treatment, resistance to osimertinib eventually occurs.	osimertinib	23-34	epidermal growth factor receptor	Homo sapiens	91-123
33744716-1	2021	INTRODUCTION: Although osimertinib overcomes the T790M mutation acquired after traditional epidermal growth factor receptor (EGFR) gene tyrosine kinase inhibitor (TKI) treatment, resistance to osimertinib eventually occurs.	osimertinib	23-34	epidermal growth factor receptor	Homo sapiens	125-129
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
33831609-1	2021	BACKGROUND: Survival data support the use of first-line osimertinib as the standard of care for epidermal growth factor receptor (EGFR)-positive non-small cell lung cancer (NSCLC).	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	96-128
33831609-1	2021	BACKGROUND: Survival data support the use of first-line osimertinib as the standard of care for epidermal growth factor receptor (EGFR)-positive non-small cell lung cancer (NSCLC).	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	130-134
33593225-1	2021	INTRODUCTION Osimertinib is a third generation anti epidermal growth factor receptor (EGFR) Tyrosine Kinase Inhibitor (TKI), that irreversibly binds to mutant EGFR, specifically to the T790M mutant EGFR.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	52-84
33593225-1	2021	INTRODUCTION Osimertinib is a third generation anti epidermal growth factor receptor (EGFR) Tyrosine Kinase Inhibitor (TKI), that irreversibly binds to mutant EGFR, specifically to the T790M mutant EGFR.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	86-90
33593225-1	2021	INTRODUCTION Osimertinib is a third generation anti epidermal growth factor receptor (EGFR) Tyrosine Kinase Inhibitor (TKI), that irreversibly binds to mutant EGFR, specifically to the T790M mutant EGFR.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	159-163
33593225-1	2021	INTRODUCTION Osimertinib is a third generation anti epidermal growth factor receptor (EGFR) Tyrosine Kinase Inhibitor (TKI), that irreversibly binds to mutant EGFR, specifically to the T790M mutant EGFR.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	159-163
33593225-5	2021	EXPERT OPINION Osimertinib is a key-player in the treatment of EGFR mutant NSCLC and will probably be used in earlier clinical settings in the future, giving rise to an emerging variety of resistance mechanisms.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	63-67
32276580-1	2021	Third generation EGFR inhibitor osimertinib was approved as the first-line treatment for EGFR T790M mutation-positive Non-Small Cell Lung Cancer (NSCLC) patients in 2017.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	17-21
32276580-1	2021	Third generation EGFR inhibitor osimertinib was approved as the first-line treatment for EGFR T790M mutation-positive Non-Small Cell Lung Cancer (NSCLC) patients in 2017.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	89-93
32276580-2	2021	However, EGFR tertiary Cys797 to Ser797 (C797S) point mutation emanate rapidly after treatment of osimertinib, which is undruggable mutation to the all existing drugs.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	9-13
33333327-1	2021	The first-line treatment of choice for patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) is an EGFR tyrosine kinase inhibitor, of which five are predominantly available in practice: gefitinib, erlotinib, afatinib, dacomitinib and osimertinib.	osimertinib	287-298	epidermal growth factor receptor	Homo sapiens	53-85
33333327-1	2021	The first-line treatment of choice for patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) is an EGFR tyrosine kinase inhibitor, of which five are predominantly available in practice: gefitinib, erlotinib, afatinib, dacomitinib and osimertinib.	osimertinib	287-298	epidermal growth factor receptor	Homo sapiens	87-91
33338652-1	2021	Single agent osimertinib is the standard of care for first-line treatment of advanced metastatic EGFR+ non-small cell lung cancer (NSCLC) and remained the only marketed third-generation (third-generation) EGFR tyrosine kinase inhibitor (TKI) until March 2020 when almonertinib (HS-10296) was approved in China for the treatment of advanced EGFR T790M+ NSCLC.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	97-101
33338652-1	2021	Single agent osimertinib is the standard of care for first-line treatment of advanced metastatic EGFR+ non-small cell lung cancer (NSCLC) and remained the only marketed third-generation (third-generation) EGFR tyrosine kinase inhibitor (TKI) until March 2020 when almonertinib (HS-10296) was approved in China for the treatment of advanced EGFR T790M+ NSCLC.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	205-209
33338652-1	2021	Single agent osimertinib is the standard of care for first-line treatment of advanced metastatic EGFR+ non-small cell lung cancer (NSCLC) and remained the only marketed third-generation (third-generation) EGFR tyrosine kinase inhibitor (TKI) until March 2020 when almonertinib (HS-10296) was approved in China for the treatment of advanced EGFR T790M+ NSCLC.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	205-209
33836373-1	2021	OBJECTIVES: Non-small cell lung cancer (NSCLC) tumors harboring common (exon19del, L858R) and uncommon (e.g. G719X, L861Q) activating epidermal growth factor receptor (EGFR) mutations are best treated with EGFR tyrosine kinase inhibitors (TKI) such as the first-generation EGFR TKI erlotinib, second-generation afatinib or third-generation osimertinib.	osimertinib	340-351	epidermal growth factor receptor	Homo sapiens	134-166
33724860-0	2021	Thermal treatment decreases resistance to osimertinib in non-small cell lung cancer through the EGFR/PI3K/AKT pathway.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	96-100
33724860-0	2021	Thermal treatment decreases resistance to osimertinib in non-small cell lung cancer through the EGFR/PI3K/AKT pathway.	osimertinib	42-53	AKT serine/threonine kinase 1	Homo sapiens	106-109
33682361-0	2021	EGFR-mutant lung adenocarcinoma associated with antisynthetase syndrome successfully treated with osimertinib.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	0-4
33682361-1	2021	Here, we report a rare case involving a 66-year-old man with epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma and antisynthetase syndrome (ASS) treated with osimertinib.	osimertinib	175-186	epidermal growth factor receptor	Homo sapiens	61-93
33682361-1	2021	Here, we report a rare case involving a 66-year-old man with epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma and antisynthetase syndrome (ASS) treated with osimertinib.	osimertinib	175-186	epidermal growth factor receptor	Homo sapiens	95-99
33682361-4	2021	Osimertinib could therefore be a treatment option for EGFR-mutant lung cancer with paraneoplastic ILD.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	54-58
33939068-0	2021	Savolitinib +- Osimertinib in Japanese Patients with Advanced Solid Malignancies or EGFRm NSCLC: Ph1b TATTON Part C. BACKGROUND: Preliminary data suggest that combining savolitinib, a potent and highly selective MET-tyrosine kinase inhibitor (TKI), with osimertinib, a third-generation, irreversible, oral epidermal growth factor receptor-TKI (EGFR-TKI), may overcome MET-based resistance to EGFR-TKIs.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	84-88
33934994-0	2021	Quantification of BIM mRNA in circulating tumor cells of osimertinib-treated patients with EGFR mutation-positive lung cancer.	osimertinib	57-68	BCL2 like 11	Homo sapiens	18-21
33934994-0	2021	Quantification of BIM mRNA in circulating tumor cells of osimertinib-treated patients with EGFR mutation-positive lung cancer.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	91-95
33934994-1	2021	BACKGROUND: The response rate for osimertinib is high among patients with untreated epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	84-116
33934994-1	2021	BACKGROUND: The response rate for osimertinib is high among patients with untreated epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	118-122
33934994-9	2021	RESULTS: We enrolled 30 EGFR mutation-positive NSCLC patients treated with osimertinib during the period from April 2018 through December 2019.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	24-28
33934994-14	2021	CONCLUSIONS: BIM-gamma mRNA overexpression in CTCs from EGFR mutation-positive NSCLC patients is a potential a biomarker for poor response to osimertinib.	osimertinib	142-153	epidermal growth factor receptor	Homo sapiens	56-60
33910930-8	2021	Screening a panel of brain-penetrating EGFR inhibitors identified osimertinib as the most potent inhibitor of the EGFR-TAZ signaling axis.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	39-43
33910930-8	2021	Screening a panel of brain-penetrating EGFR inhibitors identified osimertinib as the most potent inhibitor of the EGFR-TAZ signaling axis.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	114-118
33910930-8	2021	Screening a panel of brain-penetrating EGFR inhibitors identified osimertinib as the most potent inhibitor of the EGFR-TAZ signaling axis.	osimertinib	66-77	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	119-122
33910930-9	2021	Systemic osimertinib treatment inhibited the EGFR-TAZ axis and in vivo growth of GBM stem-like cell xenografts.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	45-49
33910930-9	2021	Systemic osimertinib treatment inhibited the EGFR-TAZ axis and in vivo growth of GBM stem-like cell xenografts.	osimertinib	9-20	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	50-53
33910930-10	2021	Overall these results show that the therapeutic efficacy of osimertinib relies on effective TAZ inhibition, thus identifying TAZ as a potential biomarker of osimertinib sensitivity.	osimertinib	60-71	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	92-95
33910930-10	2021	Overall these results show that the therapeutic efficacy of osimertinib relies on effective TAZ inhibition, thus identifying TAZ as a potential biomarker of osimertinib sensitivity.	osimertinib	60-71	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	125-128
33910930-10	2021	Overall these results show that the therapeutic efficacy of osimertinib relies on effective TAZ inhibition, thus identifying TAZ as a potential biomarker of osimertinib sensitivity.	osimertinib	157-168	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	125-128
33958875-0	2021	Combination of Osimertinib and Anlotinib May Overcome the Resistance Mediated by in cis EGFR T790M-C797S in NSCLC: A Case Report.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	88-92
33958875-1	2021	The emergence of epidermal growth factor receptor (EGFR) exon 20 p.C797S is one of the major resistance mechanisms for osimertinib.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	17-49
33958875-1	2021	The emergence of epidermal growth factor receptor (EGFR) exon 20 p.C797S is one of the major resistance mechanisms for osimertinib.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	51-55
33958875-2	2021	However, there are no standard of care for non-small cell lung cancer (NSCLC) patients after acquiring EGFR C797S currently, which brings significant challenges to post-osimertinib clinical management.	osimertinib	169-180	epidermal growth factor receptor	Homo sapiens	103-107
33958875-3	2021	In the present study, we described a 52-year-old female patient with EGFR-mutated stage IV lung adenocarcinoma, who achieved a partial response (PR) to the treatment of gefitinib and osimertinib after acquiring EGFR exon 20 p.T790M-trans-C797S at osimertinib failure.	osimertinib	183-194	epidermal growth factor receptor	Homo sapiens	69-73
33958875-3	2021	In the present study, we described a 52-year-old female patient with EGFR-mutated stage IV lung adenocarcinoma, who achieved a partial response (PR) to the treatment of gefitinib and osimertinib after acquiring EGFR exon 20 p.T790M-trans-C797S at osimertinib failure.	osimertinib	183-194	epidermal growth factor receptor	Homo sapiens	211-215
33905036-4	2021	In the current study, we found that rictor was cleaved to generate two small fragments at ~ 50 kD and ~ 130 kD in cells undergoing apoptosis upon treatment with different stimuli such as the death ligand, TRAIL, and the small molecule, AZD9291.	osimertinib	236-243	RPTOR independent companion of MTOR complex 2	Homo sapiens	36-42
33986687-2	2021	Both SH-1028 and osimertinib have a pyrimidine structure (a typical mutant-selective EGFR TKI structure).	osimertinib	17-28	epidermal growth factor receptor	Mus musculus	85-89
33976888-5	2021	We found that the first-line treatment with osimertinib was safe and resulted in a long-term response in elderly patients with de novo EGFR T790M-mutated lung adenocarcinoma.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	135-139
33896827-1	2021	BACKGROUND: Osimertinib is an epidermal growth factor receptor-tyrosine kinase inhibitor that specifically targets the T790M mutation in cancer.Unfortunately, most non-small cell lung cancer (NSCLC) patients develop osimertinib resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	30-62
33968729-0	2021	Case Report: Outcome of Osimertinib Treatment in Lung Adenocarcinoma Patients With Acquired KRAS Mutations.	osimertinib	24-35	KRAS proto-oncogene, GTPase	Homo sapiens	92-96
33968729-7	2021	Conclusion: These results provide supporting evidence that KRAS exon 3 (R68S) mutations may be associated with Osimertinib resistance in lung adenocarcinoma patients.	osimertinib	111-122	KRAS proto-oncogene, GTPase	Homo sapiens	59-63
33977727-3	2021	However, osimertinib rechallenge following osimertinib resistance in EGFR T790M-negative patient is less explored.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	69-73
33977727-4	2021	Herein, we describe a metastatic adenocarcinoma NSCLC patient with exon 19 deletion in EGFR (19del) who acquired resistance to initial gefitinib and second-line osimertinib but was successfully rechallenged with osimertinib following treatment failure with chemotherapy.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	87-91
33977727-4	2021	Herein, we describe a metastatic adenocarcinoma NSCLC patient with exon 19 deletion in EGFR (19del) who acquired resistance to initial gefitinib and second-line osimertinib but was successfully rechallenged with osimertinib following treatment failure with chemotherapy.	osimertinib	212-223	epidermal growth factor receptor	Homo sapiens	87-91
33977727-5	2021	The osimertinib rechallenge, despite the absence of EGFR T790M, was considered after the development of multiple small pulmonary lesions and an increase in EGFR exon 19 deletion.	osimertinib	4-15	epidermal growth factor receptor	Homo sapiens	156-160
33889629-1	2021	BACKGROUND: Osimertinib is the recommended first-line treatment for adult patients with epidermal growth factor receptor (EGFR) mutation positive advanced or metastatic non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	88-120
33889629-1	2021	BACKGROUND: Osimertinib is the recommended first-line treatment for adult patients with epidermal growth factor receptor (EGFR) mutation positive advanced or metastatic non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	122-126
33937055-1	2021	The acquired EGFR C797X mutation has been identified as the most notable resistance to osimertinib, and novel secondary mutations of EGFR L718 and L792 residues have also been demonstrated to confer osimertinib resistance, making the choice of medication after osimertinib treatment a quandary.	osimertinib	87-98	epidermal growth factor receptor	Homo sapiens	13-17
33937055-1	2021	The acquired EGFR C797X mutation has been identified as the most notable resistance to osimertinib, and novel secondary mutations of EGFR L718 and L792 residues have also been demonstrated to confer osimertinib resistance, making the choice of medication after osimertinib treatment a quandary.	osimertinib	199-210	epidermal growth factor receptor	Homo sapiens	133-137
33937055-1	2021	The acquired EGFR C797X mutation has been identified as the most notable resistance to osimertinib, and novel secondary mutations of EGFR L718 and L792 residues have also been demonstrated to confer osimertinib resistance, making the choice of medication after osimertinib treatment a quandary.	osimertinib	199-210	epidermal growth factor receptor	Homo sapiens	133-137
33937055-3	2021	In five lung adenocarcinoma patients resistant to later-line osimertinib, recurrent mutations at EGFR L792 and/or L718 were identified using targeted next-generation sequencing of tissue or cell-free DNA from plasma or pleural effusion.	osimertinib	61-72	epidermal growth factor receptor	Homo sapiens	97-101
33981604-0	2021	Small Cell Lung Cancer Transformation as a Resistance Mechanism to Osimertinib in Epidermal Growth Factor Receptor-Mutated Lung Adenocarcinoma: Case Report and Literature Review.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	82-114
33981604-1	2021	Introduction: Small cell lung cancer (SCLC) transformation represents a mechanism of resistance to osimertinib in EGFR-mutated lung adenocarcinoma, which dramatically impacts patients" prognosis due to high refractoriness to conventional treatments.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	114-118
33981604-2	2021	Case Description: We present the case of a patient who developed a SCLC phenotypic transformation as resistance mechanism to second-line osimertinib for T790M-positive EGFR-mutated NSCLC.	osimertinib	137-148	epidermal growth factor receptor	Homo sapiens	168-172
33848354-0	2021	VPS34 suppression reverses osimertinib resistance via simultaneously inhibiting glycolysis and autophagy.	osimertinib	27-38	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	0-5
33848354-6	2021	By demonstrating that VPS34 is the key player controlling autophagy and glycolysis simultaneously, our study may provide a new strategy for overcoming osimertinib resistance for treatment of EGFR-mutant non-small cell lung cancer (NSCLC patients.	osimertinib	151-162	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	22-27
33848354-6	2021	By demonstrating that VPS34 is the key player controlling autophagy and glycolysis simultaneously, our study may provide a new strategy for overcoming osimertinib resistance for treatment of EGFR-mutant non-small cell lung cancer (NSCLC patients.	osimertinib	151-162	epidermal growth factor receptor	Homo sapiens	191-195
33912453-10	2021	Resected EGFR-mutant NSCLC patients treated with osimertinib experienced improved DFS and a lower risk of brain recurrence than those treated with gefitinib or erlotinib.	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	9-13
33896827-1	2021	BACKGROUND: Osimertinib is an epidermal growth factor receptor-tyrosine kinase inhibitor that specifically targets the T790M mutation in cancer.Unfortunately, most non-small cell lung cancer (NSCLC) patients develop osimertinib resistance.	osimertinib	216-227	epidermal growth factor receptor	Homo sapiens	30-62
33896827-7	2021	Among them, 4 exosomal miRNAs, miR-323-3p, miR-1468-3p, miR-5189-3p and miR-6513-5p were essentially upregulated and show the potential to be markers for the discrimination of osimertinib-resistance from osimertinib-sensitive NSCLC patients with high accuracy (p< 0.0001).	osimertinib	176-187	microRNA 6513	Homo sapiens	72-80
31802642-1	2021	BACKGROUND: Osimertinib has been approved by the Food and Drug Administration (FDA) of the United States (US) for the treatment of progressive non-small cell lung cancer (NSCLC) that has acquired T790M mutation during treatment with first-line epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	305-309
33901930-0	2021	Late recurrence of lung adenocarcinoma harboring EGFR exon 20 insertion (A763_Y764insFQEA) mutation successfully treated with osimertinib.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	49-53
33414509-0	2021	Targeting DNA-PK overcomes acquired resistance to third-generation EGFR-TKI osimertinib in non-small-cell lung cancer.	osimertinib	76-87	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	10-16
33414509-1	2021	The third-generation of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), represented by osimertinib, has achieved remarkable clinical outcomes in the treatment of non-small-cell lung cancer (NSCLC) with EGFR mutation.	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	24-56
33414509-1	2021	The third-generation of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), represented by osimertinib, has achieved remarkable clinical outcomes in the treatment of non-small-cell lung cancer (NSCLC) with EGFR mutation.	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	58-62
33414509-1	2021	The third-generation of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), represented by osimertinib, has achieved remarkable clinical outcomes in the treatment of non-small-cell lung cancer (NSCLC) with EGFR mutation.	osimertinib	114-125	epidermal growth factor receptor	Homo sapiens	229-233
33414509-3	2021	In this study, we generated an osimertinib-acquired resistant lung cancer model from a NSCLC cell line H1975 harboring EGFR L858R and T790M mutations.	osimertinib	31-42	epidermal growth factor receptor	Homo sapiens	119-123
33414509-5	2021	Pharmacological inhibiting the activity or genetic knockdown the expression of DNA-PK, a key kinase in DNA damage response (DDR), sensitized the resistant cells to osimertinib.	osimertinib	164-175	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	79-85
33414509-8	2021	These findings shed new light on the mechanisms of osimertinib resistance in the aspect of DNA repair, and provide a rationale for targeting DNA-PK as a therapeutic strategy to overcome osimertinib-acquired resistance in NSCLC.	osimertinib	186-197	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	141-147
33132329-3	2021	We experienced a case of EGFR mutant lung squamous cell carcinoma in which fifth-line treatment with osimertinib was effective after T790M EGFR mutation turned positive.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	25-29
33732316-0	2021	Cost-effectiveness analysis of different sequences of osimertinib administration for epidermal growth factor receptor-mutated non-small-cell lung cancer.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	85-117
33732316-1	2021	Osimertinib is a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) that is clinically effective in patients with EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	94-98
32955628-0	2021	Retrospective analysis of osimertinib re-challenge after osimertinib-induced interstitial lung disease in patients with EGFR-mutant non-small cell lung carcinoma.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	120-124
32955628-1	2021	Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has exhibited efficacy in patients with EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-66
32955628-1	2021	Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has exhibited efficacy in patients with EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	68-72
33132329-3	2021	We experienced a case of EGFR mutant lung squamous cell carcinoma in which fifth-line treatment with osimertinib was effective after T790M EGFR mutation turned positive.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	139-143
32955628-1	2021	Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has exhibited efficacy in patients with EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	151-155
32955628-13	2021	For patients with EGFR-mutant NSCLC who experience grade 1 ILD during osimertinib therapy, osimertinib re-challenge may be suitable when no other treatments are available.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	18-22
33132329-5	2021	Osimertinib may be a promising treatment option for EGFR mutant lung squamous cell carcinoma.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	52-56
33591844-10	2021	New or revised recommendations include the following: Osimertinib is the optimal first-line treatment for patients with activating epidermal growth factor receptor mutations (exon 19 deletion, exon 21 L858R, and exon 20 T790M); alectinib or brigatinib is the optimal first-line treatment for patients with anaplastic lymphoma kinase fusions.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	131-163
33631449-9	2021	In the analysis of HCC4006 DTCs against osimertinib, we observed increased receptor-like tyrosine kinase (RYK) expression, and siRNA-mediated RYK knockdown inhibited the proliferation of DTCs.	osimertinib	40-51	receptor like tyrosine kinase	Homo sapiens	75-104
33631449-9	2021	In the analysis of HCC4006 DTCs against osimertinib, we observed increased receptor-like tyrosine kinase (RYK) expression, and siRNA-mediated RYK knockdown inhibited the proliferation of DTCs.	osimertinib	40-51	receptor like tyrosine kinase	Homo sapiens	106-109
33631449-10	2021	CONCLUSIONS: These results suggest that induction of DTCs is dose-dependent, and increased RYK expression was the mechanism of drug tolerance in HCC4006 cells against osimertinib.	osimertinib	167-178	receptor like tyrosine kinase	Homo sapiens	91-94
32969527-5	2021	Subsequent disease progression was mediated by off-target pan-EGFR inhibitor (including osimertinib)-resistant KRAS mutation and not by acquisition of EGFR-T790M.	osimertinib	88-99	KRAS proto-oncogene, GTPase	Homo sapiens	111-115
33828979-9	2021	Three patients with EGFR T790M mutations in CSF achieved iPR after second-line osimertinib treatment.	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	20-24
34012779-0	2021	Plasma pre-treatment T790M relative allelic frequency in patients with advanced EGFR-mutated non-small cell lung cancer predicts treatment response to subsequent-line osimertinib.	osimertinib	167-178	epidermal growth factor receptor	Homo sapiens	80-84
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	epidermal growth factor receptor	Homo sapiens	189-193
33741979-1	2021	Advanced non-small-cell lung cancer (NSCLC) patients with EGFR T790M-positive tumours benefit from osimertinib, an epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	58-62
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
33741979-1	2021	Advanced non-small-cell lung cancer (NSCLC) patients with EGFR T790M-positive tumours benefit from osimertinib, an epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI).	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	175-179
33741979-2	2021	Here we show that the size of the EGFR T790M-positive clone impacts response to osimertinib.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	34-38
33675607-0	2021	Afatinib therapy in case of EGFR G724S emergence as resistance mechanism to osimertinib.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	28-32
33741979-4	2021	Both baseline and longitudinal ctDNA profiling indicate that the T790M subclonal tumours are enriched for PIK3CA alterations, which we demonstrate to confer resistance to osimertinib in vitro that can be partially reversed by PI3K pathway inhibitors.	osimertinib	171-182	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	106-112
33376097-0	2021	Phase IB study of osimertinib in combination with navitoclax in EGFR-mutant NSCLC following resistance to initial EGFR therapy (ETCTN 9903).	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	64-68
33376097-0	2021	Phase IB study of osimertinib in combination with navitoclax in EGFR-mutant NSCLC following resistance to initial EGFR therapy (ETCTN 9903).	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	114-118
33376097-1	2021	INTRODUCTION: Osimertinib is an effective therapy in EGFR mutant NSCLC, but resistance invariably develops.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	53-57
33376097-15	2021	Further study of BCL-2/BCL-xL inhibition to enhance osimertinib activity is warranted.	osimertinib	52-63	BCL2 apoptosis regulator	Homo sapiens	17-22
33376097-15	2021	Further study of BCL-2/BCL-xL inhibition to enhance osimertinib activity is warranted.	osimertinib	52-63	BCL2 like 1	Homo sapiens	23-29
33723247-12	2021	Further, depletion of MSI2 in combination with EGFR inhibitors such as erlotinib, afatinib, and osimertinib selectively reduced the growth of EGFRmut NSCLC cells and xenografts.	osimertinib	96-107	musashi RNA binding protein 2	Homo sapiens	22-26
33707235-5	2021	Furthermore, Keap1 inactivation reduced the sensitivity of EGFR-driven tumors to the EGFR inhibitor osimertinib and mutations in the KEAP1 pathway were associated with decreased time on tyrosine kinase inhibitor treatment in patients.	osimertinib	100-111	kelch like ECH associated protein 1	Homo sapiens	13-18
33707235-5	2021	Furthermore, Keap1 inactivation reduced the sensitivity of EGFR-driven tumors to the EGFR inhibitor osimertinib and mutations in the KEAP1 pathway were associated with decreased time on tyrosine kinase inhibitor treatment in patients.	osimertinib	100-111	epidermal growth factor receptor	Homo sapiens	59-63
33707235-5	2021	Furthermore, Keap1 inactivation reduced the sensitivity of EGFR-driven tumors to the EGFR inhibitor osimertinib and mutations in the KEAP1 pathway were associated with decreased time on tyrosine kinase inhibitor treatment in patients.	osimertinib	100-111	epidermal growth factor receptor	Homo sapiens	85-89
33676426-0	2021	Osimertinib in advanced EGFR-T790M mutation-positive non-small cell lung cancer patients treated within the Special Use Medication Program in Spain: OSIREX-Spanish Lung Cancer Group.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	24-28
33676426-1	2021	BACKGROUND: AURA study reported 61% objective response rate and progression-free survival of 9.6 months with osimertinib in patients with EGFR/T790M+ non-small cell lung cancer.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	138-142
33676426-16	2021	CONCLUSION: This study to assess the real-world clinical impact of osimertinib showed high drug activity in pretreated advanced EGFR/T790M+ non-small cell lung cancer, with manageable adverse events.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	128-132
33675607-1	2021	Osimertinib is a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) used both as the first-line treatment of EGFR-mutated non-small cell lung cancer patients and in second-line after T790M-positive disease progression to first- or second-generation TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	94-98
33675607-1	2021	Osimertinib is a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) used both as the first-line treatment of EGFR-mutated non-small cell lung cancer patients and in second-line after T790M-positive disease progression to first- or second-generation TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	145-149
33675607-3	2021	We report the case of a patient with advanced EGFR-mutated (exon 19 deletion and T790M-positive) non-small cell lung cancer who developed disease progression to osimertinib characterized by the loss of T790M concurrently with the emergence of G724S EGFR mutation, which was tackled by subsequent afatinib treatment.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	46-50
33675607-3	2021	We report the case of a patient with advanced EGFR-mutated (exon 19 deletion and T790M-positive) non-small cell lung cancer who developed disease progression to osimertinib characterized by the loss of T790M concurrently with the emergence of G724S EGFR mutation, which was tackled by subsequent afatinib treatment.	osimertinib	161-172	epidermal growth factor receptor	Homo sapiens	249-253
33675607-4	2021	Next-generation sequencing molecular study of rebiopsy at time of progression to osimertinib revealed the persistence of EGFR exon 19 deletion, loss of T790M with a new G724S EGFR mutation; other concomitant mechanisms were excluded.	osimertinib	81-92	epidermal growth factor receptor	Homo sapiens	121-125
33675607-7	2021	Our case report contributes to increase the knowledge on acquired resistance mechanisms to osimertinib treatment, and it shows, for the first time, the efficacy of afatinib in the case of T790M loss and emergence of G724S EGFR mutation.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	222-226
33040541-2	2021	However, acquired resistance to the third-generation EGFR-TKI osimertinib is an intractable obstacle for many clinical oncologists.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	53-57
32678313-0	2021	TGFbeta2-mediated epithelial-mesenchymal transition and NF-kappaB pathway activation contribute to osimertinib resistance.	osimertinib	99-110	transforming growth factor beta 2	Homo sapiens	0-8
32678313-0	2021	TGFbeta2-mediated epithelial-mesenchymal transition and NF-kappaB pathway activation contribute to osimertinib resistance.	osimertinib	99-110	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32678313-1	2021	Osimertinib (AZD9291) has been widely used for the treatment of EGFR mutant non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	64-68
32678313-1	2021	Osimertinib (AZD9291) has been widely used for the treatment of EGFR mutant non-small cell lung cancer.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	64-68
32678313-5	2021	The EMT occurrence resulted from osimertinib-induced upregulation of TGFbeta2 that activated SMAD2.	osimertinib	33-44	transforming growth factor beta 2	Homo sapiens	69-77
32678313-5	2021	The EMT occurrence resulted from osimertinib-induced upregulation of TGFbeta2 that activated SMAD2.	osimertinib	33-44	SMAD family member 2	Homo sapiens	93-98
32678313-7	2021	In NCI-H1975 cells, osimertinib activated NF-kappaB pathway, evidenced by the increased p65 nuclear translocation, which was abolished by knockdown of TGFbeta2.	osimertinib	20-31	nuclear factor kappa B subunit 1	Homo sapiens	42-51
32678313-7	2021	In NCI-H1975 cells, osimertinib activated NF-kappaB pathway, evidenced by the increased p65 nuclear translocation, which was abolished by knockdown of TGFbeta2.	osimertinib	20-31	RELA proto-oncogene, NF-kB subunit	Homo sapiens	88-91
32678313-7	2021	In NCI-H1975 cells, osimertinib activated NF-kappaB pathway, evidenced by the increased p65 nuclear translocation, which was abolished by knockdown of TGFbeta2.	osimertinib	20-31	transforming growth factor beta 2	Homo sapiens	151-159
32678313-10	2021	These findings shed new light on distinct roles of TGFbeta2 in osimertinib-resistant cells and provide new strategies for treatment of this resistant status.	osimertinib	63-74	transforming growth factor beta 2	Homo sapiens	51-59
33199228-9	2021	CONCLUSIONS: This is the first study to explore the efficacy and safety of osimertinib combined with platinum-based chemotherapy in previously untreated NSCLC patients with EGFR-sensitizing mutations.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	173-177
33410885-2	2021	Objective: To explore the efficacy and safety of osimertinib plus bevacizumab compared with osimertinib alone in patients with lung adenocarcinoma with EGFR T790M mutation.	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	152-156
33728415-9	2021	The presence of EGFR-C797S led to >200-fold resistance in proliferation assays probing mobocertinib and osimertinib.	osimertinib	104-115	epidermal growth factor receptor	Homo sapiens	16-20
33277055-1	2021	INTRODUCTION: The use of osimertinib is associated with the risk of cancer therapy-related cardiac dysfunction (CTRCD) for EGFR-mutated non-small cell lung cancer (NSCLC) patients.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	123-127
33434619-5	2021	Furthermore afatinib, dacomitinib, and osimertinib, inhibitors of members of the epidermal growth factor receptor family (ErbB1/2/3/4), are used in the treatment of non-small cell lung cancers.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	122-133
33471376-6	2021	While EGFR L858R/T90M-mutated cell line was sensitive to osimertinib or TAS-121 in vitro, EGFR-overexpressing cell lines displayed resistance to these EGFR-TKIs.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	6-10
33475261-0	2021	Higher osimertinib introduction rate achieved by multiple repeated rebiopsy after acquired resistance to first/second generation EGFR-TKIs.	osimertinib	7-18	epidermal growth factor receptor	Homo sapiens	129-133
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
33621951-0	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	AKT serine/threonine kinase 1	Homo sapiens	82-85
33621951-3	2021	RESULTS: We first established that HCC827 and H1975 cells showed increased resistance against osimertinib when co-cultured with CAFs isolated from osimertinib-resistant patients.	osimertinib	94-105	T-box transcription factor 1	Homo sapiens	128-132
33621951-3	2021	RESULTS: We first established that HCC827 and H1975 cells showed increased resistance against osimertinib when co-cultured with CAFs isolated from osimertinib-resistant patients.	osimertinib	147-158	T-box transcription factor 1	Homo sapiens	128-132
33621951-7	2021	Subsequently, we observed that the treatment of capmatinib resulted in the re-sensitization of CAF-co-cultured H1975 and HCC827 to osimertinib, in association with reduced EMT and self-renewal ability.	osimertinib	131-142	lysine acetyltransferase 2B	Homo sapiens	95-98
33621951-10	2021	Finally, we demonstrated that the combination of capmatinib and osimertinib led to an increased tumor inhibition and significantly lower number of CAFs within the patient derived xenograft (PDX) model.	osimertinib	64-75	T-box transcription factor 1	Homo sapiens	147-151
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
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	AKT serine/threonine kinase 1	Homo sapiens	73-76
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	snail family transcriptional repressor 1	Homo sapiens	77-82
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	T-box transcription factor 1	Homo sapiens	144-148
32999231-1	2021	Osimertinib is the standard treatment for epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	42-74
32999231-1	2021	Osimertinib is the standard treatment for epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	76-80
32999231-5	2021	Treatment with other EGFR-TKIs after osimertinib-induced ILD may be an option for subsequent therapy.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	21-25
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-108
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	TNF receptor superfamily member 10a	Homo sapiens	119-122
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	TNF receptor superfamily member 10a	Homo sapiens	119-122
33574724-2	2021	The third-generation EGFR-TKIs, osimertinib and almonertinib, are now approved for the treatment of advanced NSCLC patients harboring activating EGFR mutations (first-line) and/or the resistant T790M mutation (second-line).	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	21-25
33574724-2	2021	The third-generation EGFR-TKIs, osimertinib and almonertinib, are now approved for the treatment of advanced NSCLC patients harboring activating EGFR mutations (first-line) and/or the resistant T790M mutation (second-line).	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	145-149
33574724-5	2021	This review focuses on discussing the scientific rationale for and potential of co-targeting MEK/ERK signaling in delaying and overcoming acquired resistance to third-generation EGFR-TKIs, particularly osimertinib.	osimertinib	202-213	mitogen-activated protein kinase kinase 7	Homo sapiens	93-96
33574724-5	2021	This review focuses on discussing the scientific rationale for and potential of co-targeting MEK/ERK signaling in delaying and overcoming acquired resistance to third-generation EGFR-TKIs, particularly osimertinib.	osimertinib	202-213	EPH receptor B2	Homo sapiens	97-100
33626238-11	2021	Moreover, ACER and net benefit showed that the combination of EGFR-TKI with chemotherapy and osimertinib was of more economic benefit following first-generation EGFR-TKIs.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	62-66
33626238-11	2021	Moreover, ACER and net benefit showed that the combination of EGFR-TKI with chemotherapy and osimertinib was of more economic benefit following first-generation EGFR-TKIs.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	161-165
33158763-0	2021	Emergence of NOTCH2-NTRK1 After Osimertinib in a Patient With Lung Adenocarcinoma With Neuroendocrine Differentiation.	osimertinib	32-43	notch receptor 2	Homo sapiens	13-19
33158763-0	2021	Emergence of NOTCH2-NTRK1 After Osimertinib in a Patient With Lung Adenocarcinoma With Neuroendocrine Differentiation.	osimertinib	32-43	neurotrophic receptor tyrosine kinase 1	Homo sapiens	20-25
33482349-2	2021	There have been significant advances in the management of metastatic EGFR-mutant NSCLC, from the advent of first and second generation EGFR inhibitors to, more recently, the third-generation inhibitor osimertinib.	osimertinib	201-212	epidermal growth factor receptor	Homo sapiens	69-73
33009209-0	2021	Generation of Osimertinib-Resistant Cells from EGFR L858R/T790M Mutant NSCLC Cell Line.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	47-51
33009209-4	2021	Third generation EGFR-TKI, Osimertinib exhibits high efficacy in patients with exon 19 deletion/L858R/T790M mutation but they experienced acquired resistance thereafter.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	17-21
33641720-0	2021	Osimertinib Should be the Standard of Care for the Adjuvant Therapy of Stage IB to IIIA EGFR-Mutant NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	88-92
33641721-0	2021	Osimertinib Should Not Yet Be Considered the Standard of Care for EGFR-Mutant NSCLC in the Adjuvant Setting.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	66-70
33641722-0	2021	Selpercatinib Overcomes CCDC6-RET-Mediated Resistance to Osimertinib.	osimertinib	57-68	coiled-coil domain containing 6	Homo sapiens	24-29
33641722-0	2021	Selpercatinib Overcomes CCDC6-RET-Mediated Resistance to Osimertinib.	osimertinib	57-68	ret proto-oncogene	Homo sapiens	30-33
33486418-1	2021	BACKGROUND: Resistance mechanisms following 1st line therapy with osimertinib in EGFR + NSCLC have become focus of investigation.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	81-85
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
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
33506568-0	2021	ALK rearrangements as mechanisms of acquired resistance to osimertinib in EGFR mutant non-small cell lung cancer.	osimertinib	59-70	ALK receptor tyrosine kinase	Homo sapiens	0-3
33506568-0	2021	ALK rearrangements as mechanisms of acquired resistance to osimertinib in EGFR mutant non-small cell lung cancer.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	74-78
33506568-4	2021	Here, we determined that ALK rearrangement might be an underlying mechanism contributing to acquired resistance to osimertinib.	osimertinib	115-126	ALK receptor tyrosine kinase	Homo sapiens	25-28
33506568-5	2021	In our report, a 60-year-old female patient with lung adenocarcinoma with an EGFR mutation was administered multiple treatments, including first-line gefitinib and second-line osimertinib.	osimertinib	176-187	epidermal growth factor receptor	Homo sapiens	77-81
33506568-6	2021	According to the next-generation sequencing (NGS) assay after osimertinib failure, the emergence of an ALK rearrangement was considered to be a potentially acquired resistance mechanism to osimertinib.	osimertinib	62-73	ALK receptor tyrosine kinase	Homo sapiens	103-106
33506568-9	2021	In this study, we also summarized previously reported cases and concluded that ALK rearrangement is a rare but critical resistance mechanism to osimertinib.	osimertinib	144-155	ALK receptor tyrosine kinase	Homo sapiens	79-82
33544337-1	2021	BACKGROUND: In the global FLAURA study, first-line osimertinib, a third-generation irreversible tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR), significantly improved progression-free survival (PFS) and overall survival (OS) versus comparator EGFR TKIs in patients with EGFR mutation-positive (EGFRm) advanced non-small-cell lung cancer (NSCLC).	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	131-163
33544337-1	2021	BACKGROUND: In the global FLAURA study, first-line osimertinib, a third-generation irreversible tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR), significantly improved progression-free survival (PFS) and overall survival (OS) versus comparator EGFR TKIs in patients with EGFR mutation-positive (EGFRm) advanced non-small-cell lung cancer (NSCLC).	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	165-169
33544337-1	2021	BACKGROUND: In the global FLAURA study, first-line osimertinib, a third-generation irreversible tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR), significantly improved progression-free survival (PFS) and overall survival (OS) versus comparator EGFR TKIs in patients with EGFR mutation-positive (EGFRm) advanced non-small-cell lung cancer (NSCLC).	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	271-275
33544337-1	2021	BACKGROUND: In the global FLAURA study, first-line osimertinib, a third-generation irreversible tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR), significantly improved progression-free survival (PFS) and overall survival (OS) versus comparator EGFR TKIs in patients with EGFR mutation-positive (EGFRm) advanced non-small-cell lung cancer (NSCLC).	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	271-275
33889509-11	2021	Further analysis revealed that metformin obviously prolonged the median PFS2 of osimertinib treatment among patients who progressed to prior line EGFR-TKIs due to secondary EGFR T790M mutation (cohort B).	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	146-150
33679141-0	2021	Real-World Data on Osimertinib in Chinese Patients with Pretreated, EGFR T790M Mutation Positive, Advanced Non-Small Cell Lung Cancer: A Retrospective Study.	osimertinib	19-30	epidermal growth factor receptor	Homo sapiens	68-72
33679141-1	2021	Purpose: As a third-generation EGFR TKI has been taken orally, Osimertinib effectively inhibits mutant EGFR, including T790M EGFR resistance mutations.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	31-35
33679141-1	2021	Purpose: As a third-generation EGFR TKI has been taken orally, Osimertinib effectively inhibits mutant EGFR, including T790M EGFR resistance mutations.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	103-107
33679141-1	2021	Purpose: As a third-generation EGFR TKI has been taken orally, Osimertinib effectively inhibits mutant EGFR, including T790M EGFR resistance mutations.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	103-107
33679141-2	2021	Here, we examined real-world efficacy and tolerability of Osimertinib among Chinese patients with advanced EGFR T790M-mutant NSCLC.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	107-111
33658860-3	2021	EGFR C797S and MET amplification are common mechanisms of osimertinib.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	0-4
33658860-3	2021	EGFR C797S and MET amplification are common mechanisms of osimertinib.	osimertinib	58-69	SAFB like transcription modulator	Homo sapiens	15-18
33658860-10	2021	Conclusion: EGFR C797S mutation and MET amplification are leading mechanisms for osimertinib resistance in lung cancer.	osimertinib	81-92	epidermal growth factor receptor	Homo sapiens	12-16
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
33718183-0	2021	Advanced NSCLC Patients With EGFR T790M Harboring TP53 R273C or KRAS G12V Cannot Benefit From Osimertinib Based on a Clinical Multicentre Study by Tissue and Liquid Biopsy.	osimertinib	94-105	epidermal growth factor receptor	Homo sapiens	29-33
33718183-0	2021	Advanced NSCLC Patients With EGFR T790M Harboring TP53 R273C or KRAS G12V Cannot Benefit From Osimertinib Based on a Clinical Multicentre Study by Tissue and Liquid Biopsy.	osimertinib	94-105	tumor protein p53	Homo sapiens	50-54
33718183-0	2021	Advanced NSCLC Patients With EGFR T790M Harboring TP53 R273C or KRAS G12V Cannot Benefit From Osimertinib Based on a Clinical Multicentre Study by Tissue and Liquid Biopsy.	osimertinib	94-105	KRAS proto-oncogene, GTPase	Homo sapiens	64-68
33718183-2	2021	While a large amount of patients with EGFR exon 21 p.Thr790 Met (T790M) benefited from osimertinib treatment, acquired resistance to osimertinb has subsequently become a growing challenge.	osimertinib	87-98	epidermal growth factor receptor	Homo sapiens	38-42
33718183-13	2021	Moreover, we discovered two uncommon mutations, TP53 R273C and KRAS G12V, which attenuates the effectiveness of osimertinib.	osimertinib	112-123	tumor protein p53	Homo sapiens	48-52
33718183-13	2021	Moreover, we discovered two uncommon mutations, TP53 R273C and KRAS G12V, which attenuates the effectiveness of osimertinib.	osimertinib	112-123	KRAS proto-oncogene, GTPase	Homo sapiens	63-67
33596364-0	2021	Osimertinib in EGFR-Mutated Lung Cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
33596365-0	2021	Osimertinib in EGFR-Mutated Lung Cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
33334907-1	2021	Both osimertinib and the combination of erlotinib plus ramuciumab are approved for initial therapy of advanced epidermal growth factor receptor (EGFR) mutation positive non-small cell lung cancer (NSCLC).	osimertinib	5-16	epidermal growth factor receptor	Homo sapiens	111-143
33664875-10	2021	Results: EGFR inhibitors (e.g., osimertinib) decreased DR4 levels only in EGFR mutant NSCLC cells and tumors, being tightly associated with induction of apoptosis.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	9-13
33664875-10	2021	Results: EGFR inhibitors (e.g., osimertinib) decreased DR4 levels only in EGFR mutant NSCLC cells and tumors, being tightly associated with induction of apoptosis.	osimertinib	32-43	TNF receptor superfamily member 10a	Homo sapiens	55-58
33664875-10	2021	Results: EGFR inhibitors (e.g., osimertinib) decreased DR4 levels only in EGFR mutant NSCLC cells and tumors, being tightly associated with induction of apoptosis.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	74-78
33664875-12	2021	Increased levels of DR4 were detected in cell lines with acquired osimertinib resistance and in NSCLC tissues relapsed from EGFR-targeted therapy.	osimertinib	66-77	TNF receptor superfamily member 10a	Homo sapiens	20-23
33664875-13	2021	DR4 knockdown induced apoptosis and augmented apoptosis when combined with osimertinib in both sensitive and resistant cell lines, whereas enforced DR4 expression significantly attenuated osimertinib-induced apoptosis.	osimertinib	188-199	TNF receptor superfamily member 10a	Homo sapiens	148-151
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	TNF receptor superfamily member 10a	Homo sapiens	53-56
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	mitogen-activated protein kinase kinase 7	Homo sapiens	96-99
33664875-14	2021	Mechanistically, osimertinib induced MARCH8-mediated DR4 proteasomal degradation and suppressed MEK/ERK/AP-1-dependent DR4 transcription, resulting in DR4 downregulation.	osimertinib	17-28	mitogen-activated protein kinase 1	Homo sapiens	100-103
33580193-0	2021	Impressive response to dabrafenib, trametinib, and osimertinib in a metastatic EGFR-mutant/BRAF V600E lung adenocarcinoma patient.	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	79-83
33580193-0	2021	Impressive response to dabrafenib, trametinib, and osimertinib in a metastatic EGFR-mutant/BRAF V600E lung adenocarcinoma patient.	osimertinib	51-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	91-95
33580193-1	2021	The survival outcomes of the FLAURA trial support osimertinib as the new standard of care for untreated patients harboring activating mutations in the epidermal growth factor receptor (EGFR).	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	151-183
33580193-1	2021	The survival outcomes of the FLAURA trial support osimertinib as the new standard of care for untreated patients harboring activating mutations in the epidermal growth factor receptor (EGFR).	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	185-189
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	124-128
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	osimertinib	97-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	178-182
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	osimertinib	249-260	epidermal growth factor receptor	Homo sapiens	124-128
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	osimertinib	249-260	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	178-182
33572269-5	2021	Currently, many oncologists prescribe osimertinib, a third-generation EGFR-TKI that can overcome T790M-mediated resistance, as a first-line TKI.	osimertinib	38-49	epidermal growth factor receptor	Homo sapiens	70-74
33714692-0	2021	Emergence of NOTCH2-NTRK1 After Osimertinib in a Patient With Lung Adenocarcinoma With Neuroendocrine Differentiation.	osimertinib	32-43	notch receptor 2	Homo sapiens	13-19
33714692-0	2021	Emergence of NOTCH2-NTRK1 After Osimertinib in a Patient With Lung Adenocarcinoma With Neuroendocrine Differentiation.	osimertinib	32-43	neurotrophic receptor tyrosine kinase 1	Homo sapiens	20-25
33474947-9	2021	CONCLUSIONS: Osimertinib demonstrated a superior therapeutic benefit with high efficacy and low toxicity for T790M-positive advanced NSCLC patients who were treated with early-generation EGFR-TKIs.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	187-191
32556898-3	2021	The patient received osimertinib, a third generation EGFR-TKI, as the first-line treatment, but the disease progressed during treatment.	osimertinib	21-32	epidermal growth factor receptor	Homo sapiens	53-57
33465742-0	2021	Molecular predictors of EGFR-mutant NSCLC transformation into LCNEC after frontline osimertinib: digging under the surface.	osimertinib	84-95	epidermal growth factor receptor	Homo sapiens	24-28
33122107-10	2021	In patients with T790M-negative CSF, EGFR exon 21 L858R mutation, concurrent FGF3 alteration and over 1st line osimertinib showed shortened iPFS.	osimertinib	111-122	epidermal growth factor receptor	Homo sapiens	37-41
33356419-1	2021	PURPOSE: Osimertinib is a third-generation, CNS-active, irreversible, oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that potently and selectively inhibits both EGFR-TKI-sensitizing and T790M resistance mutations.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	135-139
33976025-0	2021	[Effectiveness of Osimertinib for Postoperative Recurrence of Lung Cancer with L861Q Activating EGFR Mutation:Report of a Case].	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	96-100
33494928-0	2021	Osimertinib Leads the Way Toward Improving Outcomes of EGFR-Mutant NSCLC With Leptomeningeal Metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	55-59
33494929-0	2021	A Response to the Letter to the Editor: Osimertinib Leads the Way Towards Improving Outcomes of EGFR-Mutant NSCLC With Leptomeningeal Metastases.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	96-100
33459024-1	2021	Osimertinib is a highly potent and selective third-generation epidermal growth factor receptor (EGFR) inhibitor, which provides excellent clinical benefits and is now a standard-of-care therapy for advanced EGFR mutation-positive non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	62-94
33341538-0	2021	Osimertinib for Chinese advanced non-small cell lung cancer patients harboring diverse EGFR exon 20 insertion mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	87-91
33341538-3	2021	We performed this study to investigate the real efficacy of osimertinib for Chinese advanced NSCLC patients harboring EGFR ex20 ins mutations.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	118-122
33341538-14	2021	Osimertinib either 80 mg or 160 mg once daily showed less activity in Chinese NSCLC patients harboring diverse EGFR ex20 ins mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	111-115
33219754-0	2021	Impact of the generation of EGFR-TKIs administered as prior therapy on the efficacy of osimertinib in patients with non-small cell lung cancer harboring EGFR T790M mutation.	osimertinib	87-98	epidermal growth factor receptor	Homo sapiens	28-32
33219754-0	2021	Impact of the generation of EGFR-TKIs administered as prior therapy on the efficacy of osimertinib in patients with non-small cell lung cancer harboring EGFR T790M mutation.	osimertinib	87-98	epidermal growth factor receptor	Homo sapiens	153-157
33219754-1	2021	BACKGROUND: There are few studies that directly compare the effects of osimertinib on patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) T790M mutation between the generation of prior EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	145-177
33219754-1	2021	BACKGROUND: There are few studies that directly compare the effects of osimertinib on patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) T790M mutation between the generation of prior EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	179-183
33219754-2	2021	METHODS: We retrospectively reviewed clinical data from the medical records of consecutive patients with advanced NSCLC who had developed resistance to first- or second-generation EGFR-TKIs due to EGFR T790M mutation and were subsequently treated with osimertinib at Juntendo University Hospital.	osimertinib	252-263	epidermal growth factor receptor	Homo sapiens	197-201
33219754-4	2021	RESULTS: A total of 38 patients with NSCLC harboring EGFR T790M mutation were treated with osimertinib.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	53-57
33219754-10	2021	CONCLUSIONS: PFS of osimertinib was significantly longer in patients with NSCLC harboring EGFR T790M mutation after treatment with afatinib than in patients after treatment with first generation EGFR-TKIs.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	90-94
33219754-10	2021	CONCLUSIONS: PFS of osimertinib was significantly longer in patients with NSCLC harboring EGFR T790M mutation after treatment with afatinib than in patients after treatment with first generation EGFR-TKIs.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	195-199
33219754-11	2021	Additional mutations other than EGFR T790M may affect the efficacy of osimertinib treatment.	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	32-36
33219754-12	2021	KEY POINTS: Significant findings of the study: PFS of osimertinib was significantly longer in patients with NSCLC harboring EGFR T790M mutation after treatment with afatinib than in patients after treatment with first generation EGFR-TKIs.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	124-128
33219754-12	2021	KEY POINTS: Significant findings of the study: PFS of osimertinib was significantly longer in patients with NSCLC harboring EGFR T790M mutation after treatment with afatinib than in patients after treatment with first generation EGFR-TKIs.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	229-233
33219754-13	2021	WHAT THIS STUDY ADDS: Additional mutations other than EGFR T790M may affect the efficacy of osimertinib treatment.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	54-58
33459024-1	2021	Osimertinib is a highly potent and selective third-generation epidermal growth factor receptor (EGFR) inhibitor, which provides excellent clinical benefits and is now a standard-of-care therapy for advanced EGFR mutation-positive non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	96-100
33459024-1	2021	Osimertinib is a highly potent and selective third-generation epidermal growth factor receptor (EGFR) inhibitor, which provides excellent clinical benefits and is now a standard-of-care therapy for advanced EGFR mutation-positive non-small-cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	207-211
33504904-0	2021	Gene expression in circulating tumor cells reveals a dynamic role of EMT and PD-L1 during osimertinib treatment in NSCLC patients.	osimertinib	90-101	IL2 inducible T cell kinase	Homo sapiens	69-72
33610453-0	2021	Combining Osimertinib With Chemotherapy in EGFR-Mutant NSCLC at Progression.	osimertinib	10-21	epidermal growth factor receptor	Homo sapiens	43-47
33610453-1	2021	BACKGROUND: Osimertinib is a third-generation EGFR tyrosine kinase inhibitor that has improved survival and central nervous system (CNS) outcomes in patients with non-small cell lung cancer (NSCLC) with activating EGFR mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-50
33504904-0	2021	Gene expression in circulating tumor cells reveals a dynamic role of EMT and PD-L1 during osimertinib treatment in NSCLC patients.	osimertinib	90-101	CD274 molecule	Homo sapiens	77-82
33504904-2	2021	We studied changes in gene expression in CTC-enriched fractions of EGFR-mutant NSCLC patients under osimertinib.	osimertinib	100-111	epidermal growth factor receptor	Homo sapiens	67-71
33461557-0	2021	Intercellular transfer of exosomal wild type EGFR triggers osimertinib resistance in non-small cell lung cancer.	osimertinib	59-70	epidermal growth factor receptor	Homo sapiens	45-49
33612406-2	2021	However, only about one-half of patients who have received prior treatment with a first- or second-generation EGFR-TKI are eligible for osimertinib therapy because its indication in the second-line setting is limited to metastatic NSCLC positive for the T790M resistance mutation of EGFR.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	110-114
33612406-3	2021	The dose-escalation part of a study in which patients received osimertinib at doses of 20 to 240 mg once daily after the development of resistance to first- or second-generation EGFR-TKIs revealed a response rate of 21% and a median progression-free survival of 2.8 months for individuals whose tumors were negative for EGFR T790M.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	178-182
33612406-3	2021	The dose-escalation part of a study in which patients received osimertinib at doses of 20 to 240 mg once daily after the development of resistance to first- or second-generation EGFR-TKIs revealed a response rate of 21% and a median progression-free survival of 2.8 months for individuals whose tumors were negative for EGFR T790M.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	320-324
33612406-4	2021	We have now designed a phase II study of osimertinib for patients with EGFR mutation-positive NSCLC who develop isolated central nervous system progression (T790M-negative or unknown) after first- or second-generation EGFR-TKI therapy (cohort 1) or who develop systemic disease progression (T790M-negative) after first- or second-generation EGFR-TKI therapy and platinum-based chemotherapy (cohort 2).	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	71-75
33612406-4	2021	We have now designed a phase II study of osimertinib for patients with EGFR mutation-positive NSCLC who develop isolated central nervous system progression (T790M-negative or unknown) after first- or second-generation EGFR-TKI therapy (cohort 1) or who develop systemic disease progression (T790M-negative) after first- or second-generation EGFR-TKI therapy and platinum-based chemotherapy (cohort 2).	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	218-222
33612406-4	2021	We have now designed a phase II study of osimertinib for patients with EGFR mutation-positive NSCLC who develop isolated central nervous system progression (T790M-negative or unknown) after first- or second-generation EGFR-TKI therapy (cohort 1) or who develop systemic disease progression (T790M-negative) after first- or second-generation EGFR-TKI therapy and platinum-based chemotherapy (cohort 2).	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	218-222
33459177-1	2021	ABTRACT The epidermal growth factor receptor (EGFR) kinase inhibitors Gefitinib, Erlotinib, Afatinib and Osimertinib have been approved for the treatments of non-small cell lung cancer patients harboring sensitive EGFR mutations, but resistance arises rapidly.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	12-44
33459177-1	2021	ABTRACT The epidermal growth factor receptor (EGFR) kinase inhibitors Gefitinib, Erlotinib, Afatinib and Osimertinib have been approved for the treatments of non-small cell lung cancer patients harboring sensitive EGFR mutations, but resistance arises rapidly.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	46-50
33459177-1	2021	ABTRACT The epidermal growth factor receptor (EGFR) kinase inhibitors Gefitinib, Erlotinib, Afatinib and Osimertinib have been approved for the treatments of non-small cell lung cancer patients harboring sensitive EGFR mutations, but resistance arises rapidly.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	214-218
33461557-1	2021	BACKGROUND: Epidermal growth factor receptor (EGFR)-mutated lung cancer constitutes a major subgroup of non-small cell lung cancer (NSCLC) and osimertinib is administrated as first-line treatment.	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	12-44
33461557-1	2021	BACKGROUND: Epidermal growth factor receptor (EGFR)-mutated lung cancer constitutes a major subgroup of non-small cell lung cancer (NSCLC) and osimertinib is administrated as first-line treatment.	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	46-50
33461557-9	2021	RESULTS: Intercellular transfer of exosomal wild type EGFR protein confers osimertinib resistance to EGFR-mutated sensitive cancer cells in vitro and in vivo.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	54-58
33461557-9	2021	RESULTS: Intercellular transfer of exosomal wild type EGFR protein confers osimertinib resistance to EGFR-mutated sensitive cancer cells in vitro and in vivo.	osimertinib	75-86	epidermal growth factor receptor	Homo sapiens	101-105
33461557-10	2021	Co-culture of EGFR-mutated sensitive cells and EGFR-nonmutated resistant cells promoted osimertinib resistance phenotype in EGFR-mutated cancer cells, while depletion of exosomes from conditioned medium or blockade of exosomal EGFR by neutralizing antibody alleviated this phenotype.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	14-18
33461557-10	2021	Co-culture of EGFR-mutated sensitive cells and EGFR-nonmutated resistant cells promoted osimertinib resistance phenotype in EGFR-mutated cancer cells, while depletion of exosomes from conditioned medium or blockade of exosomal EGFR by neutralizing antibody alleviated this phenotype.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	47-51
33461557-10	2021	Co-culture of EGFR-mutated sensitive cells and EGFR-nonmutated resistant cells promoted osimertinib resistance phenotype in EGFR-mutated cancer cells, while depletion of exosomes from conditioned medium or blockade of exosomal EGFR by neutralizing antibody alleviated this phenotype.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	47-51
33461557-10	2021	Co-culture of EGFR-mutated sensitive cells and EGFR-nonmutated resistant cells promoted osimertinib resistance phenotype in EGFR-mutated cancer cells, while depletion of exosomes from conditioned medium or blockade of exosomal EGFR by neutralizing antibody alleviated this phenotype.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	47-51
33461557-11	2021	Mechanistically, osimertinib promoted the release of exosomes by upregulated a Rab GTPase (RAB17).	osimertinib	17-28	RAB17, member RAS oncogene family	Homo sapiens	91-96
33461557-13	2021	Moreover, exosomes could be internalized by EGFR-mutated cancer cells via Clathrin-dependent endocytosis and then the encapsulated exosomal wild type EGFR protein activated downstream PI3K/AKT and MAPK signaling pathways and triggered osimertinib resistance.	osimertinib	235-246	epidermal growth factor receptor	Homo sapiens	44-48
33461557-13	2021	Moreover, exosomes could be internalized by EGFR-mutated cancer cells via Clathrin-dependent endocytosis and then the encapsulated exosomal wild type EGFR protein activated downstream PI3K/AKT and MAPK signaling pathways and triggered osimertinib resistance.	osimertinib	235-246	epidermal growth factor receptor	Homo sapiens	150-154
33461557-14	2021	CONCLUSIONS: Intercellular transfer of exosomal wild type EGFR promotes osimertinib resistance in NSCLC, which may represent a novel resistant mechanism of osimertinib and provide a proof of concept for targeting exosomes to prevent and reverse the osimertinib resistance.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	58-62
33461557-14	2021	CONCLUSIONS: Intercellular transfer of exosomal wild type EGFR promotes osimertinib resistance in NSCLC, which may represent a novel resistant mechanism of osimertinib and provide a proof of concept for targeting exosomes to prevent and reverse the osimertinib resistance.	osimertinib	156-167	epidermal growth factor receptor	Homo sapiens	58-62
33461557-14	2021	CONCLUSIONS: Intercellular transfer of exosomal wild type EGFR promotes osimertinib resistance in NSCLC, which may represent a novel resistant mechanism of osimertinib and provide a proof of concept for targeting exosomes to prevent and reverse the osimertinib resistance.	osimertinib	156-167	epidermal growth factor receptor	Homo sapiens	58-62
33500828-3	2021	Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) approved for the treatment of patients with NSCLC with an epithelial growth factor receptor (EGFR) mutation though its role in the treatment of NSCLC-PitM that remains unclear.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	124-157
33246030-6	2021	A combination of miR-137 mimic and AZD9291 had stronger inhibition on GH3 cells compared with miR-137 mimic or AZD9291 alone; furthermore, miR-137 inhibitor partially reversed the inhibition of AZD9291.	osimertinib	111-118	microRNA 137	Rattus norvegicus	17-24
33246030-6	2021	A combination of miR-137 mimic and AZD9291 had stronger inhibition on GH3 cells compared with miR-137 mimic or AZD9291 alone; furthermore, miR-137 inhibitor partially reversed the inhibition of AZD9291.	osimertinib	111-118	microRNA 137	Rattus norvegicus	17-24
33246030-7	2021	p21 and p27 were shown to be involved in the miR-137- and AZD9291-mediated effects on GH3 cells.	osimertinib	58-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
33246030-7	2021	p21 and p27 were shown to be involved in the miR-137- and AZD9291-mediated effects on GH3 cells.	osimertinib	58-65	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	8-11
33500828-3	2021	Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) approved for the treatment of patients with NSCLC with an epithelial growth factor receptor (EGFR) mutation though its role in the treatment of NSCLC-PitM that remains unclear.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	159-163
33500828-9	2021	Conclusion: Osimertinib is a third-generation EGFR-TKI that has demonstrated promising results among patients with metastatic EGFR-mutated NSCLC.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-50
33500828-9	2021	Conclusion: Osimertinib is a third-generation EGFR-TKI that has demonstrated promising results among patients with metastatic EGFR-mutated NSCLC.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	126-130
32398685-0	2021	Osimertinib successfully combats EGFR-negative glioblastoma cells by inhibiting the MAPK pathway.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	33-37
33129919-1	2021	The third-generation of EGFR-TKI osimertinib has been approved as a first-line therapy in NSCLC, representing the most successful advance in molecularly targeted therapy.	osimertinib	33-44	epidermal growth factor receptor	Homo sapiens	24-28
32398685-4	2021	In this study we investigated the antitumor activity of osimertinib, an FDA-approved epidermal growth factor receptor (EGFR) inhibitor, against patient-derived primary GBM cells.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	85-117
32398685-4	2021	In this study we investigated the antitumor activity of osimertinib, an FDA-approved epidermal growth factor receptor (EGFR) inhibitor, against patient-derived primary GBM cells.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	119-123
32398685-5	2021	Using high-throughput screening approach, we screened the entire panel of FDA-approved drugs against primary cancer cells derived from glioblastoma patients, found that osimertinib (3 muM) suppressed the proliferation of a subset (10/22) of EGFR-negative GBM cells (>50% growth inhibition).	osimertinib	169-180	epidermal growth factor receptor	Homo sapiens	241-245
32541922-8	2021	Furthermore, MDL-800 (25, 50 muM) enhanced the antiproliferation of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in osimertinib-resistant HCC827 and PC9 cells as well as in patient-derived primary tumor cells, and suppressed mitogen-activated protein kinase (MAPK) pathway.	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	129-133
32398685-7	2021	We further showed that osimertinib potently inhibited the MNK kinase activities with IC50 values of 324 nM and 48.6 nM, respectively, against MNK1 and MNK2 kinases; osimertinib (0.3-3 muM) dose-dependently suppressed the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E).	osimertinib	23-34	MAPK interacting serine/threonine kinase 1	Homo sapiens	142-146
32398685-7	2021	We further showed that osimertinib potently inhibited the MNK kinase activities with IC50 values of 324 nM and 48.6 nM, respectively, against MNK1 and MNK2 kinases; osimertinib (0.3-3 muM) dose-dependently suppressed the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E).	osimertinib	23-34	MAPK interacting serine/threonine kinase 2	Homo sapiens	151-155
32398685-7	2021	We further showed that osimertinib potently inhibited the MNK kinase activities with IC50 values of 324 nM and 48.6 nM, respectively, against MNK1 and MNK2 kinases; osimertinib (0.3-3 muM) dose-dependently suppressed the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E).	osimertinib	23-34	eukaryotic translation initiation factor 4E	Homo sapiens	240-283
32398685-7	2021	We further showed that osimertinib potently inhibited the MNK kinase activities with IC50 values of 324 nM and 48.6 nM, respectively, against MNK1 and MNK2 kinases; osimertinib (0.3-3 muM) dose-dependently suppressed the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E).	osimertinib	23-34	eukaryotic translation initiation factor 4E	Homo sapiens	285-290
32398685-8	2021	In GBM patient-derived xenografts mice, oral administration of osimertinib (40 mg  kg-1  d-1, for 18 days) significantly suppressed the tumor growth (TGI = 74.5%) and inhibited eIF4E phosphorylation in tumor cells.	osimertinib	63-74	eukaryotic translation initiation factor 4E	Mus musculus	177-182
33553373-0	2021	The emergence of various genetic alterations mediated the Osimertinib resistance of a patient harboring heterozygous germline EGFR T790M: a case report.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	126-130
33553373-4	2021	This study examined a patient harboring germline EGFR T790M who acquired resistance to Osimertinib therapy.	osimertinib	87-98	epidermal growth factor receptor	Homo sapiens	49-53
32972042-0	2021	A Phase II Trial of Osimertinib as the First-Line Treatment of Non-small Cell Lung Cancer Harboring Activating EGFR Mutations in Circulating Tumor DNA: LiquidLung-O-Cohort 1.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	111-115
32972042-1	2021	Purpose: Osimertinib is a potent, irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for both EGFR-activating and T790M resistant mutation.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	64-96
32972042-1	2021	Purpose: Osimertinib is a potent, irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for both EGFR-activating and T790M resistant mutation.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	98-102
32972042-1	2021	Purpose: Osimertinib is a potent, irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for both EGFR-activating and T790M resistant mutation.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	139-143
32972042-2	2021	The treatment efficacy of osimertinib was assessed in previously untreated patients with metastatic non-small cell lung carcinoma (NSCLC) harboring activating EGFR mutations in circulating tumor DNA (ctDNA) as well as tumor DNA.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	159-163
32972042-12	2021	Conclusion: Osimertinib had favorable efficacy in the first-line treatment of metastatic NSCLC harboring activating EGFR mutations in ctDNA as well as tumor DNA.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	116-120
33028591-1	2021	Purpose Osimertinib is a potent and selective epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) of both sensitizing and T790M resistance mutations.	osimertinib	8-19	epidermal growth factor receptor	Mus musculus	106-110
33721431-0	2021	Effect of osimertinib in treating patients with first-generation EGFR-TKI-resistant advanced non-small cell lung cancer and prognostic analysis.	osimertinib	10-21	epidermal growth factor receptor	Homo sapiens	65-69
33391435-0	2021	Silencing of CASC8 inhibits non-small cell lung cancer cells function and promotes sensitivity to osimertinib via FOXM1.	osimertinib	98-109	cancer susceptibility 8	Homo sapiens	13-18
33391435-0	2021	Silencing of CASC8 inhibits non-small cell lung cancer cells function and promotes sensitivity to osimertinib via FOXM1.	osimertinib	98-109	forkhead box M1	Homo sapiens	114-119
33721431-1	2021	PURPOSE: To explore the efficacy and safety of the third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) Osimertinib in the treatment of patients with first-generation EGFR-TKI-resistant advanced non-small cell lung cancer (NSCLC).	osimertinib	138-149	epidermal growth factor receptor	Homo sapiens	128-132
33391435-4	2021	Silencing CASC8 also promoted sensitivity to osimertinib through Forkhead box M1 (FOXM1).	osimertinib	45-56	cancer susceptibility 8	Homo sapiens	10-15
33721431-1	2021	PURPOSE: To explore the efficacy and safety of the third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) Osimertinib in the treatment of patients with first-generation EGFR-TKI-resistant advanced non-small cell lung cancer (NSCLC).	osimertinib	138-149	epidermal growth factor receptor	Homo sapiens	201-205
33391435-4	2021	Silencing CASC8 also promoted sensitivity to osimertinib through Forkhead box M1 (FOXM1).	osimertinib	45-56	forkhead box M1	Homo sapiens	65-80
33721431-17	2021	CONCLUSION: Osimertinib has definite efficacy in the treatment of patients with first-generation EGFR-TKI-resistant advanced NSCLC, with a low incidence rate of tolerable adverse reactions.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	97-101
33391435-4	2021	Silencing CASC8 also promoted sensitivity to osimertinib through Forkhead box M1 (FOXM1).	osimertinib	45-56	forkhead box M1	Homo sapiens	82-87
33038514-10	2021	In addition, treatment with osimertinib enhanced expression of the anti-apoptotic protein MCL1, and knockdown of ERBB2 suppressed the expression of MCL1 in L861Q, raising the possibility of differential allele-specific cross-phosphorylation of ERBB2.	osimertinib	28-39	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	90-94
33391435-6	2021	Our study revealed for the first time that silencing CASC8 inhibited the proliferation, migration, and invasion of non-small cell lung cancer cells and promoted their sensitivity to osimertinib, suggesting that CASC8 is closely related to the occurrence and development of non-small cell lung cancer.	osimertinib	182-193	cancer susceptibility 8	Homo sapiens	53-58
33391435-6	2021	Our study revealed for the first time that silencing CASC8 inhibited the proliferation, migration, and invasion of non-small cell lung cancer cells and promoted their sensitivity to osimertinib, suggesting that CASC8 is closely related to the occurrence and development of non-small cell lung cancer.	osimertinib	182-193	cancer susceptibility 8	Homo sapiens	211-216
32467321-1	2021	AIMS: Osimertinib is a third-generation EGFR (epidermal growth factor receptor) tyrosine kinase inhibitor that is effective in non-small cell lung cancer (NSCLC) harbouring the EGFR T790M mutation.	osimertinib	6-17	epidermal growth factor receptor	Homo sapiens	40-44
32467321-1	2021	AIMS: Osimertinib is a third-generation EGFR (epidermal growth factor receptor) tyrosine kinase inhibitor that is effective in non-small cell lung cancer (NSCLC) harbouring the EGFR T790M mutation.	osimertinib	6-17	epidermal growth factor receptor	Homo sapiens	46-78
32467321-1	2021	AIMS: Osimertinib is a third-generation EGFR (epidermal growth factor receptor) tyrosine kinase inhibitor that is effective in non-small cell lung cancer (NSCLC) harbouring the EGFR T790M mutation.	osimertinib	6-17	epidermal growth factor receptor	Homo sapiens	177-181
33276184-3	2021	RESULTS: We report a patient with EGFR-mutated NSCLC who experienced the progression of leptomeningeal metastases as a disease flare shortly after the discontinuation of osimertinib despite the absence of radiological or cytological findings.	osimertinib	170-181	epidermal growth factor receptor	Homo sapiens	34-38
33131198-0	2021	Predicting osimertinib-treatment outcomes through EGFR mutant-fraction monitoring in the circulating tumor DNA of EGFR T790M-positive patients with non-small-cell lung cancer (WJOG8815L).	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	50-54
33296806-0	2021	Clinical implications of germline BCL2L11 deletion polymorphism in pretreated advanced NSCLC patients with osimertinib therapy.	osimertinib	107-118	BCL2 like 11	Homo sapiens	34-41
33296806-2	2021	Nevertheless, the impact of BIM-del in advanced NSCLC patients treated with the third-generation EGFR-TKI osimertinib remains undetermined.	osimertinib	106-117	BCL2 like 11	Homo sapiens	28-31
33296806-3	2021	This study aims to evaluate the relationship between BIM-del and therapeutic efficacy of osimertinib in pretreated NSCLC patients.	osimertinib	89-100	BCL2 like 11	Homo sapiens	53-56
33296806-14	2021	CONCLUSIONS: BIM-del is associated with poor clinical responses and outcomes, and might be a negative predictive and prognostic biomarker in EGFR T790 M NSCLC patients with osimertinib treatment.	osimertinib	173-184	BCL2 like 11	Homo sapiens	13-16
33296806-14	2021	CONCLUSIONS: BIM-del is associated with poor clinical responses and outcomes, and might be a negative predictive and prognostic biomarker in EGFR T790 M NSCLC patients with osimertinib treatment.	osimertinib	173-184	epidermal growth factor receptor	Homo sapiens	141-145
33131198-0	2021	Predicting osimertinib-treatment outcomes through EGFR mutant-fraction monitoring in the circulating tumor DNA of EGFR T790M-positive patients with non-small-cell lung cancer (WJOG8815L).	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	114-118
33131198-2	2021	Purpose of this study was to assess the predictive value of monitoring EGFR genomic alterations in circulating tumor DNA (ctDNA) from patients with NSCLC that undergo treatment with the third-generation EGFR-TKI osimertinib.	osimertinib	212-223	epidermal growth factor receptor	Homo sapiens	71-75
33200796-0	2021	Inhibition of Bcl-2 and Bcl-xL overcomes the resistance to the third-generation EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancer.	osimertinib	111-122	BCL2 apoptosis regulator	Homo sapiens	14-19
33131198-2	2021	Purpose of this study was to assess the predictive value of monitoring EGFR genomic alterations in circulating tumor DNA (ctDNA) from patients with NSCLC that undergo treatment with the third-generation EGFR-TKI osimertinib.	osimertinib	212-223	epidermal growth factor receptor	Homo sapiens	203-207
33200796-0	2021	Inhibition of Bcl-2 and Bcl-xL overcomes the resistance to the third-generation EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancer.	osimertinib	111-122	BCL2 like 1	Homo sapiens	24-30
33270169-0	2021	The Allele Frequency of EGFR Mutations Predicts Survival in Advanced EGFR T790M-Positive Non-small Cell Lung Cancer Patients Treated with Osimertinib.	osimertinib	138-149	epidermal growth factor receptor	Homo sapiens	24-28
33200796-5	2021	Furthermore, the suppression of Bcl-2 and Bcl-xL through small interfering RNA-mediated gene knockdown or using a small molecule specific inhibitor ABT-263 re-sensitized HCC827/OR cells to osimertinib treatment.	osimertinib	189-200	BCL2 apoptosis regulator	Homo sapiens	32-37
33200796-5	2021	Furthermore, the suppression of Bcl-2 and Bcl-xL through small interfering RNA-mediated gene knockdown or using a small molecule specific inhibitor ABT-263 re-sensitized HCC827/OR cells to osimertinib treatment.	osimertinib	189-200	BCL2 like 1	Homo sapiens	42-48
33060857-5	2021	Currently, the field faces an unprecedented number of combinations of activating mutations with distinct resistance mutations in parallel to the approval of osimertinib as a first-line drug for EGFR-mutant lung cancer.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	194-198
33205587-0	2021	Osimertinib combined with bevacizumab for leptomeningeal metastasis from EGFR-mutation non-small cell lung cancer: A phase II single-arm prospective clinical trial.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	73-77
33131198-6	2021	Both MFs were found to decrease during treatment, whereas rebound of the sensitizing EGFR MF was observed at PD/stop, suggesting that osimertinib targeted both T790M mutation-positive tumors and tumors with sensitizing EGFR mutations.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	85-89
33131198-6	2021	Both MFs were found to decrease during treatment, whereas rebound of the sensitizing EGFR MF was observed at PD/stop, suggesting that osimertinib targeted both T790M mutation-positive tumors and tumors with sensitizing EGFR mutations.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	219-223
33131198-8	2021	In conclusion, ctDNA monitoring for sensitizing EGFR mutations at C4 is suitable for predicting the treatment outcomes in NSCLC patients receiving osimertinib.	osimertinib	147-158	epidermal growth factor receptor	Homo sapiens	48-52
33270169-0	2021	The Allele Frequency of EGFR Mutations Predicts Survival in Advanced EGFR T790M-Positive Non-small Cell Lung Cancer Patients Treated with Osimertinib.	osimertinib	138-149	epidermal growth factor receptor	Homo sapiens	69-73
33569316-2	2021	Herein, we investigated the molecular factors and dynamic changes in ctDNA that can serve as predictors of survival outcomes of patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small cell lung cancer (NSCLC) who received osimertinib therapy after progression from prior EGFR inhibitor regimen.	osimertinib	247-258	epidermal growth factor receptor	Homo sapiens	142-174
33270169-1	2021	BACKGROUND: The allele frequency of epidermal growth factor receptor (EGFR) mutations could be a potential molecular biomarker for the outcome of osimertinib therapy.	osimertinib	146-157	epidermal growth factor receptor	Homo sapiens	36-68
33569316-2	2021	Herein, we investigated the molecular factors and dynamic changes in ctDNA that can serve as predictors of survival outcomes of patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small cell lung cancer (NSCLC) who received osimertinib therapy after progression from prior EGFR inhibitor regimen.	osimertinib	247-258	epidermal growth factor receptor	Homo sapiens	176-180
33270169-1	2021	BACKGROUND: The allele frequency of epidermal growth factor receptor (EGFR) mutations could be a potential molecular biomarker for the outcome of osimertinib therapy.	osimertinib	146-157	epidermal growth factor receptor	Homo sapiens	70-74
33270169-2	2021	OBJECTIVE: The purpose of our study was to assess the clinical relevance of the allele frequency of EGFR mutations in plasma-based circulating tumor DNA (ctDNA) before starting osimertinib therapy in patients with advanced EGFR-mutated non-small cell lung cancer (NSCLC) who had progressed under treatment with EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	177-188	epidermal growth factor receptor	Homo sapiens	223-227
33270169-2	2021	OBJECTIVE: The purpose of our study was to assess the clinical relevance of the allele frequency of EGFR mutations in plasma-based circulating tumor DNA (ctDNA) before starting osimertinib therapy in patients with advanced EGFR-mutated non-small cell lung cancer (NSCLC) who had progressed under treatment with EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	177-188	epidermal growth factor receptor	Homo sapiens	223-227
33151783-6	2021	Results: Compared with standard EGFR-TKIs, osimertinib was associated with a higher incremental cost of A$118,502, and an incremental benefit of 0.274 QALYs and 0.313 LYs.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	32-36
33392076-0	2020	Lung Adenocarcinoma Harboring EGFR Kinase Domain Duplication (EGFR-KDD) Confers Sensitivity to Osimertinib and Nivolumab: A Case Report.	osimertinib	95-106	epidermal growth factor receptor	Homo sapiens	30-60
33392076-0	2020	Lung Adenocarcinoma Harboring EGFR Kinase Domain Duplication (EGFR-KDD) Confers Sensitivity to Osimertinib and Nivolumab: A Case Report.	osimertinib	95-106	epidermal growth factor receptor	Homo sapiens	30-34
33392076-10	2020	Conclusions: Our case provided direct evidence to support the role of Osimertinib in the treatment of EGFR-KDD, as well as added valuable insights into application of immune-based therapeutics in the specific subgroups bearing EGFR alteration(s).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	102-110
33392076-10	2020	Conclusions: Our case provided direct evidence to support the role of Osimertinib in the treatment of EGFR-KDD, as well as added valuable insights into application of immune-based therapeutics in the specific subgroups bearing EGFR alteration(s).	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	102-106
33489892-2	2020	For instance, the occurrence of EGFR T790M is associated with resistance to gefitinib, erlotinib, and afatinib, while EGFR C797S causes osimertinib to lose activity.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	32-36
33489892-2	2020	For instance, the occurrence of EGFR T790M is associated with resistance to gefitinib, erlotinib, and afatinib, while EGFR C797S causes osimertinib to lose activity.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	118-122
33396393-3	2020	The acquired EGFR C797S mutation is a known mechanism that confers resistance to third-generation EGFR TKIs such as AZD9291.	osimertinib	116-123	epidermal growth factor receptor	Homo sapiens	13-17
33396393-3	2020	The acquired EGFR C797S mutation is a known mechanism that confers resistance to third-generation EGFR TKIs such as AZD9291.	osimertinib	116-123	epidermal growth factor receptor	Homo sapiens	98-102
33456471-1	2020	Osimertinib is a novel oral, potent, and irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) for treatment of advanced T790M mutation-positive advanced non-small cell lung cancer, which is commonly combined with ginsenoside Rg3 in clinic to enhance the efficacy and minimize adverse reactions.	osimertinib	0-11	epidermal growth factor receptor	Rattus norvegicus	114-118
33374971-0	2020	Efficacy of the CDK4/6 Dual Inhibitor Abemaciclib in EGFR-Mutated NSCLC Cell Lines with Different Resistance Mechanisms to Osimertinib.	osimertinib	123-134	cyclin dependent kinase 4	Homo sapiens	16-22
33324104-0	2020	Osimertinib for Front-Line Treatment of Locally Advanced or Metastatic EGFR-Mutant NSCLC Patients: Efficacy, Acquired Resistance and Perspectives for Subsequent Treatments.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	71-75
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
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	erb-b2 receptor tyrosine kinase 2	Homo sapiens	135-139
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	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	155-159
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	epidermal growth factor receptor	Homo sapiens	237-241
33511016-0	2021	AZD9291 Resistance Reversal Activity of a pH-Sensitive Nanocarrier Dual-Loaded with Chloroquine and FGFR1 Inhibitor in NSCLC.	osimertinib	0-7	fibroblast growth factor receptor 1	Homo sapiens	100-105
33280593-3	2022	The USFDA approved osimertinib to treat patients with metastatic T790M EGFR NSCLC on a regular basis in March 2017.	osimertinib	19-30	epidermal growth factor receptor	Homo sapiens	71-75
33280593-6	2022	RESULT: Osimertinib analouge 48, 50, 60, 61, 67, 75, 80, 86, 89, 92, 93, 116 and 124 were the most active and selective compounds against T790M EGFR mutants compared to Osimertinib.	osimertinib	8-19	epidermal growth factor receptor	Homo sapiens	144-148
33511016-3	2021	This study shows that autophagy and fibroblast growth factor receptor 1 signaling pathways are both activated in AZD9291 resistant NSCLC, and inhibition of them, respectively, by chloroquine (CQ) and PD173074 can synergistically reverse AZD9291 resistance.	osimertinib	113-120	fibroblast growth factor receptor 1	Homo sapiens	36-71
33511016-3	2021	This study shows that autophagy and fibroblast growth factor receptor 1 signaling pathways are both activated in AZD9291 resistant NSCLC, and inhibition of them, respectively, by chloroquine (CQ) and PD173074 can synergistically reverse AZD9291 resistance.	osimertinib	237-244	fibroblast growth factor receptor 1	Homo sapiens	36-71
33511016-8	2021	The combination of CP@NP-cRGD and AZD9291 significantly induces a higher rate of apoptosis, more G0/G1 phase arrest, and reduces proliferation of resistant cell lines by downregulation of p-ERK1/2 in vitro.	osimertinib	34-41	mitogen-activated protein kinase 3	Homo sapiens	190-196
32424780-0	2020	Osimertinib for patients with poor performance status and EGFR T790M mutation-positive advanced non-small cell lung cancer: a phase II clinical trial.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	58-62
33287368-3	2020	We established 3rd generation EGFR-TKI resistant cell lines (H1975/WR and H1975/OR) via repeated exposure to WZ4002 and osimertinib.	osimertinib	120-131	epidermal growth factor receptor	Homo sapiens	30-34
32854536-0	2020	Sequential afatinib and osimertinib in patients with EGFR mutation-positive non-small-cell lung cancer: final analysis of the GioTag study.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	53-57
32854536-6	2020	Conclusion: In real-world clinical practice, sequential afatinib and osimertinib was associated with encouraging outcomes in patients with EGFR mutation-positive NSCLC, especially in Del19-positive patients and Asian patients.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	139-143
32424780-1	2020	Osimertinib is a molecularly targeted agent used to treat non-small cell lung cancer (NSCLC) patients with an epidermal growth factor receptor (EGFR) T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	110-142
32424780-1	2020	Osimertinib is a molecularly targeted agent used to treat non-small cell lung cancer (NSCLC) patients with an epidermal growth factor receptor (EGFR) T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	144-148
32424780-14	2020	Osimertinib therapy could be beneficial for EGFR T790M mutation-positive advanced NSCLC patients with poor PS.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	44-48
32927121-0	2020	Real-world evaluation of factors for interstitial lung disease incidence and radiologic characteristics in patients with epidermal growth factor receptor T790M-positive non-small cell lung cancer treated with osimertinib in Japan.	osimertinib	209-220	epidermal growth factor receptor	Homo sapiens	121-153
32927121-1	2020	INTRODUCTION: Using real-world Japanese post-marketing data, we characterized interstitial lung disease (ILD) development during second- or later-line osimertinib treatment for epidermal growth factor receptor-mutation-positive non-small cell lung cancer.	osimertinib	151-162	epidermal growth factor receptor	Homo sapiens	177-209
33035779-0	2020	A rare EGFR mutation L747P conferred therapeutic efficacy to both gefitinib and osimertinib: A case report.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	7-11
33035779-7	2020	This case revealed that EGFR L747 P rendered both gefitinib and osimertinib therapeutically efficacious.	osimertinib	64-75	epidermal growth factor receptor	Homo sapiens	24-28
33049499-0	2020	Inhibition of ACK1 delays and overcomes acquired resistance of EGFR mutant NSCLC cells to the third generation EGFR inhibitor, osimertinib.	osimertinib	127-138	tyrosine kinase, non-receptor, 2	Mus musculus	14-18
33049499-0	2020	Inhibition of ACK1 delays and overcomes acquired resistance of EGFR mutant NSCLC cells to the third generation EGFR inhibitor, osimertinib.	osimertinib	127-138	epidermal growth factor receptor	Mus musculus	63-67
33049499-0	2020	Inhibition of ACK1 delays and overcomes acquired resistance of EGFR mutant NSCLC cells to the third generation EGFR inhibitor, osimertinib.	osimertinib	127-138	epidermal growth factor receptor	Mus musculus	111-115
33049499-1	2020	OBJECTIVES: The emergence of acquired resistance to the third generation EGFR inhibitor, osimertinib (AZD9291 or TAGRISSO ), is an unavoidable huge clinical challenge.	osimertinib	89-100	epidermal growth factor receptor	Mus musculus	73-77
33049499-1	2020	OBJECTIVES: The emergence of acquired resistance to the third generation EGFR inhibitor, osimertinib (AZD9291 or TAGRISSO ), is an unavoidable huge clinical challenge.	osimertinib	102-109	epidermal growth factor receptor	Mus musculus	73-77
33049499-1	2020	OBJECTIVES: The emergence of acquired resistance to the third generation EGFR inhibitor, osimertinib (AZD9291 or TAGRISSO ), is an unavoidable huge clinical challenge.	osimertinib	113-121	epidermal growth factor receptor	Mus musculus	73-77
33049499-2	2020	The involvement of ACK1, a non-receptor tyrosine kinase with an oncogenic function, in regulating cell response to osimertinib has not been investigated and thus is the focus of this study.	osimertinib	115-126	tyrosine kinase, non-receptor, 2	Mus musculus	19-23
33049499-8	2020	RESULTS: Inhibition of ACK1 with the novel ACK1 inhibitor, (R)-9b synergized with osimertinib in inhibiting the growth of EGFR mutant NSCLC cell lines.	osimertinib	82-93	tyrosine kinase, non-receptor, 2	Mus musculus	23-27
33049499-8	2020	RESULTS: Inhibition of ACK1 with the novel ACK1 inhibitor, (R)-9b synergized with osimertinib in inhibiting the growth of EGFR mutant NSCLC cell lines.	osimertinib	82-93	tyrosine kinase, non-receptor, 2	Mus musculus	43-47
33049499-8	2020	RESULTS: Inhibition of ACK1 with the novel ACK1 inhibitor, (R)-9b synergized with osimertinib in inhibiting the growth of EGFR mutant NSCLC cell lines.	osimertinib	82-93	epidermal growth factor receptor	Mus musculus	122-126
33049499-12	2020	Further, the (R)-9b and osimertinib combination was also effective in inhibiting the growth of EGFR mutant NSCLC cell lines with acquired resistance to osimertinib, which possess elevated levels of ACK1, and the growth of osimertinib-resistant tumors in vivo.	osimertinib	24-35	epidermal growth factor receptor	Mus musculus	95-99
33049499-12	2020	Further, the (R)-9b and osimertinib combination was also effective in inhibiting the growth of EGFR mutant NSCLC cell lines with acquired resistance to osimertinib, which possess elevated levels of ACK1, and the growth of osimertinib-resistant tumors in vivo.	osimertinib	24-35	tyrosine kinase, non-receptor, 2	Mus musculus	198-202
33049499-12	2020	Further, the (R)-9b and osimertinib combination was also effective in inhibiting the growth of EGFR mutant NSCLC cell lines with acquired resistance to osimertinib, which possess elevated levels of ACK1, and the growth of osimertinib-resistant tumors in vivo.	osimertinib	152-163	epidermal growth factor receptor	Mus musculus	95-99
33067020-0	2020	Response to Osimertinib in a NSCLC Patient Harboring EGFR V843I Germ-Line Mutation.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	53-57
33186860-0	2020	Survival outcomes and symptomatic central nervous system (CNS) metastasis in EGFR-mutant advanced non-small cell lung cancer without baseline CNS metastasis: Osimertinib vs. first-generation EGFR tyrosine kinase inhibitors.	osimertinib	158-169	epidermal growth factor receptor	Homo sapiens	77-81
33489813-0	2020	Osimertinib in combination with bevacizumab in EGFR-Mutated NSCLC with leptomeningeal metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	47-51
33489825-5	2020	More recently, ADAURA study evaluating adjuvant osimertinib demonstrated a profound reduction of the risk of recurrence in patients with stage I (>4 cm)-IIIA eNSCLC harbouring EGFR sensitizing mutations.	osimertinib	48-59	epidermal growth factor receptor	Homo sapiens	176-180
33324543-0	2020	Osimertinib Resistance With a Novel EGFR L858R/A859S/Y891D Triple Mutation in a Patient With Non-Small Cell Lung Cancer: A Case Report.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	36-40
33324543-3	2020	Here, we report a novel EGFR L858R/A859S/Y891D triple mutation in plasma-derived circulating tumor DNA (ctDNA) was identified in a 53-year-old male patient with NSCLC resistant to osimertinib treatment, using an ultra-deep (20,000x) 160-gene panel through the NGS platform.	osimertinib	180-191	epidermal growth factor receptor	Homo sapiens	24-28
33318755-7	2020	Conclusion: In this NMA, we found that osimertinib is the most efficacious and safest EGFR-TKI.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	86-90
33262603-0	2020	Case Report: A Metabolic Complete Response to Upfront Osimertinib in a Smoker Non-Small Cell Lung Cancer Patient Harbouring EGFR G719A/V769M Complex Mutation.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	124-128
33262603-3	2020	Here, we reported the case of a complete metabolic response in a patient with advanced NSCLC carrying the uncommon EGFR G719A/V769M complex mutation treated with the first-line osimertinib.	osimertinib	177-188	epidermal growth factor receptor	Homo sapiens	115-119
32773008-4	2020	The third-generation EGFR-TKIs, represented by osimertinib, are found to have significant effect on this resistance.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	21-25
33203197-1	2020	BACKGROUND: Osimertinib is approved by Food and Drug Administration for patients with advanced non-small cell lung cancer carrying EGFR-T790M mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	131-135
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
33174519-2	2022	Osimertinib is the only FDA-approved third-generation inhibitor, which has a good potency against the EGFR-T790M mutant with minimal toxicities and excellent selectivity for wild-type EGFR.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	102-106
33174519-2	2022	Osimertinib is the only FDA-approved third-generation inhibitor, which has a good potency against the EGFR-T790M mutant with minimal toxicities and excellent selectivity for wild-type EGFR.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	184-188
33174519-3	2022	EGFR tertiary Cys797 to Ser797 (C797S) point mutation emanate rapidly after the treatment of osimertinib, which is an undruggable mutation to all three existing generation drugs.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	0-4
33335671-1	2020	Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) and currently the gold-standard for the treatment of patients suffering from non-small cell lung cancer (NSCLC) harboring T790M-mutated epidermal growth factor receptor (EGFR).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	202-234
33335671-1	2020	Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) and currently the gold-standard for the treatment of patients suffering from non-small cell lung cancer (NSCLC) harboring T790M-mutated epidermal growth factor receptor (EGFR).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	236-240
33153414-4	2021	Consequently, osimertinib, a third-generation EGFR TKI, was studied and demonstrated activity against EGFR-sensitizing and resistant mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	46-50
33153414-4	2021	Consequently, osimertinib, a third-generation EGFR TKI, was studied and demonstrated activity against EGFR-sensitizing and resistant mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	102-106
33153004-6	2020	In 60% of cases, resistance to these TKIs occurs due to T790M mutation in EGFR, which is overcome 3rd generation drugs (osimertinib).	osimertinib	120-131	epidermal growth factor receptor	Homo sapiens	74-78
33173309-4	2020	A novel MYH9 (exon41)-RET (exon12) fusion and EGFR exon20 p.T790M loss were identified using plasma circulation tumor DNA (ctDNA) after osimertinib treatment, which led to rapid progression after osimertinib five months and suggested a potential resistance mechanism.	osimertinib	136-147	myosin heavy chain 9	Homo sapiens	8-12
33173309-4	2020	A novel MYH9 (exon41)-RET (exon12) fusion and EGFR exon20 p.T790M loss were identified using plasma circulation tumor DNA (ctDNA) after osimertinib treatment, which led to rapid progression after osimertinib five months and suggested a potential resistance mechanism.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	46-50
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	50-53
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	125-128
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	epidermal growth factor receptor	Homo sapiens	147-151
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	epidermal growth factor receptor	Homo sapiens	243-247
33294282-1	2020	A growing number of progression on Osimertinib among EGFR-mutated lung cancers represents a great challenge clinically.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	53-57
33294282-5	2020	Compared with the 1st-TKIs-resistant group, EGFR mutations C797S/G, L718Q/V, L792F/H were significantly more enriched in the Osimertinib-resistant cohort, whose sensitivities to Osimertinib were successfully predicted.	osimertinib	125-136	epidermal growth factor receptor	Homo sapiens	44-48
33294282-5	2020	Compared with the 1st-TKIs-resistant group, EGFR mutations C797S/G, L718Q/V, L792F/H were significantly more enriched in the Osimertinib-resistant cohort, whose sensitivities to Osimertinib were successfully predicted.	osimertinib	178-189	epidermal growth factor receptor	Homo sapiens	44-48
33294282-6	2020	Importantly, a total of 14 low-frequency EGFR mutations were exclusively or significantly observed in the Osimertinib-resistant group, 7 were predicted to dramatically reduce the binding affinity of EGFR to Osimertinib (G796S, V802F, T725M, Q791L/H, P794S/R).	osimertinib	106-117	epidermal growth factor receptor	Homo sapiens	41-45
33294282-6	2020	Importantly, a total of 14 low-frequency EGFR mutations were exclusively or significantly observed in the Osimertinib-resistant group, 7 were predicted to dramatically reduce the binding affinity of EGFR to Osimertinib (G796S, V802F, T725M, Q791L/H, P794S/R).	osimertinib	106-117	epidermal growth factor receptor	Homo sapiens	199-203
33294282-6	2020	Importantly, a total of 14 low-frequency EGFR mutations were exclusively or significantly observed in the Osimertinib-resistant group, 7 were predicted to dramatically reduce the binding affinity of EGFR to Osimertinib (G796S, V802F, T725M, Q791L/H, P794S/R).	osimertinib	207-218	epidermal growth factor receptor	Homo sapiens	41-45
33294282-6	2020	Importantly, a total of 14 low-frequency EGFR mutations were exclusively or significantly observed in the Osimertinib-resistant group, 7 were predicted to dramatically reduce the binding affinity of EGFR to Osimertinib (G796S, V802F, T725M, Q791L/H, P794S/R).	osimertinib	207-218	epidermal growth factor receptor	Homo sapiens	199-203
33294282-7	2020	Analysis of pre-Osimertinib treatment samples of two patients supported that EGFR V802F and G796S were acquired during the treatment.	osimertinib	16-27	epidermal growth factor receptor	Homo sapiens	77-81
33294282-9	2020	This study represented the largest real-world data so far investigating Osimertinib resistance in EGFR-mutated lung cancer.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	98-102
33294282-10	2020	We identified a collection of coexistent EGFR rare mutations and provided possible guidance for those patients who progressed on the first-line treatment of Osimertinib.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	41-45
32861806-0	2020	Osimertinib versus platinum-pemetrexed for patients with EGFR T790M advanced NSCLC and progression on a prior EGFR-tyrosine kinase inhibitor: AURA3 overall survival analysis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	110-114
32542461-1	2020	Background Osimertinib is one of the first-line treatments for advanced non-small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	117-149
32542461-1	2020	Background Osimertinib is one of the first-line treatments for advanced non-small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	151-155
32861806-1	2020	BACKGROUND: In AURA3 (NCT02151981), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), significantly prolonged progression-free survival and improved response in patients with EGFR T790M advanced non-small-cell lung cancer (NSCLC) and progression on prior EGFR-TKI treatment.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	68-100
32861806-1	2020	BACKGROUND: In AURA3 (NCT02151981), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), significantly prolonged progression-free survival and improved response in patients with EGFR T790M advanced non-small-cell lung cancer (NSCLC) and progression on prior EGFR-TKI treatment.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	230-234
32861806-1	2020	BACKGROUND: In AURA3 (NCT02151981), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), significantly prolonged progression-free survival and improved response in patients with EGFR T790M advanced non-small-cell lung cancer (NSCLC) and progression on prior EGFR-TKI treatment.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	230-234
32873635-3	2020	Consistent with our previous studies, we show here that long-term, moderate hypoxia promotes resistance to the EGFR TKI osimertinib (AZD9291) in the NSCLC cell line H1975, which harbors two EGFR mutations including T790M.	osimertinib	120-131	epidermal growth factor receptor	Mus musculus	111-115
32798688-0	2020	Osimertinib in CNS-progressive EGFR-mutant lung cancer: Do we need to detect T790M?	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	31-35
32928921-0	2020	Allosteric SHP2 inhibitor IACS-13909 overcomes EGFR-dependent and EGFR-independent resistance mechanisms towards osimertinib.	osimertinib	113-124	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	11-15
32873635-3	2020	Consistent with our previous studies, we show here that long-term, moderate hypoxia promotes resistance to the EGFR TKI osimertinib (AZD9291) in the NSCLC cell line H1975, which harbors two EGFR mutations including T790M.	osimertinib	133-140	epidermal growth factor receptor	Mus musculus	111-115
32928921-0	2020	Allosteric SHP2 inhibitor IACS-13909 overcomes EGFR-dependent and EGFR-independent resistance mechanisms towards osimertinib.	osimertinib	113-124	epidermal growth factor receptor	Homo sapiens	66-70
33064977-0	2020	LncRNA TSLNC8 synergizes with EGFR inhibitor osimertinib to inhibit lung cancer tumorigenesis by blocking the EGFR-STAT3 pathway.	osimertinib	45-56	epidermal growth factor receptor	Mus musculus	30-34
32928921-3	2020	The long-term effectiveness of tyrosine kinase inhibitors (TKI) such as the EGFR inhibitor osimertinib in non-small cell lung cancer (NSCLC) is limited by acquired resistance.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	76-80
32928921-4	2020	Multiple clinically identified mechanisms underlie resistance to osimertinib, including mutations in EGFR that preclude drug binding as well as EGFR-independent activation of the MAPK pathway through alternate RTK (RTK-bypass).	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	101-105
32928921-4	2020	Multiple clinically identified mechanisms underlie resistance to osimertinib, including mutations in EGFR that preclude drug binding as well as EGFR-independent activation of the MAPK pathway through alternate RTK (RTK-bypass).	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	144-148
33064977-0	2020	LncRNA TSLNC8 synergizes with EGFR inhibitor osimertinib to inhibit lung cancer tumorigenesis by blocking the EGFR-STAT3 pathway.	osimertinib	45-56	epidermal growth factor receptor	Mus musculus	110-114
33064977-0	2020	LncRNA TSLNC8 synergizes with EGFR inhibitor osimertinib to inhibit lung cancer tumorigenesis by blocking the EGFR-STAT3 pathway.	osimertinib	45-56	signal transducer and activator of transcription 3	Mus musculus	115-120
33064977-8	2020	TSLNC8 overexpression or osimertinib administration led to promotion of apoptosis and inhibition of cell proliferation, migration and invasion, as well as deactivation of the EGFR-STAT3 pathway, whereas TSLNC8 knockdown had opposite effects.	osimertinib	25-36	epidermal growth factor receptor	Mus musculus	175-179
33064977-12	2020	In this study, we revealed a TSLNC8-EGFR-STAT3 signaling axis in lung cancer, and TSLNC8 overexpression significantly enhanced the anti-tumor effects of osimertinib via inhibiting EGFR-STAT3 signaling.	osimertinib	153-164	epidermal growth factor receptor	Mus musculus	36-40
33064977-12	2020	In this study, we revealed a TSLNC8-EGFR-STAT3 signaling axis in lung cancer, and TSLNC8 overexpression significantly enhanced the anti-tumor effects of osimertinib via inhibiting EGFR-STAT3 signaling.	osimertinib	153-164	signal transducer and activator of transcription 3	Mus musculus	41-46
33064977-12	2020	In this study, we revealed a TSLNC8-EGFR-STAT3 signaling axis in lung cancer, and TSLNC8 overexpression significantly enhanced the anti-tumor effects of osimertinib via inhibiting EGFR-STAT3 signaling.	osimertinib	153-164	epidermal growth factor receptor	Mus musculus	180-184
33028495-1	2020	PURPOSE: This study aimed to evaluate the cost-effectiveness of osimertinib vs docetaxel and bevacizumab in third-line treatment in EGFR T790M resistance mutation advanced non-small cell lung cancer in China from the perspective of the health care system.	osimertinib	64-75	epidermal growth factor receptor	Homo sapiens	132-136
33028495-0	2020	Cost-effectiveness of Osimertinib vs Docetaxel-Bevacizumab in Third-Line Treatment in EGFR T790M Resistance Mutation Advanced Non-Small Cell Lung Cancer in China.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	86-90
33064977-12	2020	In this study, we revealed a TSLNC8-EGFR-STAT3 signaling axis in lung cancer, and TSLNC8 overexpression significantly enhanced the anti-tumor effects of osimertinib via inhibiting EGFR-STAT3 signaling.	osimertinib	153-164	signal transducer and activator of transcription 3	Mus musculus	185-190
33028495-4	2020	Efficacy and safety data of osimertinib vs docetaxel and bevacizumab in patients who had acquired EGFR T790M resistance mutation were derived from a key head-to-head clinical trial.	osimertinib	28-39	epidermal growth factor receptor	Homo sapiens	98-102
33028495-12	2020	IMPLICATIONS: The findings from the present analysis suggest that osimertinib could be cost-effective vs docetaxel and bevacizumab in third-line treatment in EGFR T790M resistance mutation advanced non-small cell lung cancer in China.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	158-162
32652216-0	2020	Osimertinib improves overall survival in EGFR-mutated non-small cell lung cancer patients with leptomeningeal metastases regardless of T790M mutational status.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	41-45
32845180-4	2020	We describe the methodology for this integration and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: For better accuracy in estimating the ADP, we used the prices generated from the six dimensions at scenario levels, not at the dimension-specific price (DSP) level.	osimertinib	171-182	epidermal growth factor receptor	Homo sapiens	152-156
32845191-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: The reference-based pricing dimension utilizes a six-step method: 1) selecting foreign countries based on a set of four criteria (drug is available in the foreign country, price information is available in the foreign country, foreign countries are members within the organization for Economic Co-operation and Development, pricing methods in the foreign countries involve value assessment); 2) adjusting for exchange rates; 3) generating reference price (RP) scenarios; 4) adjusting with the medical inflation rate; 5) pooling all generated RP scenarios and calculating average and standard deviation (SD); 6) and Monte Carlo Simulation (MCS) to estimate the dimension-specific DSPReference.	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32845201-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: Eight WTP scenarios based on four levels of real gross domestic product per capita (<1GDP/capita, 1xGDP/capita, 3xGDP/capita, and >3xGDP/capita) and two market conditions (monopolistic versus competitive) were assumed.	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32845204-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: The risk of efficacy failure pricing dimension utilizes a seven-step method: 1) defining risk; 2) extracting data; 3) predicting models; 4) performing Monte Carlo Simulation (MCS) to estimate risk of efficacy failure; 5) estimating ranges for a payback; 6) adjusting for medical inflation; and 7) performing Monte Carlo Simulation (MCS) to estimate the DSPRisk of efficacy failure.	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32845205-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: The safety-based pricing dimension utilizes a four-step method: 1) pooling adverse events (AE), standardizing, estimating 95%CIs, and adjusting for time; 2) estimating correction factors and corrected probabilities of AEs; 3) estimating the probability of at least one adverse event (AE) occurring and leading to treatment discontinuation; and 4) estimating ranges for payback percentages and performing Monte Carlo Simulation to estimate a DSPSafety.	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32845209-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: We propose two paybacks based on adherence: in-advance (based on clinical trial data) and in-arrear (based on real-world data).	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32845794-3	2020	We describe this dimension"s methodology and present a proof-of-concept application to the treatment of non-small cell lung cancer (NSCLC) with EGFR mutation with osimertinib.Materials and methods: CEA and CUA were performed using established methods.	osimertinib	163-174	epidermal growth factor receptor	Homo sapiens	144-148
32886557-0	2020	Cost-effectiveness analysis of osimertinib for first-line treatment of locally advanced or metastatic EGFR mutation positive non-small cell lung cancer in Singapore.	osimertinib	31-42	epidermal growth factor receptor	Homo sapiens	102-106
32652216-1	2020	INTRODUCTION: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), efficiently penetrates the blood-brain barrier.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	46-78
32652216-1	2020	INTRODUCTION: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), efficiently penetrates the blood-brain barrier.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	80-84
32652216-2	2020	Current study explored whether treatment with osimertinib leads to improved overall survival (OS) for EGFR-mutated NSCLC patients with leptomeningeal metastases (LM) compared with those not treated with osimertinib.	osimertinib	46-57	Moloney sarcoma oncogene	Mus musculus	94-96
32652216-2	2020	Current study explored whether treatment with osimertinib leads to improved overall survival (OS) for EGFR-mutated NSCLC patients with leptomeningeal metastases (LM) compared with those not treated with osimertinib.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	102-106
32652216-8	2020	However, patients treated with osimertinib showed a superior OS of 17.0 months (95% CI, 15.13-18.94) compared with those not treated with osimertinib who showed a mOS 5.5 months (95% CI 4.34-6.63) regardless of T790M mutational status (HR 0.36; 95% CI 0.28-0.47, P <0.001).	osimertinib	31-42	Moloney sarcoma oncogene	Mus musculus	61-63
32652216-10	2020	CONCLUSIONS: Osimertinib is a promising treatment option for EGFR-mutated NSCLC with LM regardless of T790M mutational status.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	61-65
33193830-2	2020	Three reasons are suggested: since rechallenge with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is covered by health insurance in Japan, EGFR-TKI rechallenge rate was higher in SOC than in the osimertinib group, which resulted in a long-term sequential administration of EGFR-TKIs; treatment discontinuation rate was high in the osimertinib group due to adverse events such as interstitial pneumonia among Japanese patients.	osimertinib	219-230	epidermal growth factor receptor	Homo sapiens	112-116
32956986-0	2020	Concurrent use of aspirin with osimertinib is associated with improved survival in advanced EGFR-mutant non-small cell lung cancer.	osimertinib	31-42	epidermal growth factor receptor	Homo sapiens	92-96
32956986-1	2020	BACKGROUND: Osimertinib is the treatment of choice for advanced EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	64-68
32956986-5	2020	METHODS: MD Anderson Cancer Center GEMINI database was retrospectively queried for EGFR-mutant NSCLC patients who received osimertinib with or without concurrent use of aspirin for progression-free survival (PFS) and overall survival (OS).	osimertinib	123-134	epidermal growth factor receptor	Homo sapiens	83-87
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	55-59
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	osimertinib	40-51	tumor protein p53	Homo sapiens	209-213
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	osimertinib	40-51	CD274 molecule	Homo sapiens	219-224
33193830-2	2020	Three reasons are suggested: since rechallenge with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is covered by health insurance in Japan, EGFR-TKI rechallenge rate was higher in SOC than in the osimertinib group, which resulted in a long-term sequential administration of EGFR-TKIs; treatment discontinuation rate was high in the osimertinib group due to adverse events such as interstitial pneumonia among Japanese patients.	osimertinib	219-230	epidermal growth factor receptor	Homo sapiens	163-167
33193830-2	2020	Three reasons are suggested: since rechallenge with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is covered by health insurance in Japan, EGFR-TKI rechallenge rate was higher in SOC than in the osimertinib group, which resulted in a long-term sequential administration of EGFR-TKIs; treatment discontinuation rate was high in the osimertinib group due to adverse events such as interstitial pneumonia among Japanese patients.	osimertinib	355-366	epidermal growth factor receptor	Homo sapiens	112-116
33193830-2	2020	Three reasons are suggested: since rechallenge with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is covered by health insurance in Japan, EGFR-TKI rechallenge rate was higher in SOC than in the osimertinib group, which resulted in a long-term sequential administration of EGFR-TKIs; treatment discontinuation rate was high in the osimertinib group due to adverse events such as interstitial pneumonia among Japanese patients.	osimertinib	355-366	epidermal growth factor receptor	Homo sapiens	163-167
33193830-6	2020	Methods: The Heat on Beat study is a randomized, open-label, multicenter, phase II study to compare OS between initial treatment with afatinib and osimertinib in treatment-naive patients with advanced or recurrent EGFR-mutant NSCLC.	osimertinib	147-158	epidermal growth factor receptor	Homo sapiens	214-218
33138052-6	2020	In thirteen (second line) osimertinib-treated patients with a (plasma or tissue) concomitant TP53 mutation at baseline, PFS was significantly shorter compared to six wild-type cases; 8.8 vs. 18.8 months, p = 0.017.	osimertinib	26-37	tumor protein p53	Homo sapiens	93-97
32955177-0	2020	Osimertinib in Resected EGFR-Mutated Non-Small-Cell Lung Cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	24-28
32955177-1	2020	BACKGROUND: Osimertinib is standard-of-care therapy for previously untreated epidermal growth factor receptor (EGFR) mutation-positive advanced non-small-cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	77-109
33113300-0	2020	Adjuvant Osimertinib in EGFR-Mutated Non-Small-Cell Lung Cancer.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	24-28
32955177-1	2020	BACKGROUND: Osimertinib is standard-of-care therapy for previously untreated epidermal growth factor receptor (EGFR) mutation-positive advanced non-small-cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	111-115
32955177-12	2020	CONCLUSIONS: In patients with stage IB to IIIA EGFR mutation-positive NSCLC, disease-free survival was significantly longer among those who received osimertinib than among those who received placebo.	osimertinib	149-160	epidermal growth factor receptor	Homo sapiens	47-51
33082305-9	2020	The EGFR-TKI Osimertinib downregulated IPO13 expression level in NSCLC cell lines with EGFR mutations, but not in EGFR wild-type ones.	osimertinib	13-24	importin 13	Homo sapiens	39-44
33193892-8	2020	Moreover, multivariate analysis indicated that BM status (P=0.015), local therapy for BM (P=0.013) and subsequent treatment of Osimertinib (P=0.008) impact significantly on OS.	osimertinib	127-138	Moloney sarcoma oncogene	Mus musculus	173-175
33082305-9	2020	The EGFR-TKI Osimertinib downregulated IPO13 expression level in NSCLC cell lines with EGFR mutations, but not in EGFR wild-type ones.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	4-8
33082305-9	2020	The EGFR-TKI Osimertinib downregulated IPO13 expression level in NSCLC cell lines with EGFR mutations, but not in EGFR wild-type ones.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	87-91
33330839-3	2020	We discovered six compounds (cepharanthine, abemaciclib, osimertinib, trimipramine, colforsin, and ingenol) to be broad spectrum inhibitors for spike-mediated entry.	osimertinib	57-68	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	144-149
33080698-0	2020	Poor effect of osimertinib on EGFR exon 20 insertion-positive lung adenocarcinoma: A case report.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	30-34
33489707-0	2021	First-line osimertinib for leptomeningeal metastasis from lung adenocarcinoma with EGFR mutation as the initial and solitary site of postoperative recurrence.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	83-87
33489707-2	2021	We present the case of a 54-year-old man with LM from lung adenocarcinoma harboring EGFR L858R point mutation, who received osimertinib as first-line therapy.	osimertinib	124-135	epidermal growth factor receptor	Homo sapiens	84-88
33489707-8	2021	Osimertinib is considered to be an effective therapeutic option for LM from lung adenocarcinoma harboring EGFR mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	106-110
33080698-1	2020	INTRODUCTION: The clinical efficacy of osimertinib for patients with lung adenocarcinoma harboring epidermal growth factor receptor (EGFR) exon 20 insertion mutations is unclear.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	99-131
33080698-1	2020	INTRODUCTION: The clinical efficacy of osimertinib for patients with lung adenocarcinoma harboring epidermal growth factor receptor (EGFR) exon 20 insertion mutations is unclear.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	133-137
33080698-8	2020	INTERVENTIONS: Daily oral administration of 80 mg osimertinib was initiated to treat the EGFR exon 20 insertion-positive lung adenocarcinoma.	osimertinib	50-61	epidermal growth factor receptor	Homo sapiens	89-93
33489705-3	2021	She started taking osimertinib (80 mg/day).	osimertinib	19-30	Src homology 2 domain containing E	Homo sapiens	0-3
33116624-0	2020	Durable Response to Osimertinib in a Chinese Patient with Metastatic Lung Adenocarcinoma Harboring a Rare EGFR L858R/D761Y Compound Mutation.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	106-110
33116624-3	2020	In the present case, we describe the clinical efficacy of icotinib and osimertinib in a metastatic lung adenocarcinoma patient carrying a highly uncommon EGFR L858R/D761Y compound mutation.	osimertinib	71-82	epidermal growth factor receptor	Homo sapiens	154-158
33116624-5	2020	To the best of our knowledge, this is the first report of durable osimertinib response in an NSCLC patient with a rare EGFR L858R/D761Y mutation.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	119-123
32634610-0	2020	A phase II, multicenter, two cohort study of 160 mg osimertinib in EGFR T790M-positive non-small cell lung cancer patients with brain metastases or leptomeningeal disease who progressed on prior EGFR TKI therapy.	osimertinib	52-63	epidermal growth factor receptor	Homo sapiens	67-71
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
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
33163272-2	2020	AZD9291 (osimertinib) represents the first-approved third generation EGFR-tyrosine kinase inhibitor (EGFR-TKI) for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and resistant T790M mutation, but faces the giant challenge of acquired resistance developed in patients in the clinic.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	69-73
33163272-2	2020	AZD9291 (osimertinib) represents the first-approved third generation EGFR-tyrosine kinase inhibitor (EGFR-TKI) for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and resistant T790M mutation, but faces the giant challenge of acquired resistance developed in patients in the clinic.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	101-105
33163272-2	2020	AZD9291 (osimertinib) represents the first-approved third generation EGFR-tyrosine kinase inhibitor (EGFR-TKI) for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and resistant T790M mutation, but faces the giant challenge of acquired resistance developed in patients in the clinic.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	69-73
33163272-2	2020	AZD9291 (osimertinib) represents the first-approved third generation EGFR-tyrosine kinase inhibitor (EGFR-TKI) for the treatment of non-small cell lung cancer (NSCLC) with activating EGFR mutations and resistant T790M mutation, but faces the giant challenge of acquired resistance developed in patients in the clinic.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	101-105
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
33163272-6	2020	The HQP8361 and AZD9291 combination synergistically decreased the survival of these HCC827/AR cell lines with enhanced induction of apoptosis that involved alteration of Bim and Mcl-1 levels via modulating their degradation.	osimertinib	16-23	BCL2 like 11	Homo sapiens	170-173
33163272-6	2020	The HQP8361 and AZD9291 combination synergistically decreased the survival of these HCC827/AR cell lines with enhanced induction of apoptosis that involved alteration of Bim and Mcl-1 levels via modulating their degradation.	osimertinib	16-23	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	178-183
32634610-14	2020	CONCLUSION: Thus, 160 mg osimertinib demonstrated promising ORR and survival benefit with a tolerable safety profile in EGFR T790M-positive NSCLC patients with CNS metastasis who progressed on prior EGFR TKIs.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	120-124
32634610-14	2020	CONCLUSION: Thus, 160 mg osimertinib demonstrated promising ORR and survival benefit with a tolerable safety profile in EGFR T790M-positive NSCLC patients with CNS metastasis who progressed on prior EGFR TKIs.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	199-203
32634610-2	2020	Osimertinib (80mg), a third generation, irreversible, oral EGFR TKI, has shown efficacy in active CNS metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	59-63
32735723-0	2020	MET amplification results in heterogeneous responses to osimertinib in EGFR-mutant lung cancer treated with erlotinib.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	71-75
32639668-9	2020	Exploratory analysis showed that OS using the 2G EGFR-TKI was superior to that of the 1G EGFR-TKIs, suggesting the potential of sequential therapy of 2G EGFR-TKI followed by osimertinib.	osimertinib	174-185	epidermal growth factor receptor	Homo sapiens	49-53
32735723-1	2020	The third generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) osimertinib is approved for untreated, or previously EGFR-TKI-treated T790M-positive EGFR-mutated non-small cell lung carcinoma (NSCLC).	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	81-85
32735723-1	2020	The third generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) osimertinib is approved for untreated, or previously EGFR-TKI-treated T790M-positive EGFR-mutated non-small cell lung carcinoma (NSCLC).	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	144-148
32735723-13	2020	Hence, MET amplification might induce heterogeneous responses to osimertinib in EGFR-mutated NSCLC.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	80-84
32847720-3	2020	In addition to the reports on neratinib and pyrotinib, osimertinib, alflutinib, AST5902, and ibrutinib were confirmed to covalently bind to the Lys-190 of human serum albumin (HSA).	osimertinib	55-66	albumin	Homo sapiens	161-174
33209443-0	2020	A reflection on the actual place of osimertinib in the treatment algorithm of EGFR-positive non-small cell lung cancer patients.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	78-82
32981603-0	2020	EGFR Exon 20 Insertion (A763_Y764insFQEA) Mutant NSCLC Is Not Identified by Roche Cobas Version 2 Tissue Testing but Has Durable Intracranial and Extracranial Response to Osimertinib.	osimertinib	171-182	epidermal growth factor receptor	Homo sapiens	0-4
32945365-8	2020	The inhibition of receptor phosphorylation with the 1st, 2nd and 3rd generation TKIs, gefitinib, afatinib, osimertinib, respectively, reduced PLCgamma1 phosphorylation, and reduced the invasive and migratory potential of 293 cells, confirming PLCgamma1 as one of the probable downstream effectors of mutant EGFR signaling.	osimertinib	107-118	phospholipase C gamma 1	Homo sapiens	142-151
32945365-8	2020	The inhibition of receptor phosphorylation with the 1st, 2nd and 3rd generation TKIs, gefitinib, afatinib, osimertinib, respectively, reduced PLCgamma1 phosphorylation, and reduced the invasive and migratory potential of 293 cells, confirming PLCgamma1 as one of the probable downstream effectors of mutant EGFR signaling.	osimertinib	107-118	phospholipase C gamma 1	Homo sapiens	243-252
32945365-8	2020	The inhibition of receptor phosphorylation with the 1st, 2nd and 3rd generation TKIs, gefitinib, afatinib, osimertinib, respectively, reduced PLCgamma1 phosphorylation, and reduced the invasive and migratory potential of 293 cells, confirming PLCgamma1 as one of the probable downstream effectors of mutant EGFR signaling.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	307-311
32800358-0	2020	A reply to "Comment on: "Osimertinib treatment for patients with EGFR exon 20 mutation positive non-small cell lung cancer".	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	65-69
32586660-0	2020	Comment on: "Osimertinib treatment for patients with EGFR exon 20 mutation positive non-small cell lung cancer".	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	53-57
32659740-0	2020	Osimertinib regressed an EGFR-mutant lung-adenocarcinoma bone-metastasis mouse model and increased long-term survival.	osimertinib	0-11	epidermal growth factor receptor	Mus musculus	25-29
32367600-9	2020	CONCLUSION: Osimertinib can be a treatment option for patients with lung ASC harboring germline EGFR T790M mutation.	osimertinib	12-23	PYD and CARD domain containing	Homo sapiens	73-76
32367600-9	2020	CONCLUSION: Osimertinib can be a treatment option for patients with lung ASC harboring germline EGFR T790M mutation.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	96-100
32812378-10	2020	KEY POINTS: SIGNIFICANT FINDINGS OF THE STUDY: Osimertinib is the only market available third-generation EGFR-TKI and it has been reported that some drugs could have drug-drug interactions with it.	osimertinib	47-58	epidermal growth factor receptor	Rattus norvegicus	105-109
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	18-25	epidermal growth factor receptor	Homo sapiens	103-135
33209639-0	2020	HER2-D16 oncogenic driver mutation confers osimertinib resistance in EGFR mutation-positive non-small cell lung cancer.	osimertinib	43-54	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
33209639-0	2020	HER2-D16 oncogenic driver mutation confers osimertinib resistance in EGFR mutation-positive non-small cell lung cancer.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	69-73
33209641-0	2020	Meningeal metastasis patients with EGFR G724S who develop resistance to osimertinib benefit from the addition of afatinib.	osimertinib	72-83	epidermal growth factor receptor	Homo sapiens	35-39
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	13-16	epidermal growth factor receptor	Homo sapiens	103-135
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	13-16	epidermal growth factor receptor	Homo sapiens	137-141
33209615-1	2020	Background: T790M relative allele frequency (RAF) in plasma, calculated by the ratio of T790M to epidermal growth factor receptor (EGFR)-sensitizing mutation allele frequencies (AF), is associated with osimertinib response in patients with progressive non-small cell lung cancer (NSCLC) post 1st generation EGFR-tyrosine kinase inhibitor (TKI) treatment.	osimertinib	202-213	epidermal growth factor receptor	Homo sapiens	97-129
33209615-1	2020	Background: T790M relative allele frequency (RAF) in plasma, calculated by the ratio of T790M to epidermal growth factor receptor (EGFR)-sensitizing mutation allele frequencies (AF), is associated with osimertinib response in patients with progressive non-small cell lung cancer (NSCLC) post 1st generation EGFR-tyrosine kinase inhibitor (TKI) treatment.	osimertinib	202-213	epidermal growth factor receptor	Homo sapiens	131-135
33209615-1	2020	Background: T790M relative allele frequency (RAF) in plasma, calculated by the ratio of T790M to epidermal growth factor receptor (EGFR)-sensitizing mutation allele frequencies (AF), is associated with osimertinib response in patients with progressive non-small cell lung cancer (NSCLC) post 1st generation EGFR-tyrosine kinase inhibitor (TKI) treatment.	osimertinib	202-213	epidermal growth factor receptor	Homo sapiens	307-311
33209615-7	2020	Conclusions: In patients with progressive NSCLC post 1st generation EGFR-TKI treatment, plasma T790M RAFs of less than 20% can be used to identify patients who carry concurrent resistance mechanisms, and can predict a poorer response to osimertinib.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	68-72
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	13-16	epidermal growth factor receptor	Homo sapiens	174-178
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	18-25	epidermal growth factor receptor	Homo sapiens	137-141
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	13-16	epidermal growth factor receptor	Homo sapiens	174-178
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	18-25	epidermal growth factor receptor	Homo sapiens	174-178
33008019-1	2020	Osimertinib (OSI, AZD9291), is a third-generation, irreversible tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations.	osimertinib	18-25	epidermal growth factor receptor	Homo sapiens	174-178
32943544-0	2020	Osimertinib, an EGFR tyrosine kinase inhibitor, exerts anti-tumor activity in preclinical NSCLC models harboring the uncommon EGFR mutations G719X or L861Q or S768I.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	16-20
33196042-0	2020	Dose escalation of osimertinib for intracranial progression in EGFR mutated non-small-cell lung cancer with brain metastases.	osimertinib	19-30	epidermal growth factor receptor	Homo sapiens	63-67
33196042-1	2020	Background: Osimertinib is a selective irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) with increased penetration across the blood-brain barrier compared with previous EGFR-TKIs, and thus, a 52% reduction in the risk of intracranial disease progression is seen when it is used as a first line of therapy compared with gefitinib and erlotinib.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	112-116
33196042-4	2020	Methods: This is a subcohort analysis from a larger nonrandomized, phase 2, open-label trial, evaluating the efficacy of osimertinib dose escalation from 80 mg to 160 mg in EGFR-mutated advanced non-small-cell lung cancer (NSCLC) patients with intracranial progression in either first- (arm A) or second-line setting (arm B for T790M+ and C for T790M-).	osimertinib	121-132	epidermal growth factor receptor	Homo sapiens	173-177
32943544-1	2020	Osimertinib is an oral, third-generation, irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations with lower activity against wild-type EGFR and has demonstrated efficacy in NSCLC CNS metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	115-119
32943544-1	2020	Osimertinib is an oral, third-generation, irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations with lower activity against wild-type EGFR and has demonstrated efficacy in NSCLC CNS metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	156-160
32943544-1	2020	Osimertinib is an oral, third-generation, irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR T790M resistance mutations with lower activity against wild-type EGFR and has demonstrated efficacy in NSCLC CNS metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	156-160
32943544-8	2020	Together this data supports clinical testing of osimertinib in patients with uncommon EGFR NSCLC.	osimertinib	48-59	epidermal growth factor receptor	Homo sapiens	86-90
32943545-0	2020	CH7233163 overcomes osimertinib resistant EGFR-Del19/T790M/C797S mutation.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	42-46
32943545-1	2020	Osimertinib is the only EGFR-tyrosine kinase inhibitor (TKI) capable of overcoming EGFR-T790M-mutated NSCLC, but osimertinib-resistant EGFR triple mutations (Del19/T790M/C797S or L858R/T790M/C797S) have been reported.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	24-28
32943545-1	2020	Osimertinib is the only EGFR-tyrosine kinase inhibitor (TKI) capable of overcoming EGFR-T790M-mutated NSCLC, but osimertinib-resistant EGFR triple mutations (Del19/T790M/C797S or L858R/T790M/C797S) have been reported.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	83-87
32943545-1	2020	Osimertinib is the only EGFR-tyrosine kinase inhibitor (TKI) capable of overcoming EGFR-T790M-mutated NSCLC, but osimertinib-resistant EGFR triple mutations (Del19/T790M/C797S or L858R/T790M/C797S) have been reported.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	83-87
32943545-9	2020	Therefore, we conclude that CH7233163 is a potentially effective therapy for osimertinib resistant patients, especially in cases of EGFR-Del19/T790M/C797S.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	132-136
32929081-0	2020	Transient IGF-1R inhibition combined with osimertinib eradicates AXL-low expressing EGFR mutated lung cancer.	osimertinib	42-53	AXL receptor tyrosine kinase	Homo sapiens	65-68
32929081-0	2020	Transient IGF-1R inhibition combined with osimertinib eradicates AXL-low expressing EGFR mutated lung cancer.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	84-88
32929081-1	2020	Drug tolerance is the basis for acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) including osimertinib, through mechanisms that still remain unclear.	osimertinib	137-148	epidermal growth factor receptor	Homo sapiens	116-120
32929081-2	2020	Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance.	osimertinib	110-121	AXL receptor tyrosine kinase	Homo sapiens	25-28
32929081-2	2020	Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	44-48
32929081-2	2020	Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance.	osimertinib	191-202	AXL receptor tyrosine kinase	Homo sapiens	25-28
32929081-2	2020	Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance.	osimertinib	191-202	epidermal growth factor receptor	Homo sapiens	44-48
32929081-4	2020	IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal.	osimertinib	105-116	insulin like growth factor 1 receptor	Homo sapiens	0-6
32929081-4	2020	IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	34-38
32929081-4	2020	IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal.	osimertinib	105-116	GRB2 associated binding protein 1	Homo sapiens	71-75
32929081-4	2020	IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal.	osimertinib	105-116	insulin receptor substrate 1	Homo sapiens	80-84
32929081-5	2020	In AXL-low-expressing EGFRmut-LC cell-derived xenograft and patient-derived xenograft models, transient IGF-1R inhibition combined with continuous osimertinib treatment could eradicate tumors and prevent regrowth even after the cessation of osimertinib.	osimertinib	241-252	insulin like growth factor 1 receptor	Homo sapiens	104-110
33014788-3	2020	Patients with T790M gain the opportunity of subsequent treatment with third-generation EGFR-TKI, osimertinib.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	87-91
33014788-12	2020	In conclusion, this study showed that patients who progressed from gefitinib treatment, bearing common EGFR mutations, and with longer EGFR-TKI treatment duration had increased incidence of T790M acquisition and, therefore, were suitable for subsequent osimertinib treatment.	osimertinib	253-264	epidermal growth factor receptor	Homo sapiens	103-107
33014788-12	2020	In conclusion, this study showed that patients who progressed from gefitinib treatment, bearing common EGFR mutations, and with longer EGFR-TKI treatment duration had increased incidence of T790M acquisition and, therefore, were suitable for subsequent osimertinib treatment.	osimertinib	253-264	epidermal growth factor receptor	Homo sapiens	135-139
32954743-0	2020	Osimertinib for EGFR-mutant lung cancer with central nervous system metastases: a meta-analysis and systematic review.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	16-20
32954743-1	2020	BACKGROUND: Osimertinib, a third-generation tyrosine kinase inhibitor (TKI), is the only Food and Drug Administration-approved third-generation epidermal growth factor receptor (EGFR)TKI.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	144-176
32954743-1	2020	BACKGROUND: Osimertinib, a third-generation tyrosine kinase inhibitor (TKI), is the only Food and Drug Administration-approved third-generation epidermal growth factor receptor (EGFR)TKI.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	178-182
32954743-4	2020	We review some of the main challenges in targeting EGFR, including lack of central nervous system penetration with most tyrosine kinase inhibitors, activity of osimertinib penetrating blood-brain barrier and the efficacy of osimertinib.	osimertinib	160-171	epidermal growth factor receptor	Homo sapiens	51-55
32954743-4	2020	We review some of the main challenges in targeting EGFR, including lack of central nervous system penetration with most tyrosine kinase inhibitors, activity of osimertinib penetrating blood-brain barrier and the efficacy of osimertinib.	osimertinib	224-235	epidermal growth factor receptor	Homo sapiens	51-55
32954743-9	2020	In untreated advanced EGFR-mutated NSCLC with CNS metastases patients, the pooled ORR and DCR of osimertinib were 71% and 93%, respectively.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	22-26
32577785-0	2020	Synergistic effects of Bcl-2 inhibitors with AZD9291 on overcoming the acquired resistance of AZD9291 in H1975 cells.	osimertinib	94-101	BCL2 apoptosis regulator	Homo sapiens	23-28
32577785-2	2020	Different mechanisms of acquired resistance to first-generation and second-generation EGFR TKIs have been widely reported, but there were few reports on the resistant mechanism of third-generation EGFR-TKI such as osimertinib (AZD9291).	osimertinib	227-234	epidermal growth factor receptor	Homo sapiens	197-201
32577785-3	2020	In the present study, significant upregulation of Bcl-2 was found in AZD9291-resistant H1975 cells (H1975AR) compared with H1975, which may constitute an important resistant mechanism of acquired resistance to AZD9291.	osimertinib	69-76	BCL2 apoptosis regulator	Homo sapiens	50-55
32577785-3	2020	In the present study, significant upregulation of Bcl-2 was found in AZD9291-resistant H1975 cells (H1975AR) compared with H1975, which may constitute an important resistant mechanism of acquired resistance to AZD9291.	osimertinib	210-217	BCL2 apoptosis regulator	Homo sapiens	50-55
32577785-4	2020	More importantly, our study showed that synergism between AZD9291 and Bcl-2 inhibitor ABT263 (0.25 muM) or ABT199 (1 muM) could effectively overcome the acquired resistance of AZD9291 in H1975AR in vitro.	osimertinib	176-183	BCL2 apoptosis regulator	Homo sapiens	70-75
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	osimertinib	101-108	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	osimertinib	101-108	nuclear factor kappa B subunit 1	Homo sapiens	235-244
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	osimertinib	156-163	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	osimertinib	156-163	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	osimertinib	156-163	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	osimertinib	27-34	H3 histone pseudogene 16	Homo sapiens	102-105
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	osimertinib	27-34	sequestosome 1	Homo sapiens	234-240
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	osimertinib	120-127	H3 histone pseudogene 16	Homo sapiens	102-105
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	osimertinib	120-127	H3 histone pseudogene 16	Homo sapiens	102-105
32498573-1	2021	OBJECTIVE: To estimate the cost-effectiveness of first line tyrosine kinase inhibitors (TKI), afatinib and osimertinib, for the treatment of epidermal growth factor receptor (EGFR) mutation-positive (Exon 19 deletion or L858R) non-small cell lung cancer (NSCLC), stages IIIB - IV in Colombia.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	175-179
32389504-0	2020	Early Detection of Multiple Resistance Mechanisms by ctDNA Profiling in a Patient With EGFR-mutant Lung Adenocarcinoma Treated With Osimertinib.	osimertinib	132-143	epidermal growth factor receptor	Homo sapiens	87-91
32755244-3	2020	AREAS COVERED: We discuss the development of third generation EGFR TKIs, focusing on osimertinib and discuss the most common resistance mechanisms under evaluation.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	62-66
32385709-1	2020	PURPOSE: Osimertinib, a third-generation epidermal growth factor receptor tyrosine-kinase inhibitor (EGFR-TKI), has demonstrated substantial clinical benefit in patients with non-small-cell lung cancer (NSCLC) who were resistant to early-generation EGFR-TKIs and had acquired a T790M mutation.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	101-105
32854916-0	2020	Erdafitinib Overcomes FGFR3-TACC3-Mediated Resistance to Osimertinib.	osimertinib	57-68	fibroblast growth factor receptor 3	Homo sapiens	22-27
32854916-0	2020	Erdafitinib Overcomes FGFR3-TACC3-Mediated Resistance to Osimertinib.	osimertinib	57-68	transforming acidic coiled-coil containing protein 3	Homo sapiens	28-33
32782526-7	2020	Several EGFR tyrosine kinase inhibitors (EGFR-TKIs) that target these mutations, including gefitinib, erlotinib, afatinib and osimertinib, have been widely used clinically.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	8-12
32666714-2	2020	Here, we present a report of a patient with adenocarcinoma harboring EGFR exon 19 deletion mutation treated with osimertinib as first-line treatment.	osimertinib	113-124	epidermal growth factor receptor	Homo sapiens	69-73
32667739-0	2020	Osimertinib for compound EGFR exon 19 deletion/T790M mutated lung squamous cell carcinoma.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	25-29
32667739-2	2020	Evidence of the effectiveness of osimertinib in SqCC with EGFR T790M mutation is limited.	osimertinib	33-44	epidermal growth factor receptor	Homo sapiens	58-62
32667739-6	2020	Osimertinib has shown good efficacy in SqCC harboring a "primary" resistance mechanism (EGFR T790M).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	88-92
32667739-10	2020	Osimertinib has shown good efficacy in SqCC harboring a "primary" resistance mechanism (EGFR T790M).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	88-92
32510788-3	2020	DDC-01-163 is also effective against osimertinib-resistant cells with L/T/C797S and L/T/L718Q EGFR mutations.	osimertinib	37-48	epidermal growth factor receptor	Mus musculus	94-98
32510788-4	2020	When combined with an ATP-site EGFR inhibitor, osimertinib, the anti-proliferative activity of DDC-01-163 against L858R/T790M EGFR-Ba/F3 cells is enhanced.	osimertinib	47-58	epidermal growth factor receptor	Mus musculus	126-130
32631532-2	2020	EGFR19D/T790M/C797S mutation is one of the primary reasons for the emergence of resistance after treatment with the third-generation EGFR inhibitors such as AZD9291, CO1686 and Olmutinib.	osimertinib	157-164	epidermal growth factor receptor	Mus musculus	0-4
32548617-0	2020	Real-world use of osimertinib for epidermal growth factor receptor T790M-positive non-small cell lung cancer in Japan.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	34-66
32548617-2	2020	METHODS: Patients with epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer treated with second-line or later oral osimertinib per the Japanese package insert (80 mg once daily) were included.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	57-61
32848385-8	2020	Results: T7-DSNPs/9291 could significantly enhance BBB penetration of AZD9291 and doxorubicin via transferrin receptor-mediated transcytosis.	osimertinib	70-77	transferrin receptor	Homo sapiens	98-118
32461525-1	2020	Some patients discontinue receiving osimertinib for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) Thr790Met (T790M) mutation due to adverse its effects.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	97-129
32461525-1	2020	Some patients discontinue receiving osimertinib for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) Thr790Met (T790M) mutation due to adverse its effects.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	131-135
32461525-3	2020	An 85-year-old Japanese woman received osimertinib as third-line therapy for NSCLC with the EGFR T790M mutation.	osimertinib	39-50	epidermal growth factor receptor	Homo sapiens	92-96
32525442-5	2020	The safety and efficacy of osimertinib (a third generation EGFR-TKIs) were confirmed by well-designed clinical trials.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	59-63
32525442-6	2020	Consequently, osimertinib was considered a first-line treatment option, particularly in patients with EGFR mutant NSCLC.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	102-106
32693293-1	2020	Osimertinib is an irreversible EGFR-tyrosine kinase inhibitor initially approved for treatment of EGFR-positive patients exhibiting a T790 M resistance mutation in the second line setting and now emerging as the new standard of care for all EGFR positive patients as first-line treatment.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	31-35
32693293-1	2020	Osimertinib is an irreversible EGFR-tyrosine kinase inhibitor initially approved for treatment of EGFR-positive patients exhibiting a T790 M resistance mutation in the second line setting and now emerging as the new standard of care for all EGFR positive patients as first-line treatment.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	98-102
32693293-1	2020	Osimertinib is an irreversible EGFR-tyrosine kinase inhibitor initially approved for treatment of EGFR-positive patients exhibiting a T790 M resistance mutation in the second line setting and now emerging as the new standard of care for all EGFR positive patients as first-line treatment.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	98-102
32693293-2	2020	Despite its efficacy, resistance to osimertinib inevitably develops and mechanisms of resistance can be grouped broadly in two categories: on-target EGFR-dependent and off-target EGFR-independent mechanisms.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	149-153
32693293-2	2020	Despite its efficacy, resistance to osimertinib inevitably develops and mechanisms of resistance can be grouped broadly in two categories: on-target EGFR-dependent and off-target EGFR-independent mechanisms.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	179-183
32693293-3	2020	EGFR-dependent resistance typically is associated with additional EGFR-mutations disrupting the osimertinib binding through changes in the binding site by allosteric/ conformational transitions; EGFR-independent mechanisms are related mostly to alternate pathway activation or aberrant downstream signalling but also to lineage plasticity leading to small cell transformation.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	0-4
32693293-3	2020	EGFR-dependent resistance typically is associated with additional EGFR-mutations disrupting the osimertinib binding through changes in the binding site by allosteric/ conformational transitions; EGFR-independent mechanisms are related mostly to alternate pathway activation or aberrant downstream signalling but also to lineage plasticity leading to small cell transformation.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	66-70
32693293-3	2020	EGFR-dependent resistance typically is associated with additional EGFR-mutations disrupting the osimertinib binding through changes in the binding site by allosteric/ conformational transitions; EGFR-independent mechanisms are related mostly to alternate pathway activation or aberrant downstream signalling but also to lineage plasticity leading to small cell transformation.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	66-70
32782544-7	2020	In conclusion, the present study analysed the effects of osimertinib in patients with advanced NSCLC with EGFR mutations, particularly T790M mutations.	osimertinib	57-68	epidermal growth factor receptor	Homo sapiens	106-110
32677256-0	2020	CDK46 inhibitor palbociclib overcomes acquired resistance to third-generation EGFR inhibitor osimertinib in non-small cell lung cancer (NSCLC).	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	78-82
32677256-3	2020	METHODS: We established osimertinib-resistant cells (H1975 OR) derived from EGFR-mutant NSCLC cells H1975.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	76-80
32677256-16	2020	The combination of CDK4/6 inhibitor palbociclib and osimertinib could overcome the acquired resistance of osimertinib.	osimertinib	106-117	cyclin dependent kinase 4	Homo sapiens	19-25
32497272-0	2020	MEK or ERK inhibition effectively abrogates emergence of acquired osimertinib resistance in the treatment of epidermal growth factor receptor-mutant lung cancers.	osimertinib	66-77	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
32497272-0	2020	MEK or ERK inhibition effectively abrogates emergence of acquired osimertinib resistance in the treatment of epidermal growth factor receptor-mutant lung cancers.	osimertinib	66-77	mitogen-activated protein kinase 1	Homo sapiens	7-10
32497272-0	2020	MEK or ERK inhibition effectively abrogates emergence of acquired osimertinib resistance in the treatment of epidermal growth factor receptor-mutant lung cancers.	osimertinib	66-77	epidermal growth factor receptor	Homo sapiens	109-141
32497272-1	2020	BACKGROUND: The majority of patients with non-small cell lung cancer (NSCLC) harboring activating epidermal growth factor receptor (EGFR) mutations respond well to osimertinib (AZD9291), a third-generation, mutation-selective EGFR inhibitor.	osimertinib	164-175	epidermal growth factor receptor	Homo sapiens	98-130
32497272-1	2020	BACKGROUND: The majority of patients with non-small cell lung cancer (NSCLC) harboring activating epidermal growth factor receptor (EGFR) mutations respond well to osimertinib (AZD9291), a third-generation, mutation-selective EGFR inhibitor.	osimertinib	164-175	epidermal growth factor receptor	Homo sapiens	132-136
32497272-1	2020	BACKGROUND: The majority of patients with non-small cell lung cancer (NSCLC) harboring activating epidermal growth factor receptor (EGFR) mutations respond well to osimertinib (AZD9291), a third-generation, mutation-selective EGFR inhibitor.	osimertinib	164-175	epidermal growth factor receptor	Homo sapiens	226-230
32497272-1	2020	BACKGROUND: The majority of patients with non-small cell lung cancer (NSCLC) harboring activating epidermal growth factor receptor (EGFR) mutations respond well to osimertinib (AZD9291), a third-generation, mutation-selective EGFR inhibitor.	osimertinib	177-184	epidermal growth factor receptor	Homo sapiens	98-130
32497272-2	2020	The current study focuses on determining whether targeting MEK/ERK signaling prevents or delays the development of acquired resistance to osimertinib.	osimertinib	138-149	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
32497272-2	2020	The current study focuses on determining whether targeting MEK/ERK signaling prevents or delays the development of acquired resistance to osimertinib.	osimertinib	138-149	mitogen-activated protein kinase 1	Homo sapiens	63-66
32497272-7	2020	RESULTS: Osimertinib combined with an MEK or ERK inhibitor synergistically decreased cell survival with enhanced induction of apoptosis in EGFR-mutant NSCLC cells but not in EGFR wild-type NSCLC cells.	osimertinib	9-20	epidermal growth factor receptor	Mus musculus	139-143
32497272-9	2020	Continuous and intermittent pharmacologic inhibition of MEK/ERK signaling delayed the emergence of osimertinib resistance both in vitro and in vivo.	osimertinib	99-110	midkine	Mus musculus	56-59
32497272-9	2020	Continuous and intermittent pharmacologic inhibition of MEK/ERK signaling delayed the emergence of osimertinib resistance both in vitro and in vivo.	osimertinib	99-110	mitogen-activated protein kinase 1	Mus musculus	60-63
32497272-10	2020	CONCLUSIONS: These results provide strong preclinical evidence in support of targeting MEK/ERK signaling as a strategy for delaying or preventing acquired resistance to osimertinib in the clinic to improve the long-term therapeutic efficacy of osimertinib.	osimertinib	169-180	midkine	Mus musculus	87-90
32497272-10	2020	CONCLUSIONS: These results provide strong preclinical evidence in support of targeting MEK/ERK signaling as a strategy for delaying or preventing acquired resistance to osimertinib in the clinic to improve the long-term therapeutic efficacy of osimertinib.	osimertinib	169-180	mitogen-activated protein kinase 1	Mus musculus	91-94
32497272-10	2020	CONCLUSIONS: These results provide strong preclinical evidence in support of targeting MEK/ERK signaling as a strategy for delaying or preventing acquired resistance to osimertinib in the clinic to improve the long-term therapeutic efficacy of osimertinib.	osimertinib	244-255	midkine	Mus musculus	87-90
32497272-10	2020	CONCLUSIONS: These results provide strong preclinical evidence in support of targeting MEK/ERK signaling as a strategy for delaying or preventing acquired resistance to osimertinib in the clinic to improve the long-term therapeutic efficacy of osimertinib.	osimertinib	244-255	mitogen-activated protein kinase 1	Mus musculus	91-94
32497272-11	2020	From a clinical standpoint, the data support the evaluation of an intermittent treatment schedule of osimertinib in combination with an MEK or ERK inhibitor in patients with EGFR-mutated NSCLC.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	174-178
32982275-0	2020	Three Novel EGFR Mutations (750_758del, I759S, T751_I759delinsS) in One Patient with Metastatic Non-Small Cell Lung Cancer Responding to Osimertinib: A Case Report.	osimertinib	137-148	epidermal growth factor receptor	Homo sapiens	12-16
32762742-0	2020	An EGFR T790M-mutated lung adenocarcinoma undergoing large-cell neuroendocrine carcinoma transformation after osimertinib therapy: a case report.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	3-7
32762742-3	2020	Epidermal growth factor receptor-dependent resistance mechanisms, bypass pathway activation, and histological transformation have been reported with osimertinib therapy.	osimertinib	149-160	epidermal growth factor receptor	Homo sapiens	0-32
32762742-4	2020	CASE PRESENTATION: We report a case of a 64-year-old Asian man with epidermal growth factor receptor T790M-positive adenocarcinoma that transformed to epidermal growth factor receptor T790M-negative large-cell neuroendocrine carcinoma after osimertinib therapy.	osimertinib	241-252	epidermal growth factor receptor	Homo sapiens	68-100
32762742-4	2020	CASE PRESENTATION: We report a case of a 64-year-old Asian man with epidermal growth factor receptor T790M-positive adenocarcinoma that transformed to epidermal growth factor receptor T790M-negative large-cell neuroendocrine carcinoma after osimertinib therapy.	osimertinib	241-252	epidermal growth factor receptor	Homo sapiens	151-183
32391625-3	2020	Osimertinib, which is third-generation EGFR-TKI, provides clinical effect even on NSCLC harboring the threonine to methionine change at codon 790 of EGFR (EGFR T790M) mutation that cause TKI resistance.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	39-43
32391625-3	2020	Osimertinib, which is third-generation EGFR-TKI, provides clinical effect even on NSCLC harboring the threonine to methionine change at codon 790 of EGFR (EGFR T790M) mutation that cause TKI resistance.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	149-153
32391625-10	2020	These findings suggest that an immunotherapy targeting a neoantigen derived from EGFR T790M/C797S mutation could be a useful novel therapeutic strategy for NSCLC patients with EGFR-TKI resistance, especially resistant to Osimertinib.	osimertinib	221-232	epidermal growth factor receptor	Homo sapiens	81-85
32353596-1	2020	BACKGROUND: Acquired resistance to osimertinib mediated by EGFR cis-C797S is now a growing challenge.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	59-63
32353596-3	2020	METHODS: In this retrospective cohort study, 15 patients with advanced lung adenocarcinoma were identified with EGFR-activating mutation/T790M/cis-C797S after osimertinib progression by targeted next-generation sequencing.	osimertinib	159-170	epidermal growth factor receptor	Homo sapiens	112-116
32521387-3	2020	MATERIALS AND METHODS: We generated EGFR TKI-resistant NSCLC cell lines with acquired resistance to erlotinib, gefitinib, and osimertinib (PC9/ER, HCC827/GR and HCC827/OR, respectively).	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	36-40
32534795-0	2020	Combined osimertinib, dabrafenib and trametinib treatment for advanced non-small-cell lung cancer patients with an osimertinib-induced BRAF V600E mutation.	osimertinib	9-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
32534795-0	2020	Combined osimertinib, dabrafenib and trametinib treatment for advanced non-small-cell lung cancer patients with an osimertinib-induced BRAF V600E mutation.	osimertinib	115-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
32534795-1	2020	INTRODUCTION: Previous studies have reported an acquiredBRAF V600E mutation as a potential resistance mechanism to osimertinib treatment in advanced NSCLC patients with an activating mutation in EGFR.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	195-199
32534795-4	2020	METHODS: Two patients with anEGFR exon 19 deletion and a T790 M mutation, both treated with osimertinib, acquired a BRAF V600E mutation at disease progression.	osimertinib	92-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
32534795-10	2020	CONCLUSION: BRAF V600E may be a resistance mechanism induced by osimertinib in EGFR-mutated advanced NSCLC.	osimertinib	64-75	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	12-16
32534795-10	2020	CONCLUSION: BRAF V600E may be a resistance mechanism induced by osimertinib in EGFR-mutated advanced NSCLC.	osimertinib	64-75	epidermal growth factor receptor	Homo sapiens	79-83
32534795-11	2020	Combined treatment using dabrafenib/trametinib concurrently with osimertinib needs to be explored for osimertinib-induced BRAF V600E mutation.	osimertinib	102-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	122-126
32540560-5	2020	Six and five patients received a combination of either first-generation (gefitinib, erlotinib, or icotinib) or third-generation (osimertinib) EGFR-TKI and crizotinib, respectively.	osimertinib	129-140	epidermal growth factor receptor	Homo sapiens	142-146
32540560-8	2020	Moreover, analysis of acquired resistance mechanisms from nine patients identified EGFR T790 M from three patients who progressed from first-generation EGFR-TKI and crizotinib, while EGFR T790 M/trans-C797S and L718Q, EGFR G724S, and CCDC6-RET fusion were detected from one patient each who progressed from osimertinib and crizotinib regimen.	osimertinib	307-318	epidermal growth factor receptor	Homo sapiens	83-87
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	0-4
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	24-28
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	24-28
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	24-28
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	24-28
32412152-1	2020	EGFR exon20-insertions (EGFR e20ins) account for up to 10% of EGFR mutations in lung cancer; however, tumors with EGFR e20ins had poor response rates to EGFR tyrosine kinase inhibitors (TKIs) including gefitinib, erlotinib, afatinib and osimertinib, and the heterogeneity of EGFR e20ins further complicate the clinical studies.	osimertinib	237-248	epidermal growth factor receptor	Homo sapiens	24-28
32567817-1	2020	Osimertinib is a third-generation, irreversible, oral epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits both EGFR-TKI sensitizing and EGFR T790M and has demonstrated efficacy in non-small cell lung cancer (NSCLC) central nervous system metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	54-86
32567817-1	2020	Osimertinib is a third-generation, irreversible, oral epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits both EGFR-TKI sensitizing and EGFR T790M and has demonstrated efficacy in non-small cell lung cancer (NSCLC) central nervous system metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	88-92
32567817-1	2020	Osimertinib is a third-generation, irreversible, oral epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits both EGFR-TKI sensitizing and EGFR T790M and has demonstrated efficacy in non-small cell lung cancer (NSCLC) central nervous system metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	170-174
32567817-6	2020	Osimertinib exposure based on Cmax and area under the plasma concentration-time curve, was 1.19-fold (90% CI: 0.6, 2.0) and 1.85-fold (90% CI: 0.9, 3.6), respectively, higher for patients with SRI vs patients with NRF, with no clear correlation between CrCL and exposure.	osimertinib	0-11	CRCL	Homo sapiens	253-257
32696212-10	2020	CONCLUSIONS: These data further emphasize that osimertinib should be a standard of care in patients with pretreated EGFR T790M-positive NSCLC.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	116-120
32495514-1	2020	INTRODUCTION: As most patients with epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) develop progressive disease after treatment with osimertinib, it is important to develop more effective treatment options.	osimertinib	167-178	epidermal growth factor receptor	Homo sapiens	36-68
32495514-1	2020	INTRODUCTION: As most patients with epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) develop progressive disease after treatment with osimertinib, it is important to develop more effective treatment options.	osimertinib	167-178	epidermal growth factor receptor	Homo sapiens	70-74
32495514-2	2020	Afatinib has been shown to be more effective in in vitro studies than osimertinib when used in cancer cell lines containing some specific EGFR mutations.	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	138-142
32495514-6	2020	DISCUSSION: A previous study indicated that afatinib inhibits lung cancer cells with specific EGFR mutations more effectively than other EGFR-TKIs such as osimertinib.	osimertinib	155-166	epidermal growth factor receptor	Homo sapiens	137-141
32953518-2	2020	Osimertinib is a third-generation EGFR-TKI, and its efficacy and safety in NSCLC patients with first-generation EGFR-TKI resistance, especially lung adenocarcinoma, are not yet clear.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-38
32272148-0	2020	Desmoglein-2 modulates tumor progression and osimertinib drug resistance through the EGFR/Src/PAK1 pathway in lung adenocarcinoma.	osimertinib	45-56	desmoglein 2	Homo sapiens	0-12
32272148-3	2020	Notably, DSG2 overexpression promoted cell proliferation and migration, and increased resistance to the EGFR tyrosine kinase inhibitor osimertinib, whereas DSG2 silencing could reverse these results.	osimertinib	135-146	desmoglein 2	Homo sapiens	9-13
32272148-6	2020	Consistent with these findings, a nude mouse xenograft model using H1975 cells demonstrated that DSG2 promoted LUAD cell growth in vivo and increased osimertinib resistance.	osimertinib	150-161	desmoglein 2	Homo sapiens	97-101
32723319-12	2020	Our results suggested that EGFR-mutated advanced NSCLC patients with >=1 risk factors were candidates for PCI or the first-line Osimertinib treatment.	osimertinib	128-139	epidermal growth factor receptor	Homo sapiens	27-31
32793495-0	2020	Longitudinal Monitoring of EGFR and PIK3CA Mutations by Saliva-Based EFIRM in Advanced NSCLC Patients With Local Ablative Therapy and Osimertinib Treatment: Two Case Reports.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	27-31
32793495-0	2020	Longitudinal Monitoring of EGFR and PIK3CA Mutations by Saliva-Based EFIRM in Advanced NSCLC Patients With Local Ablative Therapy and Osimertinib Treatment: Two Case Reports.	osimertinib	134-145	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	36-42
32674434-1	2020	The third-generation tyrosine kinase inhibitor (TKI), osimertinib, has revolutionized the treatment of patients with non-small cell lung carcinoma with epidermal growth factor receptor (EGFR)-activating mutation, and resistant to first- and second-generation TKIs.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	152-184
32674434-1	2020	The third-generation tyrosine kinase inhibitor (TKI), osimertinib, has revolutionized the treatment of patients with non-small cell lung carcinoma with epidermal growth factor receptor (EGFR)-activating mutation, and resistant to first- and second-generation TKIs.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	186-190
32641854-0	2020	Let-7c regulated epithelial-mesenchymal transition leads to osimertinib resistance in NSCLC cells with EGFR T790M mutations.	osimertinib	60-71	microRNA let-7c	Homo sapiens	0-6
32641854-0	2020	Let-7c regulated epithelial-mesenchymal transition leads to osimertinib resistance in NSCLC cells with EGFR T790M mutations.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	103-107
32641854-9	2020	Expression of let-7c was functionally relevant as EMT correlated with resistance to Osimertinib.	osimertinib	84-95	microRNA let-7c	Homo sapiens	14-20
32641854-10	2020	High let-7c expression reversed EMT and made cells sensitive to Osimertinib, and vice versa.	osimertinib	64-75	microRNA let-7c	Homo sapiens	5-11
32641854-14	2020	Our results suggest an important role of let-7c in regulating EMT and the resulting Osimertinib resistance in T790M NSCLCs.	osimertinib	84-95	microRNA let-7c	Homo sapiens	41-47
32498573-1	2021	OBJECTIVE: To estimate the cost-effectiveness of first line tyrosine kinase inhibitors (TKI), afatinib and osimertinib, for the treatment of epidermal growth factor receptor (EGFR) mutation-positive (Exon 19 deletion or L858R) non-small cell lung cancer (NSCLC), stages IIIB - IV in Colombia.	osimertinib	107-118	epidermal growth factor receptor	Homo sapiens	141-173
32498573-9	2021	The ICER of osimertinib exceeds the threshold when compared with afatinib.	osimertinib	12-23	cAMP responsive element modulator	Homo sapiens	4-8
32692221-8	2020	CONCLUSIONS: The regimens of "Gefitinib + pemetrexed + carboplatin" and "Osimertinib" were associated with the most favorable PFS and OS compared to the other therapies in advanced EGFR-mutant NSCLC patients with stable brain metastases, although the difference between these regimens and the others was not statistically significantly different.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	181-185
32839131-0	2021	Transformations First Into Squamous-Cell Carcinoma and Later Into Sarcomatoid Carcinoma After Acquired Resistance to Osimertinib in a Patient With EGFR-Mutant Lung Adenocarcinoma: Case Report.	osimertinib	117-128	epidermal growth factor receptor	Homo sapiens	147-151
32391602-0	2020	GSK-3 inhibition overcomes EMT-associated resistance to osimertinib in EGFR mutant lung cancer.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	71-75
32487567-0	2020	Osimertinib Called "Home Run" for EGFR-Mutant NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-38
32487567-1	2020	Adjuvant treatment with the tyrosine kinase inhibitor osimertinib will likely become a new standard of care in patients with EGFR-mutant non-small cell lung cancer.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	125-129
32391602-1	2020	A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutant lung cancer.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	8-12
32391602-1	2020	A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutant lung cancer.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	96-100
32391602-6	2020	These results suggest that GSK-3 inhibition may be useful to circumvent EMT-associated resistance to osimertinib in EGFR mutant lung cancer.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	116-120
32485428-4	2020	Other alterations, such as EGFR T790 M, are responsive to osimertinib, while the EGFR C797S alteration seen in osimertinib resistance demonstrates preclinical sensitivity to combined brigatinib and cetuximab.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	27-31
32485428-4	2020	Other alterations, such as EGFR T790 M, are responsive to osimertinib, while the EGFR C797S alteration seen in osimertinib resistance demonstrates preclinical sensitivity to combined brigatinib and cetuximab.	osimertinib	111-122	epidermal growth factor receptor	Homo sapiens	81-85
32387812-0	2020	Complex EGFR mutations with secondary T790M mutation confer shorter osimertinib progression-free survival and overall survival in advanced non-small cell lung cancer.	osimertinib	68-79	epidermal growth factor receptor	Homo sapiens	8-12
32662665-0	2020	Real-world osimertinib for EGFR mutation-positive non-small-cell lung cancer with acquired T790M mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	27-31
32662665-1	2020	Aim: Osimertinib is a key drug for EGFR mutation-positive non-small-cell lung cancer (NSCLC).	osimertinib	5-16	epidermal growth factor receptor	Homo sapiens	35-39
32662665-3	2020	Patients & methods: We retrospectively analyzed the clinical courses of EGFR mutation-positive NSCLC patients who were potential candidates for salvage osimertinib.	osimertinib	152-163	epidermal growth factor receptor	Homo sapiens	72-76
32662665-7	2020	Conclusion: Osimertinib is active for T790M-driven acquired resistance in EGFR-mutant NSCLC, but the detection of T790M was unsatisfactory.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	74-78
32460198-0	2020	Circulating tumor DNA analysis of EGFR-mutant non-small cell lung cancer patients receiving osimertinib following previous tyrosine kinase inhibitor treatment.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	34-38
32387812-1	2020	OBJECTIVES: Osimertinib is active against epidermal growth factor receptor (EGFR) T790M-mutated non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	42-74
32387812-1	2020	OBJECTIVES: Osimertinib is active against epidermal growth factor receptor (EGFR) T790M-mutated non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	76-80
32408132-2	2020	Osimertinib (AZD9291), a third generation EGFR TKI, has replaced earlier generation EGFR TKIs for first line treatment of EGFR mutant lung cancer due to its improved overall survival, longer progression free survival, and better tolerability compared to earlier generation inhibitors.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	42-46
32408132-2	2020	Osimertinib (AZD9291), a third generation EGFR TKI, has replaced earlier generation EGFR TKIs for first line treatment of EGFR mutant lung cancer due to its improved overall survival, longer progression free survival, and better tolerability compared to earlier generation inhibitors.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	42-46
32652816-3	2020	EGFr TKIs (such as afatinib, erlotinib, and osimertinib) reversed the acute inhibitory effect of EGF on chloride secretion induced by carbachol (CCh) across T84 human colonic epithelial cells, which correlated with the diarrhea-inducing effect of each agent clinically.	osimertinib	44-55	epidermal growth factor receptor	Homo sapiens	0-4
32652816-3	2020	EGFr TKIs (such as afatinib, erlotinib, and osimertinib) reversed the acute inhibitory effect of EGF on chloride secretion induced by carbachol (CCh) across T84 human colonic epithelial cells, which correlated with the diarrhea-inducing effect of each agent clinically.	osimertinib	44-55	epidermal growth factor	Homo sapiens	0-3
32552277-0	2020	Emerging Treatment Paradigms for EGFR-Mutant Lung Cancers Progressing on Osimertinib: A Review.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	33-37
32374485-5	2020	As osimertinib will be used more often in many EGFR-positive NSCLC patients in the future, this potentially life-threatening side effect should receive special attention, especially in first-line treatment.	osimertinib	3-14	epidermal growth factor receptor	Homo sapiens	47-51
32552277-1	2020	Since its approval in April 2018, osimertinib has been widely adopted as first-line therapy for patients with advanced EGFR-mutant non -small cell lung cancer (NSCLC).	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	119-123
32552277-3	2020	Using data compiled from 6 osimertinib-resistance series, we describe here the heterogeneous profile of EGFR-dependent and independent mechanisms of osimertinib treatment failure.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	104-108
32317208-0	2020	Discovery and biological evaluation of proteolysis targeting chimeras (PROTACs) as an EGFR degraders based on osimertinib and lenalidomide.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	86-90
32352321-0	2020	Treatment sequence of first and second generation tyrosine kinase inhibitor followed by osimertinib in EGFR-mutated non-small-cell lung cancer: a real life study.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	103-107
31911548-0	2020	Tumor Analyses Reveal Squamous Transformation and Off-Target Alterations As Early Resistance Mechanisms to First-line Osimertinib in EGFR-Mutant Lung Cancer.	osimertinib	118-129	epidermal growth factor receptor	Homo sapiens	133-137
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	ret proto-oncogene	Homo sapiens	147-150
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	165-169
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	212-216
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	227-231
32517152-1	2020	Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are used for treating EGFR-mutated lung cancer, and osimertinib is effective in cases that acquired T790M mutations after treatment with the first- and second-generation EGFR-TKIs.	osimertinib	124-135	epidermal growth factor receptor	Homo sapiens	0-32
32517152-1	2020	Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are used for treating EGFR-mutated lung cancer, and osimertinib is effective in cases that acquired T790M mutations after treatment with the first- and second-generation EGFR-TKIs.	osimertinib	124-135	epidermal growth factor receptor	Homo sapiens	61-65
32517152-8	2020	These results suggest that osimertinib was relatively safe and effective for non-small cell lung cancer that acquired T790M mutations after previous EGFR-TKI treatment, even among patients who were >=75 years old.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	149-153
31538306-0	2020	Efficacy of osimertinib for the treatment of previously EGFR TKI treated NSCLC patients: a meta-analysis.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	56-60
31538306-5	2020	Osimertinib treatment was associated with a PFS of 11.17 months [7.80, 14.55] which was longer in treatment-naive (20.30 [15.37, 25.23]) than in prior EGFR-TKI-treated (10.20 [9.60, 10.80]) patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	151-155
31538306-10	2020	CONCLUSION: Osimertinib treatment yields approximately 10 months PFS in prior EGFR-TKI-treated and 20 months in treatment-naive NSCLC patients.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	78-82
32352321-6	2020	Conclusion: These results, in line with those observed during clinical trials, confirm the effectiveness of the sequence TKI-1G/2G followed by osimertinib in EGFR-mutated non-small-cell lung cancer.	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	158-162
32493093-0	2020	Successful treatment of a patient with NSCLC carrying uncommon compound EGFR G719X and S768I mutations using osimertinib: A case report.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	72-76
32495159-1	2020	BACKGROUND: Osimertinib is a standard therapy for advanced non-small cell lung cancer (NSCLC) patients with an acquired epidermal growth factor receptor (EGFR) T790M mutation; however, the exploration of clinical characteristics that may affect prognosis and long-term survival is still lacking.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	120-152
32600081-4	2020	However, he switched to osimertinib after repeat biopsy showed EGFR exon 19 deletion and T790M mutation leading to erlotinib resistance.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	63-67
32495159-1	2020	BACKGROUND: Osimertinib is a standard therapy for advanced non-small cell lung cancer (NSCLC) patients with an acquired epidermal growth factor receptor (EGFR) T790M mutation; however, the exploration of clinical characteristics that may affect prognosis and long-term survival is still lacking.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	154-158
32495159-3	2020	PATIENTS AND METHODS: A total of 246 patients with acquired EGFR T790M mutation who were treated with osimertinib were included in this study.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	60-64
32389962-1	2020	BACKGROUND: In recent years, osimertinib has been increasingly used as a therapeutic drug for epidermal growth factor receptor(EGFR)mutation-positive lung cancer, with heart failure rarely reported as an adverse event.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	94-126
32397295-10	2020	Currently, osimertinib (which demonstrated to improve efficacy with a better tolerability in comparison with first-generation TKIs) is considered the best treatment option for patients affected by NSCLC harboring a common EGFR mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	222-226
31987959-0	2020	Pattern of recurrence analysis in metastatic EGFR-mutant NSCLC treated with Osimertinib: implications for consolidative stereotactic body radiation therapy.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	45-49
31987959-4	2020	METHODS AND MATERIALS: The serial scans of metastatic EGFR-mutant NSCLC patients treated with osimertinib were retrospectively reviewed.	osimertinib	94-105	epidermal growth factor receptor	Homo sapiens	54-58
31972351-9	2020	In the LMC model with A925L/AR cells, combined treatment with alectinib and EGFR-TKIs, such as erlotinib and osimertinib, successfully controlled progression of LMC.	osimertinib	109-120	epidermal growth factor receptor	Homo sapiens	76-80
32676311-0	2020	EGFR mutation genotypes affect efficacy and resistance mechanisms of osimertinib in T790M-positive NSCLC patients.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	0-4
32676311-1	2020	Background: Osimertinib is a potent third-generation EGFR tyrosine kinase inhibitor (TKI) with robust activity in advanced EGFR-mutant non-small cell lung cancer (NSCLC), including those with T790M resistance mutation.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	53-57
32676311-3	2020	This study aimed to evaluate whether EGFR-mutant genotypes affect the clinical outcomes and resistance mechanisms in T790M-positive NSCLC patients receiving osimertinib therapy.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	37-41
32676311-13	2020	Conclusions: Our findings indicate that the EGFR 19Del subtypes affect the clinical outcomes and resistance mechanisms to osimertinib in T790M-positive patients.	osimertinib	122-133	epidermal growth factor receptor	Homo sapiens	44-48
32641247-0	2021	Prospective Observational Study of Treatment Resistance-related Gene Screening Using Plasma Circulating Tumor DNA in Third-generation EGFR-TKI Osimertinib Therapy (Elucidator).	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	134-138
32641247-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits EGFR activating and EGFR T790M resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-78
32641247-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits EGFR activating and EGFR T790M resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	80-84
32641247-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits EGFR activating and EGFR T790M resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	157-161
32641247-1	2021	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that potently and selectively inhibits EGFR activating and EGFR T790M resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	157-161
32641247-2	2021	Osimertinib was found to be more effective than first-generation EGFR-TKIs in patients with previously untreated advanced non-small-cell lung cancer (NSCLC) harboring EGFR-positive mutations in a prior phase III trial.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	167-171
32641247-3	2021	Osimertinib is, therefore, one of the most important standard therapies for EGFR mutation-positive patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	76-80
32641247-4	2021	However, there are few reports about osimertinib resistance mechanisms in first-line EGFR-TKI therapy.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	85-89
32641247-5	2021	Understanding first-line osimertinib resistance mechanisms is essential for future therapeutic strategies in patients with NSCLC with EGFR-positive mutations.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	134-138
32374970-0	2020	Osimertinib in EGFR-Mutated Advanced NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
32374971-0	2020	Osimertinib in EGFR-Mutated Advanced NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
32374972-0	2020	Osimertinib in EGFR-Mutated Advanced NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
32374973-0	2020	Osimertinib in EGFR-Mutated Advanced NSCLC.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	15-19
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	9-20	microRNA 21	Homo sapiens	106-114
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	9-20	transforming growth factor alpha	Homo sapiens	128-135
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	9-20	ADP ribosylation factor 6	Homo sapiens	137-141
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	9-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-151
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	83-94	microRNA 21	Homo sapiens	106-114
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	83-94	transforming growth factor alpha	Homo sapiens	128-135
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	83-94	ADP ribosylation factor 6	Homo sapiens	137-141
32375124-7	2020	Besides, osimertinib-resistant exosomes could regulate gene expressions induced by osimertinib, including miRNA-21, miRNA-125b, TGFbeta, ARF6 and c-Kit.	osimertinib	83-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-151
31953310-1	2020	PURPOSE: Currently, an optimal therapeutic strategy comprising molecularly targeted agents for treating EGFR-mutated non-small cell lung cancer (NSCLC) patients with acquired resistance to osimertinib is not available.	osimertinib	189-200	epidermal growth factor receptor	Homo sapiens	104-108
31953310-6	2020	We investigated the correlation between AXL expression in tumors and clinical outcomes with osimertinib for EGFR mutated NSCLC patients with acquired resistance to initial EGFR-TKIs.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	108-112
31953310-7	2020	RESULTS: ONO-7475 sensitized AXL-overexpressing EGFR-mutant NSCLC cells to the EGFR-TKIs osimertinib and dacomitinib.	osimertinib	89-100	epidermal growth factor receptor	Homo sapiens	48-52
31953310-7	2020	RESULTS: ONO-7475 sensitized AXL-overexpressing EGFR-mutant NSCLC cells to the EGFR-TKIs osimertinib and dacomitinib.	osimertinib	89-100	epidermal growth factor receptor	Homo sapiens	79-83
31953310-9	2020	In the cell line-derived xenograft models of AXL-overexpressing EGFR mutated lung cancer treated with osimertinib, initial combination therapy of ONO-7475 and osimertinib markedly regressed tumors and delayed tumor re-growth compared to osimertinib alone or the combination after acquired resistance to osimertinib.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	64-68
31953310-9	2020	In the cell line-derived xenograft models of AXL-overexpressing EGFR mutated lung cancer treated with osimertinib, initial combination therapy of ONO-7475 and osimertinib markedly regressed tumors and delayed tumor re-growth compared to osimertinib alone or the combination after acquired resistance to osimertinib.	osimertinib	159-170	epidermal growth factor receptor	Homo sapiens	64-68
31953310-9	2020	In the cell line-derived xenograft models of AXL-overexpressing EGFR mutated lung cancer treated with osimertinib, initial combination therapy of ONO-7475 and osimertinib markedly regressed tumors and delayed tumor re-growth compared to osimertinib alone or the combination after acquired resistance to osimertinib.	osimertinib	159-170	epidermal growth factor receptor	Homo sapiens	64-68
31953310-9	2020	In the cell line-derived xenograft models of AXL-overexpressing EGFR mutated lung cancer treated with osimertinib, initial combination therapy of ONO-7475 and osimertinib markedly regressed tumors and delayed tumor re-growth compared to osimertinib alone or the combination after acquired resistance to osimertinib.	osimertinib	159-170	epidermal growth factor receptor	Homo sapiens	64-68
32354888-0	2020	Comparison of the Efficacy of EGFR Tyrosine Kinase Inhibitors Erlotinib and Low-dose Osimertinib on a PC-9-GFP EGFR Mutant Non-small-cell Lung Cancer Growing in the Brain of Nude Mice.	osimertinib	85-96	proprotein convertase subtilisin/kexin type 9	Mus musculus	102-106
32354888-2	2020	We compared the efficacy of two EGFR-tyrosine kinase inhibitors (TKIs), erlotinib and osimertinib on a PC-9-GFP EGFR mutant NSCLC growing in the brain of nude mice.	osimertinib	86-97	proprotein convertase subtilisin/kexin type 9	Mus musculus	103-107
32354888-2	2020	We compared the efficacy of two EGFR-tyrosine kinase inhibitors (TKIs), erlotinib and osimertinib on a PC-9-GFP EGFR mutant NSCLC growing in the brain of nude mice.	osimertinib	86-97	epidermal growth factor receptor	Mus musculus	112-116
32354888-6	2020	CONCLUSION: This study strongly supports the high activity of osimertinib for intracranial lesions of EGFR-mutant NSCLC.	osimertinib	62-73	epidermal growth factor receptor	Mus musculus	102-106
31972351-0	2020	Osimertinib overcomes alectinib resistance caused by amphiregulin in a leptomeningeal carcinomatosis model of ALK-rearranged lung cancer.	osimertinib	0-11	amphiregulin	Homo sapiens	53-65
31972351-0	2020	Osimertinib overcomes alectinib resistance caused by amphiregulin in a leptomeningeal carcinomatosis model of ALK-rearranged lung cancer.	osimertinib	0-11	ALK receptor tyrosine kinase	Homo sapiens	110-113
32642185-0	2020	Potential treatment strategy for the rare osimertinib resistant mutation EGFR L718Q.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	73-77
32642198-4	2020	The FLAURA study demonstrated that first-line treatment of EGFR mutant patients with osimertinib significantly improved progression free survival (PFS) over first-generation EGFR-TKIs, thus leading to its approval also in this setting.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	59-63
32642198-4	2020	The FLAURA study demonstrated that first-line treatment of EGFR mutant patients with osimertinib significantly improved progression free survival (PFS) over first-generation EGFR-TKIs, thus leading to its approval also in this setting.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	174-178
32483558-0	2020	Clonal Evolution and Heterogeneity of Osimertinib Acquired Resistance Mechanisms in EGFR Mutant Lung Cancer.	osimertinib	38-49	epidermal growth factor receptor	Homo sapiens	84-88
32483558-1	2020	Clonal evolution of osimertinib-resistance mechanisms in EGFR mutant lung adenocarcinoma is poorly understood.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	57-61
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	CD274 molecule	Homo sapiens	130-135
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	KRAS proto-oncogene, GTPase	Homo sapiens	137-141
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	estrogen receptor 1	Homo sapiens	161-165
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	A-kinase anchoring protein 12	Homo sapiens	166-172
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	makorin ring finger protein 1	Homo sapiens	174-179
32483558-6	2020	Noteworthy osimertinib-resistance mechanisms discovered include neuroendocrine differentiation without histologic transformation, PD-L1, KRAS amplification, and ESR1-AKAP12, MKRN1-BRAF fusions.	osimertinib	11-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	180-184
32351892-4	2020	Case Presentation: In this case series, we present three cases of cecal volvulus among patients with EGFR-positive NSCLC patients treated with osimertinib dosed at double the standard 80 mg dose (160 mg daily).	osimertinib	143-154	epidermal growth factor receptor	Homo sapiens	101-105
31678994-7	2020	We therefore treated mice with orthotopic xenografts using the 3rd-generation EGFR inhibitor osimertinib, with or without STAT3 knockdown.	osimertinib	93-104	epidermal growth factor receptor	Mus musculus	78-82
32207968-1	2020	Osimertinib is a covalent, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved for treating non-small cell lung cancer patients with activating EGFR mutations (Exon19del or L858R) or with the T790M resistance mutation following disease progression on first- or second-generation EGFR TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	44-76
32207968-1	2020	Osimertinib is a covalent, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved for treating non-small cell lung cancer patients with activating EGFR mutations (Exon19del or L858R) or with the T790M resistance mutation following disease progression on first- or second-generation EGFR TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	78-82
32207968-1	2020	Osimertinib is a covalent, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved for treating non-small cell lung cancer patients with activating EGFR mutations (Exon19del or L858R) or with the T790M resistance mutation following disease progression on first- or second-generation EGFR TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	190-194
32207968-1	2020	Osimertinib is a covalent, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved for treating non-small cell lung cancer patients with activating EGFR mutations (Exon19del or L858R) or with the T790M resistance mutation following disease progression on first- or second-generation EGFR TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	190-194
32207968-2	2020	The aim of this work is to rationalize and understand how osimertinib achieves mutant EGFR selectivity over the wild-type (WT) by evaluating its kinetic mechanism of action.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	86-90
32207968-3	2020	In doing so, we developed methodologies combining steady-state and pre-steady-state kinetics to determine the covalent inactivation rates (kinact) and reversible binding affinities (Ki) for osimertinib against WT, L858R, and L858R/T790M EGFR and compared these data to the inhibition kinetics of earlier generations of EGFR TKIs.	osimertinib	190-201	epidermal growth factor receptor	Homo sapiens	237-241
32207968-3	2020	In doing so, we developed methodologies combining steady-state and pre-steady-state kinetics to determine the covalent inactivation rates (kinact) and reversible binding affinities (Ki) for osimertinib against WT, L858R, and L858R/T790M EGFR and compared these data to the inhibition kinetics of earlier generations of EGFR TKIs.	osimertinib	190-201	epidermal growth factor receptor	Homo sapiens	319-323
32207968-5	2020	The Ki and kinact values reveal that osimertinib binds 3-fold tighter to and reacts 3-fold faster with L858R than WT EGFR and binds 17-fold tighter to and reacts 3-fold faster with L858R/T790M than with the WT EGFR.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	117-121
32207968-5	2020	The Ki and kinact values reveal that osimertinib binds 3-fold tighter to and reacts 3-fold faster with L858R than WT EGFR and binds 17-fold tighter to and reacts 3-fold faster with L858R/T790M than with the WT EGFR.	osimertinib	37-48	epidermal growth factor receptor	Homo sapiens	210-214
32550993-5	2020	The structure-activity relationship study revealed that CFA inhibitor 18 (NSP-037) possessed higher inhibition selectivity to the mutated EGFR over wild-type EGFR when compared to clinically approved osimertinib.	osimertinib	200-211	sperm antigen with calponin homology and coiled-coil domains 1	Homo sapiens	74-77
32489263-8	2020	Results: The published overall survival results for osimertinib, combined with its central nervous system activity, have led to osimertinib becoming the preferred first-line treatment for patients with common EGFR mutations, including those with brain metastasis.	osimertinib	128-139	epidermal growth factor receptor	Homo sapiens	209-213
32389962-1	2020	BACKGROUND: In recent years, osimertinib has been increasingly used as a therapeutic drug for epidermal growth factor receptor(EGFR)mutation-positive lung cancer, with heart failure rarely reported as an adverse event.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	127-131
32389962-11	2020	CONCLUSION: While heart failure induced by EGFR-TKIs has been rarely reported, osimertinib may cause cardiomyopathy due to human epidermal growth factor receptor type 2(HER2)inhibitory activity.	osimertinib	79-90	erb-b2 receptor tyrosine kinase 2	Homo sapiens	169-173
31887431-0	2020	Osimertinib for patients with leptomeningeal metastases associated with epidermal growth factor receptor T790M positive advanced NSCLC: the AURA LM analysis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	72-104
31887431-1	2020	BACKGROUND: Osimertinib has shown promising activity in patients with leptomeningeal metastases (LM) from epidermal growth factor receptor (EGFR) positive NSCLC at 160 mg once daily (qd) (BLOOM; NCT02228369).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	106-138
31887431-1	2020	BACKGROUND: Osimertinib has shown promising activity in patients with leptomeningeal metastases (LM) from epidermal growth factor receptor (EGFR) positive NSCLC at 160 mg once daily (qd) (BLOOM; NCT02228369).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	140-144
31887431-12	2020	CONCLUSION: Patients with EGFR T790M-positive NSCLC and radiologically-detected LM derived clinical benefit from osimertinib 80 mg qd.	osimertinib	113-124	epidermal growth factor receptor	Homo sapiens	26-30
32003107-0	2020	Overcoming acquired resistance of EGFR-mutant NSCLC cells to the third generation EGFR inhibitor, osimertinib, with the natural product honokiol.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	34-38
31941753-0	2020	IGF2 Autocrine-Mediated IGF1R Activation Is a Clinically Relevant Mechanism of Osimertinib Resistance in Lung Cancer.	osimertinib	79-90	insulin like growth factor 2	Homo sapiens	0-4
31941753-0	2020	IGF2 Autocrine-Mediated IGF1R Activation Is a Clinically Relevant Mechanism of Osimertinib Resistance in Lung Cancer.	osimertinib	79-90	insulin like growth factor 1 receptor	Homo sapiens	24-29
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	epidermal growth factor receptor	Homo sapiens	148-152
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
31941753-9	2020	Both of our established lung cancer cells and patient-derived lung cancer cells demonstrated IGF2 autocrine-mediated IGF1R pathway activation as a mechanism of osimertinib resistance.	osimertinib	160-171	insulin like growth factor 2	Homo sapiens	93-97
31941753-9	2020	Both of our established lung cancer cells and patient-derived lung cancer cells demonstrated IGF2 autocrine-mediated IGF1R pathway activation as a mechanism of osimertinib resistance.	osimertinib	160-171	insulin like growth factor 1 receptor	Homo sapiens	117-122
31941753-11	2020	Interestingly, the immunohistochemical analysis confirmed the increased IGF2 expression in lung cancer patients who were treated with osimertinib and met the established clinical definition of acquired resistance.	osimertinib	134-145	insulin like growth factor 2	Homo sapiens	72-76
31941753-13	2020	Here, we report for the first time the IGF2 autocrine-mediated IGF1R activation as a nongenetic mechanism of osimertinib resistance in lung cancer at a clinically relevant level.	osimertinib	109-120	insulin like growth factor 2	Homo sapiens	39-43
31941753-13	2020	Here, we report for the first time the IGF2 autocrine-mediated IGF1R activation as a nongenetic mechanism of osimertinib resistance in lung cancer at a clinically relevant level.	osimertinib	109-120	insulin like growth factor 1 receptor	Homo sapiens	63-68
31941753-14	2020	IMPLICATIONS: Using comprehensive protein phosphorylation array and patient-derived lung cancer cells, we found that IGF2 autocrine-mediated IGF1R pathway activation is a clinically relevant and common mechanism of acquired resistance to osimertinib.	osimertinib	238-249	insulin like growth factor 2	Homo sapiens	117-121
31941753-14	2020	IMPLICATIONS: Using comprehensive protein phosphorylation array and patient-derived lung cancer cells, we found that IGF2 autocrine-mediated IGF1R pathway activation is a clinically relevant and common mechanism of acquired resistance to osimertinib.	osimertinib	238-249	insulin like growth factor 1 receptor	Homo sapiens	141-146
32003107-0	2020	Overcoming acquired resistance of EGFR-mutant NSCLC cells to the third generation EGFR inhibitor, osimertinib, with the natural product honokiol.	osimertinib	98-109	epidermal growth factor receptor	Homo sapiens	82-86
32003107-1	2020	The development of acquired resistance to osimertinib (AZD9291 or TAGRISSOTM ), an FDA-approved third generation EGFR inhibitor for the treatment of EGFR-mutant non-small cell lung cancer (NSCLC), limits the long-term benefits for patients.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	113-117
32003107-1	2020	The development of acquired resistance to osimertinib (AZD9291 or TAGRISSOTM ), an FDA-approved third generation EGFR inhibitor for the treatment of EGFR-mutant non-small cell lung cancer (NSCLC), limits the long-term benefits for patients.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	149-153
32003107-1	2020	The development of acquired resistance to osimertinib (AZD9291 or TAGRISSOTM ), an FDA-approved third generation EGFR inhibitor for the treatment of EGFR-mutant non-small cell lung cancer (NSCLC), limits the long-term benefits for patients.	osimertinib	55-62	epidermal growth factor receptor	Homo sapiens	149-153
32420063-0	2020	EGFR mutation tracking predicts survival in advanced EGFR-mutated non-small cell lung cancer patients treated with osimertinib.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	0-4
32068351-0	2020	Severe hepatotoxicity due to osimertinib after nivolumab therapy in patients with non-small cell lung cancer harboring EGFR mutation.	osimertinib	29-40	epidermal growth factor receptor	Homo sapiens	119-123
32068351-1	2020	BACKGROUND: Osimertinib is the most promising treatment option for patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) with acquired T790M resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	81-113
32068351-1	2020	BACKGROUND: Osimertinib is the most promising treatment option for patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) with acquired T790M resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	115-119
32068351-3	2020	METHODS: In this single-institution retrospective study conducted from May 2016 to January 2019, osimertinib was administered to 47 patients with pretreated advanced NSCLC harboring the EGFR mutation.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	186-190
32420075-0	2020	An advanced non-small cell lung cancer patient with epidermal growth factor receptor sensitizing mutation responded to toripalimab in combination with chemotherapy after resistance to osimertinib: a case report.	osimertinib	184-195	epidermal growth factor receptor	Homo sapiens	52-84
32420063-0	2020	EGFR mutation tracking predicts survival in advanced EGFR-mutated non-small cell lung cancer patients treated with osimertinib.	osimertinib	115-126	epidermal growth factor receptor	Homo sapiens	53-57
32420075-1	2020	The clinical activity and favorable toxicity profile of osimertinib has led it to be approved not only for advanced non-small cell lung cancer (NSCLC) patients with T790M-positive tumors when first, or second-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment fails, but also for untreated advanced NSCLC patients with EGFR sensitizing mutation, so how to manage patients who get acquired resistance to osimertinib has becoming an emerging clinical challenge.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	280-284
32420075-1	2020	The clinical activity and favorable toxicity profile of osimertinib has led it to be approved not only for advanced non-small cell lung cancer (NSCLC) patients with T790M-positive tumors when first, or second-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment fails, but also for untreated advanced NSCLC patients with EGFR sensitizing mutation, so how to manage patients who get acquired resistance to osimertinib has becoming an emerging clinical challenge.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	359-363
32420075-2	2020	This presentation would report a case of an advanced NSCLC patient with EGFR 19DEL who received combination therapy of toripalimab and chemotherapy after resistance to first line osimertinib therapy and achieved a PFS benefit of over 8 months.	osimertinib	179-190	epidermal growth factor receptor	Homo sapiens	72-76
32420078-11	2020	Up to now, osimertinib treatment was undertaken to base on an EGFR exon 20 T790M mutation using NGS-based genotyping in cerebrospinal fluid (CSF) ctDNA.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	62-66
32420080-2	2020	AURA3 study showed that patients resistant with the first generation of EGFR-TKI and with T790M mutation still received longer progression-free survival (PFS) after treatment with the third generation of EGFR-TKI osimertinib, and osimertinib also had a good effect on brain metastasis.	osimertinib	213-224	epidermal growth factor receptor	Homo sapiens	72-76
32420080-2	2020	AURA3 study showed that patients resistant with the first generation of EGFR-TKI and with T790M mutation still received longer progression-free survival (PFS) after treatment with the third generation of EGFR-TKI osimertinib, and osimertinib also had a good effect on brain metastasis.	osimertinib	213-224	epidermal growth factor receptor	Homo sapiens	204-208
32068351-11	2020	CONCLUSIONS: The use of osimertinib immediately after nivolumab significantly increased the frequency of grade 3 or higher hepatotoxicity in patients with advanced NSCLC harboring EGFR mutation acquired T790M resistance.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	180-184
32420063-1	2020	Background: Osimertinib has become standard therapy of advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) patients and T790M-mediated resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	64-96
32420080-2	2020	AURA3 study showed that patients resistant with the first generation of EGFR-TKI and with T790M mutation still received longer progression-free survival (PFS) after treatment with the third generation of EGFR-TKI osimertinib, and osimertinib also had a good effect on brain metastasis.	osimertinib	230-241	epidermal growth factor receptor	Homo sapiens	72-76
32420080-2	2020	AURA3 study showed that patients resistant with the first generation of EGFR-TKI and with T790M mutation still received longer progression-free survival (PFS) after treatment with the third generation of EGFR-TKI osimertinib, and osimertinib also had a good effect on brain metastasis.	osimertinib	230-241	epidermal growth factor receptor	Homo sapiens	204-208
32420063-1	2020	Background: Osimertinib has become standard therapy of advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) patients and T790M-mediated resistance.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	98-102
32420080-10	2020	In this case, patient with advanced lung adenocarcinoma and EGFR mutation was resistant with the first generation of EGFR-TKI treatment, and after detection of T790M mutation, we switched to osimertinib for primary disease control, bone metastasis was still obvious, and there was still no obvious effect after pain relief, bone metabolism improvement and local radiotherapy.	osimertinib	191-202	epidermal growth factor receptor	Homo sapiens	60-64
32346403-0	2020	Switching from first or second generation EGFR-TKI to osimertinib in EGFR mutation-positive NSCLC.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	69-73
32252199-0	2020	[Mechanism of PLOD2 induced osimertinib resistance in non-small cell lung cancer HCC827 cells].	osimertinib	28-39	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	14-19
32252199-1	2020	Objective: To investigate the effects of osimertinib on proliferation, migration and invasion of procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) overexpressing HCC827 cells and explore the potential mechanism of PLOD2 induced osimertinib resistance.	osimertinib	41-52	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	97-146
32252199-1	2020	Objective: To investigate the effects of osimertinib on proliferation, migration and invasion of procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) overexpressing HCC827 cells and explore the potential mechanism of PLOD2 induced osimertinib resistance.	osimertinib	41-52	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	148-153
32252199-15	2020	Osimertinib inhibited the expression of p-EGFR, but did not affect the expressions of PLOD2, p-FAK, p-AKT, p-ERK, vimentin and E-cadherin in HCC827-PLOD2 cells.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	42-46
32252199-16	2020	Conclusion: PLOD2 confers resistance to osimertinib in HCC827 cells by regulating EMT, FAK-PI3K/AKT and MAPK signal pathways.	osimertinib	40-51	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	12-17
32257480-0	2020	Complete Remission of Multiple Brain Metastases in a Patient with EGFR-Mutated Non-Small-Cell Lung Cancer Treated with First-Line Osimertinib without Radiotherapy.	osimertinib	130-141	epidermal growth factor receptor	Homo sapiens	66-70
32257480-1	2020	Osimertinib has demonstrated efficacy against stable or asymptomatic central nervous system (CNS) metastases of epidermal growth factor receptor (EGFR) mutation-positive non-small-cell lung cancer (NSCLC) in phase 2 and 3 clinical trials that allowed prior CNS radiotherapy.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	112-144
32257480-1	2020	Osimertinib has demonstrated efficacy against stable or asymptomatic central nervous system (CNS) metastases of epidermal growth factor receptor (EGFR) mutation-positive non-small-cell lung cancer (NSCLC) in phase 2 and 3 clinical trials that allowed prior CNS radiotherapy.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	146-150
32257480-8	2020	This case demonstrated that first-line treatment with osimertinib could even achieve complete remission of multiple brain metastases comprising as many as twenty lesions of EGFR-mutated NSCLC without radiation therapy.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	173-177
32346403-2	2020	Materials & methods: Clinical records were collected from the patients who had received one of two sequential combination strategies of EGFR-TKIs: Salvage use of osimertinib for T790M-mediated acquired resistance to an prior EGFR-TKI or switch use of osimertinib where an EGFR-TKI was switched to osimertinib before disease progression.	osimertinib	162-173	epidermal growth factor receptor	Homo sapiens	136-140
32346403-4	2020	Conclusion: Switch use of osimertinib seemed to produce improved efficacy for patients with activating EGFR mutations, because of the lack of patient selection via T790M.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	103-107
31821539-9	2020	Moreover, the combination of an MEK or ERK inhibitor with a first-generation (eg, erlotinib) or second-generation (eg, afatinib) EGFR-TKI also very effectively inhibited the growth of osimertinib-resistant cells in vitro and of tumors in vivo, although these cell lines were cross-resistant to first-generation or second-generation EGFR-TKIs.	osimertinib	184-195	mitogen-activated protein kinase kinase 7	Homo sapiens	32-35
32256584-6	2020	HIF-1 signaling pathway modulating P-glycoproteins expression, PI3K-Akt pathway regulating survivin expression, and oxidative phosphorylation were upregulated, while arginine and proline metabolism regulating NO production and glycolysis/gluconeogenesis were downregulated during osimertinib resistance.	osimertinib	280-291	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-5
32256584-7	2020	Conclusion: The regulation of HIF-1 and PI3K-Akt signaling pathway, energy supply process, and amino acids metabolism are the promising therapeutic tactics for osimertinib resistance.	osimertinib	160-171	hypoxia inducible factor 1 subunit alpha	Homo sapiens	30-35
32256584-7	2020	Conclusion: The regulation of HIF-1 and PI3K-Akt signaling pathway, energy supply process, and amino acids metabolism are the promising therapeutic tactics for osimertinib resistance.	osimertinib	160-171	AKT serine/threonine kinase 1	Homo sapiens	45-48
31821539-9	2020	Moreover, the combination of an MEK or ERK inhibitor with a first-generation (eg, erlotinib) or second-generation (eg, afatinib) EGFR-TKI also very effectively inhibited the growth of osimertinib-resistant cells in vitro and of tumors in vivo, although these cell lines were cross-resistant to first-generation or second-generation EGFR-TKIs.	osimertinib	184-195	Eph receptor B2	Mus musculus	39-42
31787696-1	2020	Osimertinib is the standard therapy for epidermal-growth-factor-receptor (EGFR)-mutant lung cancers.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	40-72
31787696-1	2020	Osimertinib is the standard therapy for epidermal-growth-factor-receptor (EGFR)-mutant lung cancers.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	74-78
31821539-9	2020	Moreover, the combination of an MEK or ERK inhibitor with a first-generation (eg, erlotinib) or second-generation (eg, afatinib) EGFR-TKI also very effectively inhibited the growth of osimertinib-resistant cells in vitro and of tumors in vivo, although these cell lines were cross-resistant to first-generation or second-generation EGFR-TKIs.	osimertinib	184-195	epidermal growth factor receptor	Mus musculus	129-133
31821539-0	2020	ERK inhibition effectively overcomes acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib.	osimertinib	136-147	EPH receptor B2	Homo sapiens	0-3
31821539-0	2020	ERK inhibition effectively overcomes acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib.	osimertinib	136-147	epidermal growth factor receptor	Homo sapiens	60-92
31821539-9	2020	Moreover, the combination of an MEK or ERK inhibitor with a first-generation (eg, erlotinib) or second-generation (eg, afatinib) EGFR-TKI also very effectively inhibited the growth of osimertinib-resistant cells in vitro and of tumors in vivo, although these cell lines were cross-resistant to first-generation or second-generation EGFR-TKIs.	osimertinib	184-195	epidermal growth factor receptor	Mus musculus	332-336
31821539-1	2020	BACKGROUND: Osimertinib (AZD9291), a third-generation, mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI), is an approved drug for patients who have non-small cell lung cancer (NSCLC) with activating EGFR mutations or those harboring a resistant T790M mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	74-106
31821539-10	2020	CONCLUSIONS: The current findings emphasize the importance of targeting MEK/ERK signaling in maintaining the long-term benefit of osimertinib through overcoming acquired resistance to osimertinib, warranting further investigation of this therapeutic strategy to improve the therapeutic efficacy of osimertinib in the clinic.	osimertinib	130-141	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
31821539-1	2020	BACKGROUND: Osimertinib (AZD9291), a third-generation, mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI), is an approved drug for patients who have non-small cell lung cancer (NSCLC) with activating EGFR mutations or those harboring a resistant T790M mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	108-112
31821539-1	2020	BACKGROUND: Osimertinib (AZD9291), a third-generation, mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI), is an approved drug for patients who have non-small cell lung cancer (NSCLC) with activating EGFR mutations or those harboring a resistant T790M mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	141-145
31821539-10	2020	CONCLUSIONS: The current findings emphasize the importance of targeting MEK/ERK signaling in maintaining the long-term benefit of osimertinib through overcoming acquired resistance to osimertinib, warranting further investigation of this therapeutic strategy to improve the therapeutic efficacy of osimertinib in the clinic.	osimertinib	130-141	Eph receptor B2	Mus musculus	76-79
31821539-1	2020	BACKGROUND: Osimertinib (AZD9291), a third-generation, mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI), is an approved drug for patients who have non-small cell lung cancer (NSCLC) with activating EGFR mutations or those harboring a resistant T790M mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	141-145
31821539-10	2020	CONCLUSIONS: The current findings emphasize the importance of targeting MEK/ERK signaling in maintaining the long-term benefit of osimertinib through overcoming acquired resistance to osimertinib, warranting further investigation of this therapeutic strategy to improve the therapeutic efficacy of osimertinib in the clinic.	osimertinib	184-195	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
31821539-8	2020	RESULTS: The combination of osimertinib with an ERK inhibitor synergistically decreased the survival of osimertinib-resistant cell lines with enhanced induction of apoptosis and effectively inhibited the growth of osimertinib-resistant xenografts in nude mice.	osimertinib	104-115	Eph receptor B2	Mus musculus	48-51
31821539-8	2020	RESULTS: The combination of osimertinib with an ERK inhibitor synergistically decreased the survival of osimertinib-resistant cell lines with enhanced induction of apoptosis and effectively inhibited the growth of osimertinib-resistant xenografts in nude mice.	osimertinib	104-115	Eph receptor B2	Mus musculus	48-51
31821539-10	2020	CONCLUSIONS: The current findings emphasize the importance of targeting MEK/ERK signaling in maintaining the long-term benefit of osimertinib through overcoming acquired resistance to osimertinib, warranting further investigation of this therapeutic strategy to improve the therapeutic efficacy of osimertinib in the clinic.	osimertinib	184-195	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
32355810-0	2020	PIM1 inhibitor synergizes the anti-tumor effect of osimertinib via STAT3 dephosphorylation in EGFR-mutant non-small cell lung cancer.	osimertinib	51-62	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
32355810-0	2020	PIM1 inhibitor synergizes the anti-tumor effect of osimertinib via STAT3 dephosphorylation in EGFR-mutant non-small cell lung cancer.	osimertinib	51-62	signal transducer and activator of transcription 3	Homo sapiens	67-72
32355810-0	2020	PIM1 inhibitor synergizes the anti-tumor effect of osimertinib via STAT3 dephosphorylation in EGFR-mutant non-small cell lung cancer.	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	94-98
32355810-10	2020	It was more efficient in suppressing EGFR activation and phosphorylation of STAT3 compared with osimertinib treatment alone.	osimertinib	96-107	epidermal growth factor receptor	Homo sapiens	37-41
32355810-10	2020	It was more efficient in suppressing EGFR activation and phosphorylation of STAT3 compared with osimertinib treatment alone.	osimertinib	96-107	signal transducer and activator of transcription 3	Homo sapiens	76-81
32355810-13	2020	CX-6258 HCl is a potential molecular inhibitor to sensitize the antitumor effects of osimertinib through the inhibiting of the phosphorylation of STAT3 in NSCLC.	osimertinib	85-96	signal transducer and activator of transcription 3	Homo sapiens	146-151
31839416-1	2020	OBJECTIVES: The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR TKI) osimertinib has shown promising efficacy both in EGFR-mutant, T790M positive non-small cell lung cancer (NSCLC) patients who have become resistant to 1st or 2nd generation EGFR TKIs and patients with sensitizing EGFR mutations as the first line therapy.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	91-95
32274079-0	2020	The impact of age and performance status on the efficacy of osimertinib in patients with EGFR T790M-positive non-small cell lung cancer.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	89-93
31926441-0	2020	Osimertinib treatment for patients with EGFR exon 20 mutation positive non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	40-44
31839416-1	2020	OBJECTIVES: The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR TKI) osimertinib has shown promising efficacy both in EGFR-mutant, T790M positive non-small cell lung cancer (NSCLC) patients who have become resistant to 1st or 2nd generation EGFR TKIs and patients with sensitizing EGFR mutations as the first line therapy.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	150-154
31926441-2	2020	In vitro and preclinical animal studies have shown that osimertinib exerts antitumor activity against EGFR exon 20 mutation positive NSCLC.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	102-106
31839416-1	2020	OBJECTIVES: The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR TKI) osimertinib has shown promising efficacy both in EGFR-mutant, T790M positive non-small cell lung cancer (NSCLC) patients who have become resistant to 1st or 2nd generation EGFR TKIs and patients with sensitizing EGFR mutations as the first line therapy.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	150-154
31926441-3	2020	We report on a cohort of advanced stage NSCLC patients who harbor an EGFR exon 20 mutation and received osimertinib treatment.	osimertinib	104-115	epidermal growth factor receptor	Homo sapiens	69-73
31839416-1	2020	OBJECTIVES: The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR TKI) osimertinib has shown promising efficacy both in EGFR-mutant, T790M positive non-small cell lung cancer (NSCLC) patients who have become resistant to 1st or 2nd generation EGFR TKIs and patients with sensitizing EGFR mutations as the first line therapy.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	150-154
31926441-13	2020	CONCLUSION: Osimertinib has limited antitumor activity in patients with EGFR exon 20 mutated NSCLC, with an ORR of 5 %.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	72-76
31839416-8	2020	Some other putative resistance mechanisms to osimertinib, such as the recurrent EGFR V834 L mutation, were also identified.	osimertinib	45-56	epidermal growth factor receptor	Homo sapiens	80-84
31839416-9	2020	Moreover, pathogenic mutations of TP53 were negatively related to the efficacy of osimertinib.	osimertinib	82-93	tumor protein p53	Homo sapiens	34-38
32070867-2	2020	AZD9291 is a third-generation EGFR-TKI and approved to treat NSCLC patients harboring EGFR T790M mutation and common targetable activating EGFR mutations, but it has a limited effect for wtEGFR NSCLC.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	30-34
32070867-2	2020	AZD9291 is a third-generation EGFR-TKI and approved to treat NSCLC patients harboring EGFR T790M mutation and common targetable activating EGFR mutations, but it has a limited effect for wtEGFR NSCLC.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	86-90
32070867-2	2020	AZD9291 is a third-generation EGFR-TKI and approved to treat NSCLC patients harboring EGFR T790M mutation and common targetable activating EGFR mutations, but it has a limited effect for wtEGFR NSCLC.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	86-90
32070867-7	2020	Furthermore, ROS inhibition by NAC or GSH reversed the apoptosis induced by shikonin plus AZD9291, and recovered the ER stress activated by combination treatment, indicating that ROS mediated ER stress played a vital role in this combination therapy.	osimertinib	90-97	synuclein alpha	Homo sapiens	31-34
32067121-0	2020	EGFR T790M relative mutation purity predicts osimertinib treatment efficacy in non-small cell lung cancer patients.	osimertinib	45-56	epidermal growth factor receptor	Homo sapiens	0-4
31809241-0	2020	Osimertinib in Patients With Epidermal Growth Factor Receptor Mutation-Positive Non-Small-Cell Lung Cancer and Leptomeningeal Metastases: The BLOOM Study.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	29-61
31809241-1	2020	PURPOSE: In this phase I study (BLOOM), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), was evaluated in patients with leptomeningeal metastases (LMs) from EGFR-mutated (EGFRm) advanced non-small-cell lung cancer (NSCLC) whose disease had progressed on previous EGFR-TKI therapy.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	72-104
31809241-1	2020	PURPOSE: In this phase I study (BLOOM), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), was evaluated in patients with leptomeningeal metastases (LMs) from EGFR-mutated (EGFRm) advanced non-small-cell lung cancer (NSCLC) whose disease had progressed on previous EGFR-TKI therapy.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	106-110
31809241-1	2020	PURPOSE: In this phase I study (BLOOM), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), was evaluated in patients with leptomeningeal metastases (LMs) from EGFR-mutated (EGFRm) advanced non-small-cell lung cancer (NSCLC) whose disease had progressed on previous EGFR-TKI therapy.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	213-217
31809241-1	2020	PURPOSE: In this phase I study (BLOOM), osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), was evaluated in patients with leptomeningeal metastases (LMs) from EGFR-mutated (EGFRm) advanced non-small-cell lung cancer (NSCLC) whose disease had progressed on previous EGFR-TKI therapy.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	213-217
32067121-1	2020	BACKGROUND: Despite the impressive anti-tumor activity of osimertinib in epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer (NSCLC) patients, 30-40% of patients still show limited response.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	73-105
32067121-1	2020	BACKGROUND: Despite the impressive anti-tumor activity of osimertinib in epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer (NSCLC) patients, 30-40% of patients still show limited response.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	107-111
31825714-0	2020	Osimertinib for Patients With Non-Small-Cell Lung Cancer Harboring Uncommon EGFR Mutations: A Multicenter, Open-Label, Phase II Trial (KCSG-LU15-09).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	76-80
31825714-2	2020	Here, we report the efficacy and safety of osimertinib in patients with NSCLC harboring uncommon EGFR mutations.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	97-101
31825714-16	2020	CONCLUSION: Osimertinib demonstrated favorable activity with manageable toxicity in patients with NSCLC harboring uncommon EGFR mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	123-127
32042433-3	2020	We report a rare case of primary resistance to osimertinib, although liquid biopsy revealed EGFR T790M positivity.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	92-96
32042433-6	2020	Osimertinib was initiated when liquid biopsy showed EGFR T790M positivity.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	52-56
31955357-10	2020	The most common EGFR-TKIs used as 2L monotherapy in patients who received 1L EGFR-TKI were afatinib and osimertinib (n = 7 for both).	osimertinib	104-115	epidermal growth factor receptor	Homo sapiens	16-20
31671073-1	2020	EGFR-mutated lung adenocarcinoma patients treated with gefitinib and osimertinib show a therapeutic benefit limited by the appearance of secondary mutations, such as EGFRT790M and EGFRC797S.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	0-4
31671073-2	2020	It is generally assumed that these secondary mutations render EGFR completely unresponsive to the inhibitors, but contrary to this, we uncovered here that gefitinib and osimertinib increased STAT3 phosphorylation (p-STAT3) in EGFRT790M and EGFRC797S tumoral cells.	osimertinib	169-180	epidermal growth factor receptor	Homo sapiens	62-66
31671073-2	2020	It is generally assumed that these secondary mutations render EGFR completely unresponsive to the inhibitors, but contrary to this, we uncovered here that gefitinib and osimertinib increased STAT3 phosphorylation (p-STAT3) in EGFRT790M and EGFRC797S tumoral cells.	osimertinib	169-180	signal transducer and activator of transcription 3	Homo sapiens	191-196
31671073-2	2020	It is generally assumed that these secondary mutations render EGFR completely unresponsive to the inhibitors, but contrary to this, we uncovered here that gefitinib and osimertinib increased STAT3 phosphorylation (p-STAT3) in EGFRT790M and EGFRC797S tumoral cells.	osimertinib	169-180	signal transducer and activator of transcription 3	Homo sapiens	216-221
31671073-3	2020	Interestingly, we also found that concomitant Notch inhibition with gefitinib or osimertinib treatment induced a p-STAT3-dependent strong reduction in the levels of the transcriptional repressor HES1.	osimertinib	81-92	signal transducer and activator of transcription 3	Homo sapiens	115-120
31671073-3	2020	Interestingly, we also found that concomitant Notch inhibition with gefitinib or osimertinib treatment induced a p-STAT3-dependent strong reduction in the levels of the transcriptional repressor HES1.	osimertinib	81-92	hes family bHLH transcription factor 1	Homo sapiens	195-199
31882494-1	2020	Osimertinib is an oral, irreversible epidermal growth factor receptor inhibitor that is associated with various pulmonary manifestations including transient asymptomatic pulmonary opacities (TAPOs) and pneumonitis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	37-69
31863283-0	2020	Observational Study of Sequential Afatinib and Osimertinib in EGFR Mutation-Positive NSCLC: Patients Treated with a 40-mg Starting Dose of Afatinib.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	62-66
31810534-0	2020	First-line osimertinib treatment in patients with lung squamous cell carcinoma harboring active epidermal growth factor receptor mutations.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	96-128
31769875-0	2020	Epidermal growth factor receptor mutation analysis in tissue and plasma from the AURA3 trial: Osimertinib versus platinum-pemetrexed for T790M mutation-positive advanced non-small cell lung cancer.	osimertinib	94-105	epidermal growth factor receptor	Homo sapiens	0-32
31769875-1	2020	BACKGROUND: This study assesses different technologies for detecting epidermal growth factor receptor (EGFR) mutations from circulating tumor DNA in patients with EGFR T790M-positive advanced non-small cell lung cancer (NSCLC) from the AURA3 study (NCT02151981), and it evaluates clinical responses to osimertinib and platinum-pemetrexed according to the plasma T790M status.	osimertinib	302-313	epidermal growth factor receptor	Homo sapiens	163-167
31929495-13	2020	Because molecular biology of the surgical specimen showed epidermal growth factor receptor (EGFR)-activating mutations, he was treated with osimertinib for 2 months.	osimertinib	140-151	epidermal growth factor receptor	Homo sapiens	58-90
31929495-13	2020	Because molecular biology of the surgical specimen showed epidermal growth factor receptor (EGFR)-activating mutations, he was treated with osimertinib for 2 months.	osimertinib	140-151	epidermal growth factor receptor	Homo sapiens	92-96
32005071-0	2020	Erratum to clinical efficacy analysis of Osimertinib treatment for a patient with leptomeningeal metastasis of EGFR+ non-small cell lung cancer without the T790M mutation.	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	111-115
31999837-1	2020	BACKGROUND: The major clinical obstacle that limits the long-term benefits of treatment with osimertinib (AZD9291) in patients with epidermal growth factor receptor-mutant non-small cell lung cancer is the development of acquired resistance.	osimertinib	93-104	epidermal growth factor receptor	Homo sapiens	132-164
31999837-1	2020	BACKGROUND: The major clinical obstacle that limits the long-term benefits of treatment with osimertinib (AZD9291) in patients with epidermal growth factor receptor-mutant non-small cell lung cancer is the development of acquired resistance.	osimertinib	106-113	epidermal growth factor receptor	Homo sapiens	132-164
31999837-11	2020	Mechanistically, the combination of LBH589 and osimertinib enhanced the elevation of Bim in osimertinib-resistant cells.	osimertinib	47-58	BCL2-like 11 (apoptosis facilitator)	Mus musculus	85-88
31999837-11	2020	Mechanistically, the combination of LBH589 and osimertinib enhanced the elevation of Bim in osimertinib-resistant cells.	osimertinib	92-103	BCL2-like 11 (apoptosis facilitator)	Mus musculus	85-88
31999837-12	2020	Knockout of Bim in osimertinib-resistant cells substantially attenuated or abolished apoptosis enhanced by the LBH589 and osimertinib combination.	osimertinib	19-30	BCL2-like 11 (apoptosis facilitator)	Mus musculus	12-15
31999837-12	2020	Knockout of Bim in osimertinib-resistant cells substantially attenuated or abolished apoptosis enhanced by the LBH589 and osimertinib combination.	osimertinib	122-133	BCL2-like 11 (apoptosis facilitator)	Mus musculus	12-15
31999837-13	2020	These results collectively support a critical role of Bim elevation in the induction of apoptosis of osimertinib-resistant cells for this combination.	osimertinib	101-112	BCL2-like 11 (apoptosis facilitator)	Mus musculus	54-57
32022929-2	2020	No prospective data have been available for the efficacy of osimertinib in patients with non-small cell lung cancer (NSCLC) who develop resistance to first- or second-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) and who test positive for the TKI resistance-conferring T790M mutation of EGFR by liquid biopsy.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	178-210
32022929-2	2020	No prospective data have been available for the efficacy of osimertinib in patients with non-small cell lung cancer (NSCLC) who develop resistance to first- or second-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) and who test positive for the TKI resistance-conferring T790M mutation of EGFR by liquid biopsy.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	212-216
33271494-3	2020	This phase III clinical trial showed that the use of adjuvant osimertinib in stage IB-IIIA NSCLC patients harboring EGFR mutations had a clinically meaningful benefit.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	116-120
33276288-3	2020	Osimertinib is a TKI that was fast-tracked by the United States Food and Drug Administration in 2015 and subsequently approved for the treatment of metastatic epidermal growth factor receptor T790M mutation-positive non-small cell lung cancer.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	159-191
31838405-1	2020	BACKGROUND: In the FLAURA trial, osimertinib demonstrated superior progression-free survival and a favorable toxicity profile to erlotinib or gefitinib as initial therapy in patients with EGFR-mutated advanced non-small-cell lung cancer.	osimertinib	33-44	epidermal growth factor receptor	Homo sapiens	188-192
31751012-2	2020	A phase 3 trial compared first-line osimertinib with other EGFR-TKIs in patients with EGFR mutation-positive advanced non-small-cell lung cancer (NSCLC).	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	86-90
31751012-10	2020	CONCLUSIONS: Among patients with previously untreated advanced NSCLC with an EGFR mutation, those who received osimertinib had longer overall survival than those who received a comparator EGFR-TKI.	osimertinib	111-122	epidermal growth factor receptor	Homo sapiens	77-81
32706102-1	2020	INTRODUCTION: Osimertinib is a third-generation, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated efficacy in the treatment of EGFR-mutant non-small-cell lung cancer (NSCLC) in prospective clinical trials.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	62-94
32706102-1	2020	INTRODUCTION: Osimertinib is a third-generation, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated efficacy in the treatment of EGFR-mutant non-small-cell lung cancer (NSCLC) in prospective clinical trials.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	96-100
32706102-1	2020	INTRODUCTION: Osimertinib is a third-generation, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated efficacy in the treatment of EGFR-mutant non-small-cell lung cancer (NSCLC) in prospective clinical trials.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	179-183
32706102-2	2020	MATERIAL AND METHODS: This retrospective analysis evaluated the outcomes of 32 pretreated patients with EGFR T790M mutation who received osimertinib in clinical practice at seven centers in Poland within the Expanded Drug Access Program.	osimertinib	137-148	epidermal growth factor receptor	Homo sapiens	104-108
32706102-13	2020	CONCLUSION: These results confirm the value of osimertinib in patients with previously treated EGFR T790M-mutant NSCLC.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	95-99
33148913-5	2020	In comparison with PC-9 cells, PC-9 BIMi2- / - cells were less sensitive to apoptosis mediated by EGFR-TKIs such as gefitinib and osimertinib.	osimertinib	130-141	epidermal growth factor receptor	Homo sapiens	98-102
31557536-0	2020	Exon-16-skipping HER2 as a novel mechanism of osimertinib-resistance in EGFR L858R/T790M-positive non-small-cell lung cancer.	osimertinib	46-57	erb-b2 receptor tyrosine kinase 2	Homo sapiens	17-21
31557536-0	2020	Exon-16-skipping HER2 as a novel mechanism of osimertinib-resistance in EGFR L858R/T790M-positive non-small-cell lung cancer.	osimertinib	46-57	epidermal growth factor receptor	Homo sapiens	72-76
31557536-1	2020	BACKGROUND: Osimertinib is the current recommended treatment for EGFR T790M-positive NSCLC following EGFR-TKI therapy.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	65-69
31864554-0	2020	Capmatinib and Osimertinib Combination Therapy for EGFR-Mutant Lung Adenocarcinoma.	osimertinib	15-26	epidermal growth factor receptor	Homo sapiens	51-55
31557536-1	2020	BACKGROUND: Osimertinib is the current recommended treatment for EGFR T790M-positive NSCLC following EGFR-TKI therapy.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	101-105
31557536-3	2020	We had a patient suffering from EGFR L858R/T790M-positive NSCLC who initially responded to osimertinib therapy but eventually developed resistance.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	32-36
31557536-12	2020	HER2D16-expressing H1975 cells were resistant to osimertinib treatment.	osimertinib	49-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
31557536-13	2020	We also found mutant EGFR and HER2D16 cooperated to activate downstream signaling for osimertinib-resistance.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	21-25
31557536-16	2020	CONCLUSION: HER2D16 can contribute to osimertinib resistance through Src independent pathway.	osimertinib	38-49	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	69-72
31786475-2	2020	This study aimed to investigate the incidence of acquired T790M mutation and their outcome to subsequent osimertinib in patients of advanced NSCLC harboring uncommon EGFR mutations.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	166-170
31640894-0	2020	Response to the combination of dabrafenib, trametinib and osimertinib in a patient with EGFR-mutant NSCLC harboring an acquired BRAFV600E mutation.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	88-92
31786475-11	2020	CONCLUSIONS: Uncommon EGFR mutation showed a significantly lower incidence of acquired T790M mutation and benefited significantly less from subsequent osimertinib treatment than common EGFR mutations in patients with advanced NSCLC.	osimertinib	151-162	epidermal growth factor receptor	Homo sapiens	22-26
32173649-0	2020	Effect of Osimertinib on the expression of serum mmp-7 and mmp-9 in patients with non-small cell lung cancer.	osimertinib	10-21	matrix metallopeptidase 7	Homo sapiens	49-54
32400331-5	2020	Since 2013 six irreversible kinase inhibitors, including afatinib, ibrutinib, neratinib, dacomitinib and osimertinib, acalabrutinib have been approved by FDA for treatment of severe diseases like metastatic non-small cell lung cancer (NSCLC), mantel cell lymphoma (MCL) and HER2-positive breast cancer.	osimertinib	105-116	erb-b2 receptor tyrosine kinase 2	Homo sapiens	274-278
31494653-4	2020	RESULTS: An EGFR T790M mutation was detected in 32 non-small cell lung carcinoma patients, of whom 21 (65.6%) underwent osimertinib treatment after detection of the mutation.	osimertinib	120-131	epidermal growth factor receptor	Homo sapiens	12-16
31494653-9	2020	CONCLUSIONS: Non-small cell lung carcinoma patients in whom an EGFR T790M mutation was detected in plasma samples demonstrated a poorer response to osimertinib than those in whom the mutation was detected in tissue specimens.	osimertinib	148-159	epidermal growth factor receptor	Homo sapiens	63-67
32173649-0	2020	Effect of Osimertinib on the expression of serum mmp-7 and mmp-9 in patients with non-small cell lung cancer.	osimertinib	10-21	matrix metallopeptidase 9	Homo sapiens	59-64
32173649-1	2020	The purpose was to investigate the efficacy and safety of Osimertinib in the treatment of advanced non-small cell lung cancer and to analyze its effects on the expression of serum matrix metalloproteinase-7 (MMP-7) and matrix metallo-proteinase-9 (MMP-9).	osimertinib	58-69	matrix metallopeptidase 7	Homo sapiens	180-206
32173649-1	2020	The purpose was to investigate the efficacy and safety of Osimertinib in the treatment of advanced non-small cell lung cancer and to analyze its effects on the expression of serum matrix metalloproteinase-7 (MMP-7) and matrix metallo-proteinase-9 (MMP-9).	osimertinib	58-69	matrix metallopeptidase 7	Homo sapiens	208-213
32173649-1	2020	The purpose was to investigate the efficacy and safety of Osimertinib in the treatment of advanced non-small cell lung cancer and to analyze its effects on the expression of serum matrix metalloproteinase-7 (MMP-7) and matrix metallo-proteinase-9 (MMP-9).	osimertinib	58-69	matrix metallopeptidase 9	Homo sapiens	219-246
32173649-9	2020	In the treatment of patients with advanced non-small cell lung cancer, Osimertinib significantly reduced the expression of serum MMP-7, MMP-9, improved the clinical benefit and quality of life of patients.	osimertinib	71-82	matrix metallopeptidase 7	Homo sapiens	129-134
32173649-9	2020	In the treatment of patients with advanced non-small cell lung cancer, Osimertinib significantly reduced the expression of serum MMP-7, MMP-9, improved the clinical benefit and quality of life of patients.	osimertinib	71-82	matrix metallopeptidase 9	Homo sapiens	136-141
32650965-0	2020	ASTRIS, a large real-world study to evaluate the efficacy of osimertinib in epidermal growth factor receptor T790M mutation-positive non-small cell lung cancer patients: Clinical characteristics and genotyping methods in a Spanish cohort.	osimertinib	61-72	epidermal growth factor receptor	Homo sapiens	76-108
32650965-1	2020	PURPOSE: Osimertinib has proven efficacy in EGFR T790M mutation-positive non-small cell lung cancer (NSCLC) patients; however, its benefits have not been evaluated in a real-world setting.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	44-48
32650965-2	2020	METHODS: ASTRIS is a single-arm, open-label, multinational study to evaluate the efficacy and safety of osimertinib for the treatment of EGFR T790M mutation-positive NSCLC.	osimertinib	104-115	epidermal growth factor receptor	Homo sapiens	137-141
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	56-60
31758670-0	2020	Activation of insulin-like growth factor-1 receptor confers acquired resistance to osimertinib in non-small cell lung cancer with EGFR T790M mutation.	osimertinib	83-94	insulin like growth factor 1 receptor	Homo sapiens	14-51
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	134-138
31758670-0	2020	Activation of insulin-like growth factor-1 receptor confers acquired resistance to osimertinib in non-small cell lung cancer with EGFR T790M mutation.	osimertinib	83-94	epidermal growth factor receptor	Homo sapiens	130-134
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	134-138
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	56-60
31758670-3	2020	METHODS: We established osimertinib-resistant cells (PC9/T790M/AZDR and H1975/AZDR) derived from EGFR-mutant NSCLC cells harboring T790M mutation, and investigated the mechanism of acquired resistance to osimertinib by whole-exome sequencing and multiple phospho-receptor tyrosine kinase (RTK) array.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	97-101
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	134-138
31758670-1	2020	BACKGROUND: Osimertinib (AZD9291) is a third-generation EGFR-tyrosine kinase inhibitor (TKI) that selectively inhibits the activating EGFR mutation and T790M mutation, and is currently used globally to treat EGFR-mutant non-small cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	134-138
31758670-4	2020	A tumor specimen from an EGFR-mutant NSCLC patient with acquired resistance to osimertinib was also subjected to immunohistochemical analysis.	osimertinib	79-90	epidermal growth factor receptor	Homo sapiens	25-29
31758670-7	2020	Knockdown of IGF1R by siRNA as well as inhibition of IGF1R activation by linstinib (IGF1R inhibitor) significantly restored the sensitivity to osimertinib.	osimertinib	143-154	insulin like growth factor 1 receptor	Homo sapiens	13-18
31758670-7	2020	Knockdown of IGF1R by siRNA as well as inhibition of IGF1R activation by linstinib (IGF1R inhibitor) significantly restored the sensitivity to osimertinib.	osimertinib	143-154	insulin like growth factor 1 receptor	Homo sapiens	53-58
31758670-7	2020	Knockdown of IGF1R by siRNA as well as inhibition of IGF1R activation by linstinib (IGF1R inhibitor) significantly restored the sensitivity to osimertinib.	osimertinib	143-154	insulin like growth factor 1 receptor	Homo sapiens	53-58
31758670-8	2020	Immunohistochemical analysis revealed that the expression level of phosphorylated IGF1R was higher in the tumor specimen from the EGFR-mutant NSCLC patient with acquired resistance to osimertinib than in the specimen collected prior to the treatment.	osimertinib	184-195	insulin like growth factor 1 receptor	Homo sapiens	82-87
31758670-8	2020	Immunohistochemical analysis revealed that the expression level of phosphorylated IGF1R was higher in the tumor specimen from the EGFR-mutant NSCLC patient with acquired resistance to osimertinib than in the specimen collected prior to the treatment.	osimertinib	184-195	epidermal growth factor receptor	Homo sapiens	130-134
31758670-9	2020	CONCLUSIONS: IGF1R activation could occur following treatment with osimertinib in EGFR-mutant NSCLC with T790M mutation, and might be one of the mechanisms underlying osimertinib resistance.	osimertinib	67-78	insulin like growth factor 1 receptor	Homo sapiens	13-18
31758670-9	2020	CONCLUSIONS: IGF1R activation could occur following treatment with osimertinib in EGFR-mutant NSCLC with T790M mutation, and might be one of the mechanisms underlying osimertinib resistance.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	82-86
31758670-9	2020	CONCLUSIONS: IGF1R activation could occur following treatment with osimertinib in EGFR-mutant NSCLC with T790M mutation, and might be one of the mechanisms underlying osimertinib resistance.	osimertinib	167-178	insulin like growth factor 1 receptor	Homo sapiens	13-18
31758670-10	2020	Combined treatment of osimertinib and IGF1R inhibitor might be effective in overcoming the acquired resistance to osimertinib induced by IGF1R activation.	osimertinib	22-33	insulin like growth factor 1 receptor	Homo sapiens	137-142
31758670-10	2020	Combined treatment of osimertinib and IGF1R inhibitor might be effective in overcoming the acquired resistance to osimertinib induced by IGF1R activation.	osimertinib	114-125	insulin like growth factor 1 receptor	Homo sapiens	38-43
31758670-10	2020	Combined treatment of osimertinib and IGF1R inhibitor might be effective in overcoming the acquired resistance to osimertinib induced by IGF1R activation.	osimertinib	114-125	insulin like growth factor 1 receptor	Homo sapiens	137-142
31791326-15	2019	Combination of PTK2 inhibitor and EGFR-TKI (defactinib and osimertinib) recovered EGFR-TKI sensitivity in the EGFR-TKI-resistant NSCLC.	osimertinib	59-70	PTK2 protein tyrosine kinase 2	Mus musculus	15-19
31801598-8	2019	Ectopic overexpression of shisa3 inhibited CSC properties and the cell cycle in the lung adenocarcinoma cells resistant to gefitinib/osimertinib.	osimertinib	133-144	shisa family member 3	Homo sapiens	26-32
31791326-15	2019	Combination of PTK2 inhibitor and EGFR-TKI (defactinib and osimertinib) recovered EGFR-TKI sensitivity in the EGFR-TKI-resistant NSCLC.	osimertinib	59-70	epidermal growth factor receptor	Mus musculus	34-38
31791326-15	2019	Combination of PTK2 inhibitor and EGFR-TKI (defactinib and osimertinib) recovered EGFR-TKI sensitivity in the EGFR-TKI-resistant NSCLC.	osimertinib	59-70	epidermal growth factor receptor	Mus musculus	82-86
31171828-8	2019	We discovered that, AZD9291, a potent and selective EGFR inhibitor, disrupted the interaction of EZH2-EED, leading to impairment of PRC2 activity and downregulation of EZH2 protein.	osimertinib	20-27	epidermal growth factor receptor	Homo sapiens	52-56
31171828-8	2019	We discovered that, AZD9291, a potent and selective EGFR inhibitor, disrupted the interaction of EZH2-EED, leading to impairment of PRC2 activity and downregulation of EZH2 protein.	osimertinib	20-27	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	97-101
31171828-8	2019	We discovered that, AZD9291, a potent and selective EGFR inhibitor, disrupted the interaction of EZH2-EED, leading to impairment of PRC2 activity and downregulation of EZH2 protein.	osimertinib	20-27	embryonic ectoderm development	Homo sapiens	102-105
31171828-8	2019	We discovered that, AZD9291, a potent and selective EGFR inhibitor, disrupted the interaction of EZH2-EED, leading to impairment of PRC2 activity and downregulation of EZH2 protein.	osimertinib	20-27	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	168-172
31171828-9	2019	In addition, AZD9291 declined EZH2 mRNA expression via upregulating the expression of a tumor suppressor, miR-34a.	osimertinib	13-20	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	30-34
31171828-9	2019	In addition, AZD9291 declined EZH2 mRNA expression via upregulating the expression of a tumor suppressor, miR-34a.	osimertinib	13-20	microRNA 34a	Homo sapiens	106-113
31171828-10	2019	Our results suggest that AZD9291 can serve as a lead compound for further development of antagonist of PRC2 protein-protein interactions and EZH2 mRNA may be a direct target of miR-34a through non-canonical base pairing.	osimertinib	25-32	microRNA 34a	Homo sapiens	177-184
31832192-3	2019	Recent studies suggest that a key mechanism of acquired resistance to third-generation EGFR-TKIs (such as osimertinib) may be MET amplification and/or protein overactivation, especially when they are used as a first-line treatment.	osimertinib	106-117	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-129
31562701-0	2019	Metformin-sensitized NSCLC cells to osimertinib via AMPK-dependent autophagy inhibition.	osimertinib	36-47	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	52-56
31562701-1	2019	INTRODUCTION: The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib is a promising therapeutic option for patients with advanced non-small-cell lung cancer (NSCLC) in second-line or first-line treatment because of its applications in selectively inhibiting EGFR T790M and EGFR-tyrosine kinase inhibitor sensitizing mutations.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	35-67
31562701-1	2019	INTRODUCTION: The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib is a promising therapeutic option for patients with advanced non-small-cell lung cancer (NSCLC) in second-line or first-line treatment because of its applications in selectively inhibiting EGFR T790M and EGFR-tyrosine kinase inhibitor sensitizing mutations.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	69-73
31562701-1	2019	INTRODUCTION: The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib is a promising therapeutic option for patients with advanced non-small-cell lung cancer (NSCLC) in second-line or first-line treatment because of its applications in selectively inhibiting EGFR T790M and EGFR-tyrosine kinase inhibitor sensitizing mutations.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	286-290
31562701-1	2019	INTRODUCTION: The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib is a promising therapeutic option for patients with advanced non-small-cell lung cancer (NSCLC) in second-line or first-line treatment because of its applications in selectively inhibiting EGFR T790M and EGFR-tyrosine kinase inhibitor sensitizing mutations.	osimertinib	85-96	epidermal growth factor receptor	Homo sapiens	286-290
31562701-7	2019	CONCLUSION: Metformin inhibited autophagy and enhanced osimertinib sensitivity via inducing AMPK activation in a time-dependent manner.	osimertinib	55-66	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	92-96
32010579-3	2019	Methods: Parallel somatic mutation and DNA methylation profiling was performed on a total of 85 longitudinal plasma samples obtained from 8 stage IV osimertinib-treated EGFR T790M-positive lung adenocarcinoma patients.	osimertinib	149-160	epidermal growth factor receptor	Homo sapiens	169-173
31560541-4	2019	In this work, we optimized compound 2 by scaffold hopping and exploiting the potent inhibitory activity of various warhead groups to obtain a clinical candidate, 78 (DBPR112), which not only displayed a potent inhibitory activity against EGFRL858R/T790M double mutations but also exhibited tenfold potency better than the third-generation inhibitor, osimertinib, against EGFR and HER2 exon 20 insertion mutations.	osimertinib	350-361	epidermal growth factor receptor	Homo sapiens	238-242
31832192-3	2019	Recent studies suggest that a key mechanism of acquired resistance to third-generation EGFR-TKIs (such as osimertinib) may be MET amplification and/or protein overactivation, especially when they are used as a first-line treatment.	osimertinib	106-117	epidermal growth factor receptor	Homo sapiens	87-91
31930052-8	2019	DHA reversed the osimertinib-induced STAT3 and Src phosphorylation.	osimertinib	17-28	signal transducer and activator of transcription 3	Homo sapiens	37-42
31930052-8	2019	DHA reversed the osimertinib-induced STAT3 and Src phosphorylation.	osimertinib	17-28	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-50
31446643-0	2019	SHR-A1403, a novel c-mesenchymal-epithelial transition factor (c-Met) antibody-drug conjugate, overcomes AZD9291 resistance in non-small cell lung cancer cells overexpressing c-Met.	osimertinib	105-112	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
31446643-2	2019	Here, we introduce an effective approach for overcoming resistance to the EGFR-TKI, AZD9291, in NSCLC cells using SHR-A1403, a novel c-mesenchymal-epithelial transition factor (c-Met)-targeting antibody-drug conjugate (ADC) consisting of an anti-c-Met monoclonal antibody (c-Met mAb) conjugated to a microtubule inhibitor.	osimertinib	84-91	epidermal growth factor receptor	Homo sapiens	74-78
31446643-2	2019	Here, we introduce an effective approach for overcoming resistance to the EGFR-TKI, AZD9291, in NSCLC cells using SHR-A1403, a novel c-mesenchymal-epithelial transition factor (c-Met)-targeting antibody-drug conjugate (ADC) consisting of an anti-c-Met monoclonal antibody (c-Met mAb) conjugated to a microtubule inhibitor.	osimertinib	84-91	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
31446643-2	2019	Here, we introduce an effective approach for overcoming resistance to the EGFR-TKI, AZD9291, in NSCLC cells using SHR-A1403, a novel c-mesenchymal-epithelial transition factor (c-Met)-targeting antibody-drug conjugate (ADC) consisting of an anti-c-Met monoclonal antibody (c-Met mAb) conjugated to a microtubule inhibitor.	osimertinib	84-91	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	246-251
31446643-2	2019	Here, we introduce an effective approach for overcoming resistance to the EGFR-TKI, AZD9291, in NSCLC cells using SHR-A1403, a novel c-mesenchymal-epithelial transition factor (c-Met)-targeting antibody-drug conjugate (ADC) consisting of an anti-c-Met monoclonal antibody (c-Met mAb) conjugated to a microtubule inhibitor.	osimertinib	84-91	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	246-251
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	0-7	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	0-7	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-174
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	0-7	mitogen-activated protein kinase 3	Homo sapiens	226-232
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	237-240
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	60-67	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	60-67	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-174
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	60-67	mitogen-activated protein kinase 3	Homo sapiens	226-232
31446643-5	2019	AZD9291 resistance was partially restored by combination of AZD9291 and crizotinib only in resistant cells overexpressing phospho-c-Met, which synergistically inhibited c-Met-mediated phosphorylation of the downstream targets ERK1/2 and AKT.	osimertinib	60-67	AKT serine/threonine kinase 1	Homo sapiens	237-240
31446643-7	2019	In contrast, SHR-A1403 strongly inhibited proliferation of AZD9291-resistant HCC827 overexpressing c-Met, regardless of the levels of c-Met phosphorylation.	osimertinib	59-66	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
31446643-8	2019	SHR-A1403 bound to resistant cells overexpressing c-Met was internalized into cells and released associated microtubule inhibitor, resulting in cell-killing activity that was dependent on c-Met expression levels only, irrespective of the involvement of c-Met or EGFR signaling in AZD9291 resistance.	osimertinib	280-287	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
31446643-10	2019	Thus, our findings show that SHR-A1403 efficiently overcomes AZD9291 resistance in cells overexpressing c-Met, and further indicate that c-Met expression level is a biomarker predictive of SHR-A1403 efficacy.	osimertinib	61-68	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
31607559-0	2019	Cost-effectiveness of Osimertinib as a Second-line Treatment in Patients With EGFR-mutated Advanced Non-Small Cell Lung Cancer in China.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	78-82
31793440-4	2019	Osimertinib, a third-generation irreversible EGFR-TKI with good potential to cross the BBB, has shown significant clinical activity and acceptable safety profile in patients with EGFR-positive NSCLC brain and leptomeningeal metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	45-49
31793440-4	2019	Osimertinib, a third-generation irreversible EGFR-TKI with good potential to cross the BBB, has shown significant clinical activity and acceptable safety profile in patients with EGFR-positive NSCLC brain and leptomeningeal metastases.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	179-183
31793440-7	2019	These data have supported osimertinib to be recognized as a "preferred" first-line treatment for EGFR-positive metastatic NSCLC by the National Comprehensive Cancer Network (NCCN).	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	97-101
31454149-0	2019	DYRK1A inhibition suppresses STAT3/EGFR/Met signalling and sensitizes EGFR wild-type NSCLC cells to AZD9291.	osimertinib	100-107	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	0-6
31454149-8	2019	AZD9291 is effective to treat NSCLC patients with EGFR-sensitivity mutation and T790 M resistance mutation, but the clinical efficacy in patients with wild-type EGFR remains modest.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	50-54
31454149-9	2019	We showed that DYRK1A repression could enhance the anti-cancer effect of AZD9291 by inducing apoptosis and suppressing cell proliferation in EGFR wild-type NSCLC cells.	osimertinib	73-80	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	15-21
31454149-9	2019	We showed that DYRK1A repression could enhance the anti-cancer effect of AZD9291 by inducing apoptosis and suppressing cell proliferation in EGFR wild-type NSCLC cells.	osimertinib	73-80	epidermal growth factor receptor	Homo sapiens	141-145
31454149-10	2019	In addition, harmine could enhance the anti-NSCLC activity of AZD9291 by modulating STAT3 pathway.	osimertinib	62-69	signal transducer and activator of transcription 3	Homo sapiens	84-89
31454149-12	2019	Collectively, targeting DYRK1A might be an attractive target for AZD9291 sensitization in EGFR wild-type NSCLC patients.	osimertinib	65-72	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	24-30
31454149-12	2019	Collectively, targeting DYRK1A might be an attractive target for AZD9291 sensitization in EGFR wild-type NSCLC patients.	osimertinib	65-72	epidermal growth factor receptor	Homo sapiens	90-94
31903227-0	2019	Impact of clinical features of epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) patients on osimertinib efficacy.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	31-63
31903227-0	2019	Impact of clinical features of epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) patients on osimertinib efficacy.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	65-69
31563735-8	2019	RESULTS AND CONCLUSION: The osimertinib and anti-PD-L1 combined treatment group had the highest inflammation scores in pathologic grades of H&E staining of lung tissue and had the highest percentages of myeloperoxidase positive cells.	osimertinib	28-39	myeloperoxidase	Mus musculus	203-218
31563735-12	2019	The levels of IFN-gamma, IL-2, IL-5, TNF-alpha and IL-12p70 were increased in osimertinib and anti-PD-L1 combined treatment group.	osimertinib	78-89	interferon gamma	Mus musculus	14-23
31563735-12	2019	The levels of IFN-gamma, IL-2, IL-5, TNF-alpha and IL-12p70 were increased in osimertinib and anti-PD-L1 combined treatment group.	osimertinib	78-89	interleukin 2	Mus musculus	25-29
31563735-12	2019	The levels of IFN-gamma, IL-2, IL-5, TNF-alpha and IL-12p70 were increased in osimertinib and anti-PD-L1 combined treatment group.	osimertinib	78-89	interleukin 5	Mus musculus	31-35
31600593-0	2019	Resistance mechanisms to osimertinib in EGFR-mutated advanced non-small-cell lung cancer: A multicentric retrospective French study.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	40-44
31600593-1	2019	OBJECTIVES: The understanding of histo-molecular mechanisms associated with resistance to osimertinib is a critical step to define the optimal treatment strategy in advanced EGFR-mutated Non-Small-Cell-Lung-Cancer (NSCLC).	osimertinib	90-101	epidermal growth factor receptor	Homo sapiens	174-178
31600593-2	2019	MATERIALS AND METHODS: We performed a multicentric retrospective analysis on a cohort of consecutive patients treated with osimertinib for an advanced EGFR-mutated NSCLC and collected histo-molecular data from plasma and tumor samples at the time of progression.	osimertinib	123-134	epidermal growth factor receptor	Homo sapiens	151-155
31600593-15	2019	CONCLUSION: We confirmed the efficacy of osimertinib in patients with advanced EGFR mutation positive NSCLC.	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	79-83
31921341-0	2019	Successful osimertinib rechallenge following drug-induced pneumonitis after previous anti-PDL1 exposure.	osimertinib	11-22	CD274 molecule	Homo sapiens	90-94
31921341-1	2019	Osimertinib is a first-line treatment option for patients with metastatic non-small cell lung cancer (NSCLC) harbouring EGFR mutations.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	120-124
31921341-2	2019	Pneumonitis is a severe adverse event (AE) related to osimertinib treatment which appears to be more frequent when associated with concurrent or previous anti-PD(L)1 exposure.	osimertinib	54-65	CD274 molecule	Homo sapiens	159-165
31921341-4	2019	We herein describe a case of a 53-year-old patient with metastatic EGFR-mutated NSCLC, who developed pneumonitis after osimertinib treatment and was successfully rechallenged with 40 mg daily osimertinib, with CNS response.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	67-71
31921341-4	2019	We herein describe a case of a 53-year-old patient with metastatic EGFR-mutated NSCLC, who developed pneumonitis after osimertinib treatment and was successfully rechallenged with 40 mg daily osimertinib, with CNS response.	osimertinib	192-203	epidermal growth factor receptor	Homo sapiens	67-71
31728437-2	2019	We present a patient with adenocarcinoma of the lung harboring an uncommon EGFR Exon 21 mutation treated with osimertinib as second-line therapy.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	75-79
31645848-0	2019	Osimertinib as treatment for EGFR exon 20 insertion-positive lung adenocarcinoma.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	29-33
31645848-5	2019	Previous reports showing successful treatment of EGFR exon 20 insertion-positive lung adenocarcinoma with the standard osimertinib dose of 80 mg are limited.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	49-53
31645848-6	2019	The present case demonstrated that osimertinib could be a possible treatment option for EGFR exon 20 insertion-positive lung adenocarcinoma.	osimertinib	35-46	epidermal growth factor receptor	Homo sapiens	88-92
31857889-0	2019	Inhibition of osimertinib-resistant epidermal growth factor receptor EGFR-T790M/C797S.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	36-68
31857889-0	2019	Inhibition of osimertinib-resistant epidermal growth factor receptor EGFR-T790M/C797S.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	69-73
31642175-2	2019	In preclinical and clinical studies, the third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor osimertinib has demonstrated activity in the central nervous system (CNS), and studies are ongoing.	osimertinib	124-135	epidermal growth factor receptor	Homo sapiens	58-90
31642175-2	2019	In preclinical and clinical studies, the third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor osimertinib has demonstrated activity in the central nervous system (CNS), and studies are ongoing.	osimertinib	124-135	epidermal growth factor receptor	Homo sapiens	92-96
31642175-3	2019	We report here a case of osimertinib used at 160 mg once daily in a heavily pretreated patient with EGFR exon 20 T790M-negative advanced NSCLC with LM to achieve a partial response, including shrinkage of the LM, for up to 12 months until further progression.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	100-104
31999837-0	2020	Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589).	osimertinib	110-121	epidermal growth factor receptor	Mus musculus	34-66
31999837-0	2020	Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589).	osimertinib	135-146	epidermal growth factor receptor	Mus musculus	34-66
32010579-2	2019	In this study, we aimed to evaluate the potential of parallel serial assessment of somatic mutation and methylation profile in monitoring the response to osimertinib of epidermal growth factor receptor (EGFR) T790M-positive advanced lung adenocarcinoma patients.	osimertinib	154-165	epidermal growth factor receptor	Homo sapiens	169-201
32010579-2	2019	In this study, we aimed to evaluate the potential of parallel serial assessment of somatic mutation and methylation profile in monitoring the response to osimertinib of epidermal growth factor receptor (EGFR) T790M-positive advanced lung adenocarcinoma patients.	osimertinib	154-165	epidermal growth factor receptor	Homo sapiens	203-207
33906716-9	2019	The non-small cell lung cancer (NSCLC) in this case maintained EGFR activating mutation and lost EGFR T790M mutation was a genetic change after osimertinib treatment.	osimertinib	144-155	epidermal growth factor receptor	Homo sapiens	97-101
31865717-0	2019	Clinical efficacy analysis of Osimertinib treatment for a patient with leptomeningeal metastasis of EGFR+ non-small cell lung cancer without the T790M mutation.	osimertinib	30-41	epidermal growth factor receptor	Homo sapiens	100-104
31865717-15	2019	CONCLUSIONS: Whether EGFR+ with T790M mutation was positive or negative, osimertinib is an effective drug and can improve quality of life and prolong the survival for NSCLC patient with EGFR mutation to progress LM.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	21-25
31865717-15	2019	CONCLUSIONS: Whether EGFR+ with T790M mutation was positive or negative, osimertinib is an effective drug and can improve quality of life and prolong the survival for NSCLC patient with EGFR mutation to progress LM.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	186-190
31930052-2	2019	We explored in vitro and in vivo the effect of the epidermal growth factor receptor (EGFR) inhibitor, osimertinib, alone and in combination with dihydroartemisinin (DHA) in HNSCC.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	51-83
31930052-2	2019	We explored in vitro and in vivo the effect of the epidermal growth factor receptor (EGFR) inhibitor, osimertinib, alone and in combination with dihydroartemisinin (DHA) in HNSCC.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	85-89
31769726-0	2019	Clinical activity of the EGFR tyrosine kinase inhibitor osimertinib in EGFR-mutant glioblastoma.	osimertinib	56-67	epidermal growth factor receptor	Homo sapiens	25-29
31769726-3	2019	We report the case of a young female with heavily pretreated EGFR-mutated GBM, for whom we initiated osimertinib, an oral, third-generation tyrosine kinase inhibitor that irreversibly inhibits EGFR and has significant brain penetration.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	61-65
31769726-3	2019	We report the case of a young female with heavily pretreated EGFR-mutated GBM, for whom we initiated osimertinib, an oral, third-generation tyrosine kinase inhibitor that irreversibly inhibits EGFR and has significant brain penetration.	osimertinib	101-112	epidermal growth factor receptor	Homo sapiens	193-197
31254668-1	2019	INTRODUCTION: Osimertinib is an effective third-generation tyrosine kinase inhibitor (TKI) for EGFR-mutant lung cancers.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	95-99
31254668-3	2019	We characterized a novel EGFR mutation in exon 20 that was acquired while on osimertinib.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	25-29
31254668-4	2019	METHODS: A 79-year-old woman had disease progression during third-line treatment with osimertinib for an EGFR L858R/T790M-mutant lung cancer.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	105-109
31254668-9	2019	RESULTS: Modeling suggested that EGFR M766Q could disrupt osimertinib binding.	osimertinib	58-69	epidermal growth factor receptor	Mus musculus	33-37
31254668-13	2019	CONCLUSIONS: Acquisition of EGFR M766Q exon 20 mutation is a novel mechanism of acquired resistance to osimertinib.	osimertinib	103-114	epidermal growth factor receptor	Mus musculus	28-32
31254668-14	2019	EGFR-mutant lung cancers with an acquired EGFR M766Q mutation in the setting of osimertinib resistance may be sensitive to neratinib and poziotinib.	osimertinib	80-91	epidermal growth factor receptor	Mus musculus	0-4
31254668-14	2019	EGFR-mutant lung cancers with an acquired EGFR M766Q mutation in the setting of osimertinib resistance may be sensitive to neratinib and poziotinib.	osimertinib	80-91	epidermal growth factor receptor	Mus musculus	42-46
31563735-12	2019	The levels of IFN-gamma, IL-2, IL-5, TNF-alpha and IL-12p70 were increased in osimertinib and anti-PD-L1 combined treatment group.	osimertinib	78-89	tumor necrosis factor	Mus musculus	37-46
31563735-14	2019	Our findings indicate that osimertinib, rather than gefitinib combined with anti-PD-L1 treatment could lead to lung injury in an EGFR mutated tumor-bearing mouse model.	osimertinib	27-38	epidermal growth factor receptor	Mus musculus	129-133
31568888-5	2019	Osimertinib, a third-generation, central nervous system active EGFR-TKI which potently and selectively inhibits both EGFR-TKI sensitizing (EGFRm) and the most common EGFR T790 M resistance mutations, has shown superior efficacy versus first-generation EGFR-TKIs (gefitinib / erlotinib).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	63-67
31568888-5	2019	Osimertinib, a third-generation, central nervous system active EGFR-TKI which potently and selectively inhibits both EGFR-TKI sensitizing (EGFRm) and the most common EGFR T790 M resistance mutations, has shown superior efficacy versus first-generation EGFR-TKIs (gefitinib / erlotinib).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	117-121
31568888-5	2019	Osimertinib, a third-generation, central nervous system active EGFR-TKI which potently and selectively inhibits both EGFR-TKI sensitizing (EGFRm) and the most common EGFR T790 M resistance mutations, has shown superior efficacy versus first-generation EGFR-TKIs (gefitinib / erlotinib).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	117-121
31568888-5	2019	Osimertinib, a third-generation, central nervous system active EGFR-TKI which potently and selectively inhibits both EGFR-TKI sensitizing (EGFRm) and the most common EGFR T790 M resistance mutations, has shown superior efficacy versus first-generation EGFR-TKIs (gefitinib / erlotinib).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	117-121
31568888-6	2019	Osimertinib is now a treatment option for patients with advanced NSCLC harboring EGFRm in the first-line setting, and treatment of choice for patients with T790 M positive NSCLC following disease progression on first-line EGFR-TKIs.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	81-85
31857949-5	2019	The need to overcome this resistance mechanism led to the development of third-generation EGFR TKIs, of which osimertinib is the only one to date with regulatory approval.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	90-94
31857953-5	2019	However, newly developed TKIs with improved penetration such as osimertinib for EGFR and alectinib, ceritinib, brigatinib, or lorlatinib for ALK have demonstrated significant intracranial activity that should contribute to improved overall survival.	osimertinib	64-75	epidermal growth factor receptor	Homo sapiens	80-84
31671561-3	2019	Gefitinib, erlotinib, afatinib, and osimertinib are TK inhibitors (TKIs) that specifically target EGFR and are currently approved by the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) as first line treatment for sensitive EGFR-mutant patients.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	98-102
31671561-3	2019	Gefitinib, erlotinib, afatinib, and osimertinib are TK inhibitors (TKIs) that specifically target EGFR and are currently approved by the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) as first line treatment for sensitive EGFR-mutant patients.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	250-254
31632838-0	2019	Identification of osimertinib-resistant EGFR L792 mutations by cfDNA sequencing: oncogenic activity assessment and prevalence in large cfDNA cohort.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	40-44
31632838-2	2019	Here, we report the detection of EGFR L792 mutations, a non-covalent mechanism of osimertinib resistance, using Guardant360 cfDNA testing in a patient with metastatic EGFR-mutant non-small cell lung cancer (NSCLC) whose disease progressed on osimertinib.	osimertinib	82-93	epidermal growth factor receptor	Homo sapiens	33-37
31632838-2	2019	Here, we report the detection of EGFR L792 mutations, a non-covalent mechanism of osimertinib resistance, using Guardant360 cfDNA testing in a patient with metastatic EGFR-mutant non-small cell lung cancer (NSCLC) whose disease progressed on osimertinib.	osimertinib	82-93	epidermal growth factor receptor	Homo sapiens	167-171
31632838-2	2019	Here, we report the detection of EGFR L792 mutations, a non-covalent mechanism of osimertinib resistance, using Guardant360 cfDNA testing in a patient with metastatic EGFR-mutant non-small cell lung cancer (NSCLC) whose disease progressed on osimertinib.	osimertinib	242-253	epidermal growth factor receptor	Homo sapiens	33-37
31632838-4	2019	In vitro functional assays demonstrated that the EGFR L858R/T790M/L792F/H mutations conferred intermediate-level resistance to osimertinib.	osimertinib	127-138	epidermal growth factor receptor	Homo sapiens	49-53
31762748-0	2019	The Journey of an EGFR-Mutant Lung Adenocarcinoma through Erlotinib, Osimertinib and ABCP Immunotherapy Regimens: Sensitivity and Resistance.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	18-22
31591158-11	2019	Subgroup analyses by the two most common EGFR mutation types indicated that osimertinib was associated with the best progression free survival in patients with the exon 19 deletion, and gefitinib plus pemetrexed based chemotherapy was associated with the best progression free survival in patients with the Leu858Arg mutation.	osimertinib	76-87	epidermal growth factor receptor	Homo sapiens	41-45
31591158-12	2019	CONCLUSIONS: These results indicate that osimertinib and gefitinib plus pemetrexed based chemotherapy were associated with the best progression free survival and overall survival benefits for patients with advanced EGFR mutated NSCLC, compared with other first line treatments.	osimertinib	41-52	epidermal growth factor receptor	Homo sapiens	215-219
31581247-10	2019	CONCLUSIONS: Osimertinib seemed to be the most preferable first-line treatment in advanced EGFR-mutated NSCLC.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	91-95
31832192-4	2019	Therefore, in patients resistant to first-generation EGFR-TKIs caused by MET amplification and/or protein overactivation, the combination of osimertinib with MET or MEK inhibitors may be considered.	osimertinib	141-152	epidermal growth factor receptor	Homo sapiens	53-57
31832192-4	2019	Therefore, in patients resistant to first-generation EGFR-TKIs caused by MET amplification and/or protein overactivation, the combination of osimertinib with MET or MEK inhibitors may be considered.	osimertinib	141-152	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
31411906-7	2019	The third-generation EGFR TKI, osimertinib has been approved for patients whose tumor has become resistant through the secondary T790M resistant EGFR mutation.	osimertinib	31-42	epidermal growth factor receptor	Homo sapiens	21-25
31564718-0	2019	Resistance mechanisms to osimertinib in EGFR-mutated non-small cell lung cancer.	osimertinib	25-36	epidermal growth factor receptor	Homo sapiens	40-44
31564718-1	2019	Osimertinib is an irreversible, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is highly selective for EGFR-activating mutations as well as the EGFR T790M mutation in patients with advanced non-small cell lung cancer (NSCLC) with EGFR oncogene addiction.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	49-81
31564718-1	2019	Osimertinib is an irreversible, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is highly selective for EGFR-activating mutations as well as the EGFR T790M mutation in patients with advanced non-small cell lung cancer (NSCLC) with EGFR oncogene addiction.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	83-87
31564718-1	2019	Osimertinib is an irreversible, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is highly selective for EGFR-activating mutations as well as the EGFR T790M mutation in patients with advanced non-small cell lung cancer (NSCLC) with EGFR oncogene addiction.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	144-148
31564718-1	2019	Osimertinib is an irreversible, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is highly selective for EGFR-activating mutations as well as the EGFR T790M mutation in patients with advanced non-small cell lung cancer (NSCLC) with EGFR oncogene addiction.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	144-148
31564718-1	2019	Osimertinib is an irreversible, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is highly selective for EGFR-activating mutations as well as the EGFR T790M mutation in patients with advanced non-small cell lung cancer (NSCLC) with EGFR oncogene addiction.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	144-148
31564718-3	2019	On account of the high degree of tumour heterogeneity and adaptive cellular signalling pathways in NSCLC, the acquired osimertinib resistance is highly heterogeneous, encompassing EGFR-dependent as well as EGFR-independent mechanisms.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	180-184
31564718-3	2019	On account of the high degree of tumour heterogeneity and adaptive cellular signalling pathways in NSCLC, the acquired osimertinib resistance is highly heterogeneous, encompassing EGFR-dependent as well as EGFR-independent mechanisms.	osimertinib	119-130	epidermal growth factor receptor	Homo sapiens	206-210
31564718-5	2019	This review summarises the molecular mechanisms of resistance to osimertinib in patients with advanced EGFR-mutated NSCLC, including MET/HER2 amplification, activation of the RAS-mitogen-activated protein kinase (MAPK) or RAS-phosphatidylinositol 3-kinase (PI3K) pathways, novel fusion events and histological/phenotypic transformation, as well as discussing the current evidence regarding potential new approaches to counteract osimertinib resistance.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	103-107
31564718-5	2019	This review summarises the molecular mechanisms of resistance to osimertinib in patients with advanced EGFR-mutated NSCLC, including MET/HER2 amplification, activation of the RAS-mitogen-activated protein kinase (MAPK) or RAS-phosphatidylinositol 3-kinase (PI3K) pathways, novel fusion events and histological/phenotypic transformation, as well as discussing the current evidence regarding potential new approaches to counteract osimertinib resistance.	osimertinib	65-76	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	222-255
31314158-4	2019	Among these EGFR variants, we report that an exon 20 deletion/insertion mutation S768insVGH is resistant to erlotinib (a first-generation TKI), but sensitive to osimertinib (a third-generation TKI).	osimertinib	161-172	epidermal growth factor receptor	Mus musculus	12-16
31411906-7	2019	The third-generation EGFR TKI, osimertinib has been approved for patients whose tumor has become resistant through the secondary T790M resistant EGFR mutation.	osimertinib	31-42	epidermal growth factor receptor	Homo sapiens	145-149
31651902-0	2019	Osimertinib or EGFR-TKIs/chemotherapy in patients with EGFR-mutated advanced nonsmall cell lung cancer: A meta-analysis.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	55-59
31470227-9	2019	Accordingly, the third-generation EGFR-TKI osimertinib effectively inhibited gefitinib-resistant tumors in vivo.	osimertinib	43-54	epidermal growth factor receptor	Homo sapiens	34-38
31651902-6	2019	CONCLUSIONS: Osimertinib showed greater treatment benefit for patients with NSCLC with EGFR mutation than EGFR-TKIs/chemotherapy, especially for T790M mutation-positive patients.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	87-91
31414729-0	2019	Plasma next generation sequencing and droplet digital PCR-based detection of epidermal growth factor receptor (EGFR) mutations in patients with advanced lung cancer treated with subsequent-line osimertinib.	osimertinib	194-205	epidermal growth factor receptor	Homo sapiens	77-109
31414729-0	2019	Plasma next generation sequencing and droplet digital PCR-based detection of epidermal growth factor receptor (EGFR) mutations in patients with advanced lung cancer treated with subsequent-line osimertinib.	osimertinib	194-205	epidermal growth factor receptor	Homo sapiens	111-115
31414729-8	2019	Several possible osimertinib resistance associated mutations, including PIK3CA, BRAF and TP53 mutations, were detected by NGS in samples upon progression on osimertinib therapy.	osimertinib	17-28	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	72-78
31414729-8	2019	Several possible osimertinib resistance associated mutations, including PIK3CA, BRAF and TP53 mutations, were detected by NGS in samples upon progression on osimertinib therapy.	osimertinib	17-28	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
31414729-8	2019	Several possible osimertinib resistance associated mutations, including PIK3CA, BRAF and TP53 mutations, were detected by NGS in samples upon progression on osimertinib therapy.	osimertinib	17-28	tumor protein p53	Homo sapiens	89-93
31571928-0	2019	Treatment Response To Osimertinib In EGFR-Mutated Leptomeningeal Metastases From Non-Small Cell Lung Cancer: A Case Series.	osimertinib	22-33	epidermal growth factor receptor	Homo sapiens	37-41
31502118-0	2019	Acquired BRAF G469A Mutation as a Resistance Mechanism to First-Line Osimertinib Treatment in NSCLC Cell Lines Harboring an EGFR Exon 19 Deletion.	osimertinib	69-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
31502118-0	2019	Acquired BRAF G469A Mutation as a Resistance Mechanism to First-Line Osimertinib Treatment in NSCLC Cell Lines Harboring an EGFR Exon 19 Deletion.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	124-128
31502118-1	2019	BACKGROUND: Osimertinib is a new third-generation, epidermal growth factor receptor-tyrosine kinase inhibitor highly selective for the epidermal growth factor receptor with both activating and T790M mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	51-83
31502118-1	2019	BACKGROUND: Osimertinib is a new third-generation, epidermal growth factor receptor-tyrosine kinase inhibitor highly selective for the epidermal growth factor receptor with both activating and T790M mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	135-167
31502118-2	2019	A recent phase III trial showed a statistically significant progression-free survival benefit with osimertinib vs. gefitinib or erlotinib as first-line treatment for EGFR-mutated non-small cell lung cancer, and preliminary data are available on resistance mechanisms to first-line osimertinib therapy.	osimertinib	99-110	epidermal growth factor receptor	Homo sapiens	166-170
31502118-3	2019	OBJECTIVE: The objective of this study was to examine potential in vitro mechanisms of acquired resistance to osimertinib in a cell model carrying an EGFR exon 19 deletion.	osimertinib	110-121	epidermal growth factor receptor	Homo sapiens	150-154
31502118-8	2019	Stable transfection of PC9 and HCC827 cells with a plasmid containing BRAF G469A rendered the cells resistant to osimertinib.	osimertinib	113-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
31502118-10	2019	CONCLUSIONS: Our in vitro studies revealed the BRAF G469A-activating mutation as a potential mechanism of acquired resistance to first-line osimertinib treatment, and provide a strategy of intervention to overcome this mechanism of resistance.	osimertinib	140-151	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
31571928-4	2019	Three patients were treated with the third-generation TKI osimertinib at 80 mg daily, despite their different detection levels of T790M in the cerebrospinal fluid (CSF) and plasma, and achieved symptomatic remission, a decline of carcinoembryonic antigen (CEA) levels, and stable lesions.	osimertinib	58-69	CEA cell adhesion molecule 3	Homo sapiens	230-254
31571928-4	2019	Three patients were treated with the third-generation TKI osimertinib at 80 mg daily, despite their different detection levels of T790M in the cerebrospinal fluid (CSF) and plasma, and achieved symptomatic remission, a decline of carcinoembryonic antigen (CEA) levels, and stable lesions.	osimertinib	58-69	CEA cell adhesion molecule 3	Homo sapiens	256-259
31571928-6	2019	Recent related studies and our cases indicate that osimertinib has a positive effect on LM from EGFR-mutant NSCLC, regardless of T790M status.	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	96-100
31754333-5	2019	Results: Osimertinib plus pterostilbene yielded synergistic effects in all EGFR-mutation positive NSCLC cell lines investigated.	osimertinib	9-20	epidermal growth factor receptor	Homo sapiens	75-79
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	35-46	signal transducer and activator of transcription 3	Homo sapiens	99-104
31754333-0	2019	Osimertinib and pterostilbene in EGFR-mutation-positive non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	33-37
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	35-46	Yes1 associated transcriptional regulator	Homo sapiens	106-110
31754333-3	2019	In the present study, we treated EGFR-mutation positive cell lines with the combination of osimertinib plus a natural compound, pterostilbene, which has been reported to abrogate Src and STAT3 activation.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	33-37
31754333-3	2019	In the present study, we treated EGFR-mutation positive cell lines with the combination of osimertinib plus a natural compound, pterostilbene, which has been reported to abrogate Src and STAT3 activation.	osimertinib	91-102	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-182
31754333-3	2019	In the present study, we treated EGFR-mutation positive cell lines with the combination of osimertinib plus a natural compound, pterostilbene, which has been reported to abrogate Src and STAT3 activation.	osimertinib	91-102	signal transducer and activator of transcription 3	Homo sapiens	187-192
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	35-46	CUB domain containing protein 1	Homo sapiens	116-147
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	35-46	CUB domain containing protein 1	Homo sapiens	149-154
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	35-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	196-199
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	79-90	signal transducer and activator of transcription 3	Homo sapiens	99-104
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	79-90	Yes1 associated transcriptional regulator	Homo sapiens	106-110
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	79-90	CUB domain containing protein 1	Homo sapiens	116-147
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	79-90	CUB domain containing protein 1	Homo sapiens	149-154
31754333-7	2019	However, the double combination of osimertinib plus pterostilbene reversed the osimertinib-induced STAT3, YAP1, and CUB domain-containing protein-1 (CDCP1) phosphorylation and slightly suppressed Src phosphorylation in PC9 and H1975 cells.	osimertinib	79-90	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	196-199
31754333-8	2019	Conclusion: The results of this study indicate that pterostilbene may be used to abrogate the activated resistance pathways of single osimertinib treatment in EGFR-mutation positive NSCLC.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	159-163
31108249-9	2019	Third-generation EGFR TKI osimertinib was highly potent against EGFR exon 20 insertion-mutant cells (IC50, 14.7-62.7 nM), including EGFR H773insH, and spared wild-type EGFR cells.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	64-68
31370698-0	2019	Sequential afatinib and osimertinib in patients with EGFR mutation-positive non-small-cell lung cancer: updated analysis of the observational GioTag study.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	53-57
31370698-7	2019	Conclusion: Sequential afatinib/osimertinib was associated with encouraging OS/TTF in patients with EGFR T790M-positive non-small-cell lung cancer, especially in patients with Del19-positive tumors.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	100-104
31108249-0	2019	Preclinical Modeling of Osimertinib for NSCLC With EGFR Exon 20 Insertion Mutations.	osimertinib	24-35	epidermal growth factor receptor	Homo sapiens	51-55
31108249-5	2019	EGFR exon 20 insertion-mutant structures and couplings with osimertinib, a third-generation EGFR TKI, were modeled and compared.	osimertinib	60-71	epidermal growth factor receptor	Homo sapiens	0-4
31108249-9	2019	Third-generation EGFR TKI osimertinib was highly potent against EGFR exon 20 insertion-mutant cells (IC50, 14.7-62.7 nM), including EGFR H773insH, and spared wild-type EGFR cells.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	17-21
31108249-9	2019	Third-generation EGFR TKI osimertinib was highly potent against EGFR exon 20 insertion-mutant cells (IC50, 14.7-62.7 nM), including EGFR H773insH, and spared wild-type EGFR cells.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	64-68
31592498-8	2019	EGFR-targeted therapy with osimertinib 80 mg daily was initiated.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	0-4
31592498-11	2019	This is an illustrative case of NSCLC-PM with EGFR exon 19 deletion mutation, wherein osimertinib, a third-generation EGFR-tyrosine kinase inhibitor, eradicated the sellar metastasis and prevented the need for radiotherapy.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	46-50
31592498-11	2019	This is an illustrative case of NSCLC-PM with EGFR exon 19 deletion mutation, wherein osimertinib, a third-generation EGFR-tyrosine kinase inhibitor, eradicated the sellar metastasis and prevented the need for radiotherapy.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	118-122
31632761-0	2019	Impact of performance status and age on osimertinib efficacy in patients with EGFR-mutant T790M-positive non-small-cell lung cancer.	osimertinib	40-51	epidermal growth factor receptor	Homo sapiens	78-82
31632766-0	2019	Impact of clinical features on the efficacy of osimertinib treatment in epidermal growth factor receptor mutant non-small cell lung cancer patients with acquired resistance to tyrosine kinase inhibitors due to T790M mutation.	osimertinib	47-58	epidermal growth factor receptor	Homo sapiens	72-104
31442277-0	2019	Effectiveness and safety of osimertinib in patients with metastatic EGFR T790M-positive NSCLC: An observational real-world study.	osimertinib	28-39	epidermal growth factor receptor	Homo sapiens	68-72
31442277-1	2019	Osimertinib showed encouraging efficacy in patients with advanced EGFR T790M-positive NSCLC in previous randomized controlled trials.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	66-70
31108249-9	2019	Third-generation EGFR TKI osimertinib was highly potent against EGFR exon 20 insertion-mutant cells (IC50, 14.7-62.7 nM), including EGFR H773insH, and spared wild-type EGFR cells.	osimertinib	26-37	epidermal growth factor receptor	Homo sapiens	64-68
31108249-11	2019	In addition, osimertinib-resistant cells were established by stepwise exposure to osimertinib and harbored EGFR E762K mutation.	osimertinib	13-24	epidermal growth factor receptor	Mus musculus	107-111
31108249-12	2019	CONCLUSIONS: Osimertinib is active against EGFR exon 20 insertion-mutant NSCLC and flexibly binds within drug-binding pockets in preclinical models.	osimertinib	13-24	epidermal growth factor receptor	Mus musculus	43-47
31555510-11	2019	Conclusions: Hsp90 inhibitors and osimertinib exhibits a good efficiency to inhibit cell viability, colony formation and inhibits expression and activation of proteins involved in osimertinib-resistance and may represent an effective strategy for NSCLC with intrinsic resistance to osimertinib inhibition.	osimertinib	180-191	heat shock protein 90 alpha family class A member 1	Homo sapiens	13-18
31839713-7	2019	A synergistic interaction (CI &lt;1) was identified with combinations of 4-6.5 muM osimertinib with 30-75 muM chloroquine.	osimertinib	83-94	latexin	Homo sapiens	79-82
31319998-11	2019	After subsequent treatment with osimertinib, SCC transformation was observed with the disappearance of the EGFR p.T790 M mutation and acquired copy number loss in PTEN.	osimertinib	32-43	epidermal growth factor receptor	Homo sapiens	107-111
31319998-11	2019	After subsequent treatment with osimertinib, SCC transformation was observed with the disappearance of the EGFR p.T790 M mutation and acquired copy number loss in PTEN.	osimertinib	32-43	phosphatase and tensin homolog	Homo sapiens	163-167
30920616-0	2019	Osimertinib for patients with EGFR T790M mutation-positive non-small-cell lung cancer and a poor performance status.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	30-34
30920616-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is effective against EGFR T790M mutation-positive non-small-cell lung cancer (NSCLC) in patients who have good performance status (PS).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-78
30920616-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is effective against EGFR T790M mutation-positive non-small-cell lung cancer (NSCLC) in patients who have good performance status (PS).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	80-84
30920616-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is effective against EGFR T790M mutation-positive non-small-cell lung cancer (NSCLC) in patients who have good performance status (PS).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	144-148
30920616-3	2019	METHODS: We retrospectively evaluated the efficacy and safety of osimertinib in patients with EGFR T790M mutation-positive NSCLC who had Eastern Cooperative Oncology Group PS scores of 2-4 and who were administered 80 mg of osimertinib once daily between March 2016 and February 2017.	osimertinib	65-76	epidermal growth factor receptor	Homo sapiens	94-98
30920616-11	2019	CONCLUSIONS: Osimertinib therapy demonstrates promising efficacy and acceptable safety in patients with EGFR T790M mutation-positive NSCLC who have poor PS.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	104-108
31290421-1	2019	Osimertinib (AZD9291), a third-generation epidermal growth factor receptor (EGFR)-tyrosine-kinase inhibitor (TKI), is useful in the treatment of non-small cell lung cancer who show resistance to first-generation EGFR-TKIs and harbor T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	42-74
31290421-1	2019	Osimertinib (AZD9291), a third-generation epidermal growth factor receptor (EGFR)-tyrosine-kinase inhibitor (TKI), is useful in the treatment of non-small cell lung cancer who show resistance to first-generation EGFR-TKIs and harbor T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	76-80
31290421-1	2019	Osimertinib (AZD9291), a third-generation epidermal growth factor receptor (EGFR)-tyrosine-kinase inhibitor (TKI), is useful in the treatment of non-small cell lung cancer who show resistance to first-generation EGFR-TKIs and harbor T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	212-216
31289574-1	2019	Currently, osimertinib (AZD9291) is the only third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor approved by the Food and Drug Administration for the treatment of non-small cell lung cancer (NSCLC) with EGFR T790M mutations.	osimertinib	24-31	epidermal growth factor receptor	Homo sapiens	62-94
31289574-4	2019	The aim of the present study was to investigate the functional role of PLAC8 in AZD9291 resistance in NSCLC.	osimertinib	80-87	placenta associated 8	Homo sapiens	71-76
31289574-5	2019	The results revealed that the level of PLAC8 was significantly upregulated in AZD9291-resistant cells compared with that in parent cells.	osimertinib	78-85	placenta associated 8	Homo sapiens	39-44
31289574-7	2019	Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC.	osimertinib	268-275	aldehyde dehydrogenase 1 family member A1	Homo sapiens	27-68
31289574-7	2019	Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC.	osimertinib	268-275	aldehyde dehydrogenase 1 family member A1	Homo sapiens	70-77
31289574-7	2019	Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC.	osimertinib	268-275	placenta associated 8	Homo sapiens	134-139
31289574-7	2019	Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC.	osimertinib	268-275	aldehyde dehydrogenase 1 family member A1	Homo sapiens	185-192
31289574-7	2019	Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC.	osimertinib	268-275	placenta associated 8	Homo sapiens	258-263
31289574-8	2019	Overall, PLAC8 overexpression promoted NSCLC resistance to AZD9291, and PLAC8 may be a potential target for the reversal of AZD9291 resistance.	osimertinib	59-66	placenta associated 8	Homo sapiens	9-14
31289574-8	2019	Overall, PLAC8 overexpression promoted NSCLC resistance to AZD9291, and PLAC8 may be a potential target for the reversal of AZD9291 resistance.	osimertinib	124-131	placenta associated 8	Homo sapiens	9-14
31289574-8	2019	Overall, PLAC8 overexpression promoted NSCLC resistance to AZD9291, and PLAC8 may be a potential target for the reversal of AZD9291 resistance.	osimertinib	124-131	placenta associated 8	Homo sapiens	72-77
31261881-1	2019	Herein a novel series of histone deacetylases (HDACs) and epidermal growth factor receptor (EGFR) dual inhibitors were designed and synthesized based on the structure of the approved EGFR inhibitor osimertinib (AZD9291).	osimertinib	211-218	epidermal growth factor receptor	Homo sapiens	58-90
31261881-1	2019	Herein a novel series of histone deacetylases (HDACs) and epidermal growth factor receptor (EGFR) dual inhibitors were designed and synthesized based on the structure of the approved EGFR inhibitor osimertinib (AZD9291).	osimertinib	211-218	epidermal growth factor receptor	Homo sapiens	92-96
31261881-1	2019	Herein a novel series of histone deacetylases (HDACs) and epidermal growth factor receptor (EGFR) dual inhibitors were designed and synthesized based on the structure of the approved EGFR inhibitor osimertinib (AZD9291).	osimertinib	211-218	epidermal growth factor receptor	Homo sapiens	183-187
31555510-0	2019	Hsp90 inhibitors enhance the antitumoral effect of osimertinib in parental and osimertinib-resistant non-small cell lung cancer cell lines.	osimertinib	51-62	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
31555510-0	2019	Hsp90 inhibitors enhance the antitumoral effect of osimertinib in parental and osimertinib-resistant non-small cell lung cancer cell lines.	osimertinib	79-90	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
31555510-6	2019	Results: Our laboratory generated osimertinib resistant cell lines from PC9 cell line and overexpression or activation of several proteins was detected.	osimertinib	34-45	proprotein convertase subtilisin/kexin type 9	Homo sapiens	72-75
31555510-7	2019	Hsp90 inhibitors, ganetespib and luminespib, inhibited cell viability and colony formation in H1975, PC9 and PC9-derived osimertinib-resistant cell lines and combination of these inhibitors with osimertinib achieved to enhance this cell viability and colony formation inhibition.	osimertinib	121-132	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
31555510-7	2019	Hsp90 inhibitors, ganetespib and luminespib, inhibited cell viability and colony formation in H1975, PC9 and PC9-derived osimertinib-resistant cell lines and combination of these inhibitors with osimertinib achieved to enhance this cell viability and colony formation inhibition.	osimertinib	195-206	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
31555510-8	2019	Luminespib downregulated the expression of the several proteins involved in osimertinib-resistance and the combination of this compound plus osimertinib caused an important decrease of expression of several of these proteins, such as Stat3, Yap, Akt, EGFR and Met.	osimertinib	141-152	signal transducer and activator of transcription 3	Homo sapiens	234-239
31555510-8	2019	Luminespib downregulated the expression of the several proteins involved in osimertinib-resistance and the combination of this compound plus osimertinib caused an important decrease of expression of several of these proteins, such as Stat3, Yap, Akt, EGFR and Met.	osimertinib	141-152	Yes1 associated transcriptional regulator	Homo sapiens	241-244
31555510-8	2019	Luminespib downregulated the expression of the several proteins involved in osimertinib-resistance and the combination of this compound plus osimertinib caused an important decrease of expression of several of these proteins, such as Stat3, Yap, Akt, EGFR and Met.	osimertinib	141-152	AKT serine/threonine kinase 1	Homo sapiens	246-249
31555510-8	2019	Luminespib downregulated the expression of the several proteins involved in osimertinib-resistance and the combination of this compound plus osimertinib caused an important decrease of expression of several of these proteins, such as Stat3, Yap, Akt, EGFR and Met.	osimertinib	141-152	epidermal growth factor receptor	Homo sapiens	251-255
31555510-11	2019	Conclusions: Hsp90 inhibitors and osimertinib exhibits a good efficiency to inhibit cell viability, colony formation and inhibits expression and activation of proteins involved in osimertinib-resistance and may represent an effective strategy for NSCLC with intrinsic resistance to osimertinib inhibition.	osimertinib	180-191	heat shock protein 90 alpha family class A member 1	Homo sapiens	13-18
31839713-7	2019	A synergistic interaction (CI &lt;1) was identified with combinations of 4-6.5 muM osimertinib with 30-75 muM chloroquine.	osimertinib	83-94	latexin	Homo sapiens	106-109
31839713-8	2019	Results: A combination of osimertinib (6 muM) with chloroquine (30 muM) resulted in a 6-fold increase of LC3B-II relative to control compared to 2.5-fold increase for either drug alone.	osimertinib	26-37	latexin	Homo sapiens	41-44
31839713-8	2019	Results: A combination of osimertinib (6 muM) with chloroquine (30 muM) resulted in a 6-fold increase of LC3B-II relative to control compared to 2.5-fold increase for either drug alone.	osimertinib	26-37	latexin	Homo sapiens	67-70
31839713-9	2019	The caspase-3 expression increased 2-fold compared to a 0.5-fold decrease with chloroquine and 1.5-fold increase with osimertinib.	osimertinib	118-129	caspase 3	Homo sapiens	4-13
31637005-5	2019	In this study, we found that EGFR TKIs, including gefitinib and AZD9291, impaired lysosome-dependent degradation of SQSTM1, thus compromising their anti-cancer efficiency.	osimertinib	64-71	epidermal growth factor receptor	Homo sapiens	29-33
31637005-5	2019	In this study, we found that EGFR TKIs, including gefitinib and AZD9291, impaired lysosome-dependent degradation of SQSTM1, thus compromising their anti-cancer efficiency.	osimertinib	64-71	sequestosome 1	Homo sapiens	116-122
31637005-6	2019	By accumulating in the lysosome lumen, gefitinib and AZD9291 attenuated lysosomal acidification and impaired autolysosomal degradation of SQSTM1 owing to their intrinsic alkalinity.	osimertinib	53-60	sequestosome 1	Homo sapiens	138-144
31637005-7	2019	As a result, SQSTM1 protein was stabilized in response to gefitinib and AZD9291 treatment and conferred EGFR TKI resistance.	osimertinib	72-79	sequestosome 1	Homo sapiens	13-19
31637005-8	2019	Depleting SQSTM1 significantly increased the sensitivity of NSCLC cells to gefitinib and AZD9291 both in vitro and in vivo.	osimertinib	89-96	sequestosome 1	Homo sapiens	10-16
31092401-4	2019	Remarkably, osimertinib, an ATP-competitive covalent EGFR inhibitor, uniquely and significantly enhances the binding of JBJ-04-125-02 for mutant EGFR.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	53-57
31092401-4	2019	Remarkably, osimertinib, an ATP-competitive covalent EGFR inhibitor, uniquely and significantly enhances the binding of JBJ-04-125-02 for mutant EGFR.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	145-149
31092401-8	2019	Here, we identify a mutant EGFR allosteric inhibitor that is effective as a single agent and in combination with the EGFR TKI osimertinib.This article is highlighted in the In This Issue feature, p. 813.	osimertinib	126-137	epidermal growth factor receptor	Homo sapiens	27-31
31164318-0	2019	Response to First-Line Osimertinib Treatment in Non-Small-Cell Lung Cancer With Coexisting G719A and Primary T790M Epidermal Growth Factor Receptor Mutations.	osimertinib	23-34	epidermal growth factor receptor	Homo sapiens	115-147
31229973-0	2019	Successful osimertinib treatment in a patient who exhibited intramedullary spinal cord metastases of lung adenocarcinoma with an acquired EGFR T790M mutation.	osimertinib	11-22	epidermal growth factor receptor	Homo sapiens	138-142
31229973-2	2019	We describe a 52-year-old man with ISCMs secondary to lung adenocarcinoma who acquired the T790M mutation of the epidermal growth factor receptor (EGFR) after previous use of a first-generation EGFR tyrosine kinase inhibitor (TKI); he was successfully treated with osimertinib.	osimertinib	265-276	epidermal growth factor receptor	Homo sapiens	113-145
31229973-2	2019	We describe a 52-year-old man with ISCMs secondary to lung adenocarcinoma who acquired the T790M mutation of the epidermal growth factor receptor (EGFR) after previous use of a first-generation EGFR tyrosine kinase inhibitor (TKI); he was successfully treated with osimertinib.	osimertinib	265-276	epidermal growth factor receptor	Homo sapiens	147-151
30993382-1	2019	The T790M mutation is recognized as a typical mechanism of acquired resistance to first generation of epithermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) such as gefitinib in non-small cell lung cancer (NSCLC) patients who are commonly treated by third generation of EGFR-TKI AZD9291 (osimertinib).	osimertinib	297-304	epidermal growth factor receptor	Homo sapiens	164-168
30993382-1	2019	The T790M mutation is recognized as a typical mechanism of acquired resistance to first generation of epithermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) such as gefitinib in non-small cell lung cancer (NSCLC) patients who are commonly treated by third generation of EGFR-TKI AZD9291 (osimertinib).	osimertinib	297-304	epidermal growth factor receptor	Homo sapiens	288-292
30993382-1	2019	The T790M mutation is recognized as a typical mechanism of acquired resistance to first generation of epithermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) such as gefitinib in non-small cell lung cancer (NSCLC) patients who are commonly treated by third generation of EGFR-TKI AZD9291 (osimertinib).	osimertinib	306-317	epidermal growth factor receptor	Homo sapiens	164-168
30993382-1	2019	The T790M mutation is recognized as a typical mechanism of acquired resistance to first generation of epithermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) such as gefitinib in non-small cell lung cancer (NSCLC) patients who are commonly treated by third generation of EGFR-TKI AZD9291 (osimertinib).	osimertinib	306-317	epidermal growth factor receptor	Homo sapiens	288-292
30993382-9	2019	AZD9291 induced caspase 3/7 activation in A549, H1650, and H1650GR, but not in A549GR.	osimertinib	0-7	caspase 3	Homo sapiens	16-27
30993382-10	2019	Western blot analyses showed that p-Akt played a key role in determining the sensitivities of A549, A549GR, H1650, and H1650GR to gefitinib or AZD9291.	osimertinib	143-150	AKT serine/threonine kinase 1	Homo sapiens	36-39
30993382-11	2019	Additionally, increased expression of Twist1 was observed in all cells with acquired EGFR-TKI resistance and knockdown of Twist1 by shRNA was found to significantly enhance the sensitivity of A549GR to gefitinib or AZD9291 via reversing epithelial-mesenchymal transition and downregulating p-Akt, but not of H1975AR to AZD9291.	osimertinib	215-222	twist family bHLH transcription factor 1	Homo sapiens	38-44
30993382-11	2019	Additionally, increased expression of Twist1 was observed in all cells with acquired EGFR-TKI resistance and knockdown of Twist1 by shRNA was found to significantly enhance the sensitivity of A549GR to gefitinib or AZD9291 via reversing epithelial-mesenchymal transition and downregulating p-Akt, but not of H1975AR to AZD9291.	osimertinib	215-222	twist family bHLH transcription factor 1	Homo sapiens	122-128
30993382-11	2019	Additionally, increased expression of Twist1 was observed in all cells with acquired EGFR-TKI resistance and knockdown of Twist1 by shRNA was found to significantly enhance the sensitivity of A549GR to gefitinib or AZD9291 via reversing epithelial-mesenchymal transition and downregulating p-Akt, but not of H1975AR to AZD9291.	osimertinib	319-326	twist family bHLH transcription factor 1	Homo sapiens	38-44
30993382-11	2019	Additionally, increased expression of Twist1 was observed in all cells with acquired EGFR-TKI resistance and knockdown of Twist1 by shRNA was found to significantly enhance the sensitivity of A549GR to gefitinib or AZD9291 via reversing epithelial-mesenchymal transition and downregulating p-Akt, but not of H1975AR to AZD9291.	osimertinib	319-326	twist family bHLH transcription factor 1	Homo sapiens	122-128
30993382-12	2019	The enhanced cytotoxic effect of AZD9291 on A549GR by Twist1 knockdown in vitro was further validated by in vivo studies which showed that Twist1 knockdown could lead to significantly delayed tumor growth of A549GR xenograft with increased sensitivity to AZD9291 treatment in nude mice without any observed side toxic effects.	osimertinib	33-40	twist basic helix-loop-helix transcription factor 1	Mus musculus	54-60
30993382-12	2019	The enhanced cytotoxic effect of AZD9291 on A549GR by Twist1 knockdown in vitro was further validated by in vivo studies which showed that Twist1 knockdown could lead to significantly delayed tumor growth of A549GR xenograft with increased sensitivity to AZD9291 treatment in nude mice without any observed side toxic effects.	osimertinib	33-40	twist basic helix-loop-helix transcription factor 1	Mus musculus	139-145
30993382-12	2019	The enhanced cytotoxic effect of AZD9291 on A549GR by Twist1 knockdown in vitro was further validated by in vivo studies which showed that Twist1 knockdown could lead to significantly delayed tumor growth of A549GR xenograft with increased sensitivity to AZD9291 treatment in nude mice without any observed side toxic effects.	osimertinib	255-262	twist basic helix-loop-helix transcription factor 1	Mus musculus	54-60
30993382-12	2019	The enhanced cytotoxic effect of AZD9291 on A549GR by Twist1 knockdown in vitro was further validated by in vivo studies which showed that Twist1 knockdown could lead to significantly delayed tumor growth of A549GR xenograft with increased sensitivity to AZD9291 treatment in nude mice without any observed side toxic effects.	osimertinib	255-262	twist basic helix-loop-helix transcription factor 1	Mus musculus	139-145
30943730-0	2019	Osimertinib in the treatment of leptomeningeal disease in T790M-negative, epidermal growth factor receptor-mutated non-small cell lung cancer: a case report.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	74-106
30943730-2	2019	Osimertinib is a third generation EGFR-tyrosine kinase inhibitor (TKI) with preclinical and early clinical studies showing activity against LMC resistant to previous TKI treatments and acquired T790M mutation.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	34-38
30943730-3	2019	We report a case of osimertinib in the treatment of LMC in a T790M-negative, EGFR-mutated NSCLC with significant clinical benefit and no toxicity.	osimertinib	20-31	epidermal growth factor receptor	Homo sapiens	77-81
30943730-4	2019	Osimertinib is a potentially effective treatment for LMC associated with EGFR-mutated NSCLC regardless of T790M status and a well-tolerated treatment for poor performance status patients.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	73-77
31097094-1	2019	BACKGROUND: Osimertinib is a tyrosine kinase inhibitor (TKI) that is an essential agent for the treatment of epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	109-141
31122565-0	2019	A Novel CAV1-MET Fusion in SCLC Transformation Responds to Crizotinib and Osimertinib Treatment.	osimertinib	74-85	caveolin 1	Homo sapiens	8-12
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
31097094-1	2019	BACKGROUND: Osimertinib is a tyrosine kinase inhibitor (TKI) that is an essential agent for the treatment of epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	143-147
31097094-16	2019	CONCLUSIONS: Re-administration of osimertinib for EGFR-mutant NSCLC yielded modest activity with tolerable toxicity.	osimertinib	34-45	epidermal growth factor receptor	Homo sapiens	50-54
31124059-1	2019	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) osimertinib has become the standard treatment for patients with pretreated EGFR-mutated non-small cell lung cancer (NSCLC) who acquire the T790M resistance mutation.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	33-65
31558282-9	2019	A recent clinical trial has demonstrated that EGFRs harboring some of these less common mutations also appear to be sensitive to the third-generation EGFR TKI, osimertinib.	osimertinib	160-171	epidermal growth factor receptor	Homo sapiens	46-50
31124059-1	2019	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) osimertinib has become the standard treatment for patients with pretreated EGFR-mutated non-small cell lung cancer (NSCLC) who acquire the T790M resistance mutation.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	67-71
31124059-1	2019	BACKGROUND: The third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) osimertinib has become the standard treatment for patients with pretreated EGFR-mutated non-small cell lung cancer (NSCLC) who acquire the T790M resistance mutation.	osimertinib	105-116	epidermal growth factor receptor	Homo sapiens	180-184
31122294-0	2019	The third-generation EGFR inhibitor AZD9291 overcomes primary resistance by continuously blocking ERK signaling in glioblastoma.	osimertinib	36-43	epidermal growth factor receptor	Homo sapiens	21-25
31122294-0	2019	The third-generation EGFR inhibitor AZD9291 overcomes primary resistance by continuously blocking ERK signaling in glioblastoma.	osimertinib	36-43	mitogen-activated protein kinase 1	Homo sapiens	98-101
31122294-4	2019	The third-generation EGFR-targeted drug, AZD9291, is a novel and irreversible inhibitor.	osimertinib	41-48	epidermal growth factor receptor	Homo sapiens	21-25
31122294-12	2019	In contrast to erlotinib, AZD9291 continuously and efficiently inhibited the EGFR/ERK signaling in GBM cells.	osimertinib	26-33	epidermal growth factor receptor	Homo sapiens	77-81
31122294-12	2019	In contrast to erlotinib, AZD9291 continuously and efficiently inhibited the EGFR/ERK signaling in GBM cells.	osimertinib	26-33	mitogen-activated protein kinase 1	Homo sapiens	82-85
31088573-12	2019	CONCLUSIONS: Osimertinib seems to be a suitable therapy for treatment-naive patients with sensitizing and resistant compound EGFR mutations.	osimertinib	13-24	epidermal growth factor receptor	Homo sapiens	125-129
30763730-1	2019	INTRODUCTION: Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor (TKI).	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	48-52
30831205-7	2019	Induction of AGK/BRAF fusion in H1975 (L858R + T790M), PC9 (ex19del) and HCC827 (ex19del) cells increased phosphorylation of BRAF, MEK1/2, ERK1/2, and signal transducer and activator of transcription 3 and conferred resistance to growth inhibition by osimertinib.	osimertinib	251-262	acylglycerol kinase	Homo sapiens	13-16
30623574-7	2019	Both Erlotinib (Tarceva) and Osimertinib (AZD-9291) reduced the levels of HDM-stimulated IL-6 and IL-8 levels in BEAS-2B cells.	osimertinib	42-50	interleukin 6	Homo sapiens	89-93
30831205-7	2019	Induction of AGK/BRAF fusion in H1975 (L858R + T790M), PC9 (ex19del) and HCC827 (ex19del) cells increased phosphorylation of BRAF, MEK1/2, ERK1/2, and signal transducer and activator of transcription 3 and conferred resistance to growth inhibition by osimertinib.	osimertinib	251-262	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
30831205-7	2019	Induction of AGK/BRAF fusion in H1975 (L858R + T790M), PC9 (ex19del) and HCC827 (ex19del) cells increased phosphorylation of BRAF, MEK1/2, ERK1/2, and signal transducer and activator of transcription 3 and conferred resistance to growth inhibition by osimertinib.	osimertinib	251-262	signal transducer and activator of transcription 3	Homo sapiens	151-201
30831205-8	2019	MEK inhibition with trametinib synergized with osimertinib to block growth.	osimertinib	47-58	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
30831205-11	2019	Combined inhibition of EGFR and MEK (with osimertinib and trametinib) or BRAF (with a pan-RAF inhibitor) are potential therapeutic strategies that should be explored.	osimertinib	42-53	epidermal growth factor receptor	Homo sapiens	23-27
30831205-11	2019	Combined inhibition of EGFR and MEK (with osimertinib and trametinib) or BRAF (with a pan-RAF inhibitor) are potential therapeutic strategies that should be explored.	osimertinib	42-53	mitogen-activated protein kinase kinase 7	Homo sapiens	32-35
30856555-1	2019	The third-generation EGFR inhibitor, osimertinib (AZD9291), selectively and irreversibly inhibits EGFR activating and T790 M mutants while sparing wild-type EGFR.	osimertinib	50-57	epidermal growth factor receptor	Homo sapiens	21-25
30856555-1	2019	The third-generation EGFR inhibitor, osimertinib (AZD9291), selectively and irreversibly inhibits EGFR activating and T790 M mutants while sparing wild-type EGFR.	osimertinib	50-57	epidermal growth factor receptor	Homo sapiens	98-102
30856555-1	2019	The third-generation EGFR inhibitor, osimertinib (AZD9291), selectively and irreversibly inhibits EGFR activating and T790 M mutants while sparing wild-type EGFR.	osimertinib	50-57	epidermal growth factor receptor	Homo sapiens	98-102
30623574-7	2019	Both Erlotinib (Tarceva) and Osimertinib (AZD-9291) reduced the levels of HDM-stimulated IL-6 and IL-8 levels in BEAS-2B cells.	osimertinib	42-50	C-X-C motif chemokine ligand 8	Homo sapiens	98-102
30623574-8	2019	AZD-9291 was more effective than Erlotinib in inhibiting phospho-EGFR, and downstream phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and phopho-signal transducer and activator of transcription 3 (p-STAT3) pathway signaling.	osimertinib	0-8	epidermal growth factor receptor	Homo sapiens	65-69
30623574-8	2019	AZD-9291 was more effective than Erlotinib in inhibiting phospho-EGFR, and downstream phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and phopho-signal transducer and activator of transcription 3 (p-STAT3) pathway signaling.	osimertinib	0-8	protein tyrosine kinase 2 beta	Homo sapiens	116-132
30623574-8	2019	AZD-9291 was more effective than Erlotinib in inhibiting phospho-EGFR, and downstream phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and phopho-signal transducer and activator of transcription 3 (p-STAT3) pathway signaling.	osimertinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	139-142
30623574-8	2019	AZD-9291 was more effective than Erlotinib in inhibiting phospho-EGFR, and downstream phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and phopho-signal transducer and activator of transcription 3 (p-STAT3) pathway signaling.	osimertinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	209-214
30623574-10	2019	Our findings highlight EGFR-TKIs, Tarceva, and AZD-9291, attenuate HDM-induced inflammatory IL-6 and IL-8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway.	osimertinib	47-55	interleukin 6	Homo sapiens	92-96
30623574-10	2019	Our findings highlight EGFR-TKIs, Tarceva, and AZD-9291, attenuate HDM-induced inflammatory IL-6 and IL-8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway.	osimertinib	47-55	C-X-C motif chemokine ligand 8	Homo sapiens	101-105
30623574-10	2019	Our findings highlight EGFR-TKIs, Tarceva, and AZD-9291, attenuate HDM-induced inflammatory IL-6 and IL-8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway.	osimertinib	47-55	epidermal growth factor receptor	Homo sapiens	120-124
30885336-0	2019	Patterns of progression on osimertinib in EGFR T790M positive NSCLC: A Swiss cohort study.	osimertinib	27-38	epidermal growth factor receptor	Homo sapiens	42-46
30885336-1	2019	INTRODUCTION: Osimertinib is an EGFR tyrosine kinase inhibitor (TKI) with antitumor activity in non-small cell lung cancer (NSCLC) with EGFR T790 M mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	32-36
30885336-1	2019	INTRODUCTION: Osimertinib is an EGFR tyrosine kinase inhibitor (TKI) with antitumor activity in non-small cell lung cancer (NSCLC) with EGFR T790 M mutations.	osimertinib	14-25	epidermal growth factor receptor	Homo sapiens	136-140
30883029-1	2019	BACKGROUND: Osimertinib (AZD9291), a third-generation EGFR-tyrosine kinase inhibitor, can effectively prolong survival in non-small cell lung cancer (NSCLC) patients with EGFR mutations, particularly T790M mutations; however, acquired resistance to AZD9291 is inevitable, thus exploration of the targets of resistance is urgent.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	54-58
30807997-1	2019	The goal of the present study was to determine the efficacy of osimertinib (AZD9291), a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor for the treatment of aggressive EGFR-mutant non-small cell lung cancer (NSCLC), compared to cisplatinum (CDDP) + pemetrexed (PEM).	osimertinib	76-83	epidermal growth factor receptor	Mus musculus	105-137
30807997-1	2019	The goal of the present study was to determine the efficacy of osimertinib (AZD9291), a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor for the treatment of aggressive EGFR-mutant non-small cell lung cancer (NSCLC), compared to cisplatinum (CDDP) + pemetrexed (PEM).	osimertinib	76-83	epidermal growth factor receptor	Mus musculus	203-207
30807997-2	2019	The NSCLC cell line PC-9 expressing green fluorescence protein (PC-9-GFP) was implanted in the brain of nude mice and was treated with CDDP + PEM or AZD9291.	osimertinib	149-156	proprotein convertase subtilisin/kexin type 9	Mus musculus	64-72
30883029-1	2019	BACKGROUND: Osimertinib (AZD9291), a third-generation EGFR-tyrosine kinase inhibitor, can effectively prolong survival in non-small cell lung cancer (NSCLC) patients with EGFR mutations, particularly T790M mutations; however, acquired resistance to AZD9291 is inevitable, thus exploration of the targets of resistance is urgent.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	171-175
30512189-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is selective for both EGFR-TKI-sensitizing and T790M (threonine-to-methionine substitution at codon 790)-resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	46-78
30512189-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is selective for both EGFR-TKI-sensitizing and T790M (threonine-to-methionine substitution at codon 790)-resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	80-84
30512189-1	2019	BACKGROUND: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that is selective for both EGFR-TKI-sensitizing and T790M (threonine-to-methionine substitution at codon 790)-resistance mutations.	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	145-149
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	44-76
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	78-82
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	160-164
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	44-76
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	78-82
30502627-1	2019	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	160-164
30502627-2	2019	In this study, osimertinib was characterized as a LSD1 inhibitor for the first time with an IC50 of 3.98 +- 0.3 muM and showed LSD1 inhibitory effect at cellular level.	osimertinib	15-26	lysine demethylase 1A	Homo sapiens	50-54
30502627-2	2019	In this study, osimertinib was characterized as a LSD1 inhibitor for the first time with an IC50 of 3.98 +- 0.3 muM and showed LSD1 inhibitory effect at cellular level.	osimertinib	15-26	lysine demethylase 1A	Homo sapiens	127-131
30471155-1	2019	BACKGROUND: The cobas  epidermal growth factor receptor (EGFR) Mutation Test v2 designed for cell-free DNA (cfDNA) is approved as a companion diagnostic for osimertinib therapy.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	23-55
30471155-1	2019	BACKGROUND: The cobas  epidermal growth factor receptor (EGFR) Mutation Test v2 designed for cell-free DNA (cfDNA) is approved as a companion diagnostic for osimertinib therapy.	osimertinib	157-168	epidermal growth factor receptor	Homo sapiens	57-61
30642450-0	2019	Loss of T790M mutation is associated with early progression to osimertinib in Chinese patients with advanced NSCLC who are harboring EGFR T790M.	osimertinib	63-74	epidermal growth factor receptor	Homo sapiens	133-137
30736738-0	2019	Positive response to Icotinib in metastatic lung adenocarcinoma with acquiring EGFR Leu792H mutation after AZD9291 treatment: a case report.	osimertinib	107-114	epidermal growth factor receptor	Homo sapiens	79-83
30736738-3	2019	CASE PRESENTATION: Here we reported a NSCLC patient with EGFR sensitive mutation of deletion within EGFR exon 19, who had been resistant to icotinib and AZD9291 successively after a period of 18 months response duration.	osimertinib	153-160	epidermal growth factor receptor	Homo sapiens	57-61
30736738-3	2019	CASE PRESENTATION: Here we reported a NSCLC patient with EGFR sensitive mutation of deletion within EGFR exon 19, who had been resistant to icotinib and AZD9291 successively after a period of 18 months response duration.	osimertinib	153-160	epidermal growth factor receptor	Homo sapiens	100-104
30642450-1	2019	BACKGROUND: Osimertinib demonstrates superior efficacy in patients with non-small cell lung cancer (NSCLC) who acquired EGFR T790M mutation as resistant mechanism to upfront EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	120-124
30642450-1	2019	BACKGROUND: Osimertinib demonstrates superior efficacy in patients with non-small cell lung cancer (NSCLC) who acquired EGFR T790M mutation as resistant mechanism to upfront EGFR tyrosine kinase inhibitors (TKIs).	osimertinib	12-23	epidermal growth factor receptor	Homo sapiens	174-178
30642450-4	2019	The aim of this study is to investigate the prevalence of T790 M loss after progression to osimertinib in Chinese patients with NSCLC harboring EGFR T790 M mutation and to compare their clinical outcomes and characteristics when stratified by T790 M mutational status at osimertinib resistance.	osimertinib	91-102	epidermal growth factor receptor	Homo sapiens	144-148
30322949-0	2019	KRAS and EGFR Amplifications Mediate Resistance to Rociletinib and Osimertinib in Acquired Afatinib-Resistant NSCLC Harboring Exon 19 Deletion/T790M in EGFR.	osimertinib	67-78	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
30521113-0	2019	Overcoming T790M mutant small cell lung cancer with the third-generation EGFR-TKI osimertinib.	osimertinib	82-93	epidermal growth factor receptor	Homo sapiens	73-77
30521113-5	2019	Unexpectedly, this SCLC patient maintained a sensitive response to the third-generation EGFR-TKI osimertinib.	osimertinib	97-108	epidermal growth factor receptor	Homo sapiens	88-92
30521113-6	2019	This special case may indicate that osimertinib represents an effective target drug for SCLC patients who harbor an EGFR T790M mutation.	osimertinib	36-47	epidermal growth factor receptor	Homo sapiens	116-120
30539501-3	2019	For EGFR T790M-positive patients who progress on EGFR TKI therapy, osimertinib is an effective treatment option.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	4-8
30539501-3	2019	For EGFR T790M-positive patients who progress on EGFR TKI therapy, osimertinib is an effective treatment option.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	49-53
30539501-7	2019	EGFR T790M-positive patients subsequently received osimertinib.	osimertinib	51-62	epidermal growth factor receptor	Homo sapiens	0-4
30539501-14	2019	Osimertinib confers high response rates after afatinib failure in EGFR T790M-positive patients and its use in sequence potentially allows extended chemotherapy-free treatment.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	66-70
30145802-0	2019	AZD9291 promotes autophagy and inhibits PI3K/Akt pathway in NSCLC cancer cells.	osimertinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	45-48
30145802-1	2019	AZD9291, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is highly selective against EGFR T790M-mutant non-small cell lung cancer (NSCLC).	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	88-92
30145802-1	2019	AZD9291, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is highly selective against EGFR T790M-mutant non-small cell lung cancer (NSCLC).	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	127-131
30145802-2	2019	On investigating the growth inhibitory effects of AZD9291 on NSCLC and the underlying mechanism, we found that AZD9291 can trigger autophagy-mediated cell death in both A549 and H1975 cells by increasing the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3) and decreasing the expression of p62.	osimertinib	111-118	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	302-305
30145802-2	2019	On investigating the growth inhibitory effects of AZD9291 on NSCLC and the underlying mechanism, we found that AZD9291 can trigger autophagy-mediated cell death in both A549 and H1975 cells by increasing the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3) and decreasing the expression of p62.	osimertinib	111-118	nucleoporin 62	Homo sapiens	340-343
30145802-3	2019	In the presence of the autophagy inhibitor chloroquine, the AZD9291-induced increase in LC3 level was further augmented.	osimertinib	60-67	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	88-91
30145802-4	2019	AZD9291 decreased the levels of phosphoinositide-3 kinase (PI3K), protein kinase B (Akt), and phosphorylated Akt.	osimertinib	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	32-57
30145802-4	2019	AZD9291 decreased the levels of phosphoinositide-3 kinase (PI3K), protein kinase B (Akt), and phosphorylated Akt.	osimertinib	0-7	protein tyrosine kinase 2 beta	Homo sapiens	66-82
30145802-4	2019	AZD9291 decreased the levels of phosphoinositide-3 kinase (PI3K), protein kinase B (Akt), and phosphorylated Akt.	osimertinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	84-87
30145802-4	2019	AZD9291 decreased the levels of phosphoinositide-3 kinase (PI3K), protein kinase B (Akt), and phosphorylated Akt.	osimertinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	109-112
30145802-5	2019	AZD9291-induced cell death was enhanced by Akt knockdown, and the levels of both EGFR and phosphorylated EGFR were decreased by AZD9291.	osimertinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	43-46
30145802-5	2019	AZD9291-induced cell death was enhanced by Akt knockdown, and the levels of both EGFR and phosphorylated EGFR were decreased by AZD9291.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	81-85
30145802-5	2019	AZD9291-induced cell death was enhanced by Akt knockdown, and the levels of both EGFR and phosphorylated EGFR were decreased by AZD9291.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	105-109
30145802-5	2019	AZD9291-induced cell death was enhanced by Akt knockdown, and the levels of both EGFR and phosphorylated EGFR were decreased by AZD9291.	osimertinib	128-135	epidermal growth factor receptor	Homo sapiens	81-85
30145802-5	2019	AZD9291-induced cell death was enhanced by Akt knockdown, and the levels of both EGFR and phosphorylated EGFR were decreased by AZD9291.	osimertinib	128-135	epidermal growth factor receptor	Homo sapiens	105-109
30145802-7	2019	Thus, AZD9291 was found to induce autophagy, decrease in EGFR levels, and show a strong inhibitory effect on NSCLC both in vitro and in vivo.	osimertinib	6-13	epidermal growth factor receptor	Homo sapiens	57-61
30145802-8	2019	Furthermore, the PI3K/Akt signaling pathway was found to play a critical role in AZD9291-induced cell death.	osimertinib	81-88	AKT serine/threonine kinase 1	Homo sapiens	22-25
30240852-10	2019	CONCLUSION: In this Asian population, first-line osimertinib demonstrated a clinically meaningful improvement in PFS over an SoC EGFR TKI, with a safety profile consistent with that for the overall FLAURA study population.	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	129-133
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	99-103
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	KRAS proto-oncogene, GTPase	Homo sapiens	187-191
30322949-9	2019	After 2 months of osimertinib withdrawal, this complex was dissociated, and the EGFR signal, but not the GRB2/SOS1 signal, was activated.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	80-84
30322949-9	2019	After 2 months of osimertinib withdrawal, this complex was dissociated, and the EGFR signal, but not the GRB2/SOS1 signal, was activated.	osimertinib	18-29	growth factor receptor bound protein 2	Homo sapiens	105-109
30322949-10	2019	Concomitant inhibition of MAPK kinase and EGFR could overcome osimertinib resistance.	osimertinib	62-73	epidermal growth factor receptor	Homo sapiens	42-46
30463991-0	2019	Activation of AXL as a Preclinical Acquired Resistance Mechanism Against Osimertinib Treatment in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	73-84	AXL receptor tyrosine kinase	Homo sapiens	14-17
30463991-0	2019	Activation of AXL as a Preclinical Acquired Resistance Mechanism Against Osimertinib Treatment in EGFR-Mutant Non-Small Cell Lung Cancer Cells.	osimertinib	73-84	epidermal growth factor receptor	Homo sapiens	98-102
30463991-1	2019	Osimertinib (AZD9291) has an efficacy superior to that of standard EGFR-tyrosine kinase inhibitors for the first-line treatment of patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC).	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	145-149
30463991-1	2019	Osimertinib (AZD9291) has an efficacy superior to that of standard EGFR-tyrosine kinase inhibitors for the first-line treatment of patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	145-149
30463991-4	2019	However, the acquired resistance mechanisms when osimertinib is initially used for EGFR-mutant NSCLC remain unclear.	osimertinib	49-60	epidermal growth factor receptor	Homo sapiens	83-87
30463991-5	2019	In this study, we experimentally established acquired osimertinib-resistant cell lines from EGFR-mutant NSCLC cell lines and investigated the molecular profiles of resistant cells to uncover the mechanisms of acquired resistance.	osimertinib	54-65	epidermal growth factor receptor	Homo sapiens	92-96
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
30463991-9	2019	Acquired resistance cell lines derived from H1975 harboring the T790M mutation showed AXL upregulation, and the cell growth of these cell lines was suppressed by a combination of osimertinib and cabozantinib, an inhibitor of multiple tyrosine kinases including AXL, both in vitro and in vivo.	osimertinib	179-190	AXL receptor tyrosine kinase	Homo sapiens	86-89
30463991-9	2019	Acquired resistance cell lines derived from H1975 harboring the T790M mutation showed AXL upregulation, and the cell growth of these cell lines was suppressed by a combination of osimertinib and cabozantinib, an inhibitor of multiple tyrosine kinases including AXL, both in vitro and in vivo.	osimertinib	179-190	AXL receptor tyrosine kinase	Homo sapiens	261-264
30463991-10	2019	Our results suggest that AXL might be a therapeutic target for overcoming acquired resistance to osimertinib.	osimertinib	97-108	AXL receptor tyrosine kinase	Homo sapiens	25-28
30463991-11	2019	IMPLICATIONS: Upregulation of AXL is one of the mechanisms of acquired resistance to osimertinib, and combination of osimertinib and cabozantinib might be a key treatment for overcoming osimertinib resistance.	osimertinib	85-96	AXL receptor tyrosine kinase	Homo sapiens	30-33
30642543-11	2019	Cetuximab can potentially increase the efficacy of afatinib or osimertinib in NSCLC with EGFR exon 20 insertion mutations.	osimertinib	63-74	epidermal growth factor receptor	Mus musculus	89-93
30322949-0	2019	KRAS and EGFR Amplifications Mediate Resistance to Rociletinib and Osimertinib in Acquired Afatinib-Resistant NSCLC Harboring Exon 19 Deletion/T790M in EGFR.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	9-13
30322949-0	2019	KRAS and EGFR Amplifications Mediate Resistance to Rociletinib and Osimertinib in Acquired Afatinib-Resistant NSCLC Harboring Exon 19 Deletion/T790M in EGFR.	osimertinib	67-78	epidermal growth factor receptor	Homo sapiens	152-156
30322949-1	2019	The critical T790M mutation in EGFR, which mediates resistance to first- and second-generation EGFR tyrosine kinase inhibitors (TKI; gefitinib, erlotinib, and afatinib), has facilitated the development of third-generation mutation-selective EGFR TKIs (rociletinib and osimertinib).	osimertinib	268-279	epidermal growth factor receptor	Homo sapiens	31-35
30322949-1	2019	The critical T790M mutation in EGFR, which mediates resistance to first- and second-generation EGFR tyrosine kinase inhibitors (TKI; gefitinib, erlotinib, and afatinib), has facilitated the development of third-generation mutation-selective EGFR TKIs (rociletinib and osimertinib).	osimertinib	268-279	epidermal growth factor receptor	Homo sapiens	95-99
30322949-5	2019	Significant KRAS amplification was observed in the osimertinib-resistant cell lines, indicating a linear and reversible increase with increased osimertinib concentrations in OsiR1 and OsiR2 cells.	osimertinib	51-62	KRAS proto-oncogene, GTPase	Homo sapiens	12-16
30322949-5	2019	Significant KRAS amplification was observed in the osimertinib-resistant cell lines, indicating a linear and reversible increase with increased osimertinib concentrations in OsiR1 and OsiR2 cells.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Homo sapiens	12-16
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	epidermal growth factor receptor	Homo sapiens	8-12
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	growth factor receptor bound protein 2	Homo sapiens	25-63
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	growth factor receptor bound protein 2	Homo sapiens	65-69
30322949-8	2019	Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation.	osimertinib	134-145	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	71-97
30365094-0	2019	Osimertinib (AZD9291) increases radio-sensitivity in EGFR T790M non-small cell lung cancer.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	53-57
30111817-3	2019	Here we report that NSCLC cells with acquired resistance to gefitinib or osimertinib (AZD9291) exhibit EMT features, with a decrease in E-cadherin, and increases in vimentin and stemness, without possessing any EGFR secondary mutations.	osimertinib	86-93	cadherin 1	Homo sapiens	136-146
30365094-1	2019	Osimertinib (AZD9291) is a third generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated significant clinical benefits in patients with EGFR-sensitizing mutations or the T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	44-76
30111817-3	2019	Here we report that NSCLC cells with acquired resistance to gefitinib or osimertinib (AZD9291) exhibit EMT features, with a decrease in E-cadherin, and increases in vimentin and stemness, without possessing any EGFR secondary mutations.	osimertinib	86-93	vimentin	Homo sapiens	165-173
30365094-1	2019	Osimertinib (AZD9291) is a third generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated significant clinical benefits in patients with EGFR-sensitizing mutations or the T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	78-82
30365094-1	2019	Osimertinib (AZD9291) is a third generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated significant clinical benefits in patients with EGFR-sensitizing mutations or the T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	179-183
30111817-9	2019	The EMT features of AZD9291-resistant H1975 cells were related to the upregulation of Zeb1.	osimertinib	20-27	zinc finger E-box binding homeobox 1	Homo sapiens	86-90
30520383-4	2019	CONCLUSION: To date, in the light of the data from the FLAURA study, osimertinib represents the best first-line option in NSCLC patients with EGFR activating mutations; EGFR-TKI plus chemotherapy combination therapies, even though interesting, must still be considered investigational.	osimertinib	69-80	epidermal growth factor receptor	Homo sapiens	142-146
30111817-11	2019	Our study not only revealed a common mechanism of EMT in both gefitinib and AZD9291 resistance beyond EGFR mutations per se, but also provides a new strategy to overcome it.	osimertinib	76-83	epidermal growth factor receptor	Homo sapiens	102-106
30591099-5	2018	In addition, the third-generation TKI drugs Osimertinib (AZD9291) and Rociletinib (CO-1686) have been developed to further benefit patients with primary TKI resistance caused by T790M mutation of EGFR.	osimertinib	57-64	epidermal growth factor receptor	Homo sapiens	196-200
30171779-1	2018	AIM: We report on two Phase 1, open-label, single-arm studies assessing the effect of osimertinib on simvastatin (CYP3A substrate) and rosuvastatin (breast cancer resistance protein substrate [BCRP] substrate) exposure in patients with advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer who have progressed after treatment with an EGFR tyrosine kinase inhibitor, to determine, upon coadministration, whether osimertinib could affect the exposure of these agents.	osimertinib	86-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-119
30171779-1	2018	AIM: We report on two Phase 1, open-label, single-arm studies assessing the effect of osimertinib on simvastatin (CYP3A substrate) and rosuvastatin (breast cancer resistance protein substrate [BCRP] substrate) exposure in patients with advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer who have progressed after treatment with an EGFR tyrosine kinase inhibitor, to determine, upon coadministration, whether osimertinib could affect the exposure of these agents.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	245-277
30171779-1	2018	AIM: We report on two Phase 1, open-label, single-arm studies assessing the effect of osimertinib on simvastatin (CYP3A substrate) and rosuvastatin (breast cancer resistance protein substrate [BCRP] substrate) exposure in patients with advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer who have progressed after treatment with an EGFR tyrosine kinase inhibitor, to determine, upon coadministration, whether osimertinib could affect the exposure of these agents.	osimertinib	86-97	epidermal growth factor receptor	Homo sapiens	279-283
30291293-0	2018	Ankyrin Repeat Domain 1 Overexpression is Associated with Common Resistance to Afatinib and Osimertinib in EGFR-mutant Lung Cancer.	osimertinib	92-103	ankyrin repeat domain 1	Homo sapiens	0-23
29660496-9	2018	However, in H1975 cells, which harbor the TKI-resistant EGFRL858R/T790M mutant, osimertinib, but not erlotinib, could significantly inhibit phosphorylation of EGFR-pY-1197, STAT5A-pY694 and CAV1-pY14, suggesting these sites also predict response in TKI-resistant cells.	osimertinib	80-91	epidermal growth factor receptor	Homo sapiens	56-60
29660496-9	2018	However, in H1975 cells, which harbor the TKI-resistant EGFRL858R/T790M mutant, osimertinib, but not erlotinib, could significantly inhibit phosphorylation of EGFR-pY-1197, STAT5A-pY694 and CAV1-pY14, suggesting these sites also predict response in TKI-resistant cells.	osimertinib	80-91	signal transducer and activator of transcription 5A	Homo sapiens	173-179
29660496-9	2018	However, in H1975 cells, which harbor the TKI-resistant EGFRL858R/T790M mutant, osimertinib, but not erlotinib, could significantly inhibit phosphorylation of EGFR-pY-1197, STAT5A-pY694 and CAV1-pY14, suggesting these sites also predict response in TKI-resistant cells.	osimertinib	80-91	caveolin 1	Homo sapiens	190-194
29967248-3	2018	To overcome compensatory hyperactivation of ERK, which we previously reported, an anti-EGFR antibody (cetuximab) was combined with other antibodies, as well as with a subtherapeutic dose of osimertinib, and cancer cell apoptosis was assayed.Results: Our animal studies identified a combination of three clinically approved drugs, cetuximab, trastuzumab (an anti-HER2 mAb), and osimertinib (low dose), as an effective and long-lasting treatment that is able to prevent onset of resistance to osimertinib.	osimertinib	377-388	EPH receptor B2	Homo sapiens	44-47
29967248-3	2018	To overcome compensatory hyperactivation of ERK, which we previously reported, an anti-EGFR antibody (cetuximab) was combined with other antibodies, as well as with a subtherapeutic dose of osimertinib, and cancer cell apoptosis was assayed.Results: Our animal studies identified a combination of three clinically approved drugs, cetuximab, trastuzumab (an anti-HER2 mAb), and osimertinib (low dose), as an effective and long-lasting treatment that is able to prevent onset of resistance to osimertinib.	osimertinib	377-388	EPH receptor B2	Homo sapiens	44-47
29967253-7	2018	Furthermore, the MANO method was applied to evaluate the functional significance of 17 compound mutations within ERBB2 reported in the COSMIC database, revealing that compound mutations involving L755S were sensitive to osimertinib but insensitive to afatinib and neratinib.Conclusions: Several ERBB2 mutations showed varying sensitivities to ERBB2-targeted inhibitors.	osimertinib	220-231	erb-b2 receptor tyrosine kinase 2	Homo sapiens	113-118
30291293-0	2018	Ankyrin Repeat Domain 1 Overexpression is Associated with Common Resistance to Afatinib and Osimertinib in EGFR-mutant Lung Cancer.	osimertinib	92-103	epidermal growth factor receptor	Homo sapiens	107-111
30291293-6	2018	When ANKRD1 was silenced in the EGFR-TKIs-resistant cell lines, afatinib and osimertinib could induce apoptosis of the cell lines.	osimertinib	77-88	ankyrin repeat domain 1	Homo sapiens	5-11
30291293-6	2018	When ANKRD1 was silenced in the EGFR-TKIs-resistant cell lines, afatinib and osimertinib could induce apoptosis of the cell lines.	osimertinib	77-88	epidermal growth factor receptor	Homo sapiens	32-36
30291293-7	2018	Imatinib could inhibit ANKRD1 expression, resulting in restoration of the sensitivity to afatinib and osimertinib of EGFR-TKI-resistant cells.	osimertinib	102-113	ankyrin repeat domain 1	Homo sapiens	23-29
30291293-7	2018	Imatinib could inhibit ANKRD1 expression, resulting in restoration of the sensitivity to afatinib and osimertinib of EGFR-TKI-resistant cells.	osimertinib	102-113	epidermal growth factor receptor	Homo sapiens	117-121
29802850-4	2018	The third-generation TKIs such as AZD9291, HM61713, CO-1686 and WZ4002 can overcome T790M through covalent binding to the EGFR kinase through Cys 797, but ultimately lose their efficacy upon emergence of the C797S mutation that abolishes the covalent bonding.	osimertinib	34-41	epidermal growth factor receptor	Homo sapiens	122-126
30615755-3	2018	According to clinical test and in vivo experimental data, the efficiencies of gefitinib and erlotinib are only 37% and 12% compared to AZD9291, and 0.300 mug of EGFR inactivation requires 0.484 mug of AZD9291, 0.815 mug of gefitinib and 1.348 mug of erlotinib.	osimertinib	201-208	epidermal growth factor receptor	Homo sapiens	161-165
29797219-0	2018	Loss of EGFR confers acquired resistance to AZD9291 in an EGFR-mutant non-small cell lung cancer cell line with an epithelial-mesenchymal transition phenotype.	osimertinib	44-51	epidermal growth factor receptor	Homo sapiens	8-12
29797219-0	2018	Loss of EGFR confers acquired resistance to AZD9291 in an EGFR-mutant non-small cell lung cancer cell line with an epithelial-mesenchymal transition phenotype.	osimertinib	44-51	epidermal growth factor receptor	Homo sapiens	58-62
29797219-1	2018	PURPOSE: AZD9291 is an irreversible, small-molecule inhibitor which has potency against mutant EGFR- and T790M-resistant mutation.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	95-99
29797219-12	2018	CONCLUSIONS: Loss of EGFR could be proposed as a potential acquired resistance mechanism of AZD9291 in EGFR-mutant NSCLC cells with an EMT phenotype.	osimertinib	92-99	epidermal growth factor receptor	Homo sapiens	21-25
29797219-12	2018	CONCLUSIONS: Loss of EGFR could be proposed as a potential acquired resistance mechanism of AZD9291 in EGFR-mutant NSCLC cells with an EMT phenotype.	osimertinib	92-99	epidermal growth factor receptor	Homo sapiens	103-107
29797219-14	2018	Blocking MAPK and AKT signaling may be a potential therapeutic strategy following AZD9291 resistance.	osimertinib	82-89	AKT serine/threonine kinase 1	Homo sapiens	18-21
29907952-1	2018	The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has shown significant clinical efficacy against the EGFR T790M mutation in non-small cell lung cancer (NSCLC) patients.	osimertinib	106-113	epidermal growth factor receptor	Homo sapiens	21-53
29907952-1	2018	The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has shown significant clinical efficacy against the EGFR T790M mutation in non-small cell lung cancer (NSCLC) patients.	osimertinib	106-113	epidermal growth factor receptor	Homo sapiens	55-59
29907952-1	2018	The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has shown significant clinical efficacy against the EGFR T790M mutation in non-small cell lung cancer (NSCLC) patients.	osimertinib	106-113	epidermal growth factor receptor	Homo sapiens	167-171
29506987-1	2018	Purpose: The third-generation EGFR tyrosine kinase inhibitor osimertinib is approved to treat patients with EGFR T790M-positive non-small cell lung cancer (NSCLC) who have developed resistance to earlier-generation drugs.	osimertinib	61-72	epidermal growth factor receptor	Homo sapiens	30-34
29506987-2	2018	Acquired EGFR C797S mutation has been reported to mediate osimertinib resistance in some patients.	osimertinib	58-69	epidermal growth factor receptor	Homo sapiens	9-13
29506987-6	2018	Further analysis of the 12 matched pretreatment samples confirmed that these EGFR mutations were acquired during osimertinib treatment.	osimertinib	113-124	epidermal growth factor receptor	Homo sapiens	77-81
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
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	KRAS proto-oncogene, GTPase	Homo sapiens	61-65
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	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	71-77
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
29506987-8	2018	Besides C797 mutations, novel secondary mutations of EGFR L718 and L792 residues confer osimertinib resistance, both in vitro and in vivo, and are of great clinical and pharmaceutical relevance.	osimertinib	88-99	epidermal growth factor receptor	Homo sapiens	53-57
30358214-0	2018	Circulating tumor cells predict prognosis following secondline AZD 9291 treatment in EGFR-T790M mutant non-small cell lung cancer patients.	osimertinib	63-71	epidermal growth factor receptor	Homo sapiens	85-89
30358214-1	2018	PURPOSE: AZD9291 has been developed as third-generation epithermal growth factor receptor (EGFR)- tyrosine kinase inhibitor (TKI) with activities against T790M mutation.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	56-89
30358214-1	2018	PURPOSE: AZD9291 has been developed as third-generation epithermal growth factor receptor (EGFR)- tyrosine kinase inhibitor (TKI) with activities against T790M mutation.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	91-95
30358214-3	2018	METHODS: Enrolled patients confirmed with EGFR T790M mutation received AZD9291 80 mg orally once daily as second-line treatment.	osimertinib	71-78	epidermal growth factor receptor	Homo sapiens	42-46
29910645-3	2018	However, resistance inevitably develops, and the third-generation tki osimertinib has been approved to target the gatekeeper EGFR mutation T790M, which is responsible for resistance in 60% of cases.	osimertinib	70-81	epidermal growth factor receptor	Homo sapiens	125-129
29298799-5	2018	Interestingly, we further identified that combined treatment with osimertinib and the BET inhibitor JQ1 significantly increased the response rate in HER2-mutant NSCLC, whereas JQ1 single treatment did not show efficacy.Conclusions: Overall, our data indicated robust antitumor efficacy of osimertinib against multiple HER2 aberrations in lung cancer, either as a single agent or in combination with JQ1.	osimertinib	66-77	erb-b2 receptor tyrosine kinase 2	Mus musculus	149-153
29298799-5	2018	Interestingly, we further identified that combined treatment with osimertinib and the BET inhibitor JQ1 significantly increased the response rate in HER2-mutant NSCLC, whereas JQ1 single treatment did not show efficacy.Conclusions: Overall, our data indicated robust antitumor efficacy of osimertinib against multiple HER2 aberrations in lung cancer, either as a single agent or in combination with JQ1.	osimertinib	66-77	erb-b2 receptor tyrosine kinase 2	Mus musculus	318-322
29298799-6	2018	Our study provides a strong rationale for future clinical trials using osimertinib either alone or in combination with epigenetic drugs to target aberrant HER2 in patients with NSCLC.	osimertinib	71-82	erb-b2 receptor tyrosine kinase 2	Homo sapiens	155-159
29910649-9	2018	Conclusions: The treatment algorithm for EGFR mutation is changing with the proven efficacy of osimertinib for the acquired T790M mutation.	osimertinib	95-106	epidermal growth factor receptor	Homo sapiens	41-45
29673089-0	2018	Non-small cell lung cancer harboring a rare EGFR L747P mutation showing intrinsic resistance to both gefitinib and osimertinib (AZD9291): A case report.	osimertinib	128-135	epidermal growth factor receptor	Homo sapiens	44-48
29998228-6	2018	Osimertinib mesylate (formerly AZD-9291) is a potent third-generation TKI which irreversibly inhibits mutated EGFR alleles, including T790M.	osimertinib	31-39	epidermal growth factor receptor	Homo sapiens	110-114
32700141-0	2018	Osimertinib for Previously Treated Patients With Advanced EGFR T790M Mutation-Positive NSCLC: Tolerability and Diagnostic Methods From an Expanded Access Program.	osimertinib	0-11	epidermal growth factor receptor	Homo sapiens	58-62
32700141-1	2018	INTRODUCTION: The osimertinib (AZD9291) US Expanded Access Program (EAP) provided compassionate access to osimertinib prior to US Food and Drug Administration (FDA) approval for patients with advanced/metastatic epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer (NSCLC) following progression on tyrosine kinase inhibitors (TKIs) targeting EGFR.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	212-244
32700141-1	2018	INTRODUCTION: The osimertinib (AZD9291) US Expanded Access Program (EAP) provided compassionate access to osimertinib prior to US Food and Drug Administration (FDA) approval for patients with advanced/metastatic epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer (NSCLC) following progression on tyrosine kinase inhibitors (TKIs) targeting EGFR.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	246-250
32700141-1	2018	INTRODUCTION: The osimertinib (AZD9291) US Expanded Access Program (EAP) provided compassionate access to osimertinib prior to US Food and Drug Administration (FDA) approval for patients with advanced/metastatic epidermal growth factor receptor (EGFR) T790M-positive non-small cell lung cancer (NSCLC) following progression on tyrosine kinase inhibitors (TKIs) targeting EGFR.	osimertinib	18-29	epidermal growth factor receptor	Homo sapiens	371-375
29730192-1	2018	A series of novel 2,4-diarylaminopyrimidine derivatives of AZD9291 were discovered as L858R/T790M mutant selective epidermal growth factor receptor (EGFR) inhibitors.	osimertinib	59-66	epidermal growth factor receptor	Homo sapiens	115-147
29730192-1	2018	A series of novel 2,4-diarylaminopyrimidine derivatives of AZD9291 were discovered as L858R/T790M mutant selective epidermal growth factor receptor (EGFR) inhibitors.	osimertinib	59-66	epidermal growth factor receptor	Homo sapiens	149-153
29730192-6	2018	Docking study performed for 8a with ATP binding site of EGFR-TK showed the similar binding mode to that of AZD9291.	osimertinib	107-114	epidermal growth factor receptor	Homo sapiens	56-60
29789021-8	2018	AZD9291 was found to be an excellent treatment option and yielded the longest survival for T790M+ patients in all groups who had progressed on EGFR-TKIs; for other treatments, the prognosis of T790M- patient subgroups varied.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	143-147
28422737-7	2017	The clones were also highly sensitive to the 3rd-generation EGFR TKI AZD9291, which is cytotoxic to lung cancer cells with EGFR T790M.	osimertinib	69-76	epidermal growth factor receptor	Homo sapiens	60-64
29437786-6	2018	Modulation of CYP1A1/CYP1A2 levels markedly reduced parent drug concentrations, significantly altering metabolite pharmacokinetics (PK) in humanized mice in vivoConclusions: We demonstrate that a P450 enzyme expressed in smokers" lungs and lung tumors has the capacity to metabolise osimertinib.	osimertinib	283-294	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	14-20
29437786-6	2018	Modulation of CYP1A1/CYP1A2 levels markedly reduced parent drug concentrations, significantly altering metabolite pharmacokinetics (PK) in humanized mice in vivoConclusions: We demonstrate that a P450 enzyme expressed in smokers" lungs and lung tumors has the capacity to metabolise osimertinib.	osimertinib	283-294	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	21-27
29874151-1	2018	AIM: This study aims to develop new nanoformulations of EGFR T790M targeted inhibitor AZD9291 and paclitaxel (PTX) for combination therapy of lung cancer.	osimertinib	86-93	epidermal growth factor receptor	Homo sapiens	56-60
29332537-1	2018	AZD9291 is a novel, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), which is administered orally.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	33-65
29332537-1	2018	AZD9291 is a novel, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), which is administered orally.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	67-71
29332537-5	2018	In PC-9-IR cells, AZD9291 remarkably decreases phosphorylation levels of EGFR, extracellular regulated protein kinase (ERK), and protein kinase B (AKT).	osimertinib	18-25	epidermal growth factor receptor	Homo sapiens	73-77
29332537-5	2018	In PC-9-IR cells, AZD9291 remarkably decreases phosphorylation levels of EGFR, extracellular regulated protein kinase (ERK), and protein kinase B (AKT).	osimertinib	18-25	protein tyrosine kinase 2 beta	Homo sapiens	129-145
29332537-5	2018	In PC-9-IR cells, AZD9291 remarkably decreases phosphorylation levels of EGFR, extracellular regulated protein kinase (ERK), and protein kinase B (AKT).	osimertinib	18-25	AKT serine/threonine kinase 1	Homo sapiens	147-150
29332537-7	2018	Our findings suggest a potential therapeutic effect of AZD9291 as a radiation sensitizer in lung cancer cells with an acquired EGFR T790M mutation, providing a rationale for a clinical trial using the combination of AZD9291 and radiation in NSCLCs harboring acquired T790M mutation.	osimertinib	55-62	epidermal growth factor receptor	Homo sapiens	127-131
29212784-3	2018	Irreversible inhibitors (e.g., osimertinib/AZD9291) inhibit T790M-EGFR, but several mechanisms, including a third-site mutation, C797S, confer renewed resistance.	osimertinib	43-50	epidermal growth factor receptor	Homo sapiens	66-70
29568384-2	2018	Though WZ4002/CO-1686/AZD9291 are effective in overcoming EGFR T790M by targeting Cys797 via covalent bonding, their efficacy is again limited due to the emergence of C797S mutation.	osimertinib	22-29	epidermal growth factor receptor	Homo sapiens	58-62
28730963-0	2018	Increased Expression of IRE1alpha Associates with the Resistant Mechanism of Osimertinib (AZD9291)-resistant non-small Cell Lung Cancer HCC827/OSIR Cells.	osimertinib	90-97	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	24-33
28730963-1	2018	BACKGROUND: Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients.	osimertinib	45-52	epidermal growth factor receptor	Homo sapiens	76-108
28730963-1	2018	BACKGROUND: Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients.	osimertinib	45-52	epidermal growth factor receptor	Homo sapiens	110-114
28341106-0	2017	The APPLE Trial: Feasibility and Activity of AZD9291 (Osimertinib) Treatment on Positive PLasma T790M in EGFR-mutant NSCLC Patients.	osimertinib	45-52	epidermal growth factor receptor	Homo sapiens	105-109
28341106-2	2017	The AZD9291 (Osimertinib) Treatment on Positive PLasma T790M in EGFR-mutant NSCLC Patients (APPLE) trial is a randomized, open-label, multicenter, 3-arm, phase II study in advanced, epidermal growth factor receptor (EGFR)-mutant and EGFR tyrosine kinase inhibitor (TKI)-naive non-small-cell lung cancer (NSCLC) patients, to evaluate the best strategy for sequencing gefitinib and osimertinib treatment.	osimertinib	4-11	epidermal growth factor receptor	Homo sapiens	64-68
28341106-2	2017	The AZD9291 (Osimertinib) Treatment on Positive PLasma T790M in EGFR-mutant NSCLC Patients (APPLE) trial is a randomized, open-label, multicenter, 3-arm, phase II study in advanced, epidermal growth factor receptor (EGFR)-mutant and EGFR tyrosine kinase inhibitor (TKI)-naive non-small-cell lung cancer (NSCLC) patients, to evaluate the best strategy for sequencing gefitinib and osimertinib treatment.	osimertinib	4-11	epidermal growth factor receptor	Homo sapiens	216-220
28341106-2	2017	The AZD9291 (Osimertinib) Treatment on Positive PLasma T790M in EGFR-mutant NSCLC Patients (APPLE) trial is a randomized, open-label, multicenter, 3-arm, phase II study in advanced, epidermal growth factor receptor (EGFR)-mutant and EGFR tyrosine kinase inhibitor (TKI)-naive non-small-cell lung cancer (NSCLC) patients, to evaluate the best strategy for sequencing gefitinib and osimertinib treatment.	osimertinib	4-11	epidermal growth factor receptor	Homo sapiens	216-220
28808573-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor approved for EGFR-T790M-positive non-small cell lung cancer.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	44-76
28808573-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor approved for EGFR-T790M-positive non-small cell lung cancer.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	78-82
28808573-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor approved for EGFR-T790M-positive non-small cell lung cancer.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	123-127
29086838-10	2017	CONCLUSIONS: The accuracy and efficiency of RD-Metabolizer was further illustrated by a metabolism prediction case of AZD9291, which is a mutant-selective EGFR inhibitor.	osimertinib	118-125	epidermal growth factor receptor	Homo sapiens	155-159
29425688-1	2018	Given the successful identification of epidermal growth factor receptor EGFR T790M, the third-generation EGFR tyrosine kinase inhibitor (TKI), osimertinib (OSI, AZD9291), was developed to target EGFR T790M mutation.	osimertinib	161-168	epidermal growth factor receptor	Homo sapiens	105-109
29425688-1	2018	Given the successful identification of epidermal growth factor receptor EGFR T790M, the third-generation EGFR tyrosine kinase inhibitor (TKI), osimertinib (OSI, AZD9291), was developed to target EGFR T790M mutation.	osimertinib	161-168	epidermal growth factor receptor	Homo sapiens	105-109
29641535-0	2018	Acquired resistance to AZD9291 as an upfront treatment is dependent on ERK signaling in a preclinical model.	osimertinib	23-30	mitogen-activated protein kinase 1	Homo sapiens	71-74
29641535-1	2018	AZD9291 (osimertinib) is approved for standard care in patients with EGFR T790M-positive non-small cell lung cancer (NSCLC) after prior EGFR TKI progression.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	69-73
29641535-1	2018	AZD9291 (osimertinib) is approved for standard care in patients with EGFR T790M-positive non-small cell lung cancer (NSCLC) after prior EGFR TKI progression.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	136-140
29641535-2	2018	Furthermore, AZD9291 is now being evaluated as a first-line treatment for NSCLC patients with activation EGFR mutations.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	105-109
29641535-5	2018	AZD9291-resistant cells (PC9/AZDR) were established using EGFR inhibitor-naive PC9 cells.	osimertinib	0-7	proprotein convertase subtilisin/kexin type 9	Homo sapiens	25-28
29641535-5	2018	AZD9291-resistant cells (PC9/AZDR) were established using EGFR inhibitor-naive PC9 cells.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	58-62
29641535-5	2018	AZD9291-resistant cells (PC9/AZDR) were established using EGFR inhibitor-naive PC9 cells.	osimertinib	0-7	proprotein convertase subtilisin/kexin type 9	Homo sapiens	79-82
29641535-7	2018	Resistance to AZD9291 developed through aberrant activation of ERK signaling by an EGFR-independent mechanism.	osimertinib	14-21	mitogen-activated protein kinase 1	Homo sapiens	63-66
29641535-7	2018	Resistance to AZD9291 developed through aberrant activation of ERK signaling by an EGFR-independent mechanism.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	83-87
29641535-8	2018	The combination of a MEK inhibitor with AZD9291 restored the sensitivity of PC9/AZDR cells in vitro and in vivo.	osimertinib	40-47	proprotein convertase subtilisin/kexin type 9	Homo sapiens	76-79
29641535-10	2018	In addition, maspin expression was higher after AZD9291 treatment in PC9/AZDR cells.	osimertinib	48-55	serpin family B member 5	Homo sapiens	13-19
29641535-10	2018	In addition, maspin expression was higher after AZD9291 treatment in PC9/AZDR cells.	osimertinib	48-55	proprotein convertase subtilisin/kexin type 9	Homo sapiens	69-72
29641535-11	2018	Sustained ERK activation confers resistance to AZD9291 as a first-line therapy.	osimertinib	47-54	mitogen-activated protein kinase 1	Homo sapiens	10-13
29641535-12	2018	Thus, co-targeting EGFR and MEK may be an effective strategy to overcome resistance to AZD9291.	osimertinib	87-94	epidermal growth factor receptor	Homo sapiens	19-23
29641535-12	2018	Thus, co-targeting EGFR and MEK may be an effective strategy to overcome resistance to AZD9291.	osimertinib	87-94	mitogen-activated protein kinase kinase 7	Homo sapiens	28-31
28880013-0	2017	Osimertinib (AZD9291) decreases programmed death ligand-1 in EGFR-mutated non-small cell lung cancer cells.	osimertinib	13-20	CD274 molecule	Homo sapiens	32-57
28880013-0	2017	Osimertinib (AZD9291) decreases programmed death ligand-1 in EGFR-mutated non-small cell lung cancer cells.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	61-65
28880013-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	44-76
28880013-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	78-82
28880013-1	2017	Osimertinib (AZD9291) is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that has been approved for the treatment of EGFR-mutated non-small cell lung cancer (NSCLC).	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	160-164
28765329-0	2017	Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 Degradation.	osimertinib	34-41	epidermal growth factor receptor	Homo sapiens	62-66
28765329-0	2017	Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 Degradation.	osimertinib	34-41	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
28765329-0	2017	Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 Degradation.	osimertinib	34-41	mitogen-activated protein kinase 1	Homo sapiens	104-107
28765329-0	2017	Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 Degradation.	osimertinib	34-41	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	126-131
28765329-1	2017	Purpose: The mechanisms accounting for anticancer activity of AZD9291 (osimertinib or TAGRISSO), an approved third-generation EGFR inhibitor, in EGFR-mutant non-small cell lung cancer (NSCLC) cells and particularly for the subsequent development of acquired resistance are unclear and thus are the focus of this study.Experimental Design: AZD9219-resistant cell lines were established by exposing sensitive cell lines to AZD9291.	osimertinib	62-69	epidermal growth factor receptor	Homo sapiens	126-130
28765329-1	2017	Purpose: The mechanisms accounting for anticancer activity of AZD9291 (osimertinib or TAGRISSO), an approved third-generation EGFR inhibitor, in EGFR-mutant non-small cell lung cancer (NSCLC) cells and particularly for the subsequent development of acquired resistance are unclear and thus are the focus of this study.Experimental Design: AZD9219-resistant cell lines were established by exposing sensitive cell lines to AZD9291.	osimertinib	62-69	epidermal growth factor receptor	Homo sapiens	145-149
28765329-6	2017	Gene knockdown were achieved with siRNA or shRNA.Results: AZD9291 potently induced apoptosis in EGFR-mutant NSCLC cell lines, in which ERK phosphorylation was suppressed accompanied with Bim elevation and Mcl-1 reduction likely due to enhanced Mcl-1 degradation and increased Bim stability.	osimertinib	58-65	epidermal growth factor receptor	Homo sapiens	96-100
28765329-6	2017	Gene knockdown were achieved with siRNA or shRNA.Results: AZD9291 potently induced apoptosis in EGFR-mutant NSCLC cell lines, in which ERK phosphorylation was suppressed accompanied with Bim elevation and Mcl-1 reduction likely due to enhanced Mcl-1 degradation and increased Bim stability.	osimertinib	58-65	mitogen-activated protein kinase 1	Homo sapiens	135-138
28765329-6	2017	Gene knockdown were achieved with siRNA or shRNA.Results: AZD9291 potently induced apoptosis in EGFR-mutant NSCLC cell lines, in which ERK phosphorylation was suppressed accompanied with Bim elevation and Mcl-1 reduction likely due to enhanced Mcl-1 degradation and increased Bim stability.	osimertinib	58-65	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	205-210
28765329-6	2017	Gene knockdown were achieved with siRNA or shRNA.Results: AZD9291 potently induced apoptosis in EGFR-mutant NSCLC cell lines, in which ERK phosphorylation was suppressed accompanied with Bim elevation and Mcl-1 reduction likely due to enhanced Mcl-1 degradation and increased Bim stability.	osimertinib	58-65	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	244-249
28765329-7	2017	Blocking Bim elevation by gene knockdown or enforcing Mcl-1 expression attenuated or abolished AZD9291-induced apoptosis.	osimertinib	95-102	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	54-59
28765329-8	2017	Moreover, AZD9291 lost its ability to modulate Bim and Mcl-1 levels in AZD9291-resistant cell lines.	osimertinib	10-17	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	55-60
28765329-8	2017	Moreover, AZD9291 lost its ability to modulate Bim and Mcl-1 levels in AZD9291-resistant cell lines.	osimertinib	71-78	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	55-60
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	40-47	mitogen-activated protein kinase kinase 7	Homo sapiens	226-229
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	40-47	mitogen-activated protein kinase 1	Homo sapiens	230-233
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	40-47	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	252-257
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	320-324
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	226-229
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase 1	Homo sapiens	230-233
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	252-257
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	epidermal growth factor receptor	Homo sapiens	320-324
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	226-229
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase 1	Homo sapiens	230-233
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	252-257
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	epidermal growth factor receptor	Homo sapiens	320-324
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase kinase 7	Homo sapiens	226-229
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	mitogen-activated protein kinase 1	Homo sapiens	230-233
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	252-257
28765329-9	2017	The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression in vitro and in vivoConclusions: Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.	osimertinib	76-83	epidermal growth factor receptor	Homo sapiens	320-324
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	21-53
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	55-59
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	137-141
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	137-141
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	137-141
28577957-1	2017	OBJECTIVES: Reliable epidermal growth factor receptor (EGFR) mutation testing techniques are required to identify eligible patients with EGFR mutation/T790M positive advanced non-small cell lung cancer (NSCLC), for treatment with osimertinib (AZD9291), an oral, potent, irreversible EGFR tyrosine kinase inhibitor (TKI) selective for EGFR-TKI-sensitizing and T790M resistance mutations over wild-type EGFR.	osimertinib	243-250	epidermal growth factor receptor	Homo sapiens	137-141
28422737-7	2017	The clones were also highly sensitive to the 3rd-generation EGFR TKI AZD9291, which is cytotoxic to lung cancer cells with EGFR T790M.	osimertinib	69-76	epidermal growth factor receptor	Homo sapiens	123-127
27923714-1	2017	INTRODUCTION: AZD9291 (osimertinib) is designed for acquired T790M mutation after first- and second-generation EGFR) tyrosine kinase inhibitors have been used.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	111-115
28237877-1	2017	Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation.	osimertinib	33-40	epidermal growth factor receptor	Homo sapiens	64-96
28237877-1	2017	Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation.	osimertinib	33-40	epidermal growth factor receptor	Homo sapiens	98-102
28237877-1	2017	Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation.	osimertinib	33-40	epidermal growth factor receptor	Homo sapiens	228-232
28061471-1	2017	AZD9291, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), benefits patients with T790M mutant non-small-cell lung cancer who fail treatment with first-generation EGFR TKIs.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	28-60
28061471-1	2017	AZD9291, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), benefits patients with T790M mutant non-small-cell lung cancer who fail treatment with first-generation EGFR TKIs.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	62-66
28061471-1	2017	AZD9291, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), benefits patients with T790M mutant non-small-cell lung cancer who fail treatment with first-generation EGFR TKIs.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	205-209
28061471-3	2017	We reported an advanced lung adenocarcinoma female with EGFR exon19 deletion treated on AZD9291 after failure of erlotinib and chemotherapy.	osimertinib	88-95	epidermal growth factor receptor	Homo sapiens	56-60
27840244-1	2017	The third-generation tyrosine kinase inhibitors (TKI), AZD9291 (osimertinib) and CO-1686 (rociletinib) of epidermal growth factor receptor (EGFR) are highly active against T790M positive non-small cell lung cancer (NSCLC).	osimertinib	55-62	epidermal growth factor receptor	Homo sapiens	140-144
28219203-3	2017	Now, with the continuously emerging of new types of EGFR-TKIs and ever-increasing publication of clinical trial results on afatinib, AZD9291 and other TKIs, we have more first-line choices for patients with EGFR mutations.	osimertinib	133-140	epidermal growth factor receptor	Homo sapiens	207-211
28029074-7	2017	In this review, we discuss the molecular heterogeneity of EGFR and provide rational preclinical and clinical guidelines for testing AZD9291, a third generation, irreversible EGFR-TKI with both a high affinity for EGFRvIII and excellent brain penetration.	osimertinib	132-139	epidermal growth factor receptor	Homo sapiens	174-178
27885838-2	2017	Osimertinib (AZD9291) has been developed as 3rd generation EGFR-TKI with activities against sensitizing mutations and T790 M resistance mutation, which account for about 50% of the mechanisms of acquired resistance to 1st or 2nd generation EGFR-TKIs.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	59-63
27885838-2	2017	Osimertinib (AZD9291) has been developed as 3rd generation EGFR-TKI with activities against sensitizing mutations and T790 M resistance mutation, which account for about 50% of the mechanisms of acquired resistance to 1st or 2nd generation EGFR-TKIs.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	240-244
27751847-1	2016	BACKGROUND: Osimertinib (AZD9291) is an oral, potent, irreversible EGFR tyrosine-kinase inhibitor selective for EGFR tyrosine-kinase inhibitor sensitising mutations, and the EGFR Thr790Met resistance mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	67-71
27861144-3	2016	Osimertinib (AZD9291) is a novel EGFR tyrosine kinase inhibitor (TKI) that is potent and selective for sensitising (EGFRm) and T790M resistance mutations.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	33-37
27835594-1	2016	Osimertinib (OSI, also known as AZD9291) is the newest FDA-approved epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation.	osimertinib	32-39	epidermal growth factor receptor	Homo sapiens	68-100
27835594-1	2016	Osimertinib (OSI, also known as AZD9291) is the newest FDA-approved epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation.	osimertinib	32-39	epidermal growth factor receptor	Homo sapiens	102-106
27835594-1	2016	Osimertinib (OSI, also known as AZD9291) is the newest FDA-approved epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation.	osimertinib	32-39	epidermal growth factor receptor	Homo sapiens	187-191
27770386-4	2016	AZD9291 (osimertinib; Tagrisso) is the first and only FDA approved third-generation EGFR TKI for T790M-positive advanced NSCLC patients.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	84-88
27770386-7	2016	To overcome the acquired resistance to AZD9291, EAI045 was discovered and recently reported to be an allosteric EGFR inhibitor that overcomes T790M- and C797S-mediated resistance.	osimertinib	39-46	epidermal growth factor receptor	Homo sapiens	112-116
27751847-1	2016	BACKGROUND: Osimertinib (AZD9291) is an oral, potent, irreversible EGFR tyrosine-kinase inhibitor selective for EGFR tyrosine-kinase inhibitor sensitising mutations, and the EGFR Thr790Met resistance mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	112-116
27751847-1	2016	BACKGROUND: Osimertinib (AZD9291) is an oral, potent, irreversible EGFR tyrosine-kinase inhibitor selective for EGFR tyrosine-kinase inhibitor sensitising mutations, and the EGFR Thr790Met resistance mutation.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	112-116
27641462-2	2016	Osimertinib (AZD9291, Tagrisso ) is a third-generation, irreversible EGFR TKI, active in case of T790M mutation.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	69-73
27612423-8	2016	Third generation EGFR kinase inhibitor (AZD9291) inhibits the growth of L858R/T790M-EGFR driven cells and also induces EGFR degradation.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	17-21
27612423-8	2016	Third generation EGFR kinase inhibitor (AZD9291) inhibits the growth of L858R/T790M-EGFR driven cells and also induces EGFR degradation.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	84-88
27612423-8	2016	Third generation EGFR kinase inhibitor (AZD9291) inhibits the growth of L858R/T790M-EGFR driven cells and also induces EGFR degradation.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	84-88
27450722-1	2016	The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs; e.g., AZD9291), which selectively and irreversibly inhibit EGFR activating and T790M mutants, represent very promising therapeutic options for patients with non-small cell lung cancer (NSCLC) that has become resistant to 1st generation EGFR-TKIs due to T790M mutation.	osimertinib	97-104	epidermal growth factor receptor	Homo sapiens	80-84
27450722-1	2016	The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs; e.g., AZD9291), which selectively and irreversibly inhibit EGFR activating and T790M mutants, represent very promising therapeutic options for patients with non-small cell lung cancer (NSCLC) that has become resistant to 1st generation EGFR-TKIs due to T790M mutation.	osimertinib	97-104	epidermal growth factor receptor	Homo sapiens	150-154
27450722-1	2016	The 3rd generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs; e.g., AZD9291), which selectively and irreversibly inhibit EGFR activating and T790M mutants, represent very promising therapeutic options for patients with non-small cell lung cancer (NSCLC) that has become resistant to 1st generation EGFR-TKIs due to T790M mutation.	osimertinib	97-104	epidermal growth factor receptor	Homo sapiens	150-154
27450722-4	2016	The current study has demonstrated that Met amplification and hyperactivation is a resistance mechanism to both 1st and 3rd generation EGFR-TKIs since both erlotinib- and AZD9291-resistant HCC827 cell lines possessed amplified Met gene and hyperactivated Met, and were cross-resistant to AZD9291 or erlotinib.	osimertinib	171-178	epidermal growth factor receptor	Homo sapiens	135-139
27450722-4	2016	The current study has demonstrated that Met amplification and hyperactivation is a resistance mechanism to both 1st and 3rd generation EGFR-TKIs since both erlotinib- and AZD9291-resistant HCC827 cell lines possessed amplified Met gene and hyperactivated Met, and were cross-resistant to AZD9291 or erlotinib.	osimertinib	288-295	epidermal growth factor receptor	Homo sapiens	135-139
27450722-6	2016	Hence, we suggest that Met inhibition is also an effective strategy to overcome resistance of certain EGFR-mutated NSCLCs with Met amplification to AZD9291, warranting the further clinical validation of our findings.	osimertinib	148-155	epidermal growth factor receptor	Homo sapiens	102-106
27252416-1	2016	PURPOSE: To identify novel mechanisms of resistance to third-generation EGFR inhibitors in patients with lung adenocarcinoma that progressed under therapy with either AZD9291 or rociletinib (CO-1686).	osimertinib	167-174	epidermal growth factor receptor	Homo sapiens	72-76
27257132-0	2016	L718Q Mutation as New Mechanism of Acquired Resistance to AZD9291 in EGFR-Mutated NSCLC.	osimertinib	58-65	epidermal growth factor receptor	Homo sapiens	69-73
27439477-1	2016	Osimertinib (AZD9291) is a potent, selective, irreversible inhibitor of EGFR-sensitizing (exon 19 and L858R) and T790M-resistant mutation.	osimertinib	13-20	epidermal growth factor receptor	Mus musculus	72-76
27469903-0	2016	Liquid chromatography-tandem mass spectrometric assay for the T790M mutant EGFR inhibitor osimertinib (AZD9291) in human plasma.	osimertinib	103-110	epidermal growth factor receptor	Homo sapiens	75-79
27649127-0	2016	Osimertinib (AZD9291), a Mutant-Selective EGFR Inhibitor, Reverses ABCB1-Mediated Drug Resistance in Cancer Cells.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	42-46
27649127-0	2016	Osimertinib (AZD9291), a Mutant-Selective EGFR Inhibitor, Reverses ABCB1-Mediated Drug Resistance in Cancer Cells.	osimertinib	13-20	ATP binding cassette subfamily B member 1	Homo sapiens	67-72
27660466-3	2016	Osimertinib (AZD9291, Tagrisso ), an oral, third-generation EGFR TKI, has been designed to target the EGFR T790M mutation, while sparing wild-type EGFR.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	60-64
27660466-3	2016	Osimertinib (AZD9291, Tagrisso ), an oral, third-generation EGFR TKI, has been designed to target the EGFR T790M mutation, while sparing wild-type EGFR.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	102-106
27660466-3	2016	Osimertinib (AZD9291, Tagrisso ), an oral, third-generation EGFR TKI, has been designed to target the EGFR T790M mutation, while sparing wild-type EGFR.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	102-106
27044261-10	2016	Taken together, our results provide a potential mechanism for the sensitivity of EGFR(L858R/T790M) cells to AZD9291 and suggest that AZD9291 may be effective in cases of T790 M-positive EGFR resistance.	osimertinib	133-140	epidermal growth factor receptor	Homo sapiens	81-85
27177916-4	2016	Osimertinib (AZD9291) is a novel mono-anilino-pyrimidine third-generation EGFR TKI targeting both sensitizing and T790M EGFR-mutation which showed promising results in T790M-positive NSCLC.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	74-78
27177916-4	2016	Osimertinib (AZD9291) is a novel mono-anilino-pyrimidine third-generation EGFR TKI targeting both sensitizing and T790M EGFR-mutation which showed promising results in T790M-positive NSCLC.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	120-124
27044261-0	2016	AZD9291 overcomes T790 M-mediated resistance through degradation of EGFR(L858R/T790M) in non-small cell lung cancer cells.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	68-72
27196753-0	2016	Osimertinib (AZD9291) Enhanced the Efficacy of Chemotherapeutic Agents in ABCB1- and ABCG2-Overexpressing Cells In Vitro, In Vivo, and Ex Vivo.	osimertinib	13-20	ATP binding cassette subfamily B member 1	Homo sapiens	74-79
27044261-3	2016	Although AZD9291 is selective for both T790 M and activating EGFR mutations over wild-type EGFR, it is highly active when T790 M is present, especially EGFR(L858R/T790M), and modestly active when T790 M is absent.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	61-65
27044261-3	2016	Although AZD9291 is selective for both T790 M and activating EGFR mutations over wild-type EGFR, it is highly active when T790 M is present, especially EGFR(L858R/T790M), and modestly active when T790 M is absent.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	91-95
27044261-3	2016	Although AZD9291 is selective for both T790 M and activating EGFR mutations over wild-type EGFR, it is highly active when T790 M is present, especially EGFR(L858R/T790M), and modestly active when T790 M is absent.	osimertinib	9-16	epidermal growth factor receptor	Homo sapiens	91-95
27044261-4	2016	The aim of this study was to elucidate the underlying mechanism of the high sensitivity of NSCLC cells harboring EGFR(L858R/T790M) to AZD9291.	osimertinib	134-141	epidermal growth factor receptor	Homo sapiens	113-117
27044261-5	2016	In H1975 cells harboring EGFR(L858R/T790M), AZD9291 potently inhibited cellular growth and EGFR signaling pathways together with depletion of mutant EGFR protein.	osimertinib	44-51	epidermal growth factor receptor	Homo sapiens	25-29
27044261-5	2016	In H1975 cells harboring EGFR(L858R/T790M), AZD9291 potently inhibited cellular growth and EGFR signaling pathways together with depletion of mutant EGFR protein.	osimertinib	44-51	epidermal growth factor receptor	Homo sapiens	91-95
27044261-5	2016	In H1975 cells harboring EGFR(L858R/T790M), AZD9291 potently inhibited cellular growth and EGFR signaling pathways together with depletion of mutant EGFR protein.	osimertinib	44-51	epidermal growth factor receptor	Homo sapiens	91-95
27044261-6	2016	AZD9291-induced depletion of EGFR(L858R/T790M) protein was abrogated through inhibition of the proteasome with MG132.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	29-33
27044261-9	2016	Moreover, oral administration of AZD9291 as a single agent induced tumor regression in vivo in a H1975 tumor xenograft model and reduced EGFR(L858R/T790M) protein levels in xenograft tumors.	osimertinib	33-40	epidermal growth factor receptor	Homo sapiens	137-141
27044261-10	2016	Taken together, our results provide a potential mechanism for the sensitivity of EGFR(L858R/T790M) cells to AZD9291 and suggest that AZD9291 may be effective in cases of T790 M-positive EGFR resistance.	osimertinib	108-115	epidermal growth factor receptor	Homo sapiens	81-85
27393503-0	2016	Temporal changes of EGFR mutations and T790M levels in tumour and plasma DNA following AZD9291 treatment.	osimertinib	87-94	epidermal growth factor receptor	Homo sapiens	20-24
27393503-1	2016	AZD9291, a T790M specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has demonstrated impressive response rates in tumours harbouring the EGFR T790M resistance mutation.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	26-58
27393503-1	2016	AZD9291, a T790M specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has demonstrated impressive response rates in tumours harbouring the EGFR T790M resistance mutation.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	60-64
27393503-1	2016	AZD9291, a T790M specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has demonstrated impressive response rates in tumours harbouring the EGFR T790M resistance mutation.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	168-172
27393503-2	2016	Emergence of resistance to AZD9291 has been shown to occur through several different mechanisms including the development of new mutations (e.g. C797S) in the EGFR tyrosine kinase domain.	osimertinib	27-34	epidermal growth factor receptor	Homo sapiens	159-163
27393503-6	2016	In the first patient, both EGFR T790M and L858R became undetectable in the plasma within 1 month after treatment with AZD9291.	osimertinib	118-125	epidermal growth factor receptor	Homo sapiens	27-31
27196753-0	2016	Osimertinib (AZD9291) Enhanced the Efficacy of Chemotherapeutic Agents in ABCB1- and ABCG2-Overexpressing Cells In Vitro, In Vivo, and Ex Vivo.	osimertinib	13-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	85-90
27071706-6	2016	Osimertinib (AZD9291, TAGRISSO) was recently approved by FDA for metastatic EGFR T790M mutation-positive NSCLC.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	76-80
27448564-3	2016	AZD9291 (osimertinib, tagrisso) has been approved for treatment of the metastatic EGFR T790M mutation-positive non-small cell lung cancer.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	82-86
27169328-0	2016	Osimertinib (AZD9291) Attenuates the Function of Multidrug Resistance-Linked ATP-Binding Cassette Transporter ABCB1 in Vitro.	osimertinib	13-20	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
26902828-1	2016	PURPOSE: Osimertinib (AZD9291) 80 mg once daily is approved by the US FDA for the treatment of patients with metastatic EGFR T790M-positive NSCLC whose disease has previously progressed on EGFR-TKI therapy.	osimertinib	22-29	epidermal growth factor receptor	Homo sapiens	120-124
26749488-2	2016	Several third-generation EGFR-mutant selective TKI, such as AZD9291 (AstraZeneca), Rociletinib (Clovis), or HM61713 (Hanmi) have been developed.	osimertinib	60-67	epidermal growth factor receptor	Homo sapiens	25-29
26845230-1	2016	Mutant selective epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), such as rociletinib and AZD9291, are effective for tumors with T790M secondary mutation that become refractory to first-generation EGFR-TKI.	osimertinib	114-121	epidermal growth factor receptor	Homo sapiens	78-82
26845230-1	2016	Mutant selective epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), such as rociletinib and AZD9291, are effective for tumors with T790M secondary mutation that become refractory to first-generation EGFR-TKI.	osimertinib	114-121	epidermal growth factor receptor	Homo sapiens	221-225
26902828-1	2016	PURPOSE: Osimertinib (AZD9291) 80 mg once daily is approved by the US FDA for the treatment of patients with metastatic EGFR T790M-positive NSCLC whose disease has previously progressed on EGFR-TKI therapy.	osimertinib	22-29	epidermal growth factor receptor	Homo sapiens	189-193
26716903-0	2016	High efficacy of third generation EGFR inhibitor AZD9291 in a leptomeningeal carcinomatosis model with EGFR-mutant lung cancer cells.	osimertinib	49-56	epidermal growth factor receptor	Homo sapiens	34-38
26729184-1	2016	Osimertinib (Tagrisso( ), AZD9291) is an oral, third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) that is being developed by AstraZeneca for the treatment of advanced non-small cell lung cancer (NSCLC).	osimertinib	26-33	epidermal growth factor receptor	Homo sapiens	124-128
26958497-0	2016	AZD9291 in TKI EGFR resistance in non-small cell lung cancer and the new concept of phase I trials.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	15-19
26958497-8	2016	To date, however, only AZD9291, an oral, potent, irreversible EGFR TKI that is selective for EGFR tyrosine kinase inhibitor-sensitizing mutations and the T790M resistance mutation has shown to be not only highly active but also fairly tolerable in a large cohort of patients.	osimertinib	23-30	epidermal growth factor receptor	Homo sapiens	62-66
26958497-8	2016	To date, however, only AZD9291, an oral, potent, irreversible EGFR TKI that is selective for EGFR tyrosine kinase inhibitor-sensitizing mutations and the T790M resistance mutation has shown to be not only highly active but also fairly tolerable in a large cohort of patients.	osimertinib	23-30	epidermal growth factor receptor	Homo sapiens	93-97
26958499-0	2016	AZD9291 in epidermal growth factor receptor inhibitor-resistant non-small-cell lung cancer.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	11-43
26958499-3	2016	AZD9291 is a third generation irreversible EGFR TKI with activity against the activating EGFR mutation, the T790M acquired resistance mutation, and relative sparing of the wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	43-47
26958499-3	2016	AZD9291 is a third generation irreversible EGFR TKI with activity against the activating EGFR mutation, the T790M acquired resistance mutation, and relative sparing of the wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	89-93
26958499-3	2016	AZD9291 is a third generation irreversible EGFR TKI with activity against the activating EGFR mutation, the T790M acquired resistance mutation, and relative sparing of the wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	89-93
26958499-4	2016	AZD9291 was investigated in a phase I trial with expansion cohorts in patients with disease progression after EGFR TKI.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	110-114
26716903-0	2016	High efficacy of third generation EGFR inhibitor AZD9291 in a leptomeningeal carcinomatosis model with EGFR-mutant lung cancer cells.	osimertinib	49-56	epidermal growth factor receptor	Homo sapiens	103-107
26716903-6	2016	Moreover, treatment with a higher dose of AZD9291, also associated with inhibited phosphorylation of EGFR downstream molecule S6, regressed LMC refractory to the aforementioned EGFR-TKI treatments.	osimertinib	42-49	epidermal growth factor receptor	Homo sapiens	101-105
26716903-6	2016	Moreover, treatment with a higher dose of AZD9291, also associated with inhibited phosphorylation of EGFR downstream molecule S6, regressed LMC refractory to the aforementioned EGFR-TKI treatments.	osimertinib	42-49	epidermal growth factor receptor	Homo sapiens	177-181
26716903-7	2016	These observations suggest that the third generation EGFR-TKI AZD9291 may be an effective treatment for first or second generation EGFR-TKI resistant LMC caused by EGFR-mutant lung cancer.	osimertinib	62-69	epidermal growth factor receptor	Homo sapiens	53-57
26716903-7	2016	These observations suggest that the third generation EGFR-TKI AZD9291 may be an effective treatment for first or second generation EGFR-TKI resistant LMC caused by EGFR-mutant lung cancer.	osimertinib	62-69	epidermal growth factor receptor	Homo sapiens	131-135
26716903-7	2016	These observations suggest that the third generation EGFR-TKI AZD9291 may be an effective treatment for first or second generation EGFR-TKI resistant LMC caused by EGFR-mutant lung cancer.	osimertinib	62-69	epidermal growth factor receptor	Homo sapiens	131-135
26744526-7	2016	ALW-II-41-27 was also effective in decreasing viability of cells with acquired resistance to the third-generation EGFR TKI AZD9291.	osimertinib	123-130	epidermal growth factor receptor	Homo sapiens	114-118
26612314-0	2016	Rapid clearance of circulating tumor DNA during treatment with AZD9291 of a lung cancer patient presenting the resistance EGFR T790M mutation.	osimertinib	63-70	epidermal growth factor receptor	Homo sapiens	122-126
26775573-5	2016	Third generation EGFR inhibitors (rociletinib, AZD9291) are effective for patients who develop a resistance mutation such as T790M resistance mutation; they obtained temporary authorization for use in France in 2015.	osimertinib	47-54	epidermal growth factor receptor	Homo sapiens	17-21
26762749-0	2016	Two Cases of Small Cell Lung Cancer Transformation from EGFR Mutant Adenocarcinoma During AZD9291 Treatment.	osimertinib	90-97	epidermal growth factor receptor	Homo sapiens	56-60
27486808-1	2016	BACKGROUND: Osimertinib (AZD9291, Tagrisso) is a potent, irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	87-119
27486808-1	2016	BACKGROUND: Osimertinib (AZD9291, Tagrisso) is a potent, irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI).	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	121-125
26473643-0	2015	Mechanisms of Acquired Resistance to AZD9291: A Mutation-Selective, Irreversible EGFR Inhibitor.	osimertinib	37-44	epidermal growth factor receptor	Homo sapiens	81-85
26522274-0	2015	Binding mode of the breakthrough inhibitor AZD9291 to epidermal growth factor receptor revealed.	osimertinib	43-50	epidermal growth factor receptor	Homo sapiens	54-86
26522274-4	2015	One such agent is AstraZeneca"s "breakthrough" AZD9291 molecule that shows a 200-fold selectivity for T790M/L858R over wild type EGFR.	osimertinib	47-54	epidermal growth factor receptor	Homo sapiens	129-133
26522274-5	2015	Our X-ray crystal structure reveals the binding mode of AZD9291 to the kinase domain of wild type EGFR.	osimertinib	56-63	epidermal growth factor receptor	Homo sapiens	98-102
26473643-1	2015	INTRODUCTION: AZD9291, a third-generation and mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is active against patients with EGFR-mutant non-small-cell lung cancer (NSCLC) who failed prior treatment with EGFR TKIs.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	65-97
26473643-1	2015	INTRODUCTION: AZD9291, a third-generation and mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is active against patients with EGFR-mutant non-small-cell lung cancer (NSCLC) who failed prior treatment with EGFR TKIs.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	99-103
26473643-1	2015	INTRODUCTION: AZD9291, a third-generation and mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is active against patients with EGFR-mutant non-small-cell lung cancer (NSCLC) who failed prior treatment with EGFR TKIs.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	170-174
26473643-1	2015	INTRODUCTION: AZD9291, a third-generation and mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is active against patients with EGFR-mutant non-small-cell lung cancer (NSCLC) who failed prior treatment with EGFR TKIs.	osimertinib	14-21	epidermal growth factor receptor	Homo sapiens	170-174
26473643-3	2015	In this study, we identified the mechanisms of acquired resistance to AZD9291 in EGFR-mutant NSCLC.	osimertinib	70-77	epidermal growth factor receptor	Homo sapiens	81-85
26473643-4	2015	METHODS: Four NSCLC patients with both an EGFR exon 19 deletion and the EGFR mutation after developing acquired resistance to first-generation EGFR TKIs received AZD9291 at doses of 20 to 80 mg/day in a phase I trial (NCT01802632).	osimertinib	162-169	epidermal growth factor receptor	Homo sapiens	72-76
26473643-4	2015	METHODS: Four NSCLC patients with both an EGFR exon 19 deletion and the EGFR mutation after developing acquired resistance to first-generation EGFR TKIs received AZD9291 at doses of 20 to 80 mg/day in a phase I trial (NCT01802632).	osimertinib	162-169	epidermal growth factor receptor	Homo sapiens	72-76
26473643-8	2015	EGFR-mutant clones depopulated AZD9291-resistant tumors to below 1% (baseline, 14%-36%) in three patients with progression: one with the loss of EGFR-double mutant clones and two accompanied by transformation to small-cell carcinoma and focal fibroblast growth factor receptor 1 (FGFR1) amplification, respectively.	osimertinib	31-38	epidermal growth factor receptor	Homo sapiens	0-4
26473643-8	2015	EGFR-mutant clones depopulated AZD9291-resistant tumors to below 1% (baseline, 14%-36%) in three patients with progression: one with the loss of EGFR-double mutant clones and two accompanied by transformation to small-cell carcinoma and focal fibroblast growth factor receptor 1 (FGFR1) amplification, respectively.	osimertinib	31-38	fibroblast growth factor receptor 1	Homo sapiens	243-278
26473643-8	2015	EGFR-mutant clones depopulated AZD9291-resistant tumors to below 1% (baseline, 14%-36%) in three patients with progression: one with the loss of EGFR-double mutant clones and two accompanied by transformation to small-cell carcinoma and focal fibroblast growth factor receptor 1 (FGFR1) amplification, respectively.	osimertinib	31-38	fibroblast growth factor receptor 1	Homo sapiens	280-285
26473643-9	2015	EGFR-mutant clones remained and the EGFR ligand was overexpressed in one patient with focal progression to AZD9291.	osimertinib	107-114	epidermal growth factor receptor	Homo sapiens	36-40
26473643-10	2015	CONCLUSION: Acquired resistance mechanisms of AZD9291 in patients with EGFR-mutant NSCLC who failed treatment with first-generation EGFR TKIs include the loss of EGFR-mutant clones plus alternative pathway activation or histologic transformation and EGFR ligand-dependent activation.	osimertinib	46-53	epidermal growth factor receptor	Homo sapiens	71-75
26473643-10	2015	CONCLUSION: Acquired resistance mechanisms of AZD9291 in patients with EGFR-mutant NSCLC who failed treatment with first-generation EGFR TKIs include the loss of EGFR-mutant clones plus alternative pathway activation or histologic transformation and EGFR ligand-dependent activation.	osimertinib	46-53	epidermal growth factor receptor	Homo sapiens	132-136
26473643-10	2015	CONCLUSION: Acquired resistance mechanisms of AZD9291 in patients with EGFR-mutant NSCLC who failed treatment with first-generation EGFR TKIs include the loss of EGFR-mutant clones plus alternative pathway activation or histologic transformation and EGFR ligand-dependent activation.	osimertinib	46-53	epidermal growth factor receptor	Homo sapiens	132-136
26494259-0	2015	EGFR mutation detection in ctDNA from NSCLC patient plasma: A cross-platform comparison of leading technologies to support the clinical development of AZD9291.	osimertinib	151-158	epidermal growth factor receptor	Homo sapiens	0-4
26494259-3	2015	Plasma samples were collected from patients entering the ongoing AURA trial (NCT01802632), investigating the safety, tolerability, and efficacy of AZD9291 in patients with EGFR-sensitizing mutation-positive NSCLC.	osimertinib	147-154	epidermal growth factor receptor	Homo sapiens	172-176
26473643-10	2015	CONCLUSION: Acquired resistance mechanisms of AZD9291 in patients with EGFR-mutant NSCLC who failed treatment with first-generation EGFR TKIs include the loss of EGFR-mutant clones plus alternative pathway activation or histologic transformation and EGFR ligand-dependent activation.	osimertinib	46-53	epidermal growth factor receptor	Homo sapiens	132-136
25806323-0	2014	Clinical activity of the mutant-selective EGFR inhibitor AZD9291 in patients with EGFR inhibitor-resistant non-small cell lung cancer.	osimertinib	57-64	epidermal growth factor receptor	Homo sapiens	42-46
26798593-6	2015	Two new studies have shown that two covalent pyrimidine inhibitors-AZD9291 and rociletinib of EGFR-T790M (i.e., third generation EGFR TKIs) shown remarkable clinical activity in patients with acquired resistance to erlotinib, gefitinib and afatinib when the tumor carries EGFR-T790M in conjunction with an activating mutation.	osimertinib	67-74	epidermal growth factor receptor	Homo sapiens	94-98
26798593-6	2015	Two new studies have shown that two covalent pyrimidine inhibitors-AZD9291 and rociletinib of EGFR-T790M (i.e., third generation EGFR TKIs) shown remarkable clinical activity in patients with acquired resistance to erlotinib, gefitinib and afatinib when the tumor carries EGFR-T790M in conjunction with an activating mutation.	osimertinib	67-74	epidermal growth factor receptor	Homo sapiens	129-133
26798593-6	2015	Two new studies have shown that two covalent pyrimidine inhibitors-AZD9291 and rociletinib of EGFR-T790M (i.e., third generation EGFR TKIs) shown remarkable clinical activity in patients with acquired resistance to erlotinib, gefitinib and afatinib when the tumor carries EGFR-T790M in conjunction with an activating mutation.	osimertinib	67-74	epidermal growth factor receptor	Homo sapiens	129-133
26450446-0	2015	AZD9291 in EGFR-mutant advanced non-small-cell lung cancer patients.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	11-15
26450446-3	2015	AZD9291 is an oral, irreversible, mutant-selective EGF receptor (EGFR) tyrosine kinase inhibitor (TKI) developed to have potency against EGFR mutations, including T790M mutation, while sparing wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	51-63
26450446-3	2015	AZD9291 is an oral, irreversible, mutant-selective EGF receptor (EGFR) tyrosine kinase inhibitor (TKI) developed to have potency against EGFR mutations, including T790M mutation, while sparing wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	65-69
26450446-3	2015	AZD9291 is an oral, irreversible, mutant-selective EGF receptor (EGFR) tyrosine kinase inhibitor (TKI) developed to have potency against EGFR mutations, including T790M mutation, while sparing wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	137-141
26450446-3	2015	AZD9291 is an oral, irreversible, mutant-selective EGF receptor (EGFR) tyrosine kinase inhibitor (TKI) developed to have potency against EGFR mutations, including T790M mutation, while sparing wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	137-141
26450446-4	2015	A Phase I trial of AZD9291 in EGFR-mutant NSCLC patients, demonstrated high activity, essentially among T790M-mutant tumors, with a manageable tolerability profile.	osimertinib	19-26	epidermal growth factor receptor	Homo sapiens	30-34
26450446-5	2015	Ongoing Phase III trials are evaluating AZD9291 in EGFR-mutant patients as first-line treatment compared with erlotinib and gefitinib; and as second-line treatment compared with chemotherapy after progression on EGFR TKI in T790M-mutant tumors.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	51-55
26269204-0	2015	EGFR-independent mechanisms of acquired resistance to AZD9291 in EGFR T790M-positive NSCLC patients.	osimertinib	54-61	epidermal growth factor receptor	Homo sapiens	0-4
26269204-0	2015	EGFR-independent mechanisms of acquired resistance to AZD9291 in EGFR T790M-positive NSCLC patients.	osimertinib	54-61	epidermal growth factor receptor	Homo sapiens	65-69
26269204-1	2015	BACKGROUND: AZD9291 is an oral, irreversible, mutant-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKI), which specifically targets both sensitizing and resistant T790M mutations.	osimertinib	12-19	epidermal growth factor receptor	Homo sapiens	63-95
26269204-1	2015	BACKGROUND: AZD9291 is an oral, irreversible, mutant-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKI), which specifically targets both sensitizing and resistant T790M mutations.	osimertinib	12-19	epidermal growth factor receptor	Homo sapiens	97-101
26269204-1	2015	BACKGROUND: AZD9291 is an oral, irreversible, mutant-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKI), which specifically targets both sensitizing and resistant T790M mutations.	osimertinib	12-19	epidermal growth factor receptor	Homo sapiens	131-135
26269204-4	2015	Mutations at the EGFR C797 codon, located within the kinase-binding site, were very recently reported to be a potential mechanism of resistance to AZD9291 in T790M-positive patients.	osimertinib	147-154	epidermal growth factor receptor	Homo sapiens	17-21
25948633-1	2015	PURPOSE: Mutant selective irreversible pyrimidine-based EGFR kinase inhibitors, including WZ4002, CO-1686, and AZD9291, are effective in preclinical models and in lung cancer patients harboring the EGFR T790M gefitinib/erlotinib resistance mutation.	osimertinib	111-118	epidermal growth factor receptor	Homo sapiens	56-60
25948633-1	2015	PURPOSE: Mutant selective irreversible pyrimidine-based EGFR kinase inhibitors, including WZ4002, CO-1686, and AZD9291, are effective in preclinical models and in lung cancer patients harboring the EGFR T790M gefitinib/erlotinib resistance mutation.	osimertinib	111-118	epidermal growth factor receptor	Homo sapiens	198-202
25948633-7	2015	EGFR L718Q, L844V, and C797S cause resistance to both WZ4002 and CO-1686 while, in contrast, only EGFR C797S leads to AZD9291 resistance.	osimertinib	118-125	epidermal growth factor receptor	Homo sapiens	0-4
25948633-7	2015	EGFR L718Q, L844V, and C797S cause resistance to both WZ4002 and CO-1686 while, in contrast, only EGFR C797S leads to AZD9291 resistance.	osimertinib	118-125	epidermal growth factor receptor	Homo sapiens	98-102
26370354-8	2015	Third-generation EGFR-mutant-selective TKIs, such as AZD9291 or rociletininb, which target Thr790Met-mutant tumours, the most common mechanism of EGFR TKI resistance, have entered clinical trials, and exciting, albeit preliminary, efficacy data have been reported.	osimertinib	53-60	epidermal growth factor receptor	Homo sapiens	17-21
26370354-8	2015	Third-generation EGFR-mutant-selective TKIs, such as AZD9291 or rociletininb, which target Thr790Met-mutant tumours, the most common mechanism of EGFR TKI resistance, have entered clinical trials, and exciting, albeit preliminary, efficacy data have been reported.	osimertinib	53-60	epidermal growth factor receptor	Homo sapiens	146-150
25477325-6	2015	Using a panel of erlotinib/afatinib-resistant cells, including a novel patient-derived cell line (VP-2), we found that AZD9291 was more potent than A+C at inhibiting cell growth and EGFR signaling in this setting.	osimertinib	119-126	epidermal growth factor receptor	Homo sapiens	182-186
26629426-5	2015	Two EGFR TKIs targeting T790M, AZD9291 and rociletinib, are new active treatment options for NSCLC but differ in adverse effect profiles.	osimertinib	31-38	epidermal growth factor receptor	Homo sapiens	4-8
25870145-0	2015	Acquired Resistance to the Mutant-Selective EGFR Inhibitor AZD9291 Is Associated with Increased Dependence on RAS Signaling in Preclinical Models.	osimertinib	59-66	epidermal growth factor receptor	Homo sapiens	44-48
25870145-3	2015	We describe the detection of heterogeneous mechanisms of resistance within populations of EGFR-mutant cells (PC9 and/or NCI-H1975) with acquired resistance to current and newly developed EGFR tyrosine kinase inhibitors, including AZD9291.	osimertinib	230-237	epidermal growth factor receptor	Homo sapiens	90-94
25870145-4	2015	We report the detection of NRAS mutations, including a novel E63K mutation, and a gain of copy number of WT NRAS or WT KRAS in cell populations resistant to gefitinib, afatinib, WZ4002, or AZD9291.	osimertinib	189-196	NRAS proto-oncogene, GTPase	Homo sapiens	108-112
25870145-6	2015	In vitro, a combination of AZD9291 with selumetinib prevented emergence of resistance in PC9 cells and delayed resistance in NCI-H1975 cells.	osimertinib	27-34	proprotein convertase subtilisin/kexin type 9	Homo sapiens	89-92
25870145-8	2015	Our data support the use of a combination of AZD9291 with a MEK inhibitor to delay or prevent resistance to AZD9291 in EGFRm and/or EGFRm/T790M tumors.	osimertinib	108-115	mitogen-activated protein kinase kinase 7	Homo sapiens	60-63
25939061-0	2015	Acquired EGFR C797S mutation mediates resistance to AZD9291 in non-small cell lung cancer harboring EGFR T790M.	osimertinib	52-59	epidermal growth factor receptor	Homo sapiens	9-13
25939061-0	2015	Acquired EGFR C797S mutation mediates resistance to AZD9291 in non-small cell lung cancer harboring EGFR T790M.	osimertinib	52-59	epidermal growth factor receptor	Homo sapiens	100-104
25939061-1	2015	Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291.	osimertinib	212-219	epidermal growth factor receptor	Homo sapiens	140-172
25939061-1	2015	Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291.	osimertinib	212-219	epidermal growth factor receptor	Homo sapiens	174-178
25939061-2	2015	We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291.	osimertinib	209-216	epidermal growth factor receptor	Homo sapiens	154-158
25979928-6	2015	More recently, drugs that target EGFR T790M (e.g., rociletinib, AZD9291, and others) have entered clinical trials, with impressive results observed in phase I clinical trials.	osimertinib	64-71	epidermal growth factor receptor	Homo sapiens	33-37
25923549-0	2015	AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	11-15
25923549-2	2015	In preclinical models, the EGFR inhibitor AZD9291 has been shown to be effective against both EGFR tyrosine kinase inhibitor-sensitizing and T790M resistance mutations.	osimertinib	42-49	epidermal growth factor receptor	Homo sapiens	27-31
25923549-2	2015	In preclinical models, the EGFR inhibitor AZD9291 has been shown to be effective against both EGFR tyrosine kinase inhibitor-sensitizing and T790M resistance mutations.	osimertinib	42-49	epidermal growth factor receptor	Homo sapiens	94-98
25923549-3	2015	METHODS: We administered AZD9291 at doses of 20 to 240 mg once daily in patients with advanced lung cancer who had radiologically documented disease progression after previous treatment with EGFR tyrosine kinase inhibitors.	osimertinib	25-32	epidermal growth factor receptor	Homo sapiens	191-195
25923549-15	2015	CONCLUSIONS: AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	77-81
25923549-15	2015	CONCLUSIONS: AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors.	osimertinib	13-20	epidermal growth factor receptor	Homo sapiens	155-159
25936890-9	2015	EGFR inhibitors specifically targeting T790M resistance mutations (AZD9291, CO-1686, HM61713) are in the early stages of development.	osimertinib	67-74	epidermal growth factor receptor	Homo sapiens	0-4
25611025-7	2015	Third-generation EGFR-TKIs, AZD9291, CO-1686, and HM61713, inhibit both EGFR activating and resistance mutations, while sparing wild-type EGFR.	osimertinib	28-35	epidermal growth factor receptor	Homo sapiens	17-21
25611025-7	2015	Third-generation EGFR-TKIs, AZD9291, CO-1686, and HM61713, inhibit both EGFR activating and resistance mutations, while sparing wild-type EGFR.	osimertinib	28-35	epidermal growth factor receptor	Homo sapiens	72-76
25611025-7	2015	Third-generation EGFR-TKIs, AZD9291, CO-1686, and HM61713, inhibit both EGFR activating and resistance mutations, while sparing wild-type EGFR.	osimertinib	28-35	epidermal growth factor receptor	Homo sapiens	72-76
25806323-0	2014	Clinical activity of the mutant-selective EGFR inhibitor AZD9291 in patients with EGFR inhibitor-resistant non-small cell lung cancer.	osimertinib	57-64	epidermal growth factor receptor	Homo sapiens	82-86
25806323-6	2014	AZD9291, as a mono-anilino-pyrimidine compound, is a novel, irreversible EGFR-TKI, has proved to be more effective against both EGFR-TKI sensitizing and resistance T790M mutations in preclinical models.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	73-77
25806323-6	2014	AZD9291, as a mono-anilino-pyrimidine compound, is a novel, irreversible EGFR-TKI, has proved to be more effective against both EGFR-TKI sensitizing and resistance T790M mutations in preclinical models.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	128-132
25806323-7	2014	This phase I clinical study showed that AZD9291 has robust efficacy and is well tolerated in EGFR mutant NSCLC patients with acquired resistance to EGFR-TKIs.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	93-97
25806323-7	2014	This phase I clinical study showed that AZD9291 has robust efficacy and is well tolerated in EGFR mutant NSCLC patients with acquired resistance to EGFR-TKIs.	osimertinib	40-47	epidermal growth factor receptor	Homo sapiens	148-152
24893891-0	2014	AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	25-29
25296354-9	2014	Ongoing preclinical efforts for treating resistance have started to translate into patient care (including clinical trials of the covalent EGFR-T790M TKIs AZD9291 and CO-1686) and hold promise to further boost the median survival of patients with EGFR mutated NSCLC.	osimertinib	155-162	epidermal growth factor receptor	Homo sapiens	139-143
25296354-9	2014	Ongoing preclinical efforts for treating resistance have started to translate into patient care (including clinical trials of the covalent EGFR-T790M TKIs AZD9291 and CO-1686) and hold promise to further boost the median survival of patients with EGFR mutated NSCLC.	osimertinib	155-162	epidermal growth factor receptor	Homo sapiens	247-251
25271963-0	2014	Discovery of a potent and selective EGFR inhibitor (AZD9291) of both sensitizing and T790M resistance mutations that spares the wild type form of the receptor.	osimertinib	52-59	epidermal growth factor receptor	Homo sapiens	36-40
25271963-5	2014	We describe herein the evolution of an early, mutant selective lead to the clinical candidate AZD9291, an irreversible inhibitor of both EGFR sensitizing (EGFRm+) and T790M resistance mutations with selectivity over the wild type form of the receptor.	osimertinib	94-101	epidermal growth factor receptor	Homo sapiens	137-141
25027951-8	2014	Mutant-selective EGFR inhibitors (AZD9291, CO-1686, HM61713) that specifically target the T790M resistance mutation are in early development.	osimertinib	34-41	epidermal growth factor receptor	Homo sapiens	17-21
24893891-0	2014	AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	74-78
24893891-3	2014	AZD9291 is a novel oral, potent, and selective third-generation irreversible inhibitor of both EGFRm(+) sensitizing and T790M resistance mutants that spares wild-type EGFR.	osimertinib	0-7	epidermal growth factor receptor	Homo sapiens	95-99
24893891-7	2014	SIGNIFICANCE: We report the development of a novel structurally distinct third-generation EGFR TKI, AZD9291, that irreversibly and selectively targets both sensitizing and resistant T790M(+) mutant EGFR while harboring less activity toward wild-type EGFR.	osimertinib	100-107	epidermal growth factor receptor	Homo sapiens	90-94
24893891-7	2014	SIGNIFICANCE: We report the development of a novel structurally distinct third-generation EGFR TKI, AZD9291, that irreversibly and selectively targets both sensitizing and resistant T790M(+) mutant EGFR while harboring less activity toward wild-type EGFR.	osimertinib	100-107	epidermal growth factor receptor	Homo sapiens	198-202
24893891-7	2014	SIGNIFICANCE: We report the development of a novel structurally distinct third-generation EGFR TKI, AZD9291, that irreversibly and selectively targets both sensitizing and resistant T790M(+) mutant EGFR while harboring less activity toward wild-type EGFR.	osimertinib	100-107	epidermal growth factor receptor	Homo sapiens	198-202
25841416-4	2014	This article compares and contrasts the discovery and development of gefitinib-the first EGFR tyrosine kinase inhibitor and AZD9291, an irreversible inhibitor of both sensitizing and resistant mutated EGFR.	osimertinib	124-131	epidermal growth factor receptor	Homo sapiens	201-205