PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28029918-2	2016	METHODS: We conducted a phase 1 trial of selumetinib (AZD6244 or ARRY-142886), an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibromatosis type 1 and inoperable plexiform neurofibromas to determine the maximum tolerated dose and to evaluate plasma pharmacokinetics.	AZD 6244	41-52	mitogen-activated protein kinase kinase 1	Homo sapiens	110-135
28029918-2	2016	METHODS: We conducted a phase 1 trial of selumetinib (AZD6244 or ARRY-142886), an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibromatosis type 1 and inoperable plexiform neurofibromas to determine the maximum tolerated dose and to evaluate plasma pharmacokinetics.	AZD 6244	41-52	neurofibromin 1	Homo sapiens	157-181
28029918-2	2016	METHODS: We conducted a phase 1 trial of selumetinib (AZD6244 or ARRY-142886), an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibromatosis type 1 and inoperable plexiform neurofibromas to determine the maximum tolerated dose and to evaluate plasma pharmacokinetics.	AZD 6244	65-76	mitogen-activated protein kinase kinase 1	Homo sapiens	110-135
28029918-14	2016	CONCLUSIONS: Our early-phase data suggested that children with neurofibromatosis type 1 and inoperable plexiform neurofibromas benefited from long-term dose-adjusted treatment with selumetinib without having excess toxic effects.	AZD 6244	181-192	neurofibromin 1	Homo sapiens	63-87
27769200-2	2016	Selumetinib is an allosteric, ATP-noncompetitive inhibitor of MEK1/2, which has benn known as effective antineoplastic drugs for several malignant tumors.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	62-68
27670699-6	2016	We show that inhibition of ERK1/2 activation using selumetinib efficiently inhibits the growth of lung SCC with TRA2B-DNAH5 fusion expression.	AZD 6244	51-62	mitogen-activated protein kinase 3	Homo sapiens	27-33
27670699-6	2016	We show that inhibition of ERK1/2 activation using selumetinib efficiently inhibits the growth of lung SCC with TRA2B-DNAH5 fusion expression.	AZD 6244	51-62	serpin family B member 3	Homo sapiens	103-106
27670699-6	2016	We show that inhibition of ERK1/2 activation using selumetinib efficiently inhibits the growth of lung SCC with TRA2B-DNAH5 fusion expression.	AZD 6244	51-62	transformer 2 beta homolog	Homo sapiens	112-117
27670699-6	2016	We show that inhibition of ERK1/2 activation using selumetinib efficiently inhibits the growth of lung SCC with TRA2B-DNAH5 fusion expression.	AZD 6244	51-62	dynein axonemal heavy chain 5	Homo sapiens	118-123
27837934-1	2016	PURPOSE: Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective allosteric mitogen-activated protein kinase 1/2 inhibitor with a short t1/2.	AZD 6244	9-20	mitogen-activated protein kinase 12	Homo sapiens	89-125
27837934-1	2016	PURPOSE: Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective allosteric mitogen-activated protein kinase 1/2 inhibitor with a short t1/2.	AZD 6244	22-29	mitogen-activated protein kinase 12	Homo sapiens	89-125
27751676-0	2016	Metabolism, Excretion, and Pharmacokinetics of Selumetinib, an MEK1/2 inhibitor, in Healthy Adult Male Subjects.	AZD 6244	47-58	mitogen-activated protein kinase kinase 1	Homo sapiens	63-69
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	74-80
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	172-176
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	74-80
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	13-20	KRAS proto-oncogene, GTPase	Homo sapiens	172-176
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	74-80
27467210-3	2016	Selumetinib (AZD6244, ARRY-142886) is a potent and selective inhibitor of MEK1/2 which has demonstrated significant efficacy in combination with docetaxel in patients with KRAS mutant pretreated advanced NSCLC.	AZD 6244	22-33	KRAS proto-oncogene, GTPase	Homo sapiens	172-176
27669459-5	2016	Although the MEK inhibitor selumetinib transiently inhibited ERK signaling, which subsequently rebounded, the MEK inhibitor CKI suppressed ERK signaling in a sustained manner by preventing RAF reactivation.	AZD 6244	27-38	mitogen-activated protein kinase 1	Mus musculus	61-64
27576686-4	2016	We found that several MEK inhibitors including MEK162, AZD6244, and PD0325901 effectively decreased DR4 protein levels including cell surface DR4 in different cancer cell lines.	AZD 6244	55-62	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
27576686-4	2016	We found that several MEK inhibitors including MEK162, AZD6244, and PD0325901 effectively decreased DR4 protein levels including cell surface DR4 in different cancer cell lines.	AZD 6244	55-62	TNF receptor superfamily member 10a	Homo sapiens	100-103
27576686-4	2016	We found that several MEK inhibitors including MEK162, AZD6244, and PD0325901 effectively decreased DR4 protein levels including cell surface DR4 in different cancer cell lines.	AZD 6244	55-62	TNF receptor superfamily member 10a	Homo sapiens	142-145
27713506-10	2016	Therefore, we suggest that clinical use of a combination of the MEK/ERK inhibitor AZD6244 and cisplatin might improve sensitivity to cisplatin-based chemotherapy and outcomes in NSCLC patients who harbor high-PAK1-expressing tumors.	AZD 6244	82-89	mitogen-activated protein kinase kinase 7	Homo sapiens	64-67
27713506-10	2016	Therefore, we suggest that clinical use of a combination of the MEK/ERK inhibitor AZD6244 and cisplatin might improve sensitivity to cisplatin-based chemotherapy and outcomes in NSCLC patients who harbor high-PAK1-expressing tumors.	AZD 6244	82-89	mitogen-activated protein kinase 1	Homo sapiens	68-71
27713506-10	2016	Therefore, we suggest that clinical use of a combination of the MEK/ERK inhibitor AZD6244 and cisplatin might improve sensitivity to cisplatin-based chemotherapy and outcomes in NSCLC patients who harbor high-PAK1-expressing tumors.	AZD 6244	82-89	p21 (RAC1) activated kinase 1	Homo sapiens	209-213
27422710-3	2016	To determine whether additional adaptive resistance mechanisms may coexist, we characterized global phosphoproteomic changes after MEK inhibitor selumetinib (AZD6244) treatment in KRAS-mutant A427 and A549 lung adenocarcinoma cell lines employing mass spectrometry-based phosphoproteomics.	AZD 6244	145-156	mitogen-activated protein kinase kinase 7	Homo sapiens	131-134
27422710-3	2016	To determine whether additional adaptive resistance mechanisms may coexist, we characterized global phosphoproteomic changes after MEK inhibitor selumetinib (AZD6244) treatment in KRAS-mutant A427 and A549 lung adenocarcinoma cell lines employing mass spectrometry-based phosphoproteomics.	AZD 6244	145-156	KRAS proto-oncogene, GTPase	Homo sapiens	180-184
27422710-5	2016	Selumetinib increased phosphorylation of KSR-1, a scaffolding protein required for assembly of MAPK signaling complex, as well as altered phosphorylation of GEF-H1, a novel regulator of KSR-1 and implicated in RAS-driven MAPK activation.	AZD 6244	0-11	kinase suppressor of ras 1	Homo sapiens	41-46
27422710-5	2016	Selumetinib increased phosphorylation of KSR-1, a scaffolding protein required for assembly of MAPK signaling complex, as well as altered phosphorylation of GEF-H1, a novel regulator of KSR-1 and implicated in RAS-driven MAPK activation.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	95-99
27422710-6	2016	Moreover, selumetinib reduced inhibitory serine phosphorylation of MET at Ser985 and potentiated HGF- and EGF-induced AKT phosphorylation.	AZD 6244	10-21	AKT serine/threonine kinase 1	Homo sapiens	118-121
27769200-8	2016	Moreover, after transfection, the antagomir of miR-302a and CUL1 over-expressed plasmid into HCC1937 and MDA-MB-231 cell accompanied with the Selumetinib treatment, we detected the proliferation and migration again.	AZD 6244	142-153	microRNA 302a	Homo sapiens	47-55
27769200-8	2016	Moreover, after transfection, the antagomir of miR-302a and CUL1 over-expressed plasmid into HCC1937 and MDA-MB-231 cell accompanied with the Selumetinib treatment, we detected the proliferation and migration again.	AZD 6244	142-153	cullin 1	Homo sapiens	60-64
27769200-12	2016	As soon as we knockdown miR-302a and over-expression CUL1 in TNBC cells, the cytotoxicity of Selumetinib was reversed.	AZD 6244	93-104	microRNA 302a	Homo sapiens	24-32
27769200-12	2016	As soon as we knockdown miR-302a and over-expression CUL1 in TNBC cells, the cytotoxicity of Selumetinib was reversed.	AZD 6244	93-104	cullin 1	Homo sapiens	53-57
27769200-13	2016	CONCLUSIONS: MiR-302a targeted regulated the CUL1 expression and mediated the Selumetinib-induced cytotoxicity of triple-negative breast cancer.	AZD 6244	78-89	myosin regulatory light chain interacting protein	Homo sapiens	13-16
27469379-5	2016	Selumetinib, a MEK1/2 inhibitor, demonstrates promising efficacy in women with relapsed low-grade serous carcinoma, and further trials of MEK-inhibition are underway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	15-21
27523799-1	2016	AIM: Selumetinib is an inhibitor of MEK1/2 in Phase III development that has activity in multiple tumor types.	AZD 6244	5-16	mitogen-activated protein kinase kinase 1	Homo sapiens	36-42
27168466-8	2016	Viable iAMP21 cells from primary xenografts showed reduced viability in response to the MEK1/2 inhibitor, selumetinib, in vitro.	AZD 6244	106-117	mitogen-activated protein kinase kinase 1	Homo sapiens	88-94
27494873-5	2016	However, addition of a MEK1/2 inhibitor, selumetinib, to LDN-193189-treated cells resulted in significant inhibition of cell growth and induction of cell death.	AZD 6244	41-52	mitogen-activated protein kinase kinase 1	Homo sapiens	23-29
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	mitogen-activated protein kinase kinase 7	Homo sapiens	55-58
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	epidermal growth factor receptor	Homo sapiens	164-168
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	epidermal growth factor receptor	Homo sapiens	190-194
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	231-236
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	epidermal growth factor receptor	Homo sapiens	190-194
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	319-324
27015352-5	2016	The expression of MT-1G messenger RNA and protein is remarkably induced by sorafenib but not other clinically relevant kinase inhibitors (e.g., erlotinib, gefitinib, tivantinib, vemurafenib, selumetinib, imatinib, masitinib, and ponatinib).	AZD 6244	191-202	metallothionein 1G	Homo sapiens	18-23
27438013-0	2016	Selumetinib, an Oral Anti-Neoplastic Drug, May Attenuate Cardiac Hypertrophy via Targeting the ERK Pathway.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	95-98
27438013-2	2016	Selumetinib is a novel oral MEK inhibitor that is currently under Phase II and Phase III clinical investigation for advanced solid tumors.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	28-31
27438013-3	2016	In this study, we investigated whether Selumetinib could inhibit the aberrant ERK activation of the heart in response to stress as well as prevent cardiac hypertrophy.	AZD 6244	39-50	mitogen-activated protein kinase 1	Homo sapiens	78-81
27438013-4	2016	METHODS AND RESULTS: In an in vitro model of PE-induced cardiac hypertrophy, Selumetinib significantly inhibited the ERK activation and prevented enlargement of cardiomyocytes or reactivation of certain fetal genes.	AZD 6244	77-88	mitogen-activated protein kinase 1	Homo sapiens	117-120
27438013-5	2016	In the pathologic cardiac hypertrophy model of ascending aortic constriction, Selumetinib provided significant ERK inhibition in the stressed heart but not in the other organs.	AZD 6244	78-89	mitogen-activated protein kinase 1	Homo sapiens	111-114
27438013-8	2016	CONCLUSIONS: Selumetinib, a novel oral anti-cancer drug with good safety records in a number of Phase II clinical trials, can inhibit ERK activity in the heart and prevent cardiac hypertrophy.	AZD 6244	13-24	mitogen-activated protein kinase 1	Homo sapiens	134-137
27287717-7	2016	In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenograft tumor growth of NSCLC cells harboring activating EGFR mutations, including EGFR(T790M) Overall, our findings define IKBKE as a direct effector target of EGFR and provide a therapeutic rationale to target IKBKE as a strategy to eradicate EGFR-TKI-resistant NSCLC cells.	AZD 6244	69-76	epidermal growth factor receptor	Homo sapiens	190-194
27469379-5	2016	Selumetinib, a MEK1/2 inhibitor, demonstrates promising efficacy in women with relapsed low-grade serous carcinoma, and further trials of MEK-inhibition are underway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	15-18
27044592-5	2016	MEK inhibition with selumetinib has been evaluated as a therapeutic strategy in metastatic uveal melanoma.	AZD 6244	20-31	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
27100819-11	2016	While there has been limited success in inhibiting the protein directly, phase 2 and phase 3 clinical trials have demonstrated success in inhibiting downstream effectors, specifically MEK1 and/or MEK2 with selumetinib and trametinib (albeit with poor tolerability).	AZD 6244	206-217	mitogen-activated protein kinase kinase 1	Homo sapiens	184-188
27108842-3	2016	We report 2 patients with optic pathway gliomas who developed outer retinal layer separation visualized by optical coherence tomography while taking the MEK inhibitor selumetinib.	AZD 6244	167-178	mitogen-activated protein kinase kinase 7	Homo sapiens	153-156
27100819-11	2016	While there has been limited success in inhibiting the protein directly, phase 2 and phase 3 clinical trials have demonstrated success in inhibiting downstream effectors, specifically MEK1 and/or MEK2 with selumetinib and trametinib (albeit with poor tolerability).	AZD 6244	206-217	mitogen-activated protein kinase kinase 2	Homo sapiens	196-200
26482043-0	2016	MAPK Activation Predicts Poor Outcome and the MEK Inhibitor, Selumetinib, Reverses Antiestrogen Resistance in ER-Positive High-Grade Serous Ovarian Cancer.	AZD 6244	61-72	mitogen-activated protein kinase kinase 7	Homo sapiens	46-49
26893312-3	2016	Preclinical evidence of the activity of MEK inhibitors in KRAS-mutant NSCLC has pushed forward the clinical development of these agents (namely selumetinib and trametinib) in KRAS-mutant NSCLC particularly in combination with other agents.	AZD 6244	144-155	mitogen-activated protein kinase kinase 7	Homo sapiens	40-43
26893312-3	2016	Preclinical evidence of the activity of MEK inhibitors in KRAS-mutant NSCLC has pushed forward the clinical development of these agents (namely selumetinib and trametinib) in KRAS-mutant NSCLC particularly in combination with other agents.	AZD 6244	144-155	KRAS proto-oncogene, GTPase	Homo sapiens	58-62
26893312-3	2016	Preclinical evidence of the activity of MEK inhibitors in KRAS-mutant NSCLC has pushed forward the clinical development of these agents (namely selumetinib and trametinib) in KRAS-mutant NSCLC particularly in combination with other agents.	AZD 6244	144-155	KRAS proto-oncogene, GTPase	Homo sapiens	175-179
27196001-4	2016	We found that GC-resistant ALL cell lines had markedly higher baseline activity of MEK and small-molecule MEK1/2 inhibitor selumetinib increased GCs-induced cell death.	AZD 6244	123-134	mitogen-activated protein kinase kinase 1	Homo sapiens	106-112
27196001-11	2016	Taken together, we show that MEK inhibitor selumetinib enhances dexamethasone toxicity in GC-resistant B-ALL cells.	AZD 6244	43-54	mitogen-activated protein kinase kinase 7	Homo sapiens	29-32
28154798-4	2016	Here, we mapped global ATP-binding proteomes perturbed by two clinical MEK inhibitors, AZD6244 and MEK162, in KRAS mutant lung cancer cells as a model system harnessing a desthiobiotin-ATP probe coupled with LC-MS/MS.	AZD 6244	87-94	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
28154798-4	2016	Here, we mapped global ATP-binding proteomes perturbed by two clinical MEK inhibitors, AZD6244 and MEK162, in KRAS mutant lung cancer cells as a model system harnessing a desthiobiotin-ATP probe coupled with LC-MS/MS.	AZD 6244	87-94	KRAS proto-oncogene, GTPase	Homo sapiens	110-114
26802155-0	2016	Selumetinib with and without erlotinib in KRAS mutant and KRAS wild-type advanced nonsmall-cell lung cancer.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	42-46
26802155-0	2016	Selumetinib with and without erlotinib in KRAS mutant and KRAS wild-type advanced nonsmall-cell lung cancer.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	58-62
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	0-11	zinc fingers and homeoboxes 2	Homo sapiens	88-91
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	92-95
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	96-99
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	13-20	zinc fingers and homeoboxes 2	Homo sapiens	88-91
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	92-95
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	13-20	mitogen-activated protein kinase 1	Homo sapiens	96-99
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	22-33	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	22-33	zinc fingers and homeoboxes 2	Homo sapiens	88-91
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	22-33	mitogen-activated protein kinase kinase 7	Homo sapiens	92-95
26802155-2	2016	Selumetinib (AZD6244; ARRY-142886) is an oral selective MEK kinase inhibitor of the Ras/Raf/MEK/ERK pathway.	AZD 6244	22-33	mitogen-activated protein kinase 1	Homo sapiens	96-99
26802155-11	2016	The ORR in the KRAS mutant group was 0% (95% CI 0.0% to 33.6%) for selumetinib alone and 10% (95% CI 2.1% to 26.3%) for the combination.	AZD 6244	67-78	KRAS proto-oncogene, GTPase	Homo sapiens	15-19
26677984-5	2016	Some mice received intraperitoneal injections of the Mitogen-activated protein kinase kinase (MEK) inhibitor, selumetinib, for 14 consecutive days.	AZD 6244	110-121	midkine	Mus musculus	53-92
26677984-5	2016	Some mice received intraperitoneal injections of the Mitogen-activated protein kinase kinase (MEK) inhibitor, selumetinib, for 14 consecutive days.	AZD 6244	110-121	midkine	Mus musculus	94-97
26446942-0	2016	A Phase II Trial of AZD6244 (Selumetinib, ARRY-142886), an Oral MEK1/2 Inhibitor, in Relapsed/Refractory Multiple Myeloma.	AZD 6244	20-27	mitogen-activated protein kinase kinase 1	Homo sapiens	64-70
26446942-0	2016	A Phase II Trial of AZD6244 (Selumetinib, ARRY-142886), an Oral MEK1/2 Inhibitor, in Relapsed/Refractory Multiple Myeloma.	AZD 6244	29-40	mitogen-activated protein kinase kinase 1	Homo sapiens	64-70
26446942-1	2016	PURPOSE: AZD6244 is a MEK1/2 inhibitor with significant preclinical activity in multiple myeloma cells.	AZD 6244	9-16	mitogen-activated protein kinase kinase 1	Homo sapiens	22-28
26837474-0	2016	Study Design and Rationale for a Randomized, Placebo-Controlled, Double-Blind Study to Assess the Efficacy and Safety of Selumetinib in Combination With Docetaxel as Second-Line Treatment in Patients With KRAS-Mutant Advanced Non-Small Cell Lung Cancer (SELECT-1).	AZD 6244	121-132	KRAS proto-oncogene, GTPase	Homo sapiens	205-209
26837474-3	2016	In a recent phase II study, selumetinib (AZD6244, ARRY-142886), an oral, potent and selective, allosteric MEK1/2 inhibitor with a short half-life, combined with docetaxel, improved clinical outcome as second-line treatment for patients with KRASm NSCLC.	AZD 6244	28-39	mitogen-activated protein kinase kinase 1	Homo sapiens	106-112
26837474-3	2016	In a recent phase II study, selumetinib (AZD6244, ARRY-142886), an oral, potent and selective, allosteric MEK1/2 inhibitor with a short half-life, combined with docetaxel, improved clinical outcome as second-line treatment for patients with KRASm NSCLC.	AZD 6244	41-48	mitogen-activated protein kinase kinase 1	Homo sapiens	106-112
26683364-1	2016	We previously conducted a phase-II study with selumetinib (AZD6244), a small molecule inhibitor of MEK1/2, in advanced biliary tract cancers (BTC), where the primary endpoint was response rate.	AZD 6244	46-57	mitogen-activated protein kinase kinase 1	Homo sapiens	99-105
26683364-1	2016	We previously conducted a phase-II study with selumetinib (AZD6244), a small molecule inhibitor of MEK1/2, in advanced biliary tract cancers (BTC), where the primary endpoint was response rate.	AZD 6244	59-66	mitogen-activated protein kinase kinase 1	Homo sapiens	99-105
27231576-0	2016	A long-term surviving patient with recurrent low-grade serous ovarian carcinoma treated with the MEK1/2 inhibitor, selumetinib.	AZD 6244	115-126	mitogen-activated protein kinase kinase 1	Homo sapiens	97-103
27231576-1	2016	BACKGROUND: Selumetinib is a potent, selective, orally available, and non-ATP competitive small molecule inhibitor of mitogen-activated protein kinase kinase 1/2 (MEK1/2) that has demonstrated single agent activity in a number of solid tumor including recurrent low-grade serous ovarian carcinoma (LGSOC).	AZD 6244	12-23	mitogen-activated protein kinase kinase 1	Homo sapiens	118-161
27231576-1	2016	BACKGROUND: Selumetinib is a potent, selective, orally available, and non-ATP competitive small molecule inhibitor of mitogen-activated protein kinase kinase 1/2 (MEK1/2) that has demonstrated single agent activity in a number of solid tumor including recurrent low-grade serous ovarian carcinoma (LGSOC).	AZD 6244	12-23	mitogen-activated protein kinase kinase 1	Homo sapiens	163-169
27231576-3	2016	CASE PRESENTATION: In this case report, we present a patient with recurrent LGSOC with KRAS mutation whose tumor has not progressed and who has maintained a good general condition without severe toxicities following treatment with selumetinib for more than 7 years.	AZD 6244	231-242	KRAS proto-oncogene, GTPase	Homo sapiens	87-91
27068338-10	2016	After re-mining our sequencing data, we found that more than a half of our KRAS mutant NSCLC patients could potentially benefit from the addition of a MEK inhibitor such as selumetinib to standard chemotherapeutic agents.	AZD 6244	173-184	KRAS proto-oncogene, GTPase	Homo sapiens	75-79
27068338-10	2016	After re-mining our sequencing data, we found that more than a half of our KRAS mutant NSCLC patients could potentially benefit from the addition of a MEK inhibitor such as selumetinib to standard chemotherapeutic agents.	AZD 6244	173-184	mitogen-activated protein kinase kinase 7	Homo sapiens	151-154
27141064-16	2016	It has been reported that cancer cell lines with Kras G12v mutation are more sensitive to selumetinib than cell lines with wild-type Kras.	AZD 6244	90-101	KRAS proto-oncogene, GTPase	Homo sapiens	49-53
26666244-0	2016	A phase I study of selumetinib (AZD6244/ARRY-142866), a MEK1/2 inhibitor, in combination with cetuximab in refractory solid tumors and KRAS mutant colorectal cancer.	AZD 6244	19-30	mitogen-activated protein kinase kinase 1	Homo sapiens	56-62
26666244-3	2016	We hypothesized that targeting MEK with selumetinib could overcome resistance to cetuximab in KRAS mutant CRC.	AZD 6244	40-51	KRAS proto-oncogene, GTPase	Homo sapiens	94-98
26912134-2	2016	Selumetinib (AZD6244, ARRY-142886) potently and selectively inhibits MEK1/2, an intracellular kinase and has shown activity in ABC.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	69-75
26912134-2	2016	Selumetinib (AZD6244, ARRY-142886) potently and selectively inhibits MEK1/2, an intracellular kinase and has shown activity in ABC.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	69-75
25915848-6	2016	The mechanistic action in the cell model was further confirmed by the observation of xenograft tumors in nude mice, revealing that the PXN-mediated TKI resistance was conquered by ERK inhibitor (AZD6244) and Bcl-2 family inhibitor (obatoclax), but the TKI resistance overcome by AZD6244 is more effective than that of obatoclax.	AZD 6244	195-202	paxillin	Mus musculus	135-138
25915848-6	2016	The mechanistic action in the cell model was further confirmed by the observation of xenograft tumors in nude mice, revealing that the PXN-mediated TKI resistance was conquered by ERK inhibitor (AZD6244) and Bcl-2 family inhibitor (obatoclax), but the TKI resistance overcome by AZD6244 is more effective than that of obatoclax.	AZD 6244	279-286	paxillin	Mus musculus	135-138
26482043-0	2016	MAPK Activation Predicts Poor Outcome and the MEK Inhibitor, Selumetinib, Reverses Antiestrogen Resistance in ER-Positive High-Grade Serous Ovarian Cancer.	AZD 6244	61-72	estrogen receptor 1	Homo sapiens	110-112
26482043-15	2016	Data support further evaluation of fulvestrant and selumetinib in ER-positive HGSOC.	AZD 6244	51-62	estrogen receptor 1	Homo sapiens	66-68
26821351-4	2016	In this in-vitro study, we show that MEK inhibitors AZD6244, MEK162 and PD0325901 block cell growth in NRAS mutant neuroblastoma cell lines but not in NRAS wild-type cell lines.	AZD 6244	52-59	mitogen-activated protein kinase kinase 7	Homo sapiens	37-40
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	AZD 6244	81-88	mitogen-activated protein kinase kinase 7	Homo sapiens	52-55
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	AZD 6244	81-88	mitogen-activated protein kinase 3	Homo sapiens	126-132
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	AZD 6244	81-88	TNF receptor superfamily member 10b	Homo sapiens	161-164
26821351-4	2016	In this in-vitro study, we show that MEK inhibitors AZD6244, MEK162 and PD0325901 block cell growth in NRAS mutant neuroblastoma cell lines but not in NRAS wild-type cell lines.	AZD 6244	52-59	NRAS proto-oncogene, GTPase	Homo sapiens	103-107
26673006-4	2016	EXPERIMENTAL DESIGN: Since single agent metformin enhances proliferating signals through the RAS/RAF/MAPK pathway, and several MEK inhibitors (MEK-I) demonstrated clinical efficacy in combination with other agents in NSCLC, we tested the effects of metformin plus MEK-I (selumetinib or pimasertib) on proliferation, invasiveness, migration abilities in vitro and in vivo in LKB1 positive NSCLC models harboring KRAS wild type and mutated gene.	AZD 6244	271-282	mitogen-activated protein kinase kinase 7	Homo sapiens	127-130
26673006-4	2016	EXPERIMENTAL DESIGN: Since single agent metformin enhances proliferating signals through the RAS/RAF/MAPK pathway, and several MEK inhibitors (MEK-I) demonstrated clinical efficacy in combination with other agents in NSCLC, we tested the effects of metformin plus MEK-I (selumetinib or pimasertib) on proliferation, invasiveness, migration abilities in vitro and in vivo in LKB1 positive NSCLC models harboring KRAS wild type and mutated gene.	AZD 6244	271-282	mitogen-activated protein kinase kinase 7	Homo sapiens	143-146
26673006-4	2016	EXPERIMENTAL DESIGN: Since single agent metformin enhances proliferating signals through the RAS/RAF/MAPK pathway, and several MEK inhibitors (MEK-I) demonstrated clinical efficacy in combination with other agents in NSCLC, we tested the effects of metformin plus MEK-I (selumetinib or pimasertib) on proliferation, invasiveness, migration abilities in vitro and in vivo in LKB1 positive NSCLC models harboring KRAS wild type and mutated gene.	AZD 6244	271-282	mitogen-activated protein kinase kinase 7	Homo sapiens	143-146
26601868-7	2016	This knowledge has led to the rational development of clinical trials specifically for UM utilizing targeted inhibitors of the activated signaling pathways such as mitogen-activated protein kinase, Akt, and protein kinase C. A recent trial of the oral MEK inhibitor selumetinib was the first to show clinical benefit for any systemic therapy in a randomized fashion.	AZD 6244	266-277	AKT serine/threonine kinase 1	Homo sapiens	198-201
26601868-7	2016	This knowledge has led to the rational development of clinical trials specifically for UM utilizing targeted inhibitors of the activated signaling pathways such as mitogen-activated protein kinase, Akt, and protein kinase C. A recent trial of the oral MEK inhibitor selumetinib was the first to show clinical benefit for any systemic therapy in a randomized fashion.	AZD 6244	266-277	mitogen-activated protein kinase kinase 7	Homo sapiens	252-255
26373715-2	2016	Knockdown expression of GP130 or STAT3 sensitized cells to anti-cancer drugs doxorubicin, cisplatin, and MEK inhibitor AZD6244.	AZD 6244	119-126	Neutrophil migration (granulocyte glycoprotein)	Homo sapiens	24-29
26373715-2	2016	Knockdown expression of GP130 or STAT3 sensitized cells to anti-cancer drugs doxorubicin, cisplatin, and MEK inhibitor AZD6244.	AZD 6244	119-126	signal transducer and activator of transcription 3	Homo sapiens	33-38
26373715-2	2016	Knockdown expression of GP130 or STAT3 sensitized cells to anti-cancer drugs doxorubicin, cisplatin, and MEK inhibitor AZD6244.	AZD 6244	119-126	mitogen-activated protein kinase kinase 7	Homo sapiens	105-108
25981859-6	2015	RESULTS: Inhibition of MEK signaling by selumetinib suppressed TORC1 signaling only in the context of the BRAF-mutant both in vitro and in vivo.	AZD 6244	40-51	mitogen-activated protein kinase kinase 7	Homo sapiens	23-26
26747016-7	2016	We report two documented cases of serous chorioretinopathies secondary to the use of selumetinib, an MEK inhibitor.	AZD 6244	85-96	mitogen-activated protein kinase kinase 7	Homo sapiens	101-104
26630652-5	2015	Moreover, TAS-116 showed synergistic growth inhibitory effects with the farnesyltransferase inhibitor tipifarnib, the BRAF inhibitor dabrafenib, and the MEK inhibitor selumetinib.	AZD 6244	167-178	mitogen-activated protein kinase kinase 7	Homo sapiens	153-156
26324360-3	2015	With the goal of identifying biomarkers of sensitivity to MEK inhibitor treatment, we performed an outlier analysis of a patient who experienced a complete, durable, and ongoing (> 5 years) response to selumetinib, a non-ATP competitive MEK inhibitor.	AZD 6244	205-216	mitogen-activated protein kinase kinase 7	Homo sapiens	58-61
26324360-3	2015	With the goal of identifying biomarkers of sensitivity to MEK inhibitor treatment, we performed an outlier analysis of a patient who experienced a complete, durable, and ongoing (> 5 years) response to selumetinib, a non-ATP competitive MEK inhibitor.	AZD 6244	205-216	mitogen-activated protein kinase kinase 7	Homo sapiens	240-243
26384399-0	2015	MEK Inhibitor Selumetinib (AZD6244; ARRY-142886) Prevents Lung Metastasis in a Triple-Negative Breast Cancer Xenograft Model.	AZD 6244	14-25	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
26384399-0	2015	MEK Inhibitor Selumetinib (AZD6244; ARRY-142886) Prevents Lung Metastasis in a Triple-Negative Breast Cancer Xenograft Model.	AZD 6244	27-34	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
26384399-4	2015	Interestingly, when we treated TNBC cells with the allosteric MEK inhibitor selumetinib, cell viability was not reduced in two-dimensional culture.	AZD 6244	76-87	mitogen-activated protein kinase kinase 7	Homo sapiens	62-65
26384399-8	2015	We tested the hypothesis that targeted inhibition of the MAPK pathway by selumetinib inhibits acquisition of the breast cancer stem cell phenotype and prevents lung metastasis of TNBC.	AZD 6244	73-84	mitogen-activated protein kinase 1	Homo sapiens	57-61
26384399-9	2015	TNBC cells treated with selumetinib showed inhibition of anchorage-independent growth, an indicator of in vivo tumorigenicity (P < 0.005), and decreases in the CD44(+)CD24(-/low) fraction, ALDH1 activity, and mammosphere-forming efficiency.	AZD 6244	24-35	CD44 molecule (Indian blood group)	Homo sapiens	163-167
26384399-9	2015	TNBC cells treated with selumetinib showed inhibition of anchorage-independent growth, an indicator of in vivo tumorigenicity (P < 0.005), and decreases in the CD44(+)CD24(-/low) fraction, ALDH1 activity, and mammosphere-forming efficiency.	AZD 6244	24-35	CD24 molecule	Homo sapiens	170-174
26384399-9	2015	TNBC cells treated with selumetinib showed inhibition of anchorage-independent growth, an indicator of in vivo tumorigenicity (P < 0.005), and decreases in the CD44(+)CD24(-/low) fraction, ALDH1 activity, and mammosphere-forming efficiency.	AZD 6244	24-35	aldehyde dehydrogenase 1 family member A1	Homo sapiens	192-197
26571380-9	2015	The MEK 1/2 inhibitor, Selumetinib, inhibited proliferation of only mucin-IHCCA while the aminopeptidase-N inhibitor, Bestatin was more active against mixed-IHCCA.	AZD 6244	23-34	mitogen-activated protein kinase kinase 1	Homo sapiens	4-11
26571380-9	2015	The MEK 1/2 inhibitor, Selumetinib, inhibited proliferation of only mucin-IHCCA while the aminopeptidase-N inhibitor, Bestatin was more active against mixed-IHCCA.	AZD 6244	23-34	LOC100508689	Homo sapiens	68-73
26571380-14	2015	Cisplatin, Abraxane and the MEK 1/2 inhibitor, Selumetinib were more active against mucin-IHCCA while, Gemcitabine, Gemcitabine-Cisplatin combination, the c-erbB2 blocking antibody and bestatin worked better against mixed-IHCCA.	AZD 6244	47-58	mitogen-activated protein kinase kinase 1	Homo sapiens	28-35
26571380-14	2015	Cisplatin, Abraxane and the MEK 1/2 inhibitor, Selumetinib were more active against mucin-IHCCA while, Gemcitabine, Gemcitabine-Cisplatin combination, the c-erbB2 blocking antibody and bestatin worked better against mixed-IHCCA.	AZD 6244	47-58	LOC100508689	Homo sapiens	84-89
26571380-14	2015	Cisplatin, Abraxane and the MEK 1/2 inhibitor, Selumetinib were more active against mucin-IHCCA while, Gemcitabine, Gemcitabine-Cisplatin combination, the c-erbB2 blocking antibody and bestatin worked better against mixed-IHCCA.	AZD 6244	47-58	erb-b2 receptor tyrosine kinase 2	Homo sapiens	155-162
26567773-1	2015	AZD6244 (ARRY-142886), a highly selective MAPK-ERK kinase inhibitor, has shown excellent clinical efficacy in many tumors.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	47-50
26567773-1	2015	AZD6244 (ARRY-142886), a highly selective MAPK-ERK kinase inhibitor, has shown excellent clinical efficacy in many tumors.	AZD 6244	9-20	mitogen-activated protein kinase 1	Homo sapiens	47-50
26567773-4	2015	For absence of NRAS, KRAS and BRAF mutation, SGC7901 and BGC823 gastric cancer cells were relative resistance to AZD6244 in vitro.	AZD 6244	113-120	KRAS proto-oncogene, GTPase	Homo sapiens	21-25
26567773-4	2015	For absence of NRAS, KRAS and BRAF mutation, SGC7901 and BGC823 gastric cancer cells were relative resistance to AZD6244 in vitro.	AZD 6244	113-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
26567773-8	2015	Moreover, the anti-angiogenesis effect of AZD6244 may predominantly attribute to its modulation on VEGF through p-ERK - c-Fos - HIF-1alpha integrated signal pathways.	AZD 6244	42-49	vascular endothelial growth factor A	Homo sapiens	99-103
26567773-8	2015	Moreover, the anti-angiogenesis effect of AZD6244 may predominantly attribute to its modulation on VEGF through p-ERK - c-Fos - HIF-1alpha integrated signal pathways.	AZD 6244	42-49	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	112-117
26567773-8	2015	Moreover, the anti-angiogenesis effect of AZD6244 may predominantly attribute to its modulation on VEGF through p-ERK - c-Fos - HIF-1alpha integrated signal pathways.	AZD 6244	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-125
26567773-8	2015	Moreover, the anti-angiogenesis effect of AZD6244 may predominantly attribute to its modulation on VEGF through p-ERK - c-Fos - HIF-1alpha integrated signal pathways.	AZD 6244	42-49	hypoxia inducible factor 1 subunit alpha	Homo sapiens	128-138
26567773-10	2015	Targeting inhibition of p-ERK by AZD6244 suppress gastric cancer xenografts by blockage of angiogenesis without systemic toxicity.	AZD 6244	33-40	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	24-29
26567773-11	2015	The anti-angiogenesis effect afford by AZD6244 may attribute to its modulation on p-ERK - c-Fos - HIF-1alpha - VEGF integrated signal pathways.	AZD 6244	39-46	mitogen-activated protein kinase 1	Homo sapiens	84-87
26567773-11	2015	The anti-angiogenesis effect afford by AZD6244 may attribute to its modulation on p-ERK - c-Fos - HIF-1alpha - VEGF integrated signal pathways.	AZD 6244	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-95
26567773-11	2015	The anti-angiogenesis effect afford by AZD6244 may attribute to its modulation on p-ERK - c-Fos - HIF-1alpha - VEGF integrated signal pathways.	AZD 6244	39-46	hypoxia inducible factor 1 subunit alpha	Homo sapiens	98-108
26567773-11	2015	The anti-angiogenesis effect afford by AZD6244 may attribute to its modulation on p-ERK - c-Fos - HIF-1alpha - VEGF integrated signal pathways.	AZD 6244	39-46	vascular endothelial growth factor A	Homo sapiens	111-115
26672083-1	2015	In the January 15, 2012, issue of Clinical Cancer Research, Kirkwood and colleagues published a study comparing the MEK inhibitor selumetinib with temozolomide in unselected metastatic melanoma.	AZD 6244	130-141	mitogen-activated protein kinase kinase 7	Homo sapiens	116-119
26672083-2	2015	Although selumetinib did not improve survival or response, most responders had BRAF-activating mutations, and selumetinib has since demonstrated efficacy in BRAF-mutant melanoma.	AZD 6244	110-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	157-161
26544513-4	2015	HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901.	AZD 6244	72-79	HRas proto-oncogene, GTPase	Homo sapiens	0-4
26544513-4	2015	HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901.	AZD 6244	72-79	mitogen-activated protein kinase kinase 7	Homo sapiens	57-60
25959272-3	2015	In this study, we analyzed the effects of the MEK1/2 inhibitor selumetinib in combination with the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib in a panel of TNBC cell lines that showed different levels of sensitivity to single-agent selumetinib: SUM-149 and MDA-MB-231 cells resulted to be sensitive, whereas SUM-159, MDA-MB-468 and HCC70 cells were relatively resistant to the drug.	AZD 6244	63-74	mitogen-activated protein kinase kinase 1	Homo sapiens	46-52
25959272-4	2015	Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells.	AZD 6244	29-40	epidermal growth factor receptor	Homo sapiens	92-96
25959272-4	2015	Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells.	AZD 6244	105-116	epidermal growth factor receptor	Homo sapiens	92-96
25959272-4	2015	Treatment of TNBC cells with selumetinib produced an increase of the phosphorylation of the EGFR both in selumetinib-sensitive SUM-149, MDA-MB-231 and in selumetinib-resistant MDA-MB-468 TNBC cells.	AZD 6244	105-116	epidermal growth factor receptor	Homo sapiens	92-96
25959272-6	2015	This effect was associated with an almost complete suppression of ERK1/2 activation and a reduction of selumetinib-induced AKT phosphorylation.	AZD 6244	103-114	AKT serine/threonine kinase 1	Homo sapiens	123-126
25959272-8	2015	Taken together, our data demonstrated that blockade of the EGFR might efficiently increase the antitumor activity of selumetinib in a subgroup of TNBC and that this phenomenon might be related to the effects of such combination on both ERK1/2 and AKT activation.	AZD 6244	117-128	epidermal growth factor receptor	Homo sapiens	59-63
25959272-8	2015	Taken together, our data demonstrated that blockade of the EGFR might efficiently increase the antitumor activity of selumetinib in a subgroup of TNBC and that this phenomenon might be related to the effects of such combination on both ERK1/2 and AKT activation.	AZD 6244	117-128	mitogen-activated protein kinase 3	Homo sapiens	236-242
25959272-8	2015	Taken together, our data demonstrated that blockade of the EGFR might efficiently increase the antitumor activity of selumetinib in a subgroup of TNBC and that this phenomenon might be related to the effects of such combination on both ERK1/2 and AKT activation.	AZD 6244	117-128	AKT serine/threonine kinase 1	Homo sapiens	247-250
26443806-9	2015	When treated with the MEK inhibitor selumetinib combined with KW-2450, compared with KW-2450 alone, the 8N cell population was significantly reduced and apoptosis was increased.	AZD 6244	36-47	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
26443806-11	2015	Collectively, Aurora A and B inhibition had a significant antitumor effect against TNBC, and this antitumor effect was maximized by the combination of selumetinib with Aurora A and B inhibition.	AZD 6244	151-162	aurora kinase A	Homo sapiens	14-22
26250606-3	2015	Therefore, co-administration of inhibitors of both pathways, GSK2126458 as a dual PI3K/mTOR inhibitor, and AZD6244 as a MEK inhibitor, is able to overcome resistance and increase anti-tumor efficacy.	AZD 6244	107-114	mitogen-activated protein kinase kinase 7	Homo sapiens	120-123
26250606-8	2015	RESULTS: The combination of GSK2126458 and AZD6244 inhibited the growth of DU145 and PC3 prostate cancer cells in vitro and in vivo.	AZD 6244	43-50	chromobox 8	Homo sapiens	85-88
26250606-9	2015	GSK2126458 decreased phospho-AKT while increasing phospho-ERK and AZD6244 decreased phospho-ERK efficiently while increasing phospho-AKT.	AZD 6244	66-73	mitogen-activated protein kinase 1	Homo sapiens	92-95
26250606-9	2015	GSK2126458 decreased phospho-AKT while increasing phospho-ERK and AZD6244 decreased phospho-ERK efficiently while increasing phospho-AKT.	AZD 6244	66-73	AKT serine/threonine kinase 1	Homo sapiens	133-136
26250606-10	2015	The combination of GSK2126458 and AZD6244 decreased both phospho-AKT and phospho-ERK effectively in vitro and in vivo.	AZD 6244	34-41	AKT serine/threonine kinase 1	Homo sapiens	65-68
26250606-10	2015	The combination of GSK2126458 and AZD6244 decreased both phospho-AKT and phospho-ERK effectively in vitro and in vivo.	AZD 6244	34-41	mitogen-activated protein kinase 1	Homo sapiens	81-84
26250606-14	2015	CONCLUSIONS: The combination of GSK2126458 and AZD6244 blocks both the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways simultaneously and is an effective strategy for the treatment of CRPCs.	AZD 6244	47-54	zinc fingers and homeoboxes 2	Homo sapiens	75-78
26250606-14	2015	CONCLUSIONS: The combination of GSK2126458 and AZD6244 blocks both the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways simultaneously and is an effective strategy for the treatment of CRPCs.	AZD 6244	47-54	mitogen-activated protein kinase kinase 7	Homo sapiens	79-82
26250606-14	2015	CONCLUSIONS: The combination of GSK2126458 and AZD6244 blocks both the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways simultaneously and is an effective strategy for the treatment of CRPCs.	AZD 6244	47-54	mitogen-activated protein kinase 1	Homo sapiens	83-86
26250606-14	2015	CONCLUSIONS: The combination of GSK2126458 and AZD6244 blocks both the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways simultaneously and is an effective strategy for the treatment of CRPCs.	AZD 6244	47-54	AKT serine/threonine kinase 1	Homo sapiens	96-99
26250606-14	2015	CONCLUSIONS: The combination of GSK2126458 and AZD6244 blocks both the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways simultaneously and is an effective strategy for the treatment of CRPCs.	AZD 6244	47-54	mechanistic target of rapamycin kinase	Homo sapiens	100-104
26498922-14	2015	CONCLUSION: Perturbations of the MEK and the PI3K pathway radiosensitized tumor cells of different origins and the combination of AZD6244 and NVP-BEZ235 yielded cytostatic effects in several tumor entities.	AZD 6244	130-137	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
26622906-3	2015	In the present study, the mitogen-activated protein kinase kinase 1/2 inhibitor, AZD6244, was used in combination with gefitinib to investigate the efficacy of this treatment in NSCLC cell lines, particularly in gefitinib-resistant cells.	AZD 6244	81-88	mitogen-activated protein kinase kinase 1	Homo sapiens	26-69
26622906-5	2015	It was found that the growth inhibitory effect of combination treatment with gefitinib and AZD6244 was greater than that of gefitinib alone in the EGFR-TKI-resistant A549 cells.	AZD 6244	91-98	epidermal growth factor receptor	Homo sapiens	147-151
26622906-8	2015	Thus, a preclinical rationale exists for the use of AZD6244 to enhance the efficacy of gefitinib in patients with EGFR-TKI-resistant NSCLC.	AZD 6244	52-59	epidermal growth factor receptor	Homo sapiens	114-118
25981859-6	2015	RESULTS: Inhibition of MEK signaling by selumetinib suppressed TORC1 signaling only in the context of the BRAF-mutant both in vitro and in vivo.	AZD 6244	40-51	CREB regulated transcription coactivator 1	Homo sapiens	63-68
25981859-6	2015	RESULTS: Inhibition of MEK signaling by selumetinib suppressed TORC1 signaling only in the context of the BRAF-mutant both in vitro and in vivo.	AZD 6244	40-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
25981859-8	2015	CONCLUSIONS: Selumetinib suppressed TORC1 signaling in the context of BRAF mutation.	AZD 6244	13-24	CREB regulated transcription coactivator 1	Homo sapiens	36-41
25981859-8	2015	CONCLUSIONS: Selumetinib suppressed TORC1 signaling in the context of BRAF mutation.	AZD 6244	13-24	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
25981859-9	2015	Selumetinib caused a rapid downregulation of FANCD2 and markedly potentiated the effect of XRT.	AZD 6244	0-11	FA complementation group D2	Homo sapiens	45-51
26360058-6	2015	Treatment with the Mek1/2 inhibitor selumetinib resulted in a rapid, complete and persistent reduction of microenvironment-generated pErk1/2.	AZD 6244	36-47	mitogen-activated protein kinase kinase 1	Homo sapiens	19-25
26498922-8	2015	Our Western blot data indicated that AZD6244 and NVP-BEZ235 perturbed the MAPK and PI3K/mTOR signaling cascades, respectively.	AZD 6244	37-44	mechanistic target of rapamycin kinase	Homo sapiens	88-92
25933688-10	2015	The effect of RAS mutants was reversed when MET inhibition was combined with MEK inhibitors AZD6244 and UO126.	AZD 6244	92-99	mitogen-activated protein kinase kinase 7	Homo sapiens	77-80
25961376-3	2015	Here, we identified that Signal Transducer and Activator of Transcription 3 (STAT3) was significantly activated following the MEK inhibition using AZD6244, PD98059 and Trametinib in K-Ras mutant pancreatic and colon cancer cells.	AZD 6244	147-154	signal transducer and activator of transcription 3	Homo sapiens	25-75
25933683-0	2015	Dual blockade of PI3K/AKT/mTOR (NVP-BEZ235) and Ras/Raf/MEK (AZD6244) pathways synergistically inhibit growth of primary endometrioid endometrial carcinoma cultures, whereas NVP-BEZ235 reduces tumor growth in the corresponding xenograft models.	AZD 6244	61-68	zinc fingers and homeoboxes 2	Homo sapiens	52-55
25933683-0	2015	Dual blockade of PI3K/AKT/mTOR (NVP-BEZ235) and Ras/Raf/MEK (AZD6244) pathways synergistically inhibit growth of primary endometrioid endometrial carcinoma cultures, whereas NVP-BEZ235 reduces tumor growth in the corresponding xenograft models.	AZD 6244	61-68	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
25933683-11	2015	NVP-BEZ235 and AZD6244 reduced cell viability and induced cell cycle arrest and apoptosis, by reduction of p-AKT, p-S6, and p-ERK levels.	AZD 6244	15-22	AKT serine/threonine kinase 1	Homo sapiens	109-112
25933683-11	2015	NVP-BEZ235 and AZD6244 reduced cell viability and induced cell cycle arrest and apoptosis, by reduction of p-AKT, p-S6, and p-ERK levels.	AZD 6244	15-22	mitogen-activated protein kinase 1	Homo sapiens	126-129
26137449-4	2015	Selumetinib and vemurafenib potently inhibited cell proliferation in all cell lines, especially in those that expressed low levels of phosphorylated AKT (pAKT).	AZD 6244	0-11	AKT serine/threonine kinase 1	Homo sapiens	149-152
26137449-6	2015	Furthermore, ZSTK474 or BEZ235 combined with selumetinib to produce robust inhibition of pERK, pAKT, and pS6 expression and synergistic inhibition of NZM20 tumor growth.	AZD 6244	45-56	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	89-93
26137449-6	2015	Furthermore, ZSTK474 or BEZ235 combined with selumetinib to produce robust inhibition of pERK, pAKT, and pS6 expression and synergistic inhibition of NZM20 tumor growth.	AZD 6244	45-56	taste 2 receptor member 63 pseudogene	Homo sapiens	105-108
26137449-7	2015	The inhibitors of individual PI3K isoforms or mTORC1/2 were less effective at inhibiting cell proliferation either as single agents or in combination with selumetinib or vemurafenib, although KU-0063794 synergistically interacted with vemurafenib and increased the magnitude of cell growth inhibition with selumetinib or vemurafenib in certain cell lines.	AZD 6244	155-166	CREB regulated transcription coactivator 2	Mus musculus	46-54
25870145-5	2015	Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor.	AZD 6244	124-135	mitogen-activated protein kinase kinase 7	Homo sapiens	110-113
25870145-5	2015	Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor.	AZD 6244	124-135	epidermal growth factor receptor	Homo sapiens	208-212
25870145-5	2015	Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor.	AZD 6244	137-144	mitogen-activated protein kinase kinase 7	Homo sapiens	110-113
25870145-5	2015	Compared with parental cells, a number of resistant cell populations were more sensitive to inhibition by the MEK inhibitor selumetinib (AZD6244; ARRY-142886) when treated in combination with the originating EGFR inhibitor.	AZD 6244	137-144	epidermal growth factor receptor	Homo sapiens	208-212
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.	AZD 6244	40-51	proprotein convertase subtilisin/kexin type 9	Homo sapiens	89-92
26059332-2	2015	Treatment with selumetinib (AZD6244, ARRY-142886), a MEK1/2 inhibitor, results in antitumour effects in uveal melanoma pre-clinical models.	AZD 6244	15-26	mitogen-activated protein kinase kinase 1	Homo sapiens	53-59
26059332-2	2015	Treatment with selumetinib (AZD6244, ARRY-142886), a MEK1/2 inhibitor, results in antitumour effects in uveal melanoma pre-clinical models.	AZD 6244	28-35	mitogen-activated protein kinase kinase 1	Homo sapiens	53-59
26125448-0	2015	Impact of KRAS codon subtypes from a randomised phase II trial of selumetinib plus docetaxel in KRAS mutant advanced non-small-cell lung cancer.	AZD 6244	66-77	KRAS proto-oncogene, GTPase	Homo sapiens	96-100
26125448-1	2015	BACKGROUND: Selumetinib (AZD6244, ARRY-142886)+docetaxel increases median overall survival (OS) and significantly improves progression-free survival (PFS) and objective response rate (ORR) compared with docetaxel alone in patients with KRAS mutant, stage IIIB/IV non-small-cell lung cancer (NSCLC; NCT00890825).	AZD 6244	12-23	KRAS proto-oncogene, GTPase	Homo sapiens	236-240
26125448-3	2015	RESULTS: In patients receiving selumetinib+docetaxel and harbouring KRAS G12C or G12V mutations there were trends towards greater improvement in OS, PFS and ORR compared with other KRAS mutations.	AZD 6244	31-42	KRAS proto-oncogene, GTPase	Homo sapiens	68-72
26125448-3	2015	RESULTS: In patients receiving selumetinib+docetaxel and harbouring KRAS G12C or G12V mutations there were trends towards greater improvement in OS, PFS and ORR compared with other KRAS mutations.	AZD 6244	31-42	KRAS proto-oncogene, GTPase	Homo sapiens	181-185
26125448-4	2015	CONCLUSION: Different KRAS mutations in NSCLC may influence selumetinib/docetaxel sensitivity.	AZD 6244	60-71	KRAS proto-oncogene, GTPase	Homo sapiens	22-26
25892646-4	2015	We assessed the efficacy and safety of fulvestrant with selumetinib, a MEK 1/2 inhibitor, in advanced stage breast cancer progressing after aromatase inhibitor (AI).	AZD 6244	56-67	mitogen-activated protein kinase kinase 1	Homo sapiens	71-78
25857555-8	2015	Importantly, inhibition of ERK1/2 activation by PD0325901 (300 nM) or AZD6244 (5 or 10 microM) completely abolished the proliferative response.	AZD 6244	70-77	mitogen-activated protein kinase 3	Homo sapiens	27-33
25887099-0	2015	A phase II evaluation of selumetinib (AZD6244, ARRY-142886), a selective MEK-1/2 inhibitor in the treatment of recurrent or persistent endometrial cancer: an NRG Oncology/Gynecologic Oncology Group study.	AZD 6244	25-36	mitogen-activated protein kinase kinase 1	Homo sapiens	73-80
25887099-2	2015	We sought to evaluate the efficacy/safety of selumetinib, a selective MEK-1/2 inhibitor in women with recurrent endometrial cancer.	AZD 6244	45-56	mitogen-activated protein kinase kinase 1	Homo sapiens	70-77
25961376-3	2015	Here, we identified that Signal Transducer and Activator of Transcription 3 (STAT3) was significantly activated following the MEK inhibition using AZD6244, PD98059 and Trametinib in K-Ras mutant pancreatic and colon cancer cells.	AZD 6244	147-154	signal transducer and activator of transcription 3	Homo sapiens	77-82
25961376-3	2015	Here, we identified that Signal Transducer and Activator of Transcription 3 (STAT3) was significantly activated following the MEK inhibition using AZD6244, PD98059 and Trametinib in K-Ras mutant pancreatic and colon cancer cells.	AZD 6244	147-154	mitogen-activated protein kinase kinase 7	Homo sapiens	126-129
25961376-3	2015	Here, we identified that Signal Transducer and Activator of Transcription 3 (STAT3) was significantly activated following the MEK inhibition using AZD6244, PD98059 and Trametinib in K-Ras mutant pancreatic and colon cancer cells.	AZD 6244	147-154	KRAS proto-oncogene, GTPase	Homo sapiens	182-187
25541062-0	2015	AZD6244 inhibits cisplatin-induced ERK1/2 activation and potentiates cisplatin-associated cytotoxicity in K-ras G12D preclinical models.	AZD 6244	0-7	mitogen-activated protein kinase 3	Mus musculus	35-41
25637165-2	2015	We conducted a biomarker-driven trial of the combination of MK-2206, an allosteric AKT 1/2/3 inhibitor, and selumetinib, a MEK 1/2 inhibitor, in patients with CRC to evaluate inhibition of phosphorylated ERK (pERK) and AKT (pAKT) in paired tumor biopsies.	AZD 6244	108-119	mitogen-activated protein kinase kinase 1	Homo sapiens	123-130
25897676-1	2015	BACKGROUND: The MEK inhibitor, selumetinib, suppresses soft-tissue sarcoma (STS) cell proliferation in vitro.	AZD 6244	31-42	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
25667274-3	2015	Patients were enrolled onto a not-otherwise-specified arm and treated with standard-of-care therapies or one of the following five biomarker-matched treatment groups: erlotinib for EGFR mutations; selumetinib for KRAS, NRAS, HRAS, or BRAF mutations; MK2206 for PIK3CA, AKT, or PTEN mutations; lapatinib for ERBB2 mutations or amplifications; and sunitinib for KIT or PDGFRA mutations or amplification.	AZD 6244	197-208	KRAS proto-oncogene, GTPase	Homo sapiens	213-217
26101713-8	2015	When BYL719 was combined with a MEK inhibitor (AZD6244) in a 3D cell culture system, strong synergism on NPC cell growth was observed with attenuation of MAPK activation.	AZD 6244	47-54	mitogen-activated protein kinase kinase 7	Homo sapiens	32-35
25541062-0	2015	AZD6244 inhibits cisplatin-induced ERK1/2 activation and potentiates cisplatin-associated cytotoxicity in K-ras G12D preclinical models.	AZD 6244	0-7	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	106-111
25541062-3	2015	Using KRAS-mutant NSCLC cells and a mouse model, we evaluated the efficacy of adding the MEK1/2 inhibitor AZD6244 as an addition for cisplatin-based chemotherapy.	AZD 6244	106-113	mitogen-activated protein kinase kinase 1	Mus musculus	89-95
25541062-6	2015	The combination of cisplatin and AZD6244 yielded a superior response to cisplatin alone in K-ras mice.	AZD 6244	33-40	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	91-96
25102946-8	2015	Onset of resistance to both combinations was accompanied by upregulation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathway and addition of selumetinib, a small-molecule MEK inhibitor, could resensitize resistant cells.	AZD 6244	198-209	midkine	Mus musculus	228-231
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	149-160	granulin precursor	Homo sapiens	39-43
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	149-160	mitogen-activated protein kinase 3	Homo sapiens	128-134
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	149-160	cyclin dependent kinase 6	Homo sapiens	208-212
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	149-160	RB transcriptional corepressor 1	Homo sapiens	213-216
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	149-160	granulin precursor	Homo sapiens	259-263
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	162-169	granulin precursor	Homo sapiens	39-43
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	162-169	mitogen-activated protein kinase 3	Homo sapiens	128-134
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	162-169	cyclin dependent kinase 6	Homo sapiens	208-212
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	162-169	RB transcriptional corepressor 1	Homo sapiens	213-216
25624003-8	2015	We report here that both restoring the PGRN content, by suberoylanilide hydroxamic acid (SAHA) or chloroquine (CQ), as blocking ERK1/2 activation by selumetinib (AZD6244) or MEK162 (ARRY-162), normalized the CDK6/pRb pathway and the proliferative activity of PGRN deficient cells.	AZD 6244	162-169	granulin precursor	Homo sapiens	259-263
25624003-9	2015	Moreover, we found that SAHA and selumetinib prevented the cytosolic TDP-43 accumulation in PGRN-deficient lymphoblasts.	AZD 6244	33-44	TAR DNA binding protein	Homo sapiens	69-75
25638158-8	2015	AT/RT primary tumors expressed increased mitogen activated protein (MAP) kinase pathway activity, and the MEK inhibitor selumetinib (AZD6244) decreased AT/RT growth and increased apoptosis.	AZD 6244	120-131	mitogen-activated protein kinase kinase 7	Homo sapiens	106-109
25638158-8	2015	AT/RT primary tumors expressed increased mitogen activated protein (MAP) kinase pathway activity, and the MEK inhibitor selumetinib (AZD6244) decreased AT/RT growth and increased apoptosis.	AZD 6244	133-140	mitogen-activated protein kinase kinase 7	Homo sapiens	106-109
25342139-0	2015	BYL719, a selective inhibitor of phosphoinositide 3-Kinase alpha, enhances the effect of selumetinib (AZD6244, ARRY-142886) in KRAS-mutant non-small cell lung cancer.	AZD 6244	89-100	KRAS proto-oncogene, GTPase	Homo sapiens	127-131
25516890-2	2015	KRAS-mutant cells may exhibit resistance to the allosteric MEK1/2 inhibitor selumetinib (AZD6244; ARRY-142886) and allosteric AKT inhibitors (such as MK-2206), the combination of which may overcome resistance to both monotherapies.	AZD 6244	76-87	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
25516890-2	2015	KRAS-mutant cells may exhibit resistance to the allosteric MEK1/2 inhibitor selumetinib (AZD6244; ARRY-142886) and allosteric AKT inhibitors (such as MK-2206), the combination of which may overcome resistance to both monotherapies.	AZD 6244	76-87	mitogen-activated protein kinase kinase 1	Homo sapiens	59-65
25516890-2	2015	KRAS-mutant cells may exhibit resistance to the allosteric MEK1/2 inhibitor selumetinib (AZD6244; ARRY-142886) and allosteric AKT inhibitors (such as MK-2206), the combination of which may overcome resistance to both monotherapies.	AZD 6244	89-96	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
25342139-8	2015	At the molecular level, we found that AKT activation strongly influenced the sensitivity of KRAS-mutant NSCLC cells to selumetinib.	AZD 6244	119-130	AKT serine/threonine kinase 1	Homo sapiens	38-41
25342139-8	2015	At the molecular level, we found that AKT activation strongly influenced the sensitivity of KRAS-mutant NSCLC cells to selumetinib.	AZD 6244	119-130	KRAS proto-oncogene, GTPase	Homo sapiens	92-96
25342139-9	2015	Selumetinib upregulated phospho-AKT and phosphorylated BAD at ser136, which is responsible for intrinsic drug resistance in KRAS-mutant NSCLC cells.	AZD 6244	0-11	AKT serine/threonine kinase 1	Homo sapiens	32-35
25342139-9	2015	Selumetinib upregulated phospho-AKT and phosphorylated BAD at ser136, which is responsible for intrinsic drug resistance in KRAS-mutant NSCLC cells.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	124-128
25342139-10	2015	In contrast, inhibition of the PI3K/AKT pathway by BYL719 hindered selumetinib-induced BAD phosphorylation and increased the antitumor efficacy of selumetinib.	AZD 6244	67-78	AKT serine/threonine kinase 1	Homo sapiens	36-39
25342139-10	2015	In contrast, inhibition of the PI3K/AKT pathway by BYL719 hindered selumetinib-induced BAD phosphorylation and increased the antitumor efficacy of selumetinib.	AZD 6244	147-158	AKT serine/threonine kinase 1	Homo sapiens	36-39
25342139-12	2015	On analysis of the pharmacodynamics, selumetinib and BYL719 together resulted in effective inhibition of both p-ERK and p-AKT expression in tumor tissue.	AZD 6244	37-48	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	110-115
25342139-12	2015	On analysis of the pharmacodynamics, selumetinib and BYL719 together resulted in effective inhibition of both p-ERK and p-AKT expression in tumor tissue.	AZD 6244	37-48	AKT serine/threonine kinase 1	Homo sapiens	122-125
25342139-13	2015	CONCLUSION: Taken together, these data suggest that combination treatment with selumetinib and BYL719 is a promising therapeutic approach to overcoming resistance to MEK inhibitors.	AZD 6244	79-90	mitogen-activated protein kinase kinase 7	Homo sapiens	166-169
25326806-8	2015	Western blot analysis and immunohistochemical staining revealed that treatment with AZD6244 or BEZ235 could significantly reduce the phosphorylation level of ERK1/2 or AKT in HCT116 tumor tissues.	AZD 6244	84-91	mitogen-activated protein kinase 3	Mus musculus	158-164
25326806-8	2015	Western blot analysis and immunohistochemical staining revealed that treatment with AZD6244 or BEZ235 could significantly reduce the phosphorylation level of ERK1/2 or AKT in HCT116 tumor tissues.	AZD 6244	84-91	thymoma viral proto-oncogene 1	Mus musculus	168-171
25342139-0	2015	BYL719, a selective inhibitor of phosphoinositide 3-Kinase alpha, enhances the effect of selumetinib (AZD6244, ARRY-142886) in KRAS-mutant non-small cell lung cancer.	AZD 6244	102-109	KRAS proto-oncogene, GTPase	Homo sapiens	127-131
25342139-7	2015	RESULTS: The combination of BYL719 and selumetinib resulted in synergistic cytotoxic activity compared with the single agents alone in KRAS-mutant NSCLC cells.	AZD 6244	39-50	KRAS proto-oncogene, GTPase	Homo sapiens	135-139
25348516-4	2015	We tested the top hit in the screen, the MEK1/2 inhibitor, AZD6244, for efficacy alone or in combination with the PI3K inhibitors, BKM120 or GDC-0941, in a Kras(G12D)-driven GEMM that recapitulates the histopathogenesis of human PDAC.	AZD 6244	59-66	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
25498501-0	2015	The glucosylceramide synthase inhibitor PDMP sensitizes pancreatic cancer cells to MEK/ERK inhibitor AZD-6244.	AZD 6244	101-109	UDP-glucose ceramide glucosyltransferase	Homo sapiens	4-29
25498501-0	2015	The glucosylceramide synthase inhibitor PDMP sensitizes pancreatic cancer cells to MEK/ERK inhibitor AZD-6244.	AZD 6244	101-109	mitogen-activated protein kinase kinase 7	Homo sapiens	83-86
25498501-0	2015	The glucosylceramide synthase inhibitor PDMP sensitizes pancreatic cancer cells to MEK/ERK inhibitor AZD-6244.	AZD 6244	101-109	mitogen-activated protein kinase 1	Homo sapiens	87-90
25498501-1	2015	Here we show that d,l-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), a glycosphingolipid biosynthesis inhibitor, increases the sensitivity of pancreatic cancer cells to the novel MEK-ERK inhibitor AZD-6244.	AZD 6244	213-221	mitogen-activated protein kinase kinase 7	Homo sapiens	195-198
25498501-1	2015	Here we show that d,l-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), a glycosphingolipid biosynthesis inhibitor, increases the sensitivity of pancreatic cancer cells to the novel MEK-ERK inhibitor AZD-6244.	AZD 6244	213-221	mitogen-activated protein kinase 1	Homo sapiens	199-202
25348516-6	2015	The response profile to the MEK1/2 inhibitor, AZD6244, was an outlier, showing the highest selective efficacy in PDAC.	AZD 6244	46-53	mitogen-activated protein kinase kinase 1	Homo sapiens	28-34
25385055-4	2015	Selumetinib is one such drug, functioning as an oral, selective non-ATP-competitive MEK1/2 inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	84-90
25268371-1	2015	BACKGROUND: We completed a phase I clinical trial to test the safety and toxicity of combined treatment with cixutumumab (anti-IGF-1R antibody) and selumetinib (MEK 1/2 inhibitor).	AZD 6244	148-159	mitogen-activated protein kinase kinase 1	Homo sapiens	161-168
25268371-9	2015	CONCLUSIONS: Our study of anti-IGF-1R antibody cixutumumab and MEK 1/2 inhibitor selumetinib showed that the combination is safe and well-tolerated at these doses, with preliminary evidence of clinical benefit and pharmacodynamic evidence of target inhibition.	AZD 6244	81-92	mitogen-activated protein kinase kinase 1	Homo sapiens	63-70
25322874-0	2015	Phase II study of selumetinib (AZD6244, ARRY-142886) plus irinotecan as second-line therapy in patients with K-RAS mutated colorectal cancer.	AZD 6244	18-29	KRAS proto-oncogene, GTPase	Homo sapiens	109-114
25322874-2	2015	Selumetinib (AZD6244, ARRY-142886) is a small molecule kinase inhibitor targeting MEK kinase, downstream of RAS.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
25322874-2	2015	Selumetinib (AZD6244, ARRY-142886) is a small molecule kinase inhibitor targeting MEK kinase, downstream of RAS.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
25322874-2	2015	Selumetinib (AZD6244, ARRY-142886) is a small molecule kinase inhibitor targeting MEK kinase, downstream of RAS.	AZD 6244	22-33	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
26279420-9	2015	These effects were similar to the results observed when using the pharmacological ERKs phosphorylation inhibitor, AZD6244.	AZD 6244	114-121	mitogen activated protein kinase 3	Rattus norvegicus	82-86
25326806-2	2015	AZD6244 is a potent, selective, and orally available MEK1/2 inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Mus musculus	53-59
25385055-7	2015	Expert opinion: Given the frequency of activated MAPK signaling in multiple tumor types, the potent MEK inhibitor selumetinib had strong preclinical and early clinical rationale, particularly in those tumors harboring KRAS or BRAF mutations.	AZD 6244	114-125	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
25385055-7	2015	Expert opinion: Given the frequency of activated MAPK signaling in multiple tumor types, the potent MEK inhibitor selumetinib had strong preclinical and early clinical rationale, particularly in those tumors harboring KRAS or BRAF mutations.	AZD 6244	114-125	KRAS proto-oncogene, GTPase	Homo sapiens	218-222
25385055-7	2015	Expert opinion: Given the frequency of activated MAPK signaling in multiple tumor types, the potent MEK inhibitor selumetinib had strong preclinical and early clinical rationale, particularly in those tumors harboring KRAS or BRAF mutations.	AZD 6244	114-125	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	226-230
25297634-2	2014	We found that a subset of BRAF- and NRAS-mutant human melanomas resistant to the MEK inhibitor selumetinib displayed increased oxidative phosphorylation (OxPhos) mediated by the transcriptional coactivator PGC1alpha.	AZD 6244	95-106	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
25426865-3	2015	OBSERVATIONS: Three patients who were receiving different MEK inhibitors (selumetinib, cobimetinib, and trametinib) developed an eruption, all associated with unique duskiness.	AZD 6244	74-85	mitogen-activated protein kinase kinase 7	Homo sapiens	58-61
25297634-2	2014	We found that a subset of BRAF- and NRAS-mutant human melanomas resistant to the MEK inhibitor selumetinib displayed increased oxidative phosphorylation (OxPhos) mediated by the transcriptional coactivator PGC1alpha.	AZD 6244	95-106	NRAS proto-oncogene, GTPase	Homo sapiens	36-40
25297634-2	2014	We found that a subset of BRAF- and NRAS-mutant human melanomas resistant to the MEK inhibitor selumetinib displayed increased oxidative phosphorylation (OxPhos) mediated by the transcriptional coactivator PGC1alpha.	AZD 6244	95-106	mitogen-activated protein kinase kinase 7	Homo sapiens	81-84
25297634-2	2014	We found that a subset of BRAF- and NRAS-mutant human melanomas resistant to the MEK inhibitor selumetinib displayed increased oxidative phosphorylation (OxPhos) mediated by the transcriptional coactivator PGC1alpha.	AZD 6244	95-106	PPARG coactivator 1 alpha	Homo sapiens	206-215
25297634-3	2014	Notably, all selumetinib-resistant cells with elevated OxPhos could be resensitized by cotreatment with the mTORC1/2 inhibitor AZD8055, whereas this combination was ineffective in resistant cell lines with low OxPhos.	AZD 6244	13-24	CREB regulated transcription coactivator 1	Mus musculus	108-114
25294906-6	2014	Treatment of PTC cell lines with the MEK1/2 inhibitor selumetinib or IFN increased HLA-ABC expression.	AZD 6244	54-65	mitogen-activated protein kinase kinase 1	Homo sapiens	37-43
24935174-6	2014	KRAS amplification was associated with worse clinical outcomes, and the KRAS gene mutation predicted sensitivity to the MEK1/2 inhibitor AZD6244 in gastric cancer cell lines.	AZD 6244	137-144	KRAS proto-oncogene, GTPase	Homo sapiens	72-76
25152244-8	2014	Interestingly, acquired MEK inhibitor resistance to AZD6244 was reversed by combined treatment with AZD6244 and either MK-2206 or AZD8055.	AZD 6244	52-59	mitogen-activated protein kinase kinase 7	Homo sapiens	24-27
25152244-8	2014	Interestingly, acquired MEK inhibitor resistance to AZD6244 was reversed by combined treatment with AZD6244 and either MK-2206 or AZD8055.	AZD 6244	100-107	mitogen-activated protein kinase kinase 7	Homo sapiens	24-27
25253770-6	2014	Preclinical evaluation of the mitogen-activated protein kinase kinase 1/2 inhibitor selumetinib (AZD6244, ARRY-142886) showed significant differential sensitivity in Ras pathway-mutated ALL compared with WT cells both in vitro and in an orthotopic xenograft model engrafted with primary ALL; in the latter, reduced RAS-mutated CNS leukemia.	AZD 6244	84-95	mitogen-activated protein kinase kinase 1	Homo sapiens	30-73
25253770-6	2014	Preclinical evaluation of the mitogen-activated protein kinase kinase 1/2 inhibitor selumetinib (AZD6244, ARRY-142886) showed significant differential sensitivity in Ras pathway-mutated ALL compared with WT cells both in vitro and in an orthotopic xenograft model engrafted with primary ALL; in the latter, reduced RAS-mutated CNS leukemia.	AZD 6244	97-104	mitogen-activated protein kinase kinase 1	Homo sapiens	30-73
24935174-6	2014	KRAS amplification was associated with worse clinical outcomes, and the KRAS gene mutation predicted sensitivity to the MEK1/2 inhibitor AZD6244 in gastric cancer cell lines.	AZD 6244	137-144	mitogen-activated protein kinase kinase 1	Homo sapiens	120-126
25130256-2	2014	Here, we show that treatment of NRAS-mutant melanoma cell lines with the MEK inhibitors AZD6244 or trametinib resulted in a rebound activation of phospho-ERK (pERK).	AZD 6244	88-95	NRAS proto-oncogene, GTPase	Homo sapiens	32-36
25130256-2	2014	Here, we show that treatment of NRAS-mutant melanoma cell lines with the MEK inhibitors AZD6244 or trametinib resulted in a rebound activation of phospho-ERK (pERK).	AZD 6244	88-95	mitogen-activated protein kinase kinase 7	Homo sapiens	73-76
25130256-2	2014	Here, we show that treatment of NRAS-mutant melanoma cell lines with the MEK inhibitors AZD6244 or trametinib resulted in a rebound activation of phospho-ERK (pERK).	AZD 6244	88-95	mitogen-activated protein kinase 1	Homo sapiens	154-157
25379021-7	2014	Surprisingly, Selumetinib was able to inhibit phosphorylation of p70 S6 kinase (p70S6K) and its downstream target ribosomal protein S6 (RPS6) in sensitive cell lines.	AZD 6244	14-25	ribosomal protein S6 kinase B1	Homo sapiens	65-78
25379021-0	2014	Resistance to Selumetinib (AZD6244) in colorectal cancer cell lines is mediated by p70S6K and RPS6 activation.	AZD 6244	14-25	ribosomal protein S6 kinase B1	Homo sapiens	83-89
25379021-0	2014	Resistance to Selumetinib (AZD6244) in colorectal cancer cell lines is mediated by p70S6K and RPS6 activation.	AZD 6244	14-25	ribosomal protein S6	Homo sapiens	94-98
25379021-0	2014	Resistance to Selumetinib (AZD6244) in colorectal cancer cell lines is mediated by p70S6K and RPS6 activation.	AZD 6244	27-34	ribosomal protein S6 kinase B1	Homo sapiens	83-89
25379021-0	2014	Resistance to Selumetinib (AZD6244) in colorectal cancer cell lines is mediated by p70S6K and RPS6 activation.	AZD 6244	27-34	ribosomal protein S6	Homo sapiens	94-98
25379021-1	2014	Selumetinib (AZD6244, ARRY-142886) is a MEK1/2 inhibitor that has gained interest as an anti-tumour agent.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	40-46
25379021-1	2014	Selumetinib (AZD6244, ARRY-142886) is a MEK1/2 inhibitor that has gained interest as an anti-tumour agent.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	40-46
25379021-1	2014	Selumetinib (AZD6244, ARRY-142886) is a MEK1/2 inhibitor that has gained interest as an anti-tumour agent.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	40-46
25379021-5	2014	Selumetinib inhibited phosphorylation of ERK1/2 and RSK and had no effect on AKT phosphorylation in both sensitive and resistant cells.	AZD 6244	0-11	mitogen-activated protein kinase 3	Homo sapiens	41-47
25379021-5	2014	Selumetinib inhibited phosphorylation of ERK1/2 and RSK and had no effect on AKT phosphorylation in both sensitive and resistant cells.	AZD 6244	0-11	ribosomal protein S6 kinase A2	Homo sapiens	52-55
25275595-3	2014	In 49 melanoma cell lines, we found independent susceptibility profiles for response to the MEK1/2 inhibitor AZD6244, the PI3K/mTOR inhibitor BEZ235 and the death receptor ligand TRAIL, supporting the rationale for their association.	AZD 6244	109-116	mitogen-activated protein kinase kinase 1	Homo sapiens	92-98
25275595-4	2014	Drug interaction analysis indicated that a strong synergistic anti-tumor activity could be achieved by the three agents and the AZD6244-TRAIL association on 20/21 melanomas, including cell lines resistant to the inhibitors or to TRAIL.	AZD 6244	128-135	TNF superfamily member 10	Homo sapiens	136-141
25275595-4	2014	Drug interaction analysis indicated that a strong synergistic anti-tumor activity could be achieved by the three agents and the AZD6244-TRAIL association on 20/21 melanomas, including cell lines resistant to the inhibitors or to TRAIL.	AZD 6244	128-135	TNF superfamily member 10	Homo sapiens	229-234
25275595-7	2014	In SCID mice, the AZD6244-TRAIL association induced significant growth inhibition of a tumor resistant to TRAIL and poorly responsive to AZD6244, with no detectable adverse events on body weight and tissue histology.	AZD 6244	18-25	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	26-31
25275595-7	2014	In SCID mice, the AZD6244-TRAIL association induced significant growth inhibition of a tumor resistant to TRAIL and poorly responsive to AZD6244, with no detectable adverse events on body weight and tissue histology.	AZD 6244	18-25	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	106-111
25275595-7	2014	In SCID mice, the AZD6244-TRAIL association induced significant growth inhibition of a tumor resistant to TRAIL and poorly responsive to AZD6244, with no detectable adverse events on body weight and tissue histology.	AZD 6244	137-144	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	26-31
25199829-5	2014	Compounds targeting RAF kinases can reverse resistance to the MEK inhibitor selumetinib.	AZD 6244	76-87	zinc fingers and homeoboxes 2	Homo sapiens	20-23
25199829-5	2014	Compounds targeting RAF kinases can reverse resistance to the MEK inhibitor selumetinib.	AZD 6244	76-87	mitogen-activated protein kinase kinase 7	Homo sapiens	62-65
25199829-6	2014	MEK inhibition induces RAS activation and BRAF-RAF1 dimerization and sustains MEK-ERK signaling, which is responsible for intrinsic resistance to selumetinib.	AZD 6244	146-157	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
25199829-6	2014	MEK inhibition induces RAS activation and BRAF-RAF1 dimerization and sustains MEK-ERK signaling, which is responsible for intrinsic resistance to selumetinib.	AZD 6244	146-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
25199829-6	2014	MEK inhibition induces RAS activation and BRAF-RAF1 dimerization and sustains MEK-ERK signaling, which is responsible for intrinsic resistance to selumetinib.	AZD 6244	146-157	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
25199829-6	2014	MEK inhibition induces RAS activation and BRAF-RAF1 dimerization and sustains MEK-ERK signaling, which is responsible for intrinsic resistance to selumetinib.	AZD 6244	146-157	mitogen-activated protein kinase kinase 7	Homo sapiens	78-81
25199829-6	2014	MEK inhibition induces RAS activation and BRAF-RAF1 dimerization and sustains MEK-ERK signaling, which is responsible for intrinsic resistance to selumetinib.	AZD 6244	146-157	mitogen-activated protein kinase 1	Homo sapiens	82-85
25294906-0	2014	MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro.	AZD 6244	121-132	major histocompatibility complex, class I, C	Homo sapiens	0-3
25218145-8	2014	RESULTS: Treatment of Lmna(H222P/H222P) mice with either benazepril or selumetinib started at 8weeks of age, before the onset of detectable left ventricular dysfunction, lead to statistically significantly increased fractional shortening compared to placebo at 16weeks of age.	AZD 6244	71-82	lamin A	Mus musculus	22-26
25278770-3	2014	Selumetinib is a potent and selective inhibitor of MEK1 and MEK2, which are essential downstream molecules in the MAPK pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	51-55
25278770-3	2014	Selumetinib is a potent and selective inhibitor of MEK1 and MEK2, which are essential downstream molecules in the MAPK pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 2	Homo sapiens	60-64
25185205-1	2014	A phase II trial of the MEK inhibitor selumetinib offers hope for patients with metastatic uveal melanoma, a rare and fatal eye cancer.	AZD 6244	38-49	mitogen-activated protein kinase kinase 7	Homo sapiens	24-27
25379021-7	2014	Surprisingly, Selumetinib was able to inhibit phosphorylation of p70 S6 kinase (p70S6K) and its downstream target ribosomal protein S6 (RPS6) in sensitive cell lines.	AZD 6244	14-25	ribosomal protein S6 kinase B1	Homo sapiens	80-86
25379021-7	2014	Surprisingly, Selumetinib was able to inhibit phosphorylation of p70 S6 kinase (p70S6K) and its downstream target ribosomal protein S6 (RPS6) in sensitive cell lines.	AZD 6244	14-25	ribosomal protein S6	Homo sapiens	114-134
25379021-7	2014	Surprisingly, Selumetinib was able to inhibit phosphorylation of p70 S6 kinase (p70S6K) and its downstream target ribosomal protein S6 (RPS6) in sensitive cell lines.	AZD 6244	14-25	ribosomal protein S6	Homo sapiens	136-140
25379021-11	2014	Pharmacological inhibition of p70S6K using the PI3K/mTOR inhibitor NVP-BEZ235, the specific mTOR inhibitor Rapamycin and the specific p70S6K inhibitor PF-4708671 potentiated Selumetinib effects in resistant cells.	AZD 6244	174-185	ribosomal protein S6 kinase B1	Homo sapiens	30-36
25379021-12	2014	In addition, biological inhibition of p70S6K using siRNA rendered responsiveness to Selumetinib in resistant cell lines.	AZD 6244	84-95	ribosomal protein S6 kinase B1	Homo sapiens	38-44
25379021-14	2014	We can conclude that p70S6K and its downstream target RPS6 are potential biomarkers of resistance to Selumetinib in colorectal cancer.	AZD 6244	101-112	ribosomal protein S6 kinase B1	Homo sapiens	21-27
25379021-14	2014	We can conclude that p70S6K and its downstream target RPS6 are potential biomarkers of resistance to Selumetinib in colorectal cancer.	AZD 6244	101-112	ribosomal protein S6	Homo sapiens	54-58
25342991-4	2014	For patients with KRAS mutant NSCLC, a phase III trial of the MEK inhibitor, selumetinib, has been initiated.	AZD 6244	77-88	KRAS proto-oncogene, GTPase	Homo sapiens	18-22
25342991-4	2014	For patients with KRAS mutant NSCLC, a phase III trial of the MEK inhibitor, selumetinib, has been initiated.	AZD 6244	77-88	mitogen-activated protein kinase kinase 7	Homo sapiens	62-65
24938872-3	2014	Using microRNA (miRNA) arrays and quantitative RT-PCR, we found that miR-203 was up-regulated after AZD6244 treatment.	AZD 6244	100-107	microRNA 203a	Homo sapiens	69-76
24938872-5	2014	Furthermore, miR-203 inhibition and CUL1 overexpression reversed the cytotoxicity of AZD6244 on the MDA-MB-231 and HCC1937 cells.	AZD 6244	85-92	microRNA 203a	Homo sapiens	13-20
24938872-1	2014	The targeted small-molecule drug AZD6244 is an allosteric, ATP-noncompetitive inhibitor of MEK1/2 that has shown activity against several malignant tumors.	AZD 6244	33-40	mitogen-activated protein kinase kinase 1	Homo sapiens	91-97
24938872-5	2014	Furthermore, miR-203 inhibition and CUL1 overexpression reversed the cytotoxicity of AZD6244 on the MDA-MB-231 and HCC1937 cells.	AZD 6244	85-92	cullin 1	Homo sapiens	36-40
24938872-6	2014	Collectively, our data indicate that miR-203 mediates the AZD6244-induced cytotoxicity of breast cancer cells and that the MEK/ERK/miR-203/CUL1 signaling pathway may participate in this process.	AZD 6244	58-65	microRNA 203a	Homo sapiens	37-44
24938872-6	2014	Collectively, our data indicate that miR-203 mediates the AZD6244-induced cytotoxicity of breast cancer cells and that the MEK/ERK/miR-203/CUL1 signaling pathway may participate in this process.	AZD 6244	58-65	mitogen-activated protein kinase 1	Homo sapiens	127-130
24938872-6	2014	Collectively, our data indicate that miR-203 mediates the AZD6244-induced cytotoxicity of breast cancer cells and that the MEK/ERK/miR-203/CUL1 signaling pathway may participate in this process.	AZD 6244	58-65	microRNA 203a	Homo sapiens	131-138
24938872-6	2014	Collectively, our data indicate that miR-203 mediates the AZD6244-induced cytotoxicity of breast cancer cells and that the MEK/ERK/miR-203/CUL1 signaling pathway may participate in this process.	AZD 6244	58-65	cullin 1	Homo sapiens	139-143
24812410-6	2014	The synergistic antiproliferative effects were confirmed using other two selective MEK1/2 inhibitors, selumetinib and pimasertib, in combination with cetuximab.	AZD 6244	102-113	mitogen-activated protein kinase kinase 1	Homo sapiens	83-89
24899684-2	2014	Selective MEK inhibitors, such as selumetinib, have shown clinical benefit in uveal melanoma.	AZD 6244	34-45	mitogen-activated protein kinase kinase 7	Homo sapiens	10-13
24899684-9	2014	We also analyzed the expression of DDX43 in liver metastases of patients with uveal melanoma by RT-PCR, and found a significant overexpression of DDX43 in patients who did not benefit from selumetinib therapy.	AZD 6244	189-200	DEAD-box helicase 43	Homo sapiens	146-151
24760959-3	2014	In this study, we describe the development and use of the LC-MRM platform to study the adaptive signaling responses of melanoma cells to inhibitors of HSP90 (XL888) and MEK (AZD6244).	AZD 6244	174-181	mitogen-activated protein kinase kinase 7	Homo sapiens	169-172
24739393-3	2014	We evaluated the combination effect of the mTOR inhibitor AZD8055 and the MEK inhibitor selumetinib on human AML cell lines and primary AML samples.	AZD 6244	88-99	mitogen-activated protein kinase kinase 7	Homo sapiens	74-77
24760959-8	2014	Validation studies identified PDGF receptor beta signaling as a potential escape mechanism from MEK inhibition, which could be overcome through combined use of AZD6244 and the PDGF receptor inhibitor, crenolanib.	AZD 6244	160-167	mitogen-activated protein kinase kinase 7	Homo sapiens	96-99
24938562-2	2014	OBJECTIVE: To assess the efficacy of selumetinib, a selective, non-adenosine triphosphate competitive inhibitor of MEK1 and MEK2, in uveal melanoma.	AZD 6244	37-48	mitogen-activated protein kinase kinase 1	Homo sapiens	115-119
24938562-2	2014	OBJECTIVE: To assess the efficacy of selumetinib, a selective, non-adenosine triphosphate competitive inhibitor of MEK1 and MEK2, in uveal melanoma.	AZD 6244	37-48	mitogen-activated protein kinase kinase 2	Homo sapiens	124-128
24939055-0	2014	Antitumor activity of selective MEK1/2 inhibitor AZD6244 in combination with PI3K/mTOR inhibitor BEZ235 in gefitinib-resistant NSCLC xenograft models.	AZD 6244	49-56	mitogen-activated protein kinase kinase 1	Homo sapiens	32-38
24939055-2	2014	AZD6244 is a potent, selective, and orally available MEK1/2 inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	53-59
24939055-8	2014	Western blot analysis and immunohistochemical staining revealed that AZD6244 alone reduced ERK1/2 phosphorylation, angiogenesis, and tumor cell proliferation.	AZD 6244	69-76	mitogen-activated protein kinase 3	Homo sapiens	91-97
24243688-6	2014	In human thyroid cancer BCPAP cells harboring homozygous BRAF V600E mutation, BRAF V600E inhibitor, PLX4032, and MEK inhibitor, AZD6244, increased histone acetylation of the NIS promoter, suggesting that BRAF V600E normally maintained histone in a deacetylated state at the NIS promoter.	AZD 6244	128-135	mitogen-activated protein kinase kinase 7	Homo sapiens	113-116
24909280-1	2014	OBJECTIVE: To investigate the effect of phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002 combined with mitogen activated protein kinase kinase (MEK) inhibitor AZD6244 on the proliferation of cisplatin-resistant SKOV3/DDP ovarian cancer cell line.	AZD 6244	166-173	mitogen-activated protein kinase kinase 7	Homo sapiens	110-149
24909280-1	2014	OBJECTIVE: To investigate the effect of phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002 combined with mitogen activated protein kinase kinase (MEK) inhibitor AZD6244 on the proliferation of cisplatin-resistant SKOV3/DDP ovarian cancer cell line.	AZD 6244	166-173	mitogen-activated protein kinase kinase 7	Homo sapiens	151-154
24909280-9	2014	CONCLUSION: Combined PI3K inhibitor LY294002 and MEK inhibitor AZD6244 has synergistic effect on inhibition of SKOV3/DDP cell growth by inducing apoptosis and blocking cell cycle.	AZD 6244	63-70	mitogen-activated protein kinase kinase 7	Homo sapiens	49-52
24375836-0	2014	MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim.	AZD 6244	17-24	BCL2 like 11	Homo sapiens	94-97
24375836-1	2014	AZD6244, an ATP-uncompetitive inhibitor of mitogen-activated protein kinase 1/2 (MEK1/2), has shown activity in several malignant tumours.	AZD 6244	0-7	mitogen-activated protein kinase 12	Homo sapiens	43-79
24375836-1	2014	AZD6244, an ATP-uncompetitive inhibitor of mitogen-activated protein kinase 1/2 (MEK1/2), has shown activity in several malignant tumours.	AZD 6244	0-7	mitogen-activated protein kinase 12	Homo sapiens	81-87
24375836-8	2014	Silencing Bim decreases AZD6244-induced apoptosis and G1-phase arrest, suggesting that Bim contributes to the growth arrest.	AZD 6244	24-31	BCL2 like 11	Homo sapiens	10-13
24375836-8	2014	Silencing Bim decreases AZD6244-induced apoptosis and G1-phase arrest, suggesting that Bim contributes to the growth arrest.	AZD 6244	24-31	BCL2 like 11	Homo sapiens	87-90
24375836-9	2014	Thus, miR-92a mediates AZD6244-induced cytotoxicity of lymphoma cells by targeting Bim.	AZD 6244	23-30	BCL2 like 11	Homo sapiens	83-86
24375836-10	2014	Downregulation of miR-92a by AZD6244 is mediated by the ERK1/2-AP1 signalling pathway.	AZD 6244	29-36	mitogen-activated protein kinase 3	Homo sapiens	56-62
24375836-10	2014	Downregulation of miR-92a by AZD6244 is mediated by the ERK1/2-AP1 signalling pathway.	AZD 6244	29-36	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-66
24363449-7	2014	Finally, although the combination of MEK1/2 inhibitors with mTOR inhibitors is an attractive rational drug combination, SW620:8055R cells were actually cross-resistant to the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	192-203	mitogen-activated protein kinase kinase 1	Homo sapiens	175-181
24363449-7	2014	Finally, although the combination of MEK1/2 inhibitors with mTOR inhibitors is an attractive rational drug combination, SW620:8055R cells were actually cross-resistant to the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	205-212	mitogen-activated protein kinase kinase 1	Homo sapiens	175-181
24269278-0	2014	Modulation of endochondral ossification by MEK inhibitors PD0325901 and AZD6244 (Selumetinib).	AZD 6244	72-79	midkine	Mus musculus	43-46
24269278-0	2014	Modulation of endochondral ossification by MEK inhibitors PD0325901 and AZD6244 (Selumetinib).	AZD 6244	81-92	midkine	Mus musculus	43-46
24269278-1	2014	MEK inhibitors (MEKi) PD0325901 and AZD6244 (Selumetinib) are drugs currently under clinical investigation for cancer treatment, however the Ras-MAPK pathway is also an important mediator of normal bone cell differentiation and function.	AZD 6244	45-56	midkine	Mus musculus	0-3
24269278-3	2014	Treatment with PD0325901 or AZD6244 significantly increased Runx2 and Alkaline phosphate gene expression in calvarial osteoblasts and decreased TRAP+ cells in induced osteoclast cultures.	AZD 6244	28-35	runt related transcription factor 2	Mus musculus	60-65
24269278-10	2014	PD0325901 or AZD6244 led to increased matrix protein expression (Col2a1 and Acan) and decreased expression of catabolic factors (Mmp13 and Adamts-5).	AZD 6244	13-20	collagen, type II, alpha 1	Mus musculus	65-71
24269278-10	2014	PD0325901 or AZD6244 led to increased matrix protein expression (Col2a1 and Acan) and decreased expression of catabolic factors (Mmp13 and Adamts-5).	AZD 6244	13-20	aggrecan	Mus musculus	76-80
24269278-10	2014	PD0325901 or AZD6244 led to increased matrix protein expression (Col2a1 and Acan) and decreased expression of catabolic factors (Mmp13 and Adamts-5).	AZD 6244	13-20	matrix metallopeptidase 13	Mus musculus	129-134
24269278-10	2014	PD0325901 or AZD6244 led to increased matrix protein expression (Col2a1 and Acan) and decreased expression of catabolic factors (Mmp13 and Adamts-5).	AZD 6244	13-20	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2)	Mus musculus	139-147
24253175-8	2014	Selumetinib inhibited ASM with an IC50 of 1,750 ng/ml, but was not effective in ISO-HAS.	AZD 6244	0-11	H19 imprinted maternally expressed transcript	Homo sapiens	22-25
24567366-2	2014	Selumetinib, a MEK 1/2 inhibitor, suppresses pERK levels independent of BRAF and NRAS mutation status, and combination with docetaxel has demonstrated synergy in xenograft models.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	15-22
24567366-2	2014	Selumetinib, a MEK 1/2 inhibitor, suppresses pERK levels independent of BRAF and NRAS mutation status, and combination with docetaxel has demonstrated synergy in xenograft models.	AZD 6244	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	45-49
24567366-3	2014	The aim of this study was to assess the efficacy and safety of selumetinib plus docetaxel as first-line treatment in patients with wild-type BRAF advanced melanoma.	AZD 6244	63-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	141-145
24448821-3	2014	This mutation confers resistance to not only vemurafenib, but also to the allosteric MEK inhibitor selumetinib (AZD6244).	AZD 6244	99-110	midkine	Mus musculus	85-88
24448821-3	2014	This mutation confers resistance to not only vemurafenib, but also to the allosteric MEK inhibitor selumetinib (AZD6244).	AZD 6244	112-119	midkine	Mus musculus	85-88
24448821-7	2014	We found that the acquired MEK1-C121S mutation in BRAF-V600E mutant melanoma conferred resistance to both vemurafenib and selumetinib but not E6201.	AZD 6244	122-133	mitogen-activated protein kinase kinase 1	Mus musculus	27-31
24448821-7	2014	We found that the acquired MEK1-C121S mutation in BRAF-V600E mutant melanoma conferred resistance to both vemurafenib and selumetinib but not E6201.	AZD 6244	122-133	Braf transforming gene	Mus musculus	50-54
24406751-6	2014	Selumetinib added to docetaxel has improved outcome compared with docetaxel in a randomized phase II trial in patients with advanced KRAS-mutant NSCLC and this combination is currently studied in a phase III trial.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	133-137
24716986-9	2014	CONCLUSIONS: Compared with current chemotherapy, selumetinib has modest clinical activity as monotherapy in patients with advanced cancer, but combinations of selumetinib with cytotoxic agents in patients with BRAF or KRAS mutations hold great promise for cancer treatment.	AZD 6244	159-170	KRAS proto-oncogene, GTPase	Homo sapiens	218-222
24132923-0	2013	Development, characterization, and reversal of acquired resistance to the MEK1 inhibitor selumetinib (AZD6244) in an in vivo model of childhood astrocytoma.	AZD 6244	89-100	mitogen-activated protein kinase kinase 1	Mus musculus	74-78
24200969-7	2014	Further analysis of 46 melanoma cell lines that harbored BRAF mutation showed that 7 pathways, including TNFalpha, EGFR, IFNalpha, hypoxia, IFNgamma, STAT3, and MYC, were significantly differently expressed in AZD6244-resistant compared with responsive melanoma cells.	AZD 6244	210-217	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
24200969-8	2014	A SVM classifier built on this 7-pathway activation pattern correctly predicted the response of 10 BRAF-mutated melanoma cell lines to the MEK inhibitor AZD6244 in our experiments.	AZD 6244	153-160	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
24200969-8	2014	A SVM classifier built on this 7-pathway activation pattern correctly predicted the response of 10 BRAF-mutated melanoma cell lines to the MEK inhibitor AZD6244 in our experiments.	AZD 6244	153-160	mitogen-activated protein kinase kinase 7	Homo sapiens	139-142
24200969-9	2014	We experimentally showed that TNFalpha, EGFR, IFNalpha, and IFNgamma pathway activities were also upregulated in melanoma cell A375 compared with its sub-line DRO, while DRO was much more sensitive to AZD6244 than A375.	AZD 6244	201-208	tumor necrosis factor	Homo sapiens	30-38
24200969-9	2014	We experimentally showed that TNFalpha, EGFR, IFNalpha, and IFNgamma pathway activities were also upregulated in melanoma cell A375 compared with its sub-line DRO, while DRO was much more sensitive to AZD6244 than A375.	AZD 6244	201-208	epidermal growth factor receptor	Homo sapiens	40-44
24200969-9	2014	We experimentally showed that TNFalpha, EGFR, IFNalpha, and IFNgamma pathway activities were also upregulated in melanoma cell A375 compared with its sub-line DRO, while DRO was much more sensitive to AZD6244 than A375.	AZD 6244	201-208	interferon gamma	Homo sapiens	60-68
24178622-0	2014	Phase II study of the oral MEK inhibitor selumetinib in advanced acute myelogenous leukemia: a University of Chicago phase II consortium trial.	AZD 6244	41-52	mitogen-activated protein kinase kinase 7	Homo sapiens	27-30
24178622-2	2014	EXPERIMENTAL DESIGN: Selumetinib is an oral small-molecule inhibitor of MAP-ERK kinase (MEK)-1/2.	AZD 6244	21-32	mitogen-activated protein kinase kinase 1	Homo sapiens	72-96
24178622-16	2014	The potential association of SNP rs3733542 in exon 18 of the KIT gene with antileukemic activity of selumetinib is intriguing, but will require validation in larger trials.	AZD 6244	100-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
24132923-0	2013	Development, characterization, and reversal of acquired resistance to the MEK1 inhibitor selumetinib (AZD6244) in an in vivo model of childhood astrocytoma.	AZD 6244	102-109	mitogen-activated protein kinase kinase 1	Mus musculus	74-78
24132923-1	2013	PURPOSE: The BT-40 low-grade childhood astrocytoma xenograft model expresses mutated BRAF(V600E) and is highly sensitive to the MEK inhibitor selumetinib (AZD6244).	AZD 6244	142-153	Braf transforming gene	Mus musculus	85-90
24132923-1	2013	PURPOSE: The BT-40 low-grade childhood astrocytoma xenograft model expresses mutated BRAF(V600E) and is highly sensitive to the MEK inhibitor selumetinib (AZD6244).	AZD 6244	142-153	midkine	Mus musculus	128-131
24132923-1	2013	PURPOSE: The BT-40 low-grade childhood astrocytoma xenograft model expresses mutated BRAF(V600E) and is highly sensitive to the MEK inhibitor selumetinib (AZD6244).	AZD 6244	155-162	midkine	Mus musculus	128-131
24132923-7	2013	RESULTS: Resistance was unstable, tumors reverting to selumetinib sensitivity when passaged in untreated mice, and MEK was equally inhibited in sensitive and resistant tumors by selumetinib.	AZD 6244	178-189	midkine	Mus musculus	115-118
24132923-9	2013	Selumetinib treatment induced phosphorylation of STAT3 (Y705) only in resistant xenografts, and similar results were observed in BRAF(V600E) astrocytic cell lines intrinsically resistant to selumetinib.	AZD 6244	0-11	signal transducer and activator of transcription 3	Mus musculus	49-54
24132923-12	2013	In resistant tumors, selumetinib activated STAT3, and combined treatment with selumetinib and LLL12 induced complete responses in resistant BT-40 tumors.	AZD 6244	21-32	signal transducer and activator of transcription 3	Mus musculus	43-48
24132923-13	2013	These results suggest dual targeting BRAF (V600E) signaling and STAT3 signaling may be effective in selumetinib-resistant tumors or may retard or prevent onset of resistance.	AZD 6244	100-111	Braf transforming gene	Mus musculus	37-41
24132923-13	2013	These results suggest dual targeting BRAF (V600E) signaling and STAT3 signaling may be effective in selumetinib-resistant tumors or may retard or prevent onset of resistance.	AZD 6244	100-111	signal transducer and activator of transcription 3	Mus musculus	64-69
24045180-5	2013	In addition, the efficacy of OSI-906 combined with the MEK 1/2 inhibitor selumetinib (AZD6244, ARRY-142886) was evaluated in vivo using human colorectal cancer xenograft models.	AZD 6244	73-84	mitogen-activated protein kinase kinase 1	Homo sapiens	55-62
23602735-7	2013	AZD6244 abrogated p-ERK and GDC0941 abrogated p-AKT levels, confirming their expected target effects.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	20-23
24130864-7	2013	While BxPC-3 (KRAS wild type) and MIA PaCa-2 (KRAS mutated) cell lines were sensitive to GDC0941 and AZD6244 as single agents, synergistic inhibition of tumor cell growth and induction of apoptosis were observed in both cell lines when the two drugs were combined.	AZD 6244	101-108	KRAS proto-oncogene, GTPase	Homo sapiens	14-18
24130864-7	2013	While BxPC-3 (KRAS wild type) and MIA PaCa-2 (KRAS mutated) cell lines were sensitive to GDC0941 and AZD6244 as single agents, synergistic inhibition of tumor cell growth and induction of apoptosis were observed in both cell lines when the two drugs were combined.	AZD 6244	101-108	KRAS proto-oncogene, GTPase	Homo sapiens	46-50
24130864-8	2013	Interestingly, phosphorylation of the cap-dependent translational components, 4E-binding protein (p-4E-BP1) and S6 was found to be closely associated with sensitivity to GDC0941 and AZD6244.	AZD 6244	182-189	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	100-106
23602735-11	2013	CONCLUSION: Concomitant suppression of MEK/ERK and PI3K/AKT pathways by AZD6244 and GDC0941 abrogates compensatory mechanisms of tumor survival and causes synergistic cytotoxicity in thyroid cancer cells.	AZD 6244	72-79	mitogen-activated protein kinase kinase 7	Homo sapiens	39-42
23602735-11	2013	CONCLUSION: Concomitant suppression of MEK/ERK and PI3K/AKT pathways by AZD6244 and GDC0941 abrogates compensatory mechanisms of tumor survival and causes synergistic cytotoxicity in thyroid cancer cells.	AZD 6244	72-79	mitogen-activated protein kinase 1	Homo sapiens	43-46
23602735-11	2013	CONCLUSION: Concomitant suppression of MEK/ERK and PI3K/AKT pathways by AZD6244 and GDC0941 abrogates compensatory mechanisms of tumor survival and causes synergistic cytotoxicity in thyroid cancer cells.	AZD 6244	72-79	AKT serine/threonine kinase 1	Homo sapiens	56-59
23942066-0	2013	Acute tumour response to the MEK1/2 inhibitor selumetinib (AZD6244, ARRY-142886) evaluated by non-invasive diffusion-weighted MRI.	AZD 6244	46-57	mitogen-activated protein kinase kinase 1	Homo sapiens	29-35
23942066-2	2013	This study evaluates tumour apparent diffusion coefficient (ADC), measured by diffusion-weighted magnetic resonance imaging (DW-MRI), as a biomarker of response to the MEK1/2 inhibitor selumetinib (AZD6244, ARRY-142886) in human tumour xenografts.	AZD 6244	185-196	mitogen-activated protein kinase kinase 1	Homo sapiens	168-174
23942066-5	2013	RESULTS: Selumetinib treatment induced tumour stasis and reduced ERK1/2 phosphorylation in both WM266.4 and Colo205 tumour xenografts.	AZD 6244	9-20	mitogen-activated protein kinase 3	Homo sapiens	65-71
23942066-8	2013	CONCLUSION: Changes in ADC following treatment with the MEK1/2 inhibitor selumetinib in responsive human tumour xenografts were concomitant with induction of tumour cell death.	AZD 6244	73-84	mitogen-activated protein kinase kinase 1	Homo sapiens	56-62
23908690-7	2013	Consistent with its role in vitro, overexpression of PIB5PA and the MEK inhibitor selumetinib cooperatively inhibited melanoma tumor growth in a xenograft model.	AZD 6244	82-93	mitogen-activated protein kinase kinase 7	Homo sapiens	68-71
23757356-4	2013	EXPERIMENTAL DESIGN: In this study, we conducted unbiased gene set enrichment analysis and synthetic lethality screens with selumetinib, which identified the noncanonical Wnt/Ca++ signaling pathway as a potential mediator of resistance to the MEK1/2 inhibitor selumetinib.	AZD 6244	124-135	mitogen-activated protein kinase kinase 1	Homo sapiens	243-249
23575444-5	2013	Confirming our hypothesis, we found that MEK inhibitors including selumetinib preferentially inhibited cytokine production and alloreactivity mediated by naive and central memory human CD4(+) and CD8(+) T cells while sparing more differentiated T cells specific for the human herpesviruses cytomegalovirus and Epstein-Barr virus.	AZD 6244	66-77	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
23847359-1	2013	Selumetinib plus dacarbazine prolongs progression-free survival in BRAF-mutant melanoma.	AZD 6244	0-11	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
23847383-1	2013	Compared with temozolomide chemotherapy, the MEK inhibitor selumetinib extended progression-free survival by nearly 9 weeks in patients with melanoma of the eye participating in a phase II trial, making it the first effective drug for the rare disease.	AZD 6244	59-70	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
23735514-0	2013	Selumetinib plus dacarbazine versus placebo plus dacarbazine as first-line treatment for BRAF-mutant metastatic melanoma: a phase 2 double-blind randomised study.	AZD 6244	0-11	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
23735514-2	2013	Selumetinib, a MEK1/2 inhibitor, has shown antitumour activity in patients with BRAF-mutant melanoma and in preclinical models when combined with chemotherapy.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	15-21
23735514-2	2013	Selumetinib, a MEK1/2 inhibitor, has shown antitumour activity in patients with BRAF-mutant melanoma and in preclinical models when combined with chemotherapy.	AZD 6244	0-11	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
23735514-14	2013	INTERPRETATION: Selumetinib plus dacarbazine showed clinical activity in patients with BRAF-mutant cutaneous or unknown primary melanoma, reflected by a significant benefit in progression-free survival compared with placebo plus dacarbazine group, although no significant change in overall survival was noted.	AZD 6244	16-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
23815988-7	2013	LmnaH222P/H222P mice were treated with selumetinib, which blocks mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 that activates ERK1/2, from 16 to 20 weeks of age to assess the effects of treatment on muscle histology, ERK1/2 activity and limb grip strength.	AZD 6244	39-50	mitogen-activated protein kinase 3	Mus musculus	162-168
23826126-10	2013	MIB/MS and immunoblotting revealed that BAY 65-1942 increased MEK/ERK signaling and that this increase was prevented by co-treatment with a MEK inhibitor (AZD6244).	AZD 6244	155-162	MIB E3 ubiquitin protein ligase 1	Homo sapiens	0-3
23826126-10	2013	MIB/MS and immunoblotting revealed that BAY 65-1942 increased MEK/ERK signaling and that this increase was prevented by co-treatment with a MEK inhibitor (AZD6244).	AZD 6244	155-162	mitogen-activated protein kinase kinase 7	Homo sapiens	62-65
23826126-10	2013	MIB/MS and immunoblotting revealed that BAY 65-1942 increased MEK/ERK signaling and that this increase was prevented by co-treatment with a MEK inhibitor (AZD6244).	AZD 6244	155-162	EPH receptor B2	Homo sapiens	66-69
23826126-10	2013	MIB/MS and immunoblotting revealed that BAY 65-1942 increased MEK/ERK signaling and that this increase was prevented by co-treatment with a MEK inhibitor (AZD6244).	AZD 6244	155-162	mitogen-activated protein kinase kinase 7	Homo sapiens	140-143
23575444-5	2013	Confirming our hypothesis, we found that MEK inhibitors including selumetinib preferentially inhibited cytokine production and alloreactivity mediated by naive and central memory human CD4(+) and CD8(+) T cells while sparing more differentiated T cells specific for the human herpesviruses cytomegalovirus and Epstein-Barr virus.	AZD 6244	66-77	CD4 molecule	Homo sapiens	185-188
23575444-5	2013	Confirming our hypothesis, we found that MEK inhibitors including selumetinib preferentially inhibited cytokine production and alloreactivity mediated by naive and central memory human CD4(+) and CD8(+) T cells while sparing more differentiated T cells specific for the human herpesviruses cytomegalovirus and Epstein-Barr virus.	AZD 6244	66-77	CD8a molecule	Homo sapiens	196-199
23575444-6	2013	We then demonstrated that short-term posttransplant administration of selumetinib in a major histocompatibility complex major- and minor-mismatched murine model significantly delayed the onset of GVHD-associated mortality without compromising myeloid engraftment, demonstrating the in vivo potential of MEK inhibitors in the setting of hematopoietic stem cell transplantation.	AZD 6244	70-81	midkine	Mus musculus	303-306
23588995-3	2013	In this study, we investigated the role of transforming growth factor-alpha (TGF-alpha) in the radiosensitizing effects of selumetinib, a selective inhibitor of MEK1/2.	AZD 6244	123-134	tumor necrosis factor	Homo sapiens	43-75
23588995-3	2013	In this study, we investigated the role of transforming growth factor-alpha (TGF-alpha) in the radiosensitizing effects of selumetinib, a selective inhibitor of MEK1/2.	AZD 6244	123-134	transforming growth factor alpha	Homo sapiens	77-86
23588995-3	2013	In this study, we investigated the role of transforming growth factor-alpha (TGF-alpha) in the radiosensitizing effects of selumetinib, a selective inhibitor of MEK1/2.	AZD 6244	123-134	mitogen-activated protein kinase kinase 1	Homo sapiens	161-167
23588995-4	2013	The expression of epidermal growth factor receptor (EGFR) ligands was assessed by ELISA in both Ras wild-type and Ras mutant cells that were exposed to radiation with or without selumetinib.	AZD 6244	178-189	epidermal growth factor receptor	Homo sapiens	18-50
23588995-4	2013	The expression of epidermal growth factor receptor (EGFR) ligands was assessed by ELISA in both Ras wild-type and Ras mutant cells that were exposed to radiation with or without selumetinib.	AZD 6244	178-189	epidermal growth factor receptor	Homo sapiens	52-56
23588995-5	2013	The effects of selumetinib on the TGF-alpha/EGFR signaling cascade in response to radiation were examined by western blot analysis, clonogenic assay and by determing the yield of mitotic catastrophe.	AZD 6244	15-26	transforming growth factor alpha	Homo sapiens	34-43
23588995-5	2013	The effects of selumetinib on the TGF-alpha/EGFR signaling cascade in response to radiation were examined by western blot analysis, clonogenic assay and by determing the yield of mitotic catastrophe.	AZD 6244	15-26	epidermal growth factor receptor	Homo sapiens	44-48
23588995-6	2013	The treatment of cells with selumetinib reduced the basal and IR-induced secretion of TGF-alpha in both Ras wild-type and Ras mutant cell lines in vitro and in vivo.	AZD 6244	28-39	transforming growth factor alpha	Homo sapiens	86-95
23588995-7	2013	The reduction of TGF-alpha secretion was accompanied with a reduction in phosphorylated tumor necrosis factor-alpha converting enzyme (TACE) in the cells treated with selumetinib with or without IR.	AZD 6244	167-178	transforming growth factor alpha	Homo sapiens	17-26
23588995-7	2013	The reduction of TGF-alpha secretion was accompanied with a reduction in phosphorylated tumor necrosis factor-alpha converting enzyme (TACE) in the cells treated with selumetinib with or without IR.	AZD 6244	167-178	ADAM metallopeptidase domain 17	Homo sapiens	88-133
23588995-7	2013	The reduction of TGF-alpha secretion was accompanied with a reduction in phosphorylated tumor necrosis factor-alpha converting enzyme (TACE) in the cells treated with selumetinib with or without IR.	AZD 6244	167-178	ADAM metallopeptidase domain 17	Homo sapiens	135-139
23588995-8	2013	The treatment of cells with selumetinib with or without IR inhibited the phosphorylation of EGFR and checkpoint kinase 2 (Chk2), and reduced the expression of survivin.	AZD 6244	28-39	epidermal growth factor receptor	Homo sapiens	92-96
23588995-8	2013	The treatment of cells with selumetinib with or without IR inhibited the phosphorylation of EGFR and checkpoint kinase 2 (Chk2), and reduced the expression of survivin.	AZD 6244	28-39	checkpoint kinase 2	Homo sapiens	101-120
23588995-8	2013	The treatment of cells with selumetinib with or without IR inhibited the phosphorylation of EGFR and checkpoint kinase 2 (Chk2), and reduced the expression of survivin.	AZD 6244	28-39	checkpoint kinase 2	Homo sapiens	122-126
23588995-9	2013	Supplementation with exogenous TGF-alpha partially rescued the selumetinib-treated cells from IR-induced cell death, restored EGFR and Chk2 phosphorylation and increased survivin expression.	AZD 6244	63-74	transforming growth factor alpha	Homo sapiens	31-40
23588995-9	2013	Supplementation with exogenous TGF-alpha partially rescued the selumetinib-treated cells from IR-induced cell death, restored EGFR and Chk2 phosphorylation and increased survivin expression.	AZD 6244	63-74	epidermal growth factor receptor	Homo sapiens	126-130
23588995-9	2013	Supplementation with exogenous TGF-alpha partially rescued the selumetinib-treated cells from IR-induced cell death, restored EGFR and Chk2 phosphorylation and increased survivin expression.	AZD 6244	63-74	checkpoint kinase 2	Homo sapiens	135-139
23588995-10	2013	These data suggest that the inhibition of MEK1/2 with selumetinib may provide a mechanism to sensitize tumor cells to IR in a fashion that prevents the activation of the TGF-alpha autocrine loop following IR.	AZD 6244	54-65	mitogen-activated protein kinase kinase 1	Homo sapiens	42-48
23588995-10	2013	These data suggest that the inhibition of MEK1/2 with selumetinib may provide a mechanism to sensitize tumor cells to IR in a fashion that prevents the activation of the TGF-alpha autocrine loop following IR.	AZD 6244	54-65	transforming growth factor alpha	Homo sapiens	170-179
23530058-1	2013	MEK1/2 inhibitors such as AZD6244 are in clinical trials for the treatment of multiple cancers, including breast cancer.	AZD 6244	26-33	mitogen-activated protein kinase kinase 1	Homo sapiens	0-6
23530058-4	2013	Screening of a miRNA mimic library revealed the ability of miR-9-3p to significantly enhance AZD6244-induced extracellular signal-regulated kinase inhibition and growth arrest, while miR-9-3p had little effect on growth alone.	AZD 6244	93-100	microRNA 9-3	Homo sapiens	59-67
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	integrin subunit beta 1	Homo sapiens	4-18
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	integrin subunit beta 1	Homo sapiens	25-30
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	microRNA 9-3	Homo sapiens	56-64
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	integrin subunit beta 1	Homo sapiens	165-170
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	mitogen-activated protein kinase kinase 7	Homo sapiens	191-194
24063423-0	2013	Selumetinib in advanced non small cell lung cancer (NSCLC) harbouring KRAS mutation: endless clinical challenge to KRAS-mutant NSCLC.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	70-74
23515407-8	2013	Five of 6 NRAS-mutant cell lines were sensitive to the MEK inhibitors, selumetinib and trametinib, but not to other inhibitors tested.	AZD 6244	71-82	NRAS proto-oncogene, GTPase	Homo sapiens	10-14
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	163-174	G protein subunit alpha q	Homo sapiens	59-63
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	163-174	mitogen-activated protein kinase kinase 7	Homo sapiens	80-83
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	163-174	AKT serine/threonine kinase 1	Homo sapiens	88-91
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	163-174	mitogen-activated protein kinase kinase 7	Homo sapiens	149-152
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	176-183	G protein subunit alpha q	Homo sapiens	59-63
23443802-3	2013	In this study, using a siRNA strategy, we show that mutant GNAQ signals to both MEK and AKT, and that combined inhibition of these pathways with the MEK inhibitor selumetinib (AZD6244) and the AKT inhibitor MK2206 induced a synergistic decrease in cell viability.	AZD 6244	176-183	mitogen-activated protein kinase kinase 7	Homo sapiens	149-152
23436801-9	2013	Single-agent treatment with Torin2 in vivo did not yield significant efficacy against KRAS-driven lung tumors, but the combination of Torin2 with mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor AZD6244 yielded a significant growth inhibition.	AZD 6244	226-233	mitogen-activated protein kinase kinase 7	Homo sapiens	146-209
23436801-9	2013	Single-agent treatment with Torin2 in vivo did not yield significant efficacy against KRAS-driven lung tumors, but the combination of Torin2 with mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor AZD6244 yielded a significant growth inhibition.	AZD 6244	226-233	mitogen-activated protein kinase kinase 7	Homo sapiens	211-214
23444215-0	2013	Phase II trial of MEK inhibitor selumetinib (AZD6244, ARRY-142886) in patients with BRAFV600E/K-mutated melanoma.	AZD 6244	32-43	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
23444215-0	2013	Phase II trial of MEK inhibitor selumetinib (AZD6244, ARRY-142886) in patients with BRAFV600E/K-mutated melanoma.	AZD 6244	45-52	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
23444215-1	2013	PURPOSE: Test the hypothesis that in BRAF-mutated melanomas, clinical responses to selumetinib, a MEK inhibitor, will be restricted to tumors in which the PI3K/AKT pathway is not activated.	AZD 6244	83-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
23444215-1	2013	PURPOSE: Test the hypothesis that in BRAF-mutated melanomas, clinical responses to selumetinib, a MEK inhibitor, will be restricted to tumors in which the PI3K/AKT pathway is not activated.	AZD 6244	83-94	mitogen-activated protein kinase kinase 7	Homo sapiens	98-101
23444215-1	2013	PURPOSE: Test the hypothesis that in BRAF-mutated melanomas, clinical responses to selumetinib, a MEK inhibitor, will be restricted to tumors in which the PI3K/AKT pathway is not activated.	AZD 6244	83-94	AKT serine/threonine kinase 1	Homo sapiens	160-163
23255578-8	2013	Furthermore, AZD6244, a clinically relevant inhibitor of the ERK1/2 pathway, mitigated particle-induced inflammatory gene expression in osteoprogenitor cells and macrophages.	AZD 6244	13-20	mitogen-activated protein kinase 3	Homo sapiens	61-67
23234544-0	2013	The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance.	AZD 6244	61-72	mitogen-activated protein kinase kinase 1	Homo sapiens	44-50
23234544-0	2013	The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance.	AZD 6244	61-72	BCL2 like 11	Homo sapiens	92-95
23234544-0	2013	The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance.	AZD 6244	73-80	mitogen-activated protein kinase kinase 1	Homo sapiens	44-50
23234544-0	2013	The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance.	AZD 6244	73-80	BCL2 like 11	Homo sapiens	92-95
23234544-1	2013	Tumour cells typically exhibit a G(1) cell cycle arrest in response to the MEK1/2 [mitogen-activated protein kinase/ERK (extracellular-signal-regulated kinase) kinase 1/2] inhibitor selumetinib, but do not die, and thus they acquire resistance.	AZD 6244	182-193	mitogen-activated protein kinase kinase 1	Homo sapiens	75-81
23234544-1	2013	Tumour cells typically exhibit a G(1) cell cycle arrest in response to the MEK1/2 [mitogen-activated protein kinase/ERK (extracellular-signal-regulated kinase) kinase 1/2] inhibitor selumetinib, but do not die, and thus they acquire resistance.	AZD 6244	182-193	mitogen-activated protein kinase 3	Homo sapiens	116-119
23523553-7	2013	Here we show that four different MEK inhibitors, PD-0325901, AZD-6244, AZD-8330 and RDEA-119 that are orally available and at least in a phase I clinical trial against cancer demonstrate antiviral activity as single agents or in combination with oseltamivir.	AZD 6244	61-69	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
23508762-4	2013	Therefore, in the current study, we investigated the effect of inhibiting the growth factor receptor pathways with a MEK-1/2 inhibitor selumetinib (AZD6244, ARRY-142866).	AZD 6244	135-146	receptor-like tyrosine kinase	Mus musculus	78-100
23508762-4	2013	Therefore, in the current study, we investigated the effect of inhibiting the growth factor receptor pathways with a MEK-1/2 inhibitor selumetinib (AZD6244, ARRY-142866).	AZD 6244	135-146	mitogen-activated protein kinase kinase 1	Mus musculus	117-124
23508762-4	2013	Therefore, in the current study, we investigated the effect of inhibiting the growth factor receptor pathways with a MEK-1/2 inhibitor selumetinib (AZD6244, ARRY-142866).	AZD 6244	148-155	receptor-like tyrosine kinase	Mus musculus	78-100
23508762-13	2013	The treatment of mice with selumetinib resulted in downregulation of activated MAPK, along with p-mTOR, which likely resulted in upregulation of ERalpha.	AZD 6244	27-38	mechanistic target of rapamycin kinase	Mus musculus	98-102
23508762-13	2013	The treatment of mice with selumetinib resulted in downregulation of activated MAPK, along with p-mTOR, which likely resulted in upregulation of ERalpha.	AZD 6244	27-38	estrogen receptor 1 (alpha)	Mus musculus	145-152
23508762-14	2013	Our results suggest that inhibition of the growth factor receptor pathway with selumetinib can reverse anastrozole resistance.	AZD 6244	79-90	receptor-like tyrosine kinase	Mus musculus	43-65
24063423-0	2013	Selumetinib in advanced non small cell lung cancer (NSCLC) harbouring KRAS mutation: endless clinical challenge to KRAS-mutant NSCLC.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	115-119
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	89-143
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	159-163
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	233-237
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	89-143
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	13-20	KRAS proto-oncogene, GTPase	Homo sapiens	159-163
24063423-8	2013	Selumetinib (AZD6244; ARRY-142886) is an oral, tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers and currently in clinical development.	AZD 6244	13-20	KRAS proto-oncogene, GTPase	Homo sapiens	233-237
24063423-10	2013	Recently, in a randomised, phase II trial selumetinib plus docetaxel has proven to improve progression free survival compared to docetaxel alone in previously treated patients with advanced KRAS-mutant NSCLC.	AZD 6244	42-53	KRAS proto-oncogene, GTPase	Homo sapiens	190-194
22972589-2	2013	The authors hypothesized that the presence of BRAF or NRAS mutations would correlate with clinical benefit among patients who received treatment with combination regimens that included the MEK inhibitor selumetinib.	AZD 6244	203-214	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
22972589-2	2013	The authors hypothesized that the presence of BRAF or NRAS mutations would correlate with clinical benefit among patients who received treatment with combination regimens that included the MEK inhibitor selumetinib.	AZD 6244	203-214	NRAS proto-oncogene, GTPase	Homo sapiens	54-58
22972589-2	2013	The authors hypothesized that the presence of BRAF or NRAS mutations would correlate with clinical benefit among patients who received treatment with combination regimens that included the MEK inhibitor selumetinib.	AZD 6244	203-214	mitogen-activated protein kinase kinase 7	Homo sapiens	189-192
22972589-11	2013	CONCLUSIONS: Higher response rates and longer TTP were observed with selumetinib-containing regimens in patients who had tumors that harbored a BRAF mutation compared with patients who had wild-type BRAF.	AZD 6244	69-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	144-148
22972589-11	2013	CONCLUSIONS: Higher response rates and longer TTP were observed with selumetinib-containing regimens in patients who had tumors that harbored a BRAF mutation compared with patients who had wild-type BRAF.	AZD 6244	69-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	199-203
23414467-0	2013	Selumetinib: a promising pharmacologic approach for KRAS-mutant advanced non-small-cell lung cancer.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	52-56
23406027-4	2013	METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer.	AZD 6244	94-105	mitogen-activated protein kinase kinase 2	Homo sapiens	79-83
23406027-4	2013	METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer.	AZD 6244	107-114	mitogen-activated protein kinase kinase 1	Homo sapiens	55-74
23406027-4	2013	METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer.	AZD 6244	107-114	mitogen-activated protein kinase kinase 2	Homo sapiens	79-83
23406027-4	2013	METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer.	AZD 6244	116-127	mitogen-activated protein kinase kinase 1	Homo sapiens	55-74
23406027-4	2013	METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer.	AZD 6244	116-127	mitogen-activated protein kinase kinase 2	Homo sapiens	79-83
23406027-10	2013	Selumetinib increased the uptake of iodine-124 in 12 of the 20 patients (4 of 9 patients with BRAF mutations and 5 of 5 patients with NRAS mutations).	AZD 6244	0-11	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
23406027-10	2013	Selumetinib increased the uptake of iodine-124 in 12 of the 20 patients (4 of 9 patients with BRAF mutations and 5 of 5 patients with NRAS mutations).	AZD 6244	0-11	NRAS proto-oncogene, GTPase	Homo sapiens	134-138
23414467-1	2013	Selumetinib is a potent and selective inhibitor of MEK1 and 2 that is currently being clinically developed for the treatment of several human malignancies.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	51-61
23414467-4	2013	Importantly, as a MEK inhibitor, selumetinib could be particularly effective in tumors with a hyperactivated Ras/Raf/MEK/ERK pathway, which might be the case of KRAS-mutant non-small-cell lung cancers (NSCLCs).	AZD 6244	33-44	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
23414467-4	2013	Importantly, as a MEK inhibitor, selumetinib could be particularly effective in tumors with a hyperactivated Ras/Raf/MEK/ERK pathway, which might be the case of KRAS-mutant non-small-cell lung cancers (NSCLCs).	AZD 6244	33-44	zinc fingers and homeoboxes 2	Homo sapiens	113-116
23414467-4	2013	Importantly, as a MEK inhibitor, selumetinib could be particularly effective in tumors with a hyperactivated Ras/Raf/MEK/ERK pathway, which might be the case of KRAS-mutant non-small-cell lung cancers (NSCLCs).	AZD 6244	33-44	mitogen-activated protein kinase kinase 7	Homo sapiens	117-120
23414467-4	2013	Importantly, as a MEK inhibitor, selumetinib could be particularly effective in tumors with a hyperactivated Ras/Raf/MEK/ERK pathway, which might be the case of KRAS-mutant non-small-cell lung cancers (NSCLCs).	AZD 6244	33-44	mitogen-activated protein kinase 1	Homo sapiens	121-124
23414467-4	2013	Importantly, as a MEK inhibitor, selumetinib could be particularly effective in tumors with a hyperactivated Ras/Raf/MEK/ERK pathway, which might be the case of KRAS-mutant non-small-cell lung cancers (NSCLCs).	AZD 6244	33-44	KRAS proto-oncogene, GTPase	Homo sapiens	161-165
23414467-5	2013	Accordingly, a recent randomized Phase II study evaluating docetaxel plus selumetinib or placebo in KRAS-mutant pretreated advanced NSCLC patients has demonstrated a significant improvement in terms of response rate, progression-free survival and patient-reported outcomes in favor of the combination arm.	AZD 6244	74-85	KRAS proto-oncogene, GTPase	Homo sapiens	100-104
23261356-2	2013	We therefore assessed the safety and activity of selumetinib, an inhibitor of MEK1/2, for patients with this cancer.	AZD 6244	49-60	mitogen-activated protein kinase kinase 1	Homo sapiens	78-84
22565394-0	2013	Activity of the MEK inhibitor selumetinib (AZD6244; ARRY-142886) in nasopharyngeal cancer cell lines.	AZD 6244	30-41	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
22565394-0	2013	Activity of the MEK inhibitor selumetinib (AZD6244; ARRY-142886) in nasopharyngeal cancer cell lines.	AZD 6244	43-50	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
22565394-0	2013	Activity of the MEK inhibitor selumetinib (AZD6244; ARRY-142886) in nasopharyngeal cancer cell lines.	AZD 6244	52-63	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
22565394-1	2013	This study evaluated the preclinical activity of selumetinib (AZD6244, ARRY-142866), an inhibitor of the mitogen-activated protein kinase kinase (MAPKK or MEK1/2) in 6 nasopharyngeal cancer (NPC) cell lines.	AZD 6244	49-60	mitogen-activated protein kinase kinase 1	Homo sapiens	155-161
22565394-6	2013	At a concentration of 0.5 muM and 5 muM, selumetinib induced apoptosis (as indicated by cleaved PARP expression and caspase 3 induction), and G(0)/G(1) cycle arrest in HONE-1-EBV and HK1-LMP1(B95.8) cells.	AZD 6244	41-52	collagen type XI alpha 2 chain	Homo sapiens	96-100
22565394-6	2013	At a concentration of 0.5 muM and 5 muM, selumetinib induced apoptosis (as indicated by cleaved PARP expression and caspase 3 induction), and G(0)/G(1) cycle arrest in HONE-1-EBV and HK1-LMP1(B95.8) cells.	AZD 6244	41-52	caspase 3	Homo sapiens	116-125
22565394-6	2013	At a concentration of 0.5 muM and 5 muM, selumetinib induced apoptosis (as indicated by cleaved PARP expression and caspase 3 induction), and G(0)/G(1) cycle arrest in HONE-1-EBV and HK1-LMP1(B95.8) cells.	AZD 6244	41-52	hexokinase 1	Homo sapiens	183-186
22565394-7	2013	The combination of selumetinib (at IC(25) concentration) and the EGFR tyrosine kinase inhibitor, gefitinib (at concentrations of 0.1, 3 and 9 muM) resulted in synergistic growth inhibition in HK1-LMP1(B95.8) cells.	AZD 6244	19-30	hexokinase 1	Homo sapiens	192-195
23102728-9	2013	MEK inhibitors, either AZD6244 or CI1040, inhibited ERK phosphorylation and sensitized gefitinib-induced cytotoxicity in PC-9/gef cells.	AZD 6244	23-30	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
23102728-9	2013	MEK inhibitors, either AZD6244 or CI1040, inhibited ERK phosphorylation and sensitized gefitinib-induced cytotoxicity in PC-9/gef cells.	AZD 6244	23-30	EPH receptor B2	Homo sapiens	52-55
23102728-9	2013	MEK inhibitors, either AZD6244 or CI1040, inhibited ERK phosphorylation and sensitized gefitinib-induced cytotoxicity in PC-9/gef cells.	AZD 6244	23-30	proprotein convertase subtilisin/kexin type 9	Homo sapiens	121-125
23320839-8	2013	RESULTS: Both Raf1 inhibitor (GW5074) and MEK inhibitors (U0126 and AZD6244) suppressed HCC cell growth in a dose dependent manner.	AZD 6244	68-75	mitogen-activated protein kinase kinase 7	Homo sapiens	42-45
22310287-5	2013	We have discovered that in melanoma cells MEK inhibition by selumetinib (AZD6244, ARRY-142886) or PD184352, while efficiently suppressing proliferation, stimulates increased invasiveness.	AZD 6244	60-71	mitogen-activated protein kinase kinase 7	Homo sapiens	42-45
23234544-7	2013	Finally, cancer cells in which acquired resistance to selumetinib arises through BRAF(V600E) amplification remained sensitive to ABT-263, whereas selumetinib-resistant HCT116 cells (KRAS(G13D) amplification) were cross-resistant to ABT-263.	AZD 6244	54-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-86
23234544-8	2013	Thus the combination of a BCL2 inhibitor and an ERK1/2 pathway inhibitor is synthetic lethal in ERK1/2-addicted tumour cells, delays the onset of acquired resistance and in some cases overcomes acquired resistance to selumetinib.	AZD 6244	217-228	BCL2 apoptosis regulator	Homo sapiens	26-30
23234544-8	2013	Thus the combination of a BCL2 inhibitor and an ERK1/2 pathway inhibitor is synthetic lethal in ERK1/2-addicted tumour cells, delays the onset of acquired resistance and in some cases overcomes acquired resistance to selumetinib.	AZD 6244	217-228	mitogen-activated protein kinase 3	Homo sapiens	48-54
23250956-3	2013	METHODS: We assessed the cytotoxicity to MEK inhibitors (PD184352 and selumetinib) in melanoma cells by toluidine-blue staining, caspase 3 cleavage, and melanoma-sphere growth.	AZD 6244	70-81	midkine	Mus musculus	41-44
22310287-5	2013	We have discovered that in melanoma cells MEK inhibition by selumetinib (AZD6244, ARRY-142886) or PD184352, while efficiently suppressing proliferation, stimulates increased invasiveness.	AZD 6244	73-80	mitogen-activated protein kinase kinase 7	Homo sapiens	42-45
23250956-3	2013	METHODS: We assessed the cytotoxicity to MEK inhibitors (PD184352 and selumetinib) in melanoma cells by toluidine-blue staining, caspase 3 cleavage, and melanoma-sphere growth.	AZD 6244	70-81	caspase 3	Mus musculus	129-138
22310287-10	2013	Moreover, the combination of saracatinib and selumetinib effectively suppressed the growth and invasion of melanoma cells in a 3D environment, suggesting that combined inhibition of MEK and SRC is a promising approach to improve the efficacy of targeting the ERK/MAP kinase pathway in melanoma.	AZD 6244	45-56	mitogen-activated protein kinase kinase 7	Homo sapiens	182-185
22310287-10	2013	Moreover, the combination of saracatinib and selumetinib effectively suppressed the growth and invasion of melanoma cells in a 3D environment, suggesting that combined inhibition of MEK and SRC is a promising approach to improve the efficacy of targeting the ERK/MAP kinase pathway in melanoma.	AZD 6244	45-56	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	190-193
23250956-12	2013	Moreover, SMURF2 depletion sensitized melanoma cells to the cytotoxic effects of selumetinib, leading to cell death at concentrations approximately 100-fold lower than the concentration required to induce cell death in SMURF2-expressing cells.	AZD 6244	81-92	SMAD specific E3 ubiquitin protein ligase 2	Mus musculus	10-16
23250956-12	2013	Moreover, SMURF2 depletion sensitized melanoma cells to the cytotoxic effects of selumetinib, leading to cell death at concentrations approximately 100-fold lower than the concentration required to induce cell death in SMURF2-expressing cells.	AZD 6244	81-92	SMAD specific E3 ubiquitin protein ligase 2	Mus musculus	219-225
22310287-10	2013	Moreover, the combination of saracatinib and selumetinib effectively suppressed the growth and invasion of melanoma cells in a 3D environment, suggesting that combined inhibition of MEK and SRC is a promising approach to improve the efficacy of targeting the ERK/MAP kinase pathway in melanoma.	AZD 6244	45-56	mitogen-activated protein kinase 1	Homo sapiens	259-262
23250956-13	2013	Mice treated with selumetinib alone at a dosage of 10mg/kg body weight once daily produced no response, but in combination with SMURF2 depletion, selumetinib suppressed tumor growth by 97.9% (95% confidence interval = 38.65% to 155.50%, P = .005).	AZD 6244	146-157	SMAD specific E3 ubiquitin protein ligase 2	Mus musculus	128-134
23200175-0	2013	Selumetinib plus docetaxel for KRAS-mutant advanced non-small-cell lung cancer: a randomised, multicentre, placebo-controlled, phase 2 study.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	31-35
23091117-0	2013	Sequence dependence of MEK inhibitor AZD6244 combined with gemcitabine for the treatment of biliary cancer.	AZD 6244	37-44	mitogen-activated protein kinase kinase 7	Homo sapiens	23-26
23091117-3	2013	We therefore tested the sequence dependence of the combination of gemcitabine and the MEK inhibitor AZD6244 using a series of biliary cancer models.	AZD 6244	100-107	mitogen-activated protein kinase kinase 7	Homo sapiens	86-89
23320839-12	2013	MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation.	AZD 6244	25-32	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
23320839-12	2013	MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation.	AZD 6244	25-32	mitogen-activated protein kinase 1	Homo sapiens	60-63
23320839-12	2013	MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation.	AZD 6244	25-32	ATP binding cassette subfamily C member 1	Homo sapiens	86-90
23320839-12	2013	MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation.	AZD 6244	25-32	ATP binding cassette subfamily C member 1	Homo sapiens	147-151
23320839-12	2013	MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation.	AZD 6244	25-32	ATP binding cassette subfamily C member 3	Homo sapiens	156-160
23320839-14	2013	MEK inhibirors U0126 and AZD6244 reduced MRP1 as well as MRP3 expression, and may contribute partially to the sensitization.	AZD 6244	25-32	ATP binding cassette subfamily C member 1	Homo sapiens	41-45
23320839-14	2013	MEK inhibirors U0126 and AZD6244 reduced MRP1 as well as MRP3 expression, and may contribute partially to the sensitization.	AZD 6244	25-32	ATP binding cassette subfamily C member 3	Homo sapiens	57-61
23362510-6	2012	Pharmacological blockade of ERK1/2 pathway with MEK1/2 inhibitors, U0126 and selumetinib (AZD6244) significantly attenuated the pro-apoptotic effects of field electric stimulation on the mutated LMNA iPSC-CMs.	AZD 6244	77-88	mitogen-activated protein kinase 3	Homo sapiens	28-34
23362510-6	2012	Pharmacological blockade of ERK1/2 pathway with MEK1/2 inhibitors, U0126 and selumetinib (AZD6244) significantly attenuated the pro-apoptotic effects of field electric stimulation on the mutated LMNA iPSC-CMs.	AZD 6244	77-88	lamin A/C	Homo sapiens	195-199
23362510-6	2012	Pharmacological blockade of ERK1/2 pathway with MEK1/2 inhibitors, U0126 and selumetinib (AZD6244) significantly attenuated the pro-apoptotic effects of field electric stimulation on the mutated LMNA iPSC-CMs.	AZD 6244	90-97	mitogen-activated protein kinase 3	Homo sapiens	28-34
23362510-6	2012	Pharmacological blockade of ERK1/2 pathway with MEK1/2 inhibitors, U0126 and selumetinib (AZD6244) significantly attenuated the pro-apoptotic effects of field electric stimulation on the mutated LMNA iPSC-CMs.	AZD 6244	90-97	lamin A/C	Homo sapiens	195-199
23200175-2	2013	Selumetinib is an inhibitor of MEK1/MEK2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	31-35
23200175-2	2013	Selumetinib is an inhibitor of MEK1/MEK2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers.	AZD 6244	0-11	mitogen-activated protein kinase kinase 2	Homo sapiens	36-40
23200175-2	2013	Selumetinib is an inhibitor of MEK1/MEK2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	56-60
23200175-2	2013	Selumetinib is an inhibitor of MEK1/MEK2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
23200175-3	2013	We did a prospective, randomised, phase 2 trial to assess selumetinib plus docetaxel in previously treated patients with advanced KRAS-mutant NSCLC.	AZD 6244	58-69	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
23200175-16	2013	INTERPRETATION: Selumetinib plus docetaxel has promising efficacy, albeit with a higher number of adverse events than with docetaxel alone, in previously treated advanced KRAS-mutant NSCLC.	AZD 6244	16-27	KRAS proto-oncogene, GTPase	Homo sapiens	171-175
23200175-17	2013	These findings warrant further clinical investigation of selumetinib plus docetaxel in KRAS-mutant NSCLC.	AZD 6244	57-68	KRAS proto-oncogene, GTPase	Homo sapiens	87-91
22821509-6	2012	Increased proliferation due to strong activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) is caused by overexpression/activation of platelet-derived growth factor receptor-beta (PDGFR-beta) and ErbB2/3 which we successfully blocked with AZD6244, sorafenib, or lapatinib.	AZD 6244	250-257	erb-b2 receptor tyrosine kinase 2	Homo sapiens	207-214
22915752-7	2012	Overexpression of an active form of MEK1 resulted in ERK activation and downregulation of BRCA1, whereas the MEK inhibitor AZD6244 increased BRCA1/2 expression and reversed the effects of MEK1.	AZD 6244	123-130	BRCA1 DNA repair associated	Homo sapiens	141-146
22915752-7	2012	Overexpression of an active form of MEK1 resulted in ERK activation and downregulation of BRCA1, whereas the MEK inhibitor AZD6244 increased BRCA1/2 expression and reversed the effects of MEK1.	AZD 6244	123-130	mitogen-activated protein kinase kinase 1	Homo sapiens	188-192
22895053-3	2012	As a follow-up to that study, treatment of BRAF-mutant and NRAS-mutant melanoma lines with WNT3A and the MEK inhibitor AZD6244 also induces apoptosis.	AZD 6244	119-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
22895053-3	2012	As a follow-up to that study, treatment of BRAF-mutant and NRAS-mutant melanoma lines with WNT3A and the MEK inhibitor AZD6244 also induces apoptosis.	AZD 6244	119-126	NRAS proto-oncogene, GTPase	Homo sapiens	59-63
22895053-3	2012	As a follow-up to that study, treatment of BRAF-mutant and NRAS-mutant melanoma lines with WNT3A and the MEK inhibitor AZD6244 also induces apoptosis.	AZD 6244	119-126	mitogen-activated protein kinase kinase 7	Homo sapiens	105-108
22895053-5	2012	Apoptosis-resistant NRAS-mutant lines can sensitize to AZD6244 by pretreatment with AXIN1 siRNA, similar to what we previously reported in BRAF-mutant cell lines.	AZD 6244	55-62	NRAS proto-oncogene, GTPase	Homo sapiens	20-24
22895053-5	2012	Apoptosis-resistant NRAS-mutant lines can sensitize to AZD6244 by pretreatment with AXIN1 siRNA, similar to what we previously reported in BRAF-mutant cell lines.	AZD 6244	55-62	axin 1	Homo sapiens	84-89
22895053-5	2012	Apoptosis-resistant NRAS-mutant lines can sensitize to AZD6244 by pretreatment with AXIN1 siRNA, similar to what we previously reported in BRAF-mutant cell lines.	AZD 6244	55-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	139-143
22293660-0	2012	A prolonged complete response in a patient with BRAF-mutated melanoma stage IV treated with the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	113-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
22821509-6	2012	Increased proliferation due to strong activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) is caused by overexpression/activation of platelet-derived growth factor receptor-beta (PDGFR-beta) and ErbB2/3 which we successfully blocked with AZD6244, sorafenib, or lapatinib.	AZD 6244	250-257	mitogen-activated protein kinase 1	Homo sapiens	52-93
22821509-6	2012	Increased proliferation due to strong activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) is caused by overexpression/activation of platelet-derived growth factor receptor-beta (PDGFR-beta) and ErbB2/3 which we successfully blocked with AZD6244, sorafenib, or lapatinib.	AZD 6244	250-257	mitogen-activated protein kinase 3	Homo sapiens	95-101
22821509-6	2012	Increased proliferation due to strong activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) is caused by overexpression/activation of platelet-derived growth factor receptor-beta (PDGFR-beta) and ErbB2/3 which we successfully blocked with AZD6244, sorafenib, or lapatinib.	AZD 6244	250-257	platelet derived growth factor receptor beta	Homo sapiens	145-189
22821509-6	2012	Increased proliferation due to strong activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) is caused by overexpression/activation of platelet-derived growth factor receptor-beta (PDGFR-beta) and ErbB2/3 which we successfully blocked with AZD6244, sorafenib, or lapatinib.	AZD 6244	250-257	platelet derived growth factor receptor alpha	Homo sapiens	191-201
22293660-0	2012	A prolonged complete response in a patient with BRAF-mutated melanoma stage IV treated with the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	113-124	mitogen-activated protein kinase kinase 1	Homo sapiens	96-102
22293660-0	2012	A prolonged complete response in a patient with BRAF-mutated melanoma stage IV treated with the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	126-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
22293660-0	2012	A prolonged complete response in a patient with BRAF-mutated melanoma stage IV treated with the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	126-133	mitogen-activated protein kinase kinase 1	Homo sapiens	96-102
22293660-2	2012	Selumetinib (AZD6244) is an oral, selective, non-ATP-competitive inhibitor of MEK1/2.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	78-84
22293660-2	2012	Selumetinib (AZD6244) is an oral, selective, non-ATP-competitive inhibitor of MEK1/2.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	78-84
22641227-0	2012	Combination of the ERK inhibitor AZD6244 and low-dose sorafenib in a             xenograft model of human renal cell carcinoma.	AZD 6244	33-40	mitogen-activated protein kinase 1	Homo sapiens	19-22
22641227-3	2012	In this study, we examined the             antitumor and antiangiogenic activities of low-dose sorafenib in combination with             the MEK inhibitor AZD6244 (sorafenib/AZD6244) in a preclinical model of RCC.	AZD 6244	155-162	mitogen-activated protein kinase kinase 7	Homo sapiens	141-144
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	kinase insert domain receptor	Homo sapiens	85-92
22573716-3	2012	In 19 GBM cell lines, we found that treatment with the clinically available MEK inhibitors PD0325901 or AZD6244 decreased levels of phospho-ERK, the downstream effector of MEK, regardless of NF1 status.	AZD 6244	104-111	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
22765220-11	2012	Inhibition of ERK signaling in MCF7-Six1 cells with MEK1/2 inhibitors, U0126 and AZD6244, restores the TIC population of luminal breast cancer cells back to that observed in control cells.	AZD 6244	81-88	mitogen-activated protein kinase 1	Homo sapiens	14-17
22765220-11	2012	Inhibition of ERK signaling in MCF7-Six1 cells with MEK1/2 inhibitors, U0126 and AZD6244, restores the TIC population of luminal breast cancer cells back to that observed in control cells.	AZD 6244	81-88	SIX homeobox 1	Homo sapiens	36-40
22765220-11	2012	Inhibition of ERK signaling in MCF7-Six1 cells with MEK1/2 inhibitors, U0126 and AZD6244, restores the TIC population of luminal breast cancer cells back to that observed in control cells.	AZD 6244	81-88	mitogen-activated protein kinase kinase 1	Homo sapiens	52-58
22765220-12	2012	Administration of AZD6244 dramatically inhibits tumor formation efficiency and metastasis in cells that express high levels of Six1 ectopically or endogenously.	AZD 6244	18-25	SIX homeobox 1	Homo sapiens	127-131
22573716-3	2012	In 19 GBM cell lines, we found that treatment with the clinically available MEK inhibitors PD0325901 or AZD6244 decreased levels of phospho-ERK, the downstream effector of MEK, regardless of NF1 status.	AZD 6244	104-111	mitogen-activated protein kinase 1	Homo sapiens	140-143
22573716-3	2012	In 19 GBM cell lines, we found that treatment with the clinically available MEK inhibitors PD0325901 or AZD6244 decreased levels of phospho-ERK, the downstream effector of MEK, regardless of NF1 status.	AZD 6244	104-111	mitogen-activated protein kinase kinase 7	Homo sapiens	172-175
22573716-3	2012	In 19 GBM cell lines, we found that treatment with the clinically available MEK inhibitors PD0325901 or AZD6244 decreased levels of phospho-ERK, the downstream effector of MEK, regardless of NF1 status.	AZD 6244	104-111	neurofibromin 1	Homo sapiens	191-194
22569000-0	2012	Intrinsic resistance to selumetinib, a selective inhibitor of MEK1/2, by cAMP-dependent protein kinase A activation in human lung and colorectal cancer cells.	AZD 6244	24-35	mitogen-activated protein kinase kinase 1	Homo sapiens	62-68
22550165-5	2012	EXPERIMENTAL DESIGN: We conducted microarray analysis of uveal melanoma cell lines with GNAQ mutations treated with the MEK inhibitor selumetinib.	AZD 6244	134-145	G protein subunit alpha q	Homo sapiens	88-92
22550165-5	2012	EXPERIMENTAL DESIGN: We conducted microarray analysis of uveal melanoma cell lines with GNAQ mutations treated with the MEK inhibitor selumetinib.	AZD 6244	134-145	mitogen-activated protein kinase kinase 7	Homo sapiens	120-123
22550165-10	2012	Furthermore, we show that selumetinib treatment regulates the expression of these genes in tumor tissues of patients with metastatic GNAQ/11 mutant uveal melanoma.	AZD 6244	26-37	G protein subunit alpha q	Homo sapiens	133-137
22550165-11	2012	CONCLUSIONS: Our findings define a subset of transcriptionally regulated genes by selumetinib in GNAQ mutant cells and provide new insights into understanding the biologic effect of MEK inhibition in this disease.	AZD 6244	82-93	G protein subunit alpha q	Homo sapiens	97-101
22550165-11	2012	CONCLUSIONS: Our findings define a subset of transcriptionally regulated genes by selumetinib in GNAQ mutant cells and provide new insights into understanding the biologic effect of MEK inhibition in this disease.	AZD 6244	82-93	mitogen-activated protein kinase kinase 7	Homo sapiens	182-185
22869096-6	2012	Furthermore, sublethal doses of IPA3 or ectopic expression of dominant-negative PAK1 sensitized Ras-mutated cells to GDC-0897 and AZD6244, which otherwise have reduced efficiency against cells with activated Ras.	AZD 6244	130-137	p21 (RAC1) activated kinase 1	Homo sapiens	80-84
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	platelet derived growth factor receptor beta	Homo sapiens	94-104
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	mitogen-activated protein kinase 1	Homo sapiens	109-112
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	ribosomal protein S6 kinase A1	Homo sapiens	114-120
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	ribosomal protein S6 kinase B1	Homo sapiens	122-128
22641227-10	2012	Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation             of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma.	AZD 6244	10-17	cyclin dependent kinase 2	Homo sapiens	130-135
22641227-11	2012	Sorafenib/AZD6244             also caused upregulation of p27, Bad and Bim but downregulation of survivin and             cyclin B1.	AZD 6244	10-17	dynactin subunit 6	Homo sapiens	58-61
22641227-11	2012	Sorafenib/AZD6244             also caused upregulation of p27, Bad and Bim but downregulation of survivin and             cyclin B1.	AZD 6244	10-17	cyclin B1	Homo sapiens	122-131
21594619-1	2012	Selumetinib is a potent, selective MEK inhibitor with efficacy in several tumor models.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
22569000-2	2012	Selumetinib is a selective inhibitor of MEK1/2, which is currently in clinical development.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	40-46
22271687-0	2012	Enhanced apoptosis and tumor growth suppression elicited by combination of MEK (selumetinib) and mTOR kinase inhibitors (AZD8055).	AZD 6244	80-91	mitogen-activated protein kinase kinase 7	Homo sapiens	75-78
23372439-0	2012	(18)F-FLT-PET for Response Evaluation of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with Solid Tumors.	AZD 6244	55-66	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
23372439-0	2012	(18)F-FLT-PET for Response Evaluation of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with Solid Tumors.	AZD 6244	68-75	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	86-95
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	0-11	zinc fingers and homeoboxes 2	Homo sapiens	109-112
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	86-89
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	117-120
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	86-95
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	13-20	zinc fingers and homeoboxes 2	Homo sapiens	109-112
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	86-89
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	13-20	mitogen-activated protein kinase 1	Homo sapiens	117-120
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	86-95
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	22-33	zinc fingers and homeoboxes 2	Homo sapiens	109-112
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	22-33	mitogen-activated protein kinase kinase 7	Homo sapiens	86-89
23372439-1	2012	Selumetinib (AZD6244, ARRY-142886) is a potent, selective, uncompetitive inhibitor of MEK 1 / 2, part of the RAF/MEK/ERK protein kinase signal cascade, which is responsible for tumor.	AZD 6244	22-33	mitogen-activated protein kinase 1	Homo sapiens	117-120
22415236-2	2012	This study evaluated the MEK inhibitors AZD6244 and PD0325901, alone and in combination with the dual mTOR/PI3K inhibitor NVP-BEZ235 or the PI3K inhibitor GDC-0941, in three colorectal cancer cell lines.	AZD 6244	40-47	mitogen-activated protein kinase kinase 7	Homo sapiens	25-28
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	AZD 6244	48-55	mitogen-activated protein kinase kinase 1	Homo sapiens	9-15
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	AZD 6244	48-55	checkpoint kinase 1	Homo sapiens	96-100
22271687-2	2012	In this study, we investigated the therapeutic effects of combining the MAPK extracellular signal-regulated kinase (MEK)1/2 inhibitor selumetinib (AZD6244) with the dual mTORC1 and mTORC2 inhibitor (AZD8055).	AZD 6244	134-145	mitogen-activated protein kinase kinase 1	Homo sapiens	72-123
22451620-2	2012	Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary thyroid carcinoma and shows limited single-agent activity in the patients with tumors that harbor the (V600E)BRAF mutation.	AZD 6244	6-17	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	193-197
22275507-10	2012	Immunohistochemistry of tumor tissues revealed that selumetinib alone or with cediranib reduced ERK phosphorylation, angiogenesis, and tumor cell proliferation and increased apoptosis.	AZD 6244	52-63	mitogen-activated protein kinase 1	Homo sapiens	96-99
22394161-4	2012	Selumetinib is an orally available, selective non-ATP-competitive MEK1 and MEK2 inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	66-70
22394161-4	2012	Selumetinib is an orally available, selective non-ATP-competitive MEK1 and MEK2 inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 2	Homo sapiens	75-79
22394161-5	2012	AREAS COVERED: In this review, the authors discuss the rationale for MEK inhibition therapy in melanoma and summarize data from the preclinical and clinical studies of selumetinib for advanced melanoma.	AZD 6244	168-179	mitogen-activated protein kinase kinase 7	Homo sapiens	69-72
22394161-7	2012	The results of early clinical studies of selumetinib suggest that selumetinib may have a role in melanoma therapy, especially in certain subsets of patients, such as those whose tumor harbors a BRAF mutation.	AZD 6244	66-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	194-198
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	mitogen activated protein kinase 3	Rattus norvegicus	41-47
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	nerve growth factor	Rattus norvegicus	68-71
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	brain-derived neurotrophic factor	Rattus norvegicus	85-89
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	nerve growth factor	Rattus norvegicus	120-123
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	brain-derived neurotrophic factor	Rattus norvegicus	137-141
22280975-5	2012	AZD6244, a potent selective inhibitor of ERK1/2 activation, blocked NGF induction of BDNF mRNA in vitro suggesting that NGF induction of BDNF is mediated by ERK1/2.	AZD 6244	0-7	mitogen activated protein kinase 3	Rattus norvegicus	157-163
22425996-5	2012	This trial aims to determine if the MEK inhibitor selumetinib (AZD6244) increases the efficacy of docetaxel, a standard of care chemotherapy.	AZD 6244	50-61	mitogen-activated protein kinase kinase 7	Homo sapiens	36-39
22425996-5	2012	This trial aims to determine if the MEK inhibitor selumetinib (AZD6244) increases the efficacy of docetaxel, a standard of care chemotherapy.	AZD 6244	63-70	mitogen-activated protein kinase kinase 7	Homo sapiens	36-39
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	110-114
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	119-123
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	transformation related protein 53, pseudogene	Mus musculus	128-131
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	119-123
22275507-2	2012	Selumetinib is a potent, selective, and orally available MEK1/2 inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	57-63
22395615-5	2012	These two mechanisms of extracellular signal-regulated kinase reactivation are sensitive to the MEK1/2 inhibitor AZD6244/selumetinib or its combination with the B-RAF inhibitor vemurafenib.	AZD 6244	113-120	mitogen-activated protein kinase kinase 1	Homo sapiens	96-102
22395615-5	2012	These two mechanisms of extracellular signal-regulated kinase reactivation are sensitive to the MEK1/2 inhibitor AZD6244/selumetinib or its combination with the B-RAF inhibitor vemurafenib.	AZD 6244	121-132	mitogen-activated protein kinase kinase 1	Homo sapiens	96-102
22082529-1	2012	Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT.	AZD 6244	79-86	KRAS proto-oncogene, GTPase	Homo sapiens	26-30
22082529-1	2012	Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT.	AZD 6244	79-86	mitogen-activated protein kinase kinase 7	Homo sapiens	90-93
22082529-1	2012	Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT.	AZD 6244	79-86	epidermal growth factor receptor	Homo sapiens	139-143
22082529-1	2012	Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT.	AZD 6244	79-86	AKT serine/threonine kinase 1	Homo sapiens	144-147
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	29-36	ERBB receptor feedback inhibitor 1	Homo sapiens	63-87
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	29-36	ERBB receptor feedback inhibitor 1	Homo sapiens	89-93
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	29-36	epidermal growth factor receptor	Homo sapiens	130-134
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	29-36	epidermal growth factor receptor	Homo sapiens	182-186
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	29-36	AKT serine/threonine kinase 1	Homo sapiens	191-194
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	139-146	ERBB receptor feedback inhibitor 1	Homo sapiens	63-87
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	139-146	ERBB receptor feedback inhibitor 1	Homo sapiens	89-93
22082529-3	2012	We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells.	AZD 6244	139-146	epidermal growth factor receptor	Homo sapiens	130-134
22082529-4	2012	Reconstitution or knockdown of MIG6 expression affected cancer cell responses to AZD6244.	AZD 6244	81-88	ERBB receptor feedback inhibitor 1	Homo sapiens	31-35
22082529-5	2012	Treatment with a combination of EGFR inhibitor and AZD6244 inhibited cell proliferation synergistically without activation of AKT in AZD6244-resistant cells.	AZD 6244	133-140	epidermal growth factor receptor	Homo sapiens	32-36
22510747-0	2012	Skeletal muscle anabolism is a side effect of therapy with the MEK inhibitor: selumetinib in patients with cholangiocarcinoma.	AZD 6244	78-89	mitogen-activated protein kinase kinase 7	Homo sapiens	63-66
22343622-0	2012	The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
22343622-0	2012	The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.	AZD 6244	35-42	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
22343622-4	2012	The MEK1/2 inhibitor selumetinib has been shown to have anti-tumour activity and induce apoptotic cell death as a monotherapy.	AZD 6244	21-32	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
22275507-12	2012	Selumetinib also inhibited lung tumor VEGF production and VEGFR signaling.	AZD 6244	0-11	vascular endothelial growth factor A	Homo sapiens	38-42
22275507-12	2012	Selumetinib also inhibited lung tumor VEGF production and VEGFR signaling.	AZD 6244	0-11	kinase insert domain receptor	Homo sapiens	58-63
22260668-3	2012	We have used colorectal cancer cell lines harbouring mutations in B-Raf or K-Ras to model acquired resistance to the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	134-145	mitogen-activated protein kinase kinase 1	Homo sapiens	117-123
22260668-3	2012	We have used colorectal cancer cell lines harbouring mutations in B-Raf or K-Ras to model acquired resistance to the MEK1/2 inhibitor selumetinib (AZD6244).	AZD 6244	147-154	mitogen-activated protein kinase kinase 1	Homo sapiens	117-123
22260668-4	2012	Selumetinib-resistant cells were refractory to other MEK1/2 inhibitors in cell proliferation assays and exhibited a marked increase in MEK1/2 and ERK1/2 activity and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	53-59
22260668-4	2012	Selumetinib-resistant cells were refractory to other MEK1/2 inhibitors in cell proliferation assays and exhibited a marked increase in MEK1/2 and ERK1/2 activity and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	135-141
22260668-4	2012	Selumetinib-resistant cells were refractory to other MEK1/2 inhibitors in cell proliferation assays and exhibited a marked increase in MEK1/2 and ERK1/2 activity and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase 3	Homo sapiens	146-152
22260668-4	2012	Selumetinib-resistant cells were refractory to other MEK1/2 inhibitors in cell proliferation assays and exhibited a marked increase in MEK1/2 and ERK1/2 activity and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-11	cyclin D1	Homo sapiens	166-175
22144664-9	2012	Furthermore, erlotinib-sensitive cell lines were also sensitive to the MEK inhibitor selumetinib (AZD6244), which is under clinical development.	AZD 6244	85-96	midkine	Mus musculus	71-74
22173548-4	2012	The activity of selumetinib and vorinostat against the KRAS-mutant SW620 and SW480 CRC cell lines was studied in vitro and in vivo.	AZD 6244	16-27	KRAS proto-oncogene, GTPase	Homo sapiens	55-59
22173548-11	2012	CONCLUSION: These data indicate that the rationally based combination of the mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor, selumetinib, with the HDAC inhibitor vorinostat results in synergistic antiproliferative activity against KRAS-mutant CRC cell lines in vitro.	AZD 6244	159-170	KRAS proto-oncogene, GTPase	Homo sapiens	265-269
22068161-0	2012	Treatment with selumetinib preserves cardiac function and improves survival in cardiomyopathy caused by mutation in the lamin A/C gene.	AZD 6244	15-26	lamin A/C	Homo sapiens	120-129
22068161-6	2012	Selumetinib is an inhibitor of ERK1/2 signalling and has been given safely to human subjects in clinical trials for cancer.	AZD 6244	0-11	mitogen-activated protein kinase 3	Homo sapiens	31-37
22068161-7	2012	Systemic treatment with selumetinib inhibited cardiac ERK1/2 phosphorylation and blocked increased expression of RNAs encoding natriuretic peptide precursors and proteins involved in sarcomere architecture that occurred in placebo-treated mice.	AZD 6244	24-35	mitogen-activated protein kinase 3	Mus musculus	54-60
22068161-10	2012	CONCLUSION: Our results suggest that selumetinib or other related inhibitors that have been safely administered to humans in clinical trials could potentially be used to treat LMNA cardiomyopathy.	AZD 6244	37-48	lamin A/C	Homo sapiens	176-180
22090271-0	2012	The Akt inhibitor MK2206 synergizes, but perifosine antagonizes, the BRAF(V600E) inhibitor PLX4032 and the MEK1/2 inhibitor AZD6244 in the inhibition of thyroid cancer cells.	AZD 6244	124-131	AKT serine/threonine kinase 1	Homo sapiens	4-7
22090271-0	2012	The Akt inhibitor MK2206 synergizes, but perifosine antagonizes, the BRAF(V600E) inhibitor PLX4032 and the MEK1/2 inhibitor AZD6244 in the inhibition of thyroid cancer cells.	AZD 6244	124-131	mitogen-activated protein kinase kinase 1	Homo sapiens	107-113
22090271-2	2012	EXPERIMENTAL DESIGN: We tested the combinations of the Akt inhibitors MK2206 or perifosine with the BRAF(V600E) inhibitor PLX4032 or the MEK1/2 inhibitor AZD6244 in thyroid cancer cells harboring both the BRAF(V600E) and PIK3CA mutations.	AZD 6244	154-161	mitogen-activated protein kinase kinase 1	Homo sapiens	137-143
22144664-0	2012	MEK1/2 inhibitor selumetinib (AZD6244) inhibits growth of ovarian clear cell carcinoma in a PEA-15-dependent manner in a mouse xenograft model.	AZD 6244	17-28	mitogen-activated protein kinase kinase 1	Mus musculus	0-6
22144664-0	2012	MEK1/2 inhibitor selumetinib (AZD6244) inhibits growth of ovarian clear cell carcinoma in a PEA-15-dependent manner in a mouse xenograft model.	AZD 6244	17-28	proliferation and apoptosis adaptor protein 15A	Mus musculus	92-98
22144664-0	2012	MEK1/2 inhibitor selumetinib (AZD6244) inhibits growth of ovarian clear cell carcinoma in a PEA-15-dependent manner in a mouse xenograft model.	AZD 6244	30-37	mitogen-activated protein kinase kinase 1	Mus musculus	0-6
22144664-0	2012	MEK1/2 inhibitor selumetinib (AZD6244) inhibits growth of ovarian clear cell carcinoma in a PEA-15-dependent manner in a mouse xenograft model.	AZD 6244	30-37	proliferation and apoptosis adaptor protein 15A	Mus musculus	92-98
22048237-0	2012	Phase II, open-label, randomized trial of the MEK1/2 inhibitor selumetinib as monotherapy versus temozolomide in patients with advanced melanoma.	AZD 6244	63-74	mitogen-activated protein kinase kinase 1	Homo sapiens	46-52
22048237-1	2012	PURPOSE: To compare the efficacy and tolerability of the mitogen-activated protein (MAP)/extracellular signal-regulated (ERK) kinase (MEK) 1/2 inhibitor selumetinib versus temozolomide in chemotherapy-naive patients with unresectable stage III/IV melanoma.	AZD 6244	153-164	mitogen-activated protein kinase kinase 1	Homo sapiens	89-142
22048237-8	2012	However, five of the six selumetinib partial responders were BRAF mutated.	AZD 6244	25-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
22048237-11	2012	Five of six patients with partial response to selumetinib had BRAF mutant tumors.	AZD 6244	46-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
22336587-10	2012	These indicate us that MTDH is a candidate marker to predict the clinical efficacy of AZD6244 and targeting MTDH could overcome the resistance to AZD6244 in breast cancer cells.	AZD 6244	86-93	metadherin	Homo sapiens	23-27
22336587-10	2012	These indicate us that MTDH is a candidate marker to predict the clinical efficacy of AZD6244 and targeting MTDH could overcome the resistance to AZD6244 in breast cancer cells.	AZD 6244	146-153	metadherin	Homo sapiens	23-27
22336587-10	2012	These indicate us that MTDH is a candidate marker to predict the clinical efficacy of AZD6244 and targeting MTDH could overcome the resistance to AZD6244 in breast cancer cells.	AZD 6244	146-153	metadherin	Homo sapiens	108-112
22144664-9	2012	Furthermore, erlotinib-sensitive cell lines were also sensitive to the MEK inhibitor selumetinib (AZD6244), which is under clinical development.	AZD 6244	98-105	midkine	Mus musculus	71-74
22336587-0	2012	Inhibition of metadherin sensitizes breast cancer cells to AZD6244.	AZD 6244	59-66	metadherin	Homo sapiens	14-24
22336587-2	2012	AZD6244 is a novel ATP-uncompetitive inhibitor to MAP/ERK kinase (MEK) 1/2 which has been demonstrated to be potent, selective and safe in the clinical trials and previous studies.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	54-74
22336587-5	2012	Here we report that the resistance to AZD6244 can be reserved by downregulating MTDH in breast cancer cell lines.	AZD 6244	38-45	metadherin	Homo sapiens	80-84
22336587-6	2012	When the MTDH was downregulated, the breast cancer cells exhibited a significantly increased sensitivity to AZD6244 as measured by MTT assay.	AZD 6244	108-115	metadherin	Homo sapiens	9-13
22336587-7	2012	After treated with AZD6244 the MTDH-knockdown cells showed more apoptosis rate and growth inhibition.	AZD 6244	19-26	metadherin	Homo sapiens	31-35
22336587-9	2012	In conclusion knockdown MTDH can enhance the breast cancer cells sensitivity to AZD6244 via regulating the expression and activity of FOXO3a.	AZD 6244	80-87	metadherin	Homo sapiens	24-28
22336587-9	2012	In conclusion knockdown MTDH can enhance the breast cancer cells sensitivity to AZD6244 via regulating the expression and activity of FOXO3a.	AZD 6244	80-87	forkhead box O3	Homo sapiens	134-140
22144664-10	2012	Knockdown of PEA-15 expression resulted in reversal of selumetinib-sensitive cells to resistant cells, implying that PEA-15 contributes to selumetinib sensitivity.	AZD 6244	55-66	proliferation and apoptosis adaptor protein 15A	Mus musculus	13-19
22808163-4	2012	While synergistic reductions in cell viability were observed with AZD8055/selumetinib in both BRAF and GNAQ mutant cell lines, apoptosis was preferentially induced in BRAF mutant cells only.	AZD 6244	74-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
22144664-10	2012	Knockdown of PEA-15 expression resulted in reversal of selumetinib-sensitive cells to resistant cells, implying that PEA-15 contributes to selumetinib sensitivity.	AZD 6244	139-150	proliferation and apoptosis adaptor protein 15A	Mus musculus	13-19
22808163-4	2012	While synergistic reductions in cell viability were observed with AZD8055/selumetinib in both BRAF and GNAQ mutant cell lines, apoptosis was preferentially induced in BRAF mutant cells only.	AZD 6244	74-85	G protein subunit alpha q	Homo sapiens	103-107
22144664-10	2012	Knockdown of PEA-15 expression resulted in reversal of selumetinib-sensitive cells to resistant cells, implying that PEA-15 contributes to selumetinib sensitivity.	AZD 6244	139-150	proliferation and apoptosis adaptor protein 15A	Mus musculus	117-123
22144664-13	2012	Our findings indicate that the MEK-ERK pathway is a potential target for EGFR-overexpressing CCC and indicate that selumetinib and erlotinib are worth exploring as therapeutic agents for CCC.	AZD 6244	115-126	midkine	Mus musculus	31-34
22144664-13	2012	Our findings indicate that the MEK-ERK pathway is a potential target for EGFR-overexpressing CCC and indicate that selumetinib and erlotinib are worth exploring as therapeutic agents for CCC.	AZD 6244	115-126	mitogen-activated protein kinase 1	Mus musculus	35-38
22144664-13	2012	Our findings indicate that the MEK-ERK pathway is a potential target for EGFR-overexpressing CCC and indicate that selumetinib and erlotinib are worth exploring as therapeutic agents for CCC.	AZD 6244	115-126	epidermal growth factor receptor	Mus musculus	73-77
22363658-9	2012	Our data also showed that growth factor EGF treatment decreased DPEP1 expression and MEK1/2 inhibitor AZD6244 increased DPEP1 expression in vitro, indicating a potential mechanism for DPEP1 gene regulation.	AZD 6244	102-109	mitogen-activated protein kinase kinase 1	Homo sapiens	85-91
22363658-9	2012	Our data also showed that growth factor EGF treatment decreased DPEP1 expression and MEK1/2 inhibitor AZD6244 increased DPEP1 expression in vitro, indicating a potential mechanism for DPEP1 gene regulation.	AZD 6244	102-109	dipeptidase 1	Homo sapiens	120-125
22363658-9	2012	Our data also showed that growth factor EGF treatment decreased DPEP1 expression and MEK1/2 inhibitor AZD6244 increased DPEP1 expression in vitro, indicating a potential mechanism for DPEP1 gene regulation.	AZD 6244	102-109	dipeptidase 1	Homo sapiens	120-125
21953275-0	2011	A phase I, open-label, randomized crossover study to assess the effect of dosing of the MEK 1/2 inhibitor Selumetinib (AZD6244; ARRY-142866) in the presence and absence of food in patients with advanced solid tumors.	AZD 6244	106-117	mitogen-activated protein kinase kinase 1	Homo sapiens	88-95
21899882-7	2011	AZD6244 treatment, a potent inhibitor of the ERK pathway, attenuated particle mediated inflammatory osteolysis both in vivo and in vitro.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	45-48
21628402-0	2011	The novel anti-MEK small molecule AZD6244 induces BIM-dependent and AKT-independent apoptosis in diffuse large B-cell lymphoma.	AZD 6244	34-41	mitogen-activated protein kinase kinase 7	Homo sapiens	15-18
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	57-68	checkpoint kinase 1	Homo sapiens	18-22
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	57-68	mitogen-activated protein kinase kinase 1	Homo sapiens	27-33
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	57-68	CD34 molecule	Homo sapiens	187-191
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	70-77	checkpoint kinase 1	Homo sapiens	18-22
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	70-77	mitogen-activated protein kinase kinase 1	Homo sapiens	27-33
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	70-77	CD34 molecule	Homo sapiens	187-191
20978926-0	2011	Dermatologic side effects associated with the MEK 1/2 inhibitor selumetinib (AZD6244, ARRY-142886).	AZD 6244	64-75	mitogen-activated protein kinase kinase 1	Homo sapiens	46-53
20978926-0	2011	Dermatologic side effects associated with the MEK 1/2 inhibitor selumetinib (AZD6244, ARRY-142886).	AZD 6244	77-84	mitogen-activated protein kinase kinase 1	Homo sapiens	46-53
20978926-1	2011	BACKGROUND: Selumetinib (AZD6244, ARRY-142886) is a second generation MEK inhibitor that is currently in clinical trials for various solid malignancies.	AZD 6244	12-23	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
20978926-1	2011	BACKGROUND: Selumetinib (AZD6244, ARRY-142886) is a second generation MEK inhibitor that is currently in clinical trials for various solid malignancies.	AZD 6244	25-32	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
21828154-5	2011	RESULTS: BRAF-mutant UM cells were sensitive to both PLX4720 and AZD6244, undergoing cell cycle arrest but not apoptosis.	AZD 6244	65-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
21828154-6	2011	UM cells with a Galpha-protein mutation (GNAQ or GNA11) were mildly sensitive to AZD6244 but completely resistant to PLX4720.	AZD 6244	81-88	succinate-CoA ligase GDP/ADP-forming subunit alpha	Homo sapiens	16-22
21828154-6	2011	UM cells with a Galpha-protein mutation (GNAQ or GNA11) were mildly sensitive to AZD6244 but completely resistant to PLX4720.	AZD 6244	81-88	G protein subunit alpha q	Homo sapiens	41-45
21828154-6	2011	UM cells with a Galpha-protein mutation (GNAQ or GNA11) were mildly sensitive to AZD6244 but completely resistant to PLX4720.	AZD 6244	81-88	G protein subunit alpha 11	Homo sapiens	49-54
21828154-8	2011	The combination of AZD6244 with PLX4720 had synergistic anticancer activity in BRAF-mutant cells but not in Galpha-mutant cells.	AZD 6244	19-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	79-83
21828154-9	2011	The Akt inhibitor MK2206 sensitized BRAF-mutant cells to both PLX4720 and AZD6244 and sensitized Galpha-mutant cells to AZD6244 but did not overcome the resistance of the Galpha-mutant cells to PLX4720.	AZD 6244	74-81	AKT serine/threonine kinase 1	Homo sapiens	4-7
21828154-9	2011	The Akt inhibitor MK2206 sensitized BRAF-mutant cells to both PLX4720 and AZD6244 and sensitized Galpha-mutant cells to AZD6244 but did not overcome the resistance of the Galpha-mutant cells to PLX4720.	AZD 6244	120-127	AKT serine/threonine kinase 1	Homo sapiens	4-7
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	38-45	mitogen-activated protein kinase kinase 1	Homo sapiens	9-15
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	38-45	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	47-58	mitogen-activated protein kinase kinase 1	Homo sapiens	9-15
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	47-58	checkpoint kinase 1	Homo sapiens	86-90
21690569-3	2011	We previously reported radiosensitization with selumetinib, an inhibitor of MEK1/2.	AZD 6244	47-58	mitogen-activated protein kinase kinase 1	Homo sapiens	76-82
21690569-13	2011	Enhancement of 5-FU cytotoxicity and 5-FU mediated radiosensitization with selumetinib treatment was accompanied by an increase in mitotic catastrophe and apoptosis, and reductions in Stat3 phosphorylation and survivin expression.	AZD 6244	75-86	signal transducer and activator of transcription 3	Homo sapiens	184-189
22808163-6	2012	We went on to discover that GNAQ promotes relative resistance to AZD8055/selumetinib-induced apoptosis in GNAQ mutant cells.	AZD 6244	73-84	G protein subunit alpha q	Homo sapiens	28-32
22808163-6	2012	We went on to discover that GNAQ promotes relative resistance to AZD8055/selumetinib-induced apoptosis in GNAQ mutant cells.	AZD 6244	73-84	G protein subunit alpha q	Homo sapiens	106-110
21910575-0	2011	Inhibitor of MEK1/2, selumetinib, for biliary tract cancer.	AZD 6244	21-32	mitogen-activated protein kinase kinase 1	Homo sapiens	13-19
21910575-4	2011	Selumetinib is an inhibitor of MEK1/2 targeting the RAS/RAF/MEK/extracellular signal-related kinase pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	31-37
21910575-4	2011	Selumetinib is an inhibitor of MEK1/2 targeting the RAS/RAF/MEK/extracellular signal-related kinase pathway.	AZD 6244	0-11	zinc fingers and homeoboxes 2	Homo sapiens	56-59
21910575-4	2011	Selumetinib is an inhibitor of MEK1/2 targeting the RAS/RAF/MEK/extracellular signal-related kinase pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	31-34
20127139-0	2011	A Phase II, open-label, randomised study to assess the efficacy and safety of the MEK1/2 inhibitor AZD6244 (ARRY-142886) versus capecitabine monotherapy in patients with colorectal cancer who have failed one or two prior chemotherapeutic regimens.	AZD 6244	99-106	mitogen-activated protein kinase kinase 1	Homo sapiens	82-88
20127139-1	2011	OBJECTIVES: To assess the efficacy and safety of the MEK1/2 inhibitor AZD6244 (ARRY-142886) in patients with metastatic colorectal cancer who had failed one or two previous chemotherapeutic regimens that included oxaliplatin and/or irinotecan.	AZD 6244	70-77	mitogen-activated protein kinase kinase 1	Homo sapiens	53-59
21946352-6	2011	Melanoma cells expressing mutant GRM3 had reduced cell growth and cellular migration after short hairpin RNA-mediated knockdown of GRM3 or treatment with a selective MEK inhibitor, AZD-6244, which is currently being used in phase 2 clinical trials.	AZD 6244	181-189	glutamate metabotropic receptor 3	Homo sapiens	33-37
21946352-6	2011	Melanoma cells expressing mutant GRM3 had reduced cell growth and cellular migration after short hairpin RNA-mediated knockdown of GRM3 or treatment with a selective MEK inhibitor, AZD-6244, which is currently being used in phase 2 clinical trials.	AZD 6244	181-189	mitogen-activated protein kinase kinase 7	Homo sapiens	166-169
21628402-0	2011	The novel anti-MEK small molecule AZD6244 induces BIM-dependent and AKT-independent apoptosis in diffuse large B-cell lymphoma.	AZD 6244	34-41	AKT serine/threonine kinase 1	Homo sapiens	68-71
21628402-2	2011	The novel 2nd generation anti-MEK small molecule, AZD6244, down-regulated its direct downstream target, phospho-ERK (pERK) in germinal center and nongerminal center diffuse large B-cell lymphoma (DLBCL) cell lines and primary cells.	AZD 6244	50-57	mitogen-activated protein kinase kinase 7	Homo sapiens	30-33
21628402-2	2011	The novel 2nd generation anti-MEK small molecule, AZD6244, down-regulated its direct downstream target, phospho-ERK (pERK) in germinal center and nongerminal center diffuse large B-cell lymphoma (DLBCL) cell lines and primary cells.	AZD 6244	50-57	mitogen-activated protein kinase 1	Homo sapiens	112-115
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	mitogen-activated protein kinase 1	Homo sapiens	39-42
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	solute carrier family 16 member 1	Homo sapiens	95-100
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	102-107
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	BCL2 apoptosis regulator	Homo sapiens	109-114
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	116-121
21628402-4	2011	Consequently, several lymphoma-related ERK substrates were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.	AZD 6244	77-84	cyclin dependent kinase 1	Homo sapiens	127-131
21628402-11	2011	Altogether, these findings show that the novel anti-MEK agent, AZD6244, induced apoptosis in DLBCL and that cell death was BIM-dependent.	AZD 6244	63-70	mitogen-activated protein kinase kinase 7	Homo sapiens	52-55
21750552-10	2011	In contrast, treatment with MSC19363669B and selumetinib, two selective MEK inhibitors, caused inhibition of cell proliferation, invasion, migration, anchorage-independent growth in vitro and of tumour growth in vivo of all four TKI-R CALU-3 cell lines.	AZD 6244	45-56	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
21727212-0	2011	Nilotinib alone or in combination with selumetinib is a drug candidate for neurofibromatosis type 2.	AZD 6244	39-50	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	75-99
21727212-9	2011	In addition, nilotinib combined with the MEK1/2 inhibitor selumetinib (AZD6244) at low concentrations displayed stronger efficiency toward tumor growth inhibition, compared with nilotinib alone.	AZD 6244	58-69	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
21727212-9	2011	In addition, nilotinib combined with the MEK1/2 inhibitor selumetinib (AZD6244) at low concentrations displayed stronger efficiency toward tumor growth inhibition, compared with nilotinib alone.	AZD 6244	71-78	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
21519015-0	2011	Phase II study of the mitogen-activated protein kinase 1/2 inhibitor selumetinib in patients with advanced hepatocellular carcinoma.	AZD 6244	69-80	mitogen-activated protein kinase 12	Homo sapiens	22-58
21519015-3	2011	Selumetinib is an orally available inhibitor of MEK tyrosine kinase activity.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	48-51
21519026-2	2011	Selumetinib is an inhibitor of MEK1/2, so this trial was designed to determine the safety and efficacy of selumetinib in BC.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	31-37
21447798-2	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	KRAS proto-oncogene, GTPase	Homo sapiens	250-254
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	92-99	mitogen-activated protein kinase kinase 7	Homo sapiens	44-61
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	92-99	mitogen-activated protein kinase kinase 7	Homo sapiens	63-66
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	92-99	KRAS proto-oncogene, GTPase	Homo sapiens	305-309
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	92-99	KRAS proto-oncogene, GTPase	Homo sapiens	365-369
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	184-191	mitogen-activated protein kinase kinase 7	Homo sapiens	44-61
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	184-191	mitogen-activated protein kinase kinase 7	Homo sapiens	63-66
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	184-191	KRAS proto-oncogene, GTPase	Homo sapiens	305-309
21385921-8	2011	Combination treatments of erlotinib and two MAP kinase kinase (MEK) inhibitors, RDEA119 and AZD6244, showed significant synergistic effect for both combinations (RDEA119-erlotinib and AZD6244-erlotinib) compared with the corresponding single drug treatments in pancreatic cancer cell lines with wild-type KRAS (BxPC-3 and Hs 700T) but not in cell lines with mutant KRAS (MIA PaCa-2 and PANC-1).	AZD 6244	184-191	KRAS proto-oncogene, GTPase	Homo sapiens	365-369
21444672-1	2011	AZD6244 is a small molecule inhibitor of the MEK (MAP/ERK kinase) pathway currently in clinical trials.	AZD 6244	0-7	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
21444672-3	2011	To define molecular mechanisms of MEK inhibitor resistance, we analyzed responses of 38 lung cancer cell lines following AZD6244 treatment and their genome-wide gene expression profiles and identified a panel of genes correlated with sensitivity or resistance to AZD6244 treatment.	AZD 6244	263-270	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
21444672-5	2011	Inhibition of this pathway by JSI-124, a STAT3-specific small molecule inhibitor, or with STAT3-specific siRNA sensitized lung cancer cells to AZD6244 and induced apoptosis.	AZD 6244	143-150	signal transducer and activator of transcription 3	Homo sapiens	90-95
21444672-6	2011	Moreover, combining a STAT3 inhibitor with AZD6244 induced expression of BIM and PARP cleavage, whereas activation of the STAT3 pathway inhibited BIM expression and elicited resistance to MEK inhibitors.	AZD 6244	43-50	poly(ADP-ribose) polymerase 1	Homo sapiens	81-85
21444672-7	2011	We found that the STAT3-regulated microRNA miR-17 played a critical role in MEK inhibitor resistance, such that miR-17 inhibition sensitized resistant cells to AZD6244 by inducing BIM and PARP cleavage.	AZD 6244	160-167	signal transducer and activator of transcription 3	Homo sapiens	18-23
21444672-7	2011	We found that the STAT3-regulated microRNA miR-17 played a critical role in MEK inhibitor resistance, such that miR-17 inhibition sensitized resistant cells to AZD6244 by inducing BIM and PARP cleavage.	AZD 6244	160-167	microRNA 17	Homo sapiens	43-49
21444672-7	2011	We found that the STAT3-regulated microRNA miR-17 played a critical role in MEK inhibitor resistance, such that miR-17 inhibition sensitized resistant cells to AZD6244 by inducing BIM and PARP cleavage.	AZD 6244	160-167	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
21444672-7	2011	We found that the STAT3-regulated microRNA miR-17 played a critical role in MEK inhibitor resistance, such that miR-17 inhibition sensitized resistant cells to AZD6244 by inducing BIM and PARP cleavage.	AZD 6244	160-167	microRNA 17	Homo sapiens	112-118
21444672-7	2011	We found that the STAT3-regulated microRNA miR-17 played a critical role in MEK inhibitor resistance, such that miR-17 inhibition sensitized resistant cells to AZD6244 by inducing BIM and PARP cleavage.	AZD 6244	160-167	poly(ADP-ribose) polymerase 1	Homo sapiens	188-192
21444672-8	2011	Together, these results indicated that STAT3-mediated overexpression of miR-17 blocked BIM expression and caused resistance to AZD6244.	AZD 6244	127-134	signal transducer and activator of transcription 3	Homo sapiens	39-44
21444672-8	2011	Together, these results indicated that STAT3-mediated overexpression of miR-17 blocked BIM expression and caused resistance to AZD6244.	AZD 6244	127-134	microRNA 17	Homo sapiens	72-78
21444672-9	2011	Our findings suggest novel approaches to overcome resistance to MEK inhibitors by combining AZD6244 with STAT3 or miR-17 inhibitors.	AZD 6244	92-99	mitogen-activated protein kinase kinase 7	Homo sapiens	64-67
21447798-2	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	mitogen-activated protein kinase kinase 1	Homo sapiens	38-44
21447798-2	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	217-221
21447798-2	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	153-160	mitogen-activated protein kinase kinase 1	Homo sapiens	38-44
21447798-3	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	128-134
21447798-3	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	136-182
21447798-3	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	cyclin D1	Homo sapiens	206-215
21447798-6	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF(600E).	AZD 6244	42-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
21447798-6	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF(600E).	AZD 6244	42-49	mitogen-activated protein kinase kinase 1	Homo sapiens	112-118
21447798-6	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF(600E).	AZD 6244	42-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	123-127
21447798-6	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF(600E).	AZD 6244	42-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	123-127
21447798-7	2011	Knockdown of KRAS reversed AZD6244 resistance in HCT116 cells as well as reduced the activation of ERK1/2 and protein kinase B; however, the combined inhibition of ERK1/2 and phosphatidylinositol 3-kinase signaling had little effect on AZD6244 resistance, suggesting that additional KRAS effector pathways contribute to this process.	AZD 6244	27-34	KRAS proto-oncogene, GTPase	Homo sapiens	13-17
21447798-7	2011	Knockdown of KRAS reversed AZD6244 resistance in HCT116 cells as well as reduced the activation of ERK1/2 and protein kinase B; however, the combined inhibition of ERK1/2 and phosphatidylinositol 3-kinase signaling had little effect on AZD6244 resistance, suggesting that additional KRAS effector pathways contribute to this process.	AZD 6244	236-243	KRAS proto-oncogene, GTPase	Homo sapiens	13-17
21238821-0	2011	Disseminated follicular eruption during therapy with the MEK inhibitor AZD6244.	AZD 6244	71-78	mitogen-activated protein kinase kinase 7	Homo sapiens	57-60
21209378-8	2011	The NRAS(Q61K) mutation sensitized Hut78 cells toward growth inhibition by the MEK inhibitors U0126, AZD6244, and PD0325901.	AZD 6244	101-108	NRAS proto-oncogene, GTPase	Homo sapiens	4-8
21209378-8	2011	The NRAS(Q61K) mutation sensitized Hut78 cells toward growth inhibition by the MEK inhibitors U0126, AZD6244, and PD0325901.	AZD 6244	101-108	mitogen-activated protein kinase kinase 7	Homo sapiens	79-82
20407895-1	2011	PURPOSE: AZD6244 (ARRY-142886) (AstraZeneca, Macclesfield, UK) is a novel small molecule MEK1/2 inhibitor that is currently being tested in Phase II trials.	AZD 6244	9-16	mitogen-activated protein kinase kinase 1	Mus musculus	89-95
21286012-0	2011	Could HBx protein expression affect signal pathway inhibition by gefitinib or selumetinib, a MEK inhibitor, in hepatocellular carcinoma cell lines?	AZD 6244	78-89	mitogen-activated protein kinase kinase 7	Homo sapiens	93-96
21286012-6	2011	Selumetinib (MEK inhibitor) reduced pERK level and beta-catenin activity but pAkt expression was rather elevated by selumetinib in these cells.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	13-16
21286012-6	2011	Selumetinib (MEK inhibitor) reduced pERK level and beta-catenin activity but pAkt expression was rather elevated by selumetinib in these cells.	AZD 6244	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	36-40
21286012-6	2011	Selumetinib (MEK inhibitor) reduced pERK level and beta-catenin activity but pAkt expression was rather elevated by selumetinib in these cells.	AZD 6244	0-11	catenin beta 1	Homo sapiens	51-63
21286012-7	2011	Reduction of pERK levels was much stronger with selumetinib than gefitinib in both cells.	AZD 6244	48-59	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	13-17
21215703-5	2011	We further reveal that AZD6244, a clinical trial drug that inhibits RAF1-ERK signaling, could prevent breast cancer progression by eliminating BTICs.	AZD 6244	23-30	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
21215703-5	2011	We further reveal that AZD6244, a clinical trial drug that inhibits RAF1-ERK signaling, could prevent breast cancer progression by eliminating BTICs.	AZD 6244	23-30	mitogen-activated protein kinase 1	Homo sapiens	73-76
21118963-7	2011	Inhibition of MEK by AS703026 or AZD6244 also suppressed cetuximab-resistant colorectal cancer cells attributed to K-ras mutation both in vitro and in vivo.	AZD 6244	33-40	KRAS proto-oncogene, GTPase	Homo sapiens	115-120
22194965-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: The sensitivity to vemurafenib or the MEK inhibitor AZD6244 was tested in sensitive and resistant human melanoma cell lines exploring differences in activation-associated phosphorylation levels of major signaling molecules, leading to the testing of co-inhibition of the AKT/mTOR pathway genetically and pharmacologically.	AZD 6244	84-91	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
21118963-0	2011	MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy.	AZD 6244	31-38	KRAS proto-oncogene, GTPase	Homo sapiens	70-74
21118963-0	2011	MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy.	AZD 6244	31-38	epidermal growth factor receptor	Homo sapiens	122-126
21118963-3	2011	In this study, we investigated the ability of two MEK inhibitors currently in clinical trials, AS703026 and AZD6244, to address the challenge posed by the resistance of K-ras mutated colorectal cancers to EGFR mAb.	AZD 6244	108-115	KRAS proto-oncogene, GTPase	Homo sapiens	169-174
21118963-3	2011	In this study, we investigated the ability of two MEK inhibitors currently in clinical trials, AS703026 and AZD6244, to address the challenge posed by the resistance of K-ras mutated colorectal cancers to EGFR mAb.	AZD 6244	108-115	epidermal growth factor receptor	Homo sapiens	205-209
21118963-6	2011	In contrast, AS703026 and AZD6244 effectively inhibited the growth of D-MUT cells in vitro and in vivo by specific inhibition of the key MEK downstream target kinase ERK.	AZD 6244	26-33	mitogen-activated protein kinase kinase 7	Homo sapiens	137-140
21118963-6	2011	In contrast, AS703026 and AZD6244 effectively inhibited the growth of D-MUT cells in vitro and in vivo by specific inhibition of the key MEK downstream target kinase ERK.	AZD 6244	26-33	mitogen-activated protein kinase 1	Homo sapiens	166-169
21674991-3	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	mitogen-activated protein kinase kinase 1	Homo sapiens	38-44
21674991-8	2011	Knockdown of KRAS reversed AZD6244 resistance in HCT116 cells as well as reduced the activation of ERK1/2 and protein kinase B; however, the combined inhibition of ERK1/2 and phosphatidylinositol 3-kinase signaling had little effect on AZD6244 resistance, suggesting that additional KRAS effector pathways contribute to this process.	AZD 6244	236-243	KRAS proto-oncogene, GTPase	Homo sapiens	13-17
21674991-3	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	217-221
21674991-3	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	140-151	KRAS proto-oncogene, GTPase	Homo sapiens	250-254
21674991-3	2011	We modeled acquired resistance to the MEK1/2 (mitogen-activated or extracellular signal-regulated protein kinase kinases 1 and 2) inhibitor selumetinib (AZD6244) in colorectal cancer cell lines harboring mutations in BRAF (COLO205 and HT29 lines) or KRAS (HCT116 and LoVo lines).	AZD 6244	153-160	mitogen-activated protein kinase kinase 1	Homo sapiens	38-44
21674991-4	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	128-134
21674991-4	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	136-182
21674991-4	2011	AZD6244-resistant derivatives were refractory to AZD6244-induced cell cycle arrest and death and exhibited a marked increase in ERK1/2 (extracellular signal-regulated kinases 1 and 2) pathway signaling and cyclin D1 abundance when assessed in the absence of inhibitor.	AZD 6244	0-7	cyclin D1	Homo sapiens	206-215
21674991-7	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF600E.	AZD 6244	42-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
21674991-7	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF600E.	AZD 6244	42-49	mitogen-activated protein kinase kinase 1	Homo sapiens	112-118
21674991-7	2011	Inhibition of BRAF reversed resistance to AZD6244 in COLO205 cells, which suggested that combined inhibition of MEK1/2 and BRAF may reduce the likelihood of acquired resistance in tumors with BRAF600E.	AZD 6244	42-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	123-127
21674991-8	2011	Knockdown of KRAS reversed AZD6244 resistance in HCT116 cells as well as reduced the activation of ERK1/2 and protein kinase B; however, the combined inhibition of ERK1/2 and phosphatidylinositol 3-kinase signaling had little effect on AZD6244 resistance, suggesting that additional KRAS effector pathways contribute to this process.	AZD 6244	27-34	KRAS proto-oncogene, GTPase	Homo sapiens	13-17
20814675-12	2010	MEK inhibitors, including UO126 and AZD6244, reduced B7-H1 expression and restored CTL-mediated lysis of blast cells.	AZD 6244	36-43	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
21169255-6	2010	We studied in vitro activity of a novel dual PI3K/mTOR inhibitor NVP-BEZ235 and activity of the combination of NVP-BEZ235 and the MAP/ERK kinase (MEK) inhibitor AZD6244.	AZD 6244	161-168	mitogen-activated protein kinase kinase 7	Homo sapiens	146-149
21169255-12	2010	Synergism was seen when combining NVP-BEZ235 and AZD6244, with resultant increases in poly(ADP-ribose) polymerase and caspase-2 cleavage.	AZD 6244	49-56	poly(ADP-ribose) polymerase 1	Homo sapiens	86-113
21169255-12	2010	Synergism was seen when combining NVP-BEZ235 and AZD6244, with resultant increases in poly(ADP-ribose) polymerase and caspase-2 cleavage.	AZD 6244	49-56	caspase 2	Homo sapiens	118-127
20814675-12	2010	MEK inhibitors, including UO126 and AZD6244, reduced B7-H1 expression and restored CTL-mediated lysis of blast cells.	AZD 6244	36-43	CD274 antigen	Mus musculus	53-58
20802351-1	2010	INTRODUCTION: AZD6244 (ARRY-142886) is a potent, selective MEK inhibitor.	AZD 6244	14-21	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
21098728-3	2010	To identify potential mechanisms of acquired drug resistance, we generated clones resistant to the allosteric MEK inhibitor AZD6244 from two BRAF V600E mutant colorectal cancer cell lines that are highly sensitive to MEK or BRAF inhibition.	AZD 6244	124-131	mitogen-activated protein kinase kinase 7	Homo sapiens	110-113
21098728-3	2010	To identify potential mechanisms of acquired drug resistance, we generated clones resistant to the allosteric MEK inhibitor AZD6244 from two BRAF V600E mutant colorectal cancer cell lines that are highly sensitive to MEK or BRAF inhibition.	AZD 6244	124-131	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	141-145
21098728-4	2010	These AZD6244-resistant (AR) clones, which exhibited cross-resistance to BRAF inhibitors, acquired resistance through amplification of the BRAF gene.	AZD 6244	6-13	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
21098728-4	2010	These AZD6244-resistant (AR) clones, which exhibited cross-resistance to BRAF inhibitors, acquired resistance through amplification of the BRAF gene.	AZD 6244	6-13	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	139-143
21098728-7	2010	In cell lines, BRAF amplification increased the abundance of phosphorylated MEK and impaired the ability of AZD6244 to inhibit ERK (extracellular signal-regulated kinase) phosphorylation.	AZD 6244	108-115	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	15-19
21098728-7	2010	In cell lines, BRAF amplification increased the abundance of phosphorylated MEK and impaired the ability of AZD6244 to inhibit ERK (extracellular signal-regulated kinase) phosphorylation.	AZD 6244	108-115	mitogen-activated protein kinase 1	Homo sapiens	127-130
21098728-7	2010	In cell lines, BRAF amplification increased the abundance of phosphorylated MEK and impaired the ability of AZD6244 to inhibit ERK (extracellular signal-regulated kinase) phosphorylation.	AZD 6244	108-115	mitogen-activated protein kinase 1	Homo sapiens	132-169
21098728-8	2010	The ability of AZD6244 to inhibit ERK phosphorylation in AR cells was restored by treatment with a BRAF inhibitor at low concentrations that reduced the abundance of phosphorylated MEK to amounts observed in parental cells.	AZD 6244	15-22	mitogen-activated protein kinase 1	Homo sapiens	34-37
21098728-8	2010	The ability of AZD6244 to inhibit ERK phosphorylation in AR cells was restored by treatment with a BRAF inhibitor at low concentrations that reduced the abundance of phosphorylated MEK to amounts observed in parental cells.	AZD 6244	15-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
21098728-8	2010	The ability of AZD6244 to inhibit ERK phosphorylation in AR cells was restored by treatment with a BRAF inhibitor at low concentrations that reduced the abundance of phosphorylated MEK to amounts observed in parental cells.	AZD 6244	15-22	mitogen-activated protein kinase kinase 7	Homo sapiens	181-184
20923857-0	2010	Identification of predictive markers of response to the MEK1/2 inhibitor selumetinib (AZD6244) in K-ras-mutated colorectal cancer.	AZD 6244	73-84	mitogen-activated protein kinase kinase 1	Homo sapiens	56-62
20923857-0	2010	Identification of predictive markers of response to the MEK1/2 inhibitor selumetinib (AZD6244) in K-ras-mutated colorectal cancer.	AZD 6244	73-84	KRAS proto-oncogene, GTPase	Homo sapiens	98-103
20923857-0	2010	Identification of predictive markers of response to the MEK1/2 inhibitor selumetinib (AZD6244) in K-ras-mutated colorectal cancer.	AZD 6244	86-93	mitogen-activated protein kinase kinase 1	Homo sapiens	56-62
20923857-0	2010	Identification of predictive markers of response to the MEK1/2 inhibitor selumetinib (AZD6244) in K-ras-mutated colorectal cancer.	AZD 6244	86-93	KRAS proto-oncogene, GTPase	Homo sapiens	98-103
20923857-3	2010	The aim of this study was to develop and characterize predictive biomarkers of response to the MEK1/2 inhibitor AZD6244 in CRC in order to maximize the clinical utility of this agent.	AZD 6244	112-119	mitogen-activated protein kinase kinase 1	Homo sapiens	95-101
20923857-9	2010	Baseline gene array data from CRC cell lines and xenografts were used to develop a k-top scoring pair (k-TSP) classifier, which predicted with 71% accuracy which of a test set of patient-derived K-ras mutant CRC explants would respond to AZD6244, providing the basis for a patient-selective clinical trial.	AZD 6244	238-245	thrombospondin 1	Homo sapiens	105-108
20923857-9	2010	Baseline gene array data from CRC cell lines and xenografts were used to develop a k-top scoring pair (k-TSP) classifier, which predicted with 71% accuracy which of a test set of patient-derived K-ras mutant CRC explants would respond to AZD6244, providing the basis for a patient-selective clinical trial.	AZD 6244	238-245	KRAS proto-oncogene, GTPase	Homo sapiens	195-200
21124782-1	2010	AZD6244 and MK2206 are targeted small-molecule drugs that inhibit MEK and AKT respectively.	AZD 6244	0-7	mitogen-activated protein kinase kinase 7	Homo sapiens	66-69
21124782-1	2010	AZD6244 and MK2206 are targeted small-molecule drugs that inhibit MEK and AKT respectively.	AZD 6244	0-7	AKT serine/threonine kinase 1	Homo sapiens	74-77
21124782-3	2010	Our previous work showed the importance of activated AKT in mediating resistance of non-small cell lung cancer (NSCLC) to AZD6244.	AZD 6244	122-129	AKT serine/threonine kinase 1	Homo sapiens	53-56
21124782-12	2010	The AZD6244-MK2206 combination therapy resulted in effective inhibition of both p-ERK and p-AKT expression in tumor tissue.	AZD 6244	4-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	80-85
21124782-12	2010	The AZD6244-MK2206 combination therapy resulted in effective inhibition of both p-ERK and p-AKT expression in tumor tissue.	AZD 6244	4-11	AKT serine/threonine kinase 1	Homo sapiens	92-95
20959481-0	2010	Basal and treatment-induced activation of AKT mediates resistance to cell death by AZD6244 (ARRY-142886) in Braf-mutant human cutaneous melanoma cells.	AZD 6244	83-90	AKT serine/threonine kinase 1	Homo sapiens	42-45
20959481-0	2010	Basal and treatment-induced activation of AKT mediates resistance to cell death by AZD6244 (ARRY-142886) in Braf-mutant human cutaneous melanoma cells.	AZD 6244	83-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
20959481-2	2010	AZD6244 is a selective MEK1/2 inhibitor that markedly reduces tumor P-MAPK levels, but it produces few clinical responses in melanoma patients.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	23-29
20959481-7	2010	RPPA characterization of the time-dependent changes in signaling pathways revealed that AZD6244 produced durable and potent inhibition of P-MAPK in sensitive and resistant Braf-mutant cell lines, but several resistant lines showed AZD6244-induced activation of AKT.	AZD 6244	88-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	172-176
20959481-7	2010	RPPA characterization of the time-dependent changes in signaling pathways revealed that AZD6244 produced durable and potent inhibition of P-MAPK in sensitive and resistant Braf-mutant cell lines, but several resistant lines showed AZD6244-induced activation of AKT.	AZD 6244	88-95	AKT serine/threonine kinase 1	Homo sapiens	261-264
20959481-7	2010	RPPA characterization of the time-dependent changes in signaling pathways revealed that AZD6244 produced durable and potent inhibition of P-MAPK in sensitive and resistant Braf-mutant cell lines, but several resistant lines showed AZD6244-induced activation of AKT.	AZD 6244	231-238	AKT serine/threonine kinase 1	Homo sapiens	261-264
20959481-8	2010	In contrast, sensitive cell lines showed AZD6244 treatment-induced upregulation of PTEN protein and mRNA expression.	AZD 6244	41-48	phosphatase and tensin homolog	Homo sapiens	83-87
20959481-9	2010	Inhibition of AKT, TORC1/2, or insulin-like growth factor I receptor blocked AZD6244-induced activation of AKT and resulted in synergistic cell killing with AZD6244.	AZD 6244	77-84	AKT serine/threonine kinase 1	Homo sapiens	14-17
20959481-9	2010	Inhibition of AKT, TORC1/2, or insulin-like growth factor I receptor blocked AZD6244-induced activation of AKT and resulted in synergistic cell killing with AZD6244.	AZD 6244	77-84	CREB regulated transcription coactivator 1	Homo sapiens	19-68
20959481-9	2010	Inhibition of AKT, TORC1/2, or insulin-like growth factor I receptor blocked AZD6244-induced activation of AKT and resulted in synergistic cell killing with AZD6244.	AZD 6244	77-84	AKT serine/threonine kinase 1	Homo sapiens	107-110
20959481-9	2010	Inhibition of AKT, TORC1/2, or insulin-like growth factor I receptor blocked AZD6244-induced activation of AKT and resulted in synergistic cell killing with AZD6244.	AZD 6244	157-164	AKT serine/threonine kinase 1	Homo sapiens	14-17
20959481-9	2010	Inhibition of AKT, TORC1/2, or insulin-like growth factor I receptor blocked AZD6244-induced activation of AKT and resulted in synergistic cell killing with AZD6244.	AZD 6244	157-164	CREB regulated transcription coactivator 1	Homo sapiens	19-68
20959481-10	2010	These findings identify basal and treatment-induced regulation of the PI3K-AKT pathway as a critical regulator of AZD6244 sensitivity in Braf-mutant cutaneous melanoma cells and the novel regulation of PTEN expression by AZD6244 in sensitive cells, and suggest new combinatorial approaches for patients.	AZD 6244	114-121	AKT serine/threonine kinase 1	Homo sapiens	75-78
20959481-10	2010	These findings identify basal and treatment-induced regulation of the PI3K-AKT pathway as a critical regulator of AZD6244 sensitivity in Braf-mutant cutaneous melanoma cells and the novel regulation of PTEN expression by AZD6244 in sensitive cells, and suggest new combinatorial approaches for patients.	AZD 6244	114-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
20959481-10	2010	These findings identify basal and treatment-induced regulation of the PI3K-AKT pathway as a critical regulator of AZD6244 sensitivity in Braf-mutant cutaneous melanoma cells and the novel regulation of PTEN expression by AZD6244 in sensitive cells, and suggest new combinatorial approaches for patients.	AZD 6244	221-228	phosphatase and tensin homolog	Homo sapiens	202-206
20802351-1	2010	INTRODUCTION: AZD6244 (ARRY-142886) is a potent, selective MEK inhibitor.	AZD 6244	23-34	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
20802351-13	2010	Based on preclinical data and recent clinical observations, further development of AZD6244 in NSCLC should focus on BRAF or RAS mutation-positive patients and/or AZD6244-based combination regimens.	AZD 6244	83-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
20806365-1	2010	BACKGROUND: AZD6244 (ARRY-142886) is a potent small molecule inhibitor of MEK1/2 that is in phase 2 clinical development.	AZD 6244	12-19	mitogen-activated protein kinase kinase 1	Homo sapiens	74-80
20806365-9	2010	Pharmacodynamic studies indicated at this dose and schedule AZD6244 completely inhibited ERK1/2 phosphorylation.	AZD 6244	60-67	mitogen-activated protein kinase 3	Homo sapiens	89-95
20806365-12	2010	CONCLUSIONS: At the dose and schedule of administration used, AZD6244 as a single agent had limited in vitro and in vivo activity against the PPTP tumor panels despite inhibition of MEK1/2 activity.	AZD 6244	62-69	mitogen-activated protein kinase kinase 1	Homo sapiens	182-188
20806365-13	2010	However, AZD6244 was highly active against BT-40 JPA xenografts that harbor constitutively activated BRAF, causing complete regressions.	AZD 6244	9-16	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
20885957-1	2010	AZD6244 (ARRY-142886) is an inhibitor of MEK1/2 and can inhibit cell proliferation or induce apoptosis in a cell-type dependent manner.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
20885957-1	2010	AZD6244 (ARRY-142886) is an inhibitor of MEK1/2 and can inhibit cell proliferation or induce apoptosis in a cell-type dependent manner.	AZD 6244	9-20	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
20885957-9	2010	In addition, we found that transfection of constitutively active AKT up-regulated p-Thr32-FOXO3a and p-Ser253-FOXO3a expression and inhibited AZD6244-induced Bim expression in sensitive cells.	AZD 6244	142-149	BCL2 like 11	Homo sapiens	158-161
20885957-4	2010	We found that AZD6244 elicited a large increase of Bim proteins and a smaller increase of PUMA and NOXA proteins, and induced cell death in sensitive lung cancer cell lines, but had no effect on other Bcl-2 related proteins in those cell lines.	AZD 6244	14-21	BCL2 like 11	Homo sapiens	51-54
20885957-10	2010	These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244.	AZD 6244	55-62	BCL2 like 11	Homo sapiens	24-27
20885957-10	2010	These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244.	AZD 6244	55-62	forkhead box O3	Homo sapiens	124-130
20885957-5	2010	Knockdown of Bim by siRNA greatly increased the IC(50) and reduced apoptosis for AZD6244 treated cells.	AZD 6244	81-88	BCL2 like 11	Homo sapiens	13-16
20885957-10	2010	These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244.	AZD 6244	212-219	AKT serine/threonine kinase 1	Homo sapiens	120-123
20885957-6	2010	We also found that levels of endogenous p-Thr32-FOXO3a and p-Ser253-FOXO3a were lower in AZD6244-sensitive cells than in AZD6244-resistant cells.	AZD 6244	89-96	forkhead box O3	Homo sapiens	48-54
20885957-10	2010	These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244.	AZD 6244	212-219	forkhead box O3	Homo sapiens	124-130
20885957-10	2010	These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244.	AZD 6244	212-219	BCL2 like 11	Homo sapiens	154-157
20885957-6	2010	We also found that levels of endogenous p-Thr32-FOXO3a and p-Ser253-FOXO3a were lower in AZD6244-sensitive cells than in AZD6244-resistant cells.	AZD 6244	89-96	forkhead box O3	Homo sapiens	68-74
20885957-6	2010	We also found that levels of endogenous p-Thr32-FOXO3a and p-Ser253-FOXO3a were lower in AZD6244-sensitive cells than in AZD6244-resistant cells.	AZD 6244	121-128	forkhead box O3	Homo sapiens	48-54
20885957-6	2010	We also found that levels of endogenous p-Thr32-FOXO3a and p-Ser253-FOXO3a were lower in AZD6244-sensitive cells than in AZD6244-resistant cells.	AZD 6244	121-128	forkhead box O3	Homo sapiens	68-74
20885957-7	2010	In the sensitive cells, AZD6244 induced FOXO3a nuclear translocation required for Bim activation.	AZD 6244	24-31	forkhead box O3	Homo sapiens	40-46
20885957-7	2010	In the sensitive cells, AZD6244 induced FOXO3a nuclear translocation required for Bim activation.	AZD 6244	24-31	BCL2 like 11	Homo sapiens	82-85
20885957-8	2010	Moreover, the silencing of FOXO3a by siRNA abrogated AZD6244-induced cell apoptosis.	AZD 6244	53-60	forkhead box O3	Homo sapiens	27-33
20885957-9	2010	In addition, we found that transfection of constitutively active AKT up-regulated p-Thr32-FOXO3a and p-Ser253-FOXO3a expression and inhibited AZD6244-induced Bim expression in sensitive cells.	AZD 6244	142-149	AKT serine/threonine kinase 1	Homo sapiens	65-68
20221697-1	2010	We previously showed that the MEK inhibitor AZD6244 induced apoptosis in acute myelogenous leukemia (AML) HL60 cells.	AZD 6244	44-51	mitogen-activated protein kinase kinase 7	Homo sapiens	30-33
20221697-3	2010	This study found that exposure of HL60 cells to AZD6244 down-regulated the levels of phosphor (p)-4E-binding protein 1 (4E-BP1), a substrate of mammalian target of rapamycin complex 1 (mTORC1), and anti-apoptotic protein Mcl-1.	AZD 6244	48-55	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	120-126
20221697-7	2010	Moreover, we found that blockade of mTORC1 by RAD001 synergistically enhanced the action of AZD6244 in leukemia cells.	AZD 6244	92-99	CREB regulated transcription coactivator 1	Mus musculus	36-42
20221697-3	2010	This study found that exposure of HL60 cells to AZD6244 down-regulated the levels of phosphor (p)-4E-binding protein 1 (4E-BP1), a substrate of mammalian target of rapamycin complex 1 (mTORC1), and anti-apoptotic protein Mcl-1.	AZD 6244	48-55	CREB regulated transcription coactivator 1	Mus musculus	185-191
20221697-3	2010	This study found that exposure of HL60 cells to AZD6244 down-regulated the levels of phosphor (p)-4E-binding protein 1 (4E-BP1), a substrate of mammalian target of rapamycin complex 1 (mTORC1), and anti-apoptotic protein Mcl-1.	AZD 6244	48-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	221-226
20221697-5	2010	These observations prompted us to hypothesize that down-regulation od 4E-BP1 and Mcl-1 might play an important role in AZD6244-mediated apoptosis.	AZD 6244	119-126	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	70-76
20221697-5	2010	These observations prompted us to hypothesize that down-regulation od 4E-BP1 and Mcl-1 might play an important role in AZD6244-mediated apoptosis.	AZD 6244	119-126	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	81-86
20221697-6	2010	As expected, down-regulation of 4E-BP1 by an siRNA sensitized EOL-1 cells to AZD6244-mediated apoptosis in parallel with down-regulation of Mcl-1.	AZD 6244	77-84	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	32-38
20484037-2	2010	In this study, we characterized a mechanism of drug resistance that arises to AZD6244, an established mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 inhibitor currently being evaluated in cancer clinical trials.	AZD 6244	78-85	mitogen-activated protein kinase kinase 1	Homo sapiens	102-182
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	223-230	forkhead box O3	Homo sapiens	84-90
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	223-230	forkhead box O3	Homo sapiens	100-106
20587667-0	2010	Identification of common predictive markers of in vitro response to the Mek inhibitor selumetinib (AZD6244; ARRY-142886) in human breast cancer and non-small cell lung cancer cell lines.	AZD 6244	86-97	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
20587667-0	2010	Identification of common predictive markers of in vitro response to the Mek inhibitor selumetinib (AZD6244; ARRY-142886) in human breast cancer and non-small cell lung cancer cell lines.	AZD 6244	99-106	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
20587667-1	2010	Selumetinib (AZD6244; ARRY-142886) is a tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2 currently in clinical development.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	82-122
20587667-1	2010	Selumetinib (AZD6244; ARRY-142886) is a tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2 currently in clinical development.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	124-127
20587667-1	2010	Selumetinib (AZD6244; ARRY-142886) is a tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2 currently in clinical development.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	82-122
20587667-1	2010	Selumetinib (AZD6244; ARRY-142886) is a tight-binding, uncompetitive inhibitor of mitogen-activated protein kinase kinases (MEK) 1 and 2 currently in clinical development.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	124-127
20587667-7	2010	In total, these results suggest that clinical trials of selumetinib in breast cancer and NSCLC might select patients whose tumors harbor raf and ras mutations, respectively.	AZD 6244	56-67	zinc fingers and homeoboxes 2	Homo sapiens	137-140
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	223-230	forkhead box O3	Homo sapiens	100-106
20484037-6	2010	Our findings define FOXO3a as candidate marker to predict the clinical efficacy of AZD6244.	AZD 6244	83-90	forkhead box O3	Homo sapiens	20-26
20484037-3	2010	AZD6244 enhanced the expression of transcription factor FOXO3a, which suppressed cancer cell proliferation.	AZD 6244	0-7	forkhead box O3	Homo sapiens	56-62
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	3-10	forkhead box O3	Homo sapiens	84-90
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	3-10	forkhead box O3	Homo sapiens	100-106
20484037-4	2010	In AZD6244-resistant cancer cells, we observed the impaired nuclear localization of FOXO3a, reduced FOXO3a-mediated transcriptional activity, and decreased the expression of FOXO3a target gene Bim after cell treatment with AZD6244.	AZD 6244	3-10	forkhead box O3	Homo sapiens	100-106
19634052-0	2010	Case studies showing clinical signs and management of cutaneous  toxicity of the MEK1/2 inhibitor AZD6244 (ARRY-142886) in patients  with solid tumours.	AZD 6244	98-105	mitogen-activated protein kinase kinase 1	Homo sapiens	81-87
20215513-0	2010	Transcriptional pathway signatures predict MEK addiction and response to selumetinib (AZD6244).	AZD 6244	86-93	mitogen-activated protein kinase kinase 7	Homo sapiens	43-46
20215513-1	2010	Selumetinib (AZD6244, ARRY-142886) is a selective, non-ATP-competitive inhibitor of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-1/2.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	84-164
20215513-1	2010	Selumetinib (AZD6244, ARRY-142886) is a selective, non-ATP-competitive inhibitor of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-1/2.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	84-164
20215513-1	2010	Selumetinib (AZD6244, ARRY-142886) is a selective, non-ATP-competitive inhibitor of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-1/2.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	84-164
20215513-6	2010	Where the MEK pathway is activated but the cells remain resistant to selumetinib, we identified a 13-gene signature that implicates the existence of compensatory signaling from RAS effectors other than PI3K.	AZD 6244	69-80	mitogen-activated protein kinase kinase 7	Homo sapiens	10-13
20103661-2	2010	AZD6244 blocks MEK1/2, inhibiting ERK phosphorylation.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	15-21
20103661-2	2010	AZD6244 blocks MEK1/2, inhibiting ERK phosphorylation.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	34-37
20103661-17	2010	CONCLUSIONS: AZD6244-associated skin reactions partly overlap with those observed upon epidermal growth factor receptor inhibition.	AZD 6244	13-20	epidermal growth factor receptor	Homo sapiens	87-119
20215498-2	2010	In this study, antileukemic effects of combined MEK inhibition by AZD6244 and nongenotoxic p53 activation by MDM2 antagonist Nutlin-3a were investigated.	AZD 6244	66-73	mitogen-activated protein kinase kinase 7	Homo sapiens	48-51
20215498-3	2010	Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01).	AZD 6244	51-58	mitogen-activated protein kinase kinase 7	Homo sapiens	25-28
20215498-3	2010	Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01).	AZD 6244	51-58	MDM2 proto-oncogene	Homo sapiens	33-37
20215498-3	2010	Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01).	AZD 6244	51-58	RUNX family transcription factor 2	Homo sapiens	201-205
20101735-5	2010	RESULTS: We report here that pharmacological inhibition of the MEK/ERK pathway by AZD6244 enhanced the antitumor and antiangiogenic activities of mTOR inhibitor RAPA in both orthotopic and ectopic models of HCC.	AZD 6244	82-89	mitogen-activated protein kinase kinase 7	Homo sapiens	63-66
20101735-5	2010	RESULTS: We report here that pharmacological inhibition of the MEK/ERK pathway by AZD6244 enhanced the antitumor and antiangiogenic activities of mTOR inhibitor RAPA in both orthotopic and ectopic models of HCC.	AZD 6244	82-89	mitogen-activated protein kinase 1	Homo sapiens	67-70
20101735-5	2010	RESULTS: We report here that pharmacological inhibition of the MEK/ERK pathway by AZD6244 enhanced the antitumor and antiangiogenic activities of mTOR inhibitor RAPA in both orthotopic and ectopic models of HCC.	AZD 6244	82-89	mechanistic target of rapamycin kinase	Homo sapiens	146-150
20179232-0	2010	The first-in-human study of the hydrogen sulfate (Hyd-sulfate) capsule of the MEK1/2 inhibitor AZD6244 (ARRY-142886): a phase I open-label multicenter trial in patients with advanced cancer.	AZD 6244	95-102	mitogen-activated protein kinase kinase 1	Homo sapiens	78-84
20179232-0	2010	The first-in-human study of the hydrogen sulfate (Hyd-sulfate) capsule of the MEK1/2 inhibitor AZD6244 (ARRY-142886): a phase I open-label multicenter trial in patients with advanced cancer.	AZD 6244	104-115	mitogen-activated protein kinase kinase 1	Homo sapiens	78-84
19910069-7	2010	Pharmacological inhibition of the MEK/ERK pathway by AZD6244 enhanced the anti-tumor effect of sorafenib in both orthotopic and ectopic models of HCC.	AZD 6244	53-60	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
19910069-7	2010	Pharmacological inhibition of the MEK/ERK pathway by AZD6244 enhanced the anti-tumor effect of sorafenib in both orthotopic and ectopic models of HCC.	AZD 6244	53-60	mitogen-activated protein kinase 1	Homo sapiens	38-41
19548087-2	2009	This study explored the impact of the MEK inhibitor AZD6244 on the effect of cytarabien (AraC), one of the most commonly used anti-leukemia agents, to induce growth arrest and apoptosis of AML cells.	AZD 6244	52-59	mitogen-activated protein kinase kinase 7	Homo sapiens	38-41
19804833-0	2010	Targeting ERK1/2 activation and proliferation in human primary schwannoma cells with MEK1/2 inhibitor AZD6244.	AZD 6244	102-109	mitogen-activated protein kinase 3	Homo sapiens	10-16
19804833-0	2010	Targeting ERK1/2 activation and proliferation in human primary schwannoma cells with MEK1/2 inhibitor AZD6244.	AZD 6244	102-109	mitogen-activated protein kinase kinase 1	Homo sapiens	85-91
19804833-5	2010	Here, we targeted MEK1/2 known as a convergence point for multiple cascades towards ERK1/2 activation and cell proliferation, using MEK1/2 inhibitor AZD6244 (ARRY-142886; Astra Zeneca).	AZD 6244	149-156	mitogen-activated protein kinase kinase 1	Homo sapiens	18-24
19804833-5	2010	Here, we targeted MEK1/2 known as a convergence point for multiple cascades towards ERK1/2 activation and cell proliferation, using MEK1/2 inhibitor AZD6244 (ARRY-142886; Astra Zeneca).	AZD 6244	149-156	mitogen-activated protein kinase 3	Homo sapiens	84-90
19804833-5	2010	Here, we targeted MEK1/2 known as a convergence point for multiple cascades towards ERK1/2 activation and cell proliferation, using MEK1/2 inhibitor AZD6244 (ARRY-142886; Astra Zeneca).	AZD 6244	149-156	mitogen-activated protein kinase kinase 1	Homo sapiens	132-138
19804833-6	2010	We show that AZD6244 at low concentration completely abolished platelet-derived growth factor-DD-mediated ERK1/2 activation and cell proliferation in human primary schwannoma cells.	AZD 6244	13-20	mitogen-activated protein kinase 3	Homo sapiens	106-112
19637312-0	2009	Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY-142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines.	AZD 6244	45-52	mitogen-activated protein kinase kinase 1	Homo sapiens	28-34
19637312-0	2009	Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY-142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines.	AZD 6244	45-52	mitogen-activated protein kinase 3	Homo sapiens	91-97
19637312-2	2009	The MEK1/2-selective inhibitor, AZD6244 (ARRY-142886), blocks ERK1/2 activation and is currently undergoing clinical evaluation.	AZD 6244	32-39	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
19637312-2	2009	The MEK1/2-selective inhibitor, AZD6244 (ARRY-142886), blocks ERK1/2 activation and is currently undergoing clinical evaluation.	AZD 6244	32-39	mitogen-activated protein kinase 3	Homo sapiens	62-68
19637312-2	2009	The MEK1/2-selective inhibitor, AZD6244 (ARRY-142886), blocks ERK1/2 activation and is currently undergoing clinical evaluation.	AZD 6244	41-52	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
19637312-2	2009	The MEK1/2-selective inhibitor, AZD6244 (ARRY-142886), blocks ERK1/2 activation and is currently undergoing clinical evaluation.	AZD 6244	41-52	mitogen-activated protein kinase 3	Homo sapiens	62-68
19637312-6	2009	Cell lines that were resistant to AZD6244 exhibited low or no ERK1/2 activation or exhibited coincident activation of ERK1/2 and protein kinase B (PKB), the latter indicative of activation of the PI3K pathway.	AZD 6244	34-41	protein tyrosine kinase 2 beta	Homo sapiens	129-145
19637312-6	2009	Cell lines that were resistant to AZD6244 exhibited low or no ERK1/2 activation or exhibited coincident activation of ERK1/2 and protein kinase B (PKB), the latter indicative of activation of the PI3K pathway.	AZD 6244	34-41	protein tyrosine kinase 2 beta	Homo sapiens	147-150
19637312-7	2009	In cell lines with coincident ERK1/2 and PKB activation, sensitivity to AZD6244 could be re-imposed by any of the 3 distinct PI3K/mTOR inhibitors.	AZD 6244	72-79	mitogen-activated protein kinase 3	Homo sapiens	30-36
19637312-7	2009	In cell lines with coincident ERK1/2 and PKB activation, sensitivity to AZD6244 could be re-imposed by any of the 3 distinct PI3K/mTOR inhibitors.	AZD 6244	72-79	protein tyrosine kinase 2 beta	Homo sapiens	41-44
19637312-7	2009	In cell lines with coincident ERK1/2 and PKB activation, sensitivity to AZD6244 could be re-imposed by any of the 3 distinct PI3K/mTOR inhibitors.	AZD 6244	72-79	mechanistic target of rapamycin kinase	Homo sapiens	130-134
19637312-8	2009	We conclude that AZD6244 is effective in colorectal cancer cell lines with BRAF or KRAS mutations.	AZD 6244	17-24	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	75-79
19637312-8	2009	We conclude that AZD6244 is effective in colorectal cancer cell lines with BRAF or KRAS mutations.	AZD 6244	17-24	KRAS proto-oncogene, GTPase	Homo sapiens	83-87
19637312-9	2009	Sensitivity to MEK1/2 inhibition correlates with a biochemical signature; those cells with high ERK1/2 activity (whether mutant for BRAF or KRAS) evolve a dependency upon that pathway and tend to be sensitive to AZD6244 but this can be offset by high PI3K-dependent signalling.	AZD 6244	212-219	mitogen-activated protein kinase kinase 1	Homo sapiens	15-21
19637312-9	2009	Sensitivity to MEK1/2 inhibition correlates with a biochemical signature; those cells with high ERK1/2 activity (whether mutant for BRAF or KRAS) evolve a dependency upon that pathway and tend to be sensitive to AZD6244 but this can be offset by high PI3K-dependent signalling.	AZD 6244	212-219	mitogen-activated protein kinase 3	Homo sapiens	96-102
19637312-9	2009	Sensitivity to MEK1/2 inhibition correlates with a biochemical signature; those cells with high ERK1/2 activity (whether mutant for BRAF or KRAS) evolve a dependency upon that pathway and tend to be sensitive to AZD6244 but this can be offset by high PI3K-dependent signalling.	AZD 6244	212-219	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
19637312-9	2009	Sensitivity to MEK1/2 inhibition correlates with a biochemical signature; those cells with high ERK1/2 activity (whether mutant for BRAF or KRAS) evolve a dependency upon that pathway and tend to be sensitive to AZD6244 but this can be offset by high PI3K-dependent signalling.	AZD 6244	212-219	KRAS proto-oncogene, GTPase	Homo sapiens	140-144
19783898-0	2009	High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	74-81	AKT serine/threonine kinase 1	Homo sapiens	14-17
19783898-0	2009	High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	74-81	mitogen-activated protein kinase kinase 7	Homo sapiens	60-63
19783898-0	2009	High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	83-94	AKT serine/threonine kinase 1	Homo sapiens	14-17
19783898-0	2009	High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	83-94	mitogen-activated protein kinase kinase 7	Homo sapiens	60-63
19783898-3	2009	By determining the dose-responses of 35 human lung cancer cell lines to MEK-specific inhibitor AZD6244, we identified subsets of lung cancer cell lines that are either sensitive or resistant to this agent.	AZD 6244	95-102	mitogen-activated protein kinase kinase 7	Homo sapiens	72-75
19783898-4	2009	Subsequent molecular characterization showed that treatment with AZD6244 suppressed ERK phosphorylation in both sensitive and resistant cells, suggesting that resistance is not mediated by the activities of MEK/ERK themselves.	AZD 6244	65-72	mitogen-activated protein kinase 1	Homo sapiens	84-87
19783898-6	2009	Stable transfection of dominant-negative AKT into resistant cells by retroviral infection restored their susceptibility to AZD6244.	AZD 6244	123-130	AKT serine/threonine kinase 1	Homo sapiens	41-44
19783898-7	2009	These results indicate that phosphorylated AKT may be a biomarker of response to AZD6244 and that modulation of AKT activity may be a useful approach to overcome resistance to MEK inhibitors.	AZD 6244	81-88	AKT serine/threonine kinase 1	Homo sapiens	43-46
19783898-7	2009	These results indicate that phosphorylated AKT may be a biomarker of response to AZD6244 and that modulation of AKT activity may be a useful approach to overcome resistance to MEK inhibitors.	AZD 6244	81-88	mitogen-activated protein kinase kinase 7	Homo sapiens	176-179
19844848-4	2009	A case study of the investigational drug selumetinib (AstraZeneca plc) is also discussed.	AZD 6244	41-52	heparan sulfate proteoglycan 2	Homo sapiens	66-69
20009539-6	2009	AZD6244 but not rapamycin exhibited a significant anti-angiogenic effect, as shown by tumor VEGF ELISA assay and CD31 analysis.	AZD 6244	0-7	vascular endothelial growth factor A	Homo sapiens	92-96
19723757-3	2009	EXPERIMENTAL DESIGN: The MEK inhibitor AZD6244 (ARRY-142886) and mTOR inhibitor rapamycin were tested separately and in combination in 10 differentiated thyroid cancer and anaplastic thyroid cancer cell lines and in a xenograft model for evidence of pathway inhibition, growth inhibition, apoptosis, and long-range adaptation and resistance.	AZD 6244	39-46	mitogen-activated protein kinase kinase 7	Homo sapiens	25-28
19915144-6	2009	One such mutation, MEK1(P124L), was identified in a resistant metastatic focus that emerged in a melanoma patient treated with AZD6244.	AZD 6244	127-134	mitogen-activated protein kinase kinase 1	Homo sapiens	19-23
19915144-8	2009	However, exposing BRAF-mutant melanoma cells to AZD6244 and PLX4720 in combination prevented emergence of resistant clones.	AZD 6244	48-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	18-22
19861964-0	2009	Detection of BRAF mutations in the tumour and serum of patients enrolled in the AZD6244 (ARRY-142886) advanced melanoma phase II study.	AZD 6244	80-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
19843666-2	2009	AZD6244 is a potent and selective inhibitor of mitogen-activated protein kinase (MAPK) kinase 1/2 (MEK1/2), a critical enzyme within the MAPK/extracellular signal-regulated kinase (ERK) signaling pathway that regulates the proliferation and survival of tumor cells.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	99-105
19843666-10	2009	Furthermore, hypoxia-inducible factor-1 alpha, GLUT-1, and vascular endothelial growth factor levels were reduced by AZD6244, and there was a significant decrease in vascular perfusion in the tumors given combination treatment when compared with the other treatment groups.	AZD 6244	117-124	hypoxia inducible factor 1 subunit alpha	Homo sapiens	13-45
19843666-10	2009	Furthermore, hypoxia-inducible factor-1 alpha, GLUT-1, and vascular endothelial growth factor levels were reduced by AZD6244, and there was a significant decrease in vascular perfusion in the tumors given combination treatment when compared with the other treatment groups.	AZD 6244	117-124	solute carrier family 2 member 1	Homo sapiens	47-53
19843666-10	2009	Furthermore, hypoxia-inducible factor-1 alpha, GLUT-1, and vascular endothelial growth factor levels were reduced by AZD6244, and there was a significant decrease in vascular perfusion in the tumors given combination treatment when compared with the other treatment groups.	AZD 6244	117-124	vascular endothelial growth factor A	Homo sapiens	59-93
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	45-48
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	287-290
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	292-296
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	321-326
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	AZD 6244	0-7	BCL2 like 1	Homo sapiens	331-337
19422044-1	2009	We have recently reported that the mitogen-activated protein kinase/ERK kinase (MEK) inhibitor AZD6244 (ARRY-142886) strikingly potentiated the effects of histone deacetylase inhibitor to induce growth arrest and apoptosis of acute myelogeneous leukemia (AML) cells in association with enhanced upregulation of p21(waf1).	AZD 6244	95-102	mitogen-activated protein kinase kinase 7	Homo sapiens	80-83
19422044-1	2009	We have recently reported that the mitogen-activated protein kinase/ERK kinase (MEK) inhibitor AZD6244 (ARRY-142886) strikingly potentiated the effects of histone deacetylase inhibitor to induce growth arrest and apoptosis of acute myelogeneous leukemia (AML) cells in association with enhanced upregulation of p21(waf1).	AZD 6244	95-102	cyclin dependent kinase inhibitor 1A	Homo sapiens	311-314
19422044-1	2009	We have recently reported that the mitogen-activated protein kinase/ERK kinase (MEK) inhibitor AZD6244 (ARRY-142886) strikingly potentiated the effects of histone deacetylase inhibitor to induce growth arrest and apoptosis of acute myelogeneous leukemia (AML) cells in association with enhanced upregulation of p21(waf1).	AZD 6244	95-102	cyclin dependent kinase inhibitor 1A	Homo sapiens	315-319
19422044-4	2009	In parallel, 5-AzadC induced expression of p21(waf1) in AML cells, which was potently enhanced in the presence of AZD6244.	AZD 6244	114-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	43-46
19422044-4	2009	In parallel, 5-AzadC induced expression of p21(waf1) in AML cells, which was potently enhanced in the presence of AZD6244.	AZD 6244	114-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	47-51
19755509-7	2009	The results from Western blots and phosphoprotein arrays showed that, in MEK inhibitor resistant cell lines, AKT was activated through the EGFR/HER3/PI3K pathway following AZD6244 (ARRY-142886) treatment.	AZD 6244	172-179	epidermal growth factor receptor	Homo sapiens	139-143
19755509-7	2009	The results from Western blots and phosphoprotein arrays showed that, in MEK inhibitor resistant cell lines, AKT was activated through the EGFR/HER3/PI3K pathway following AZD6244 (ARRY-142886) treatment.	AZD 6244	172-179	mitogen-activated protein kinase kinase 7	Homo sapiens	73-76
19723882-6	2009	The combination of sorafenib and MAP/ERK kinase inhibitor AZD6244 enhances the effectiveness of each compound alone.	AZD 6244	58-65	mitogen-activated protein kinase 1	Mus musculus	37-40
19755509-7	2009	The results from Western blots and phosphoprotein arrays showed that, in MEK inhibitor resistant cell lines, AKT was activated through the EGFR/HER3/PI3K pathway following AZD6244 (ARRY-142886) treatment.	AZD 6244	172-179	erb-b2 receptor tyrosine kinase 3	Homo sapiens	144-148
19755509-7	2009	The results from Western blots and phosphoprotein arrays showed that, in MEK inhibitor resistant cell lines, AKT was activated through the EGFR/HER3/PI3K pathway following AZD6244 (ARRY-142886) treatment.	AZD 6244	172-179	AKT serine/threonine kinase 1	Homo sapiens	109-112
17983653-4	2008	In this study, we found that AZD6244 (ARRY-142886), a novel inhibitor of MEK1/2 kinases, effectively inhibited the proliferation of acute biphenotypic leukemia MV4-11 and acute monocytic leukemia MOLM13 cells.	AZD 6244	29-36	mitogen-activated protein kinase kinase 1	Homo sapiens	73-79
18676837-0	2008	BRAF V600E disrupts AZD6244-induced abrogation of negative feedback pathways between extracellular signal-regulated kinase and Raf proteins.	AZD 6244	20-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
18676837-0	2008	BRAF V600E disrupts AZD6244-induced abrogation of negative feedback pathways between extracellular signal-regulated kinase and Raf proteins.	AZD 6244	20-27	zinc fingers and homeoboxes 2	Homo sapiens	127-130
18676837-1	2008	AZD6244 (ARRY 142886) is a potent and selective mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor currently in early clinical trials.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	82-86
18676837-1	2008	AZD6244 (ARRY 142886) is a potent and selective mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor currently in early clinical trials.	AZD 6244	0-7	mitogen-activated protein kinase 1	Homo sapiens	127-130
18676837-1	2008	AZD6244 (ARRY 142886) is a potent and selective mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor currently in early clinical trials.	AZD 6244	0-7	mitogen-activated protein kinase kinase 7	Homo sapiens	140-143
18676837-3	2008	AZD6244 induced G(0)-G(1) cell cycle arrest in sensitive cell lines that primarily included cells containing the BRAF V600E mutation.	AZD 6244	0-7	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
18676837-5	2008	In the majority of cell lines tested, including those with K-ras or non-V600E BRAF mutations, AZD6244 induced the accumulation of phospho-MEK, an effect not observed in the most sensitive BRAF V600E-containing cells.	AZD 6244	94-101	KRAS proto-oncogene, GTPase	Homo sapiens	59-64
18676837-5	2008	In the majority of cell lines tested, including those with K-ras or non-V600E BRAF mutations, AZD6244 induced the accumulation of phospho-MEK, an effect not observed in the most sensitive BRAF V600E-containing cells.	AZD 6244	94-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	78-82
18676837-5	2008	In the majority of cell lines tested, including those with K-ras or non-V600E BRAF mutations, AZD6244 induced the accumulation of phospho-MEK, an effect not observed in the most sensitive BRAF V600E-containing cells.	AZD 6244	94-101	mitogen-activated protein kinase kinase 7	Homo sapiens	138-141
18676837-5	2008	In the majority of cell lines tested, including those with K-ras or non-V600E BRAF mutations, AZD6244 induced the accumulation of phospho-MEK, an effect not observed in the most sensitive BRAF V600E-containing cells.	AZD 6244	94-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	188-192
18676837-9	2008	Specific suppression of endogenous BRAF V600E does not confer resistance to AZD6244 but enhances sensitivity to AZD6244.	AZD 6244	112-119	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	35-39
18381570-7	2008	Similar effects were obtained with the MEK inhibitor AZD6244.	AZD 6244	53-60	mitogen-activated protein kinase kinase 7	Homo sapiens	39-42
18381570-11	2008	AZD6244 was more potent at inhibiting growth of NPA (BRAF +) than Cal62 (KRAS +) xenografts.	AZD 6244	0-7	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	53-57
19366835-0	2009	In vitro and in vivo radiosensitization with AZD6244 (ARRY-142886), an inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2 kinase.	AZD 6244	45-52	mitogen-activated protein kinase 3	Homo sapiens	117-158
19366835-10	2009	Cells treated with AZD6244 had an increased mitotic index and decreased Chk1 phosphorylation at 1 and 2 hours after irradiation.	AZD 6244	19-26	checkpoint kinase 1	Homo sapiens	72-76
18806830-4	2008	However, treatment with the MEK1/2 inhibitors U0126, PD184352 or the novel clinical candidate AZD6244 (ARRY-142886) overcomes growth factor independence, causing CRC cell death.	AZD 6244	94-101	mitogen-activated protein kinase kinase 1	Homo sapiens	28-34
18632602-6	2008	A selective MEK inhibitor, AZD6244, inhibits mutant-induced ERK activity in 293T cells and growth of mutant-bearing Ba/F3 cells.	AZD 6244	27-34	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
18632602-6	2008	A selective MEK inhibitor, AZD6244, inhibits mutant-induced ERK activity in 293T cells and growth of mutant-bearing Ba/F3 cells.	AZD 6244	27-34	mitogen-activated protein kinase 1	Homo sapiens	60-63
17983653-6	2008	AZD6244 potently down-regulated the levels of phospho-ERK1/2 and its downstream effector, p-p70S6K, in the MV4-11 and MOLM13 cells as measured by Western blot analysis.	AZD 6244	0-7	ribosomal protein S6 kinase B1	Homo sapiens	92-98
17983653-7	2008	Interestingly, when AZD6244 was combined with sunitinib, a FLT3 kinase inhibitor, growth inhibition and apoptosis of both MV4-11 and MOLM13 cells were synergistically enhanced in association with further down-regulation of phospho-ERK1/2 and p-p70S6K in these cells.	AZD 6244	20-27	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
17983653-7	2008	Interestingly, when AZD6244 was combined with sunitinib, a FLT3 kinase inhibitor, growth inhibition and apoptosis of both MV4-11 and MOLM13 cells were synergistically enhanced in association with further down-regulation of phospho-ERK1/2 and p-p70S6K in these cells.	AZD 6244	20-27	ribosomal protein S6 kinase B1	Homo sapiens	244-250
18172275-3	2008	This study addresses the anti-melanoma activity of the MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	69-76	midkine	Mus musculus	55-58
18390968-0	2008	Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers.	AZD 6244	132-139	mitogen-activated protein kinase kinase 1	Homo sapiens	78-119
18390968-1	2008	PURPOSE: To assess the tolerability, pharmacokinetics (PKs), and pharmacodynamics (PDs) of the mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancer.	AZD 6244	155-162	mitogen-activated protein kinase kinase 1	Homo sapiens	95-144
18347148-1	2008	The present studies were initiated to determine in greater molecular detail how MEK1/2 inhibitors [PD184352 and AZD6244 (ARRY-142886)] interact with UCN-01 (7-hydroxystaurosporine) to kill mammary carcinoma cells in vitro and radiosensitize mammary tumors in vitro and in vivo and whether farnesyl transferase inhibitors interact with UCN-01 to kill mammary carcinoma cells in vitro and in vivo.	AZD 6244	112-119	mitogen-activated protein kinase kinase 1	Homo sapiens	80-86
18347148-1	2008	The present studies were initiated to determine in greater molecular detail how MEK1/2 inhibitors [PD184352 and AZD6244 (ARRY-142886)] interact with UCN-01 (7-hydroxystaurosporine) to kill mammary carcinoma cells in vitro and radiosensitize mammary tumors in vitro and in vivo and whether farnesyl transferase inhibitors interact with UCN-01 to kill mammary carcinoma cells in vitro and in vivo.	AZD 6244	112-119	urocortin	Homo sapiens	149-152
18347148-1	2008	The present studies were initiated to determine in greater molecular detail how MEK1/2 inhibitors [PD184352 and AZD6244 (ARRY-142886)] interact with UCN-01 (7-hydroxystaurosporine) to kill mammary carcinoma cells in vitro and radiosensitize mammary tumors in vitro and in vivo and whether farnesyl transferase inhibitors interact with UCN-01 to kill mammary carcinoma cells in vitro and in vivo.	AZD 6244	112-119	urocortin	Homo sapiens	335-338
18347148-3	2008	In vitro colony formation studies showed that UCN-01 interacted synergistically with the MEK1/2 inhibitors PD184352 or AZD6244 and the farnesyl transferase inhibitors FTI277 and R115,777 to kill human mammary carcinoma cells.	AZD 6244	119-126	urocortin	Homo sapiens	46-49
18172275-3	2008	This study addresses the anti-melanoma activity of the MEK inhibitor AZD6244 (ARRY-142886).	AZD 6244	78-89	midkine	Mus musculus	55-58
18172275-10	2008	AZD6244 treatment decreased phospho-ERK in the tumors and significantly suppressed tumor growth.	AZD 6244	0-7	mitogen-activated protein kinase 1	Mus musculus	36-39
18172275-12	2008	Further studies showed that co-administration of AZD6244 (30 mg/kg) with docetaxel (15 mg/kg) led to tumor regression, indicating the potential for MEK inhibitor/chemotherapy drug combinations.	AZD 6244	49-56	midkine	Mus musculus	148-151
17878251-5	2007	RESULTS: AZD6244 potently inhibited MEK 1/2 activity in thyroid cancer cell lines regardless of BRAF mutation status, as evidenced by reduced ERK phosphorylation.	AZD 6244	9-16	mitogen-activated protein kinase kinase 1	Homo sapiens	36-43
17878251-0	2007	Selective growth inhibition in BRAF mutant thyroid cancer by the mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244.	AZD 6244	119-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
17878251-5	2007	RESULTS: AZD6244 potently inhibited MEK 1/2 activity in thyroid cancer cell lines regardless of BRAF mutation status, as evidenced by reduced ERK phosphorylation.	AZD 6244	9-16	mitogen-activated protein kinase 1	Homo sapiens	142-145
17878251-0	2007	Selective growth inhibition in BRAF mutant thyroid cancer by the mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244.	AZD 6244	119-126	mitogen-activated protein kinase kinase 1	Homo sapiens	65-106
17878251-8	2007	Nude mouse xenograft tumors derived from the BRAF mutant line ARO exhibited dose-dependent growth inhibition by AZD6244, with effective treatment at 10 mg/kg by oral gavage.	AZD 6244	112-119	Braf transforming gene	Mus musculus	45-49
17878251-4	2007	EXPERIMENTAL DESIGN: After treatment with the potent MEK 1/2 inhibitor AZD6244, MEK inhibition and cell growth were examined in four BRAF mutant (V600E) and two BRAF wild-type thyroid cancer cell lines and in xenografts from a BRAF mutant cell line.	AZD 6244	71-78	mitogen-activated protein kinase kinase 1	Homo sapiens	53-60
17878251-10	2007	CONCLUSION: AZD6244 inhibits the MEK-ERK pathway across a spectrum of thyroid cancer cells.	AZD 6244	12-19	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
17878251-10	2007	CONCLUSION: AZD6244 inhibits the MEK-ERK pathway across a spectrum of thyroid cancer cells.	AZD 6244	12-19	mitogen-activated protein kinase 1	Homo sapiens	37-40
17876044-4	2007	AZD6244-inhibited tumor growth was associated with increased apoptosis, inactivation of ERK1/2, inhibition of cell proliferation, and down-regulation of cell cycle regulators, including cyclin D1, cdc-2, cyclin-dependent kinases 2 and 4, cyclin B1, and c-Myc.	AZD 6244	0-7	mitogen-activated protein kinase 3	Mus musculus	88-94
17854307-4	2007	It was found that AZD6244, a mitogen-activated or extracellular signal-regulated protein kinase (MEK) inhibitor, blocked OCL differentiation and formation in a dose-dependent manner, evidenced by decreased alphaVbeta3-integrin expression and tartrate-resistant acid phosphatase positive (TRAP+) cells.	AZD 6244	18-25	mitogen-activated protein kinase kinase 7	Homo sapiens	97-100
17854307-6	2007	Major MM growth and survival factors produced by OCLs including B-cell activation factor (BAFF) and a proliferation-inducing ligand (APRIL), as well as macrophage inflammatory protein (MIP-1alpha), which mediates OCL differentiation and MM, were also significantly inhibited by AZD6244.	AZD 6244	278-285	C-C motif chemokine ligand 3	Homo sapiens	185-195
17854307-7	2007	In addition to ERK inhibition, NFATc1 (nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1) and c-fos were both downregulated, suggesting that AZD6244 targets a later stage of OCL differentiation.	AZD 6244	165-172	nuclear factor of activated T cells 1	Homo sapiens	31-37
17854307-7	2007	In addition to ERK inhibition, NFATc1 (nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1) and c-fos were both downregulated, suggesting that AZD6244 targets a later stage of OCL differentiation.	AZD 6244	165-172	nuclear factor of activated T cells 1	Homo sapiens	39-112
17854307-7	2007	In addition to ERK inhibition, NFATc1 (nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1) and c-fos were both downregulated, suggesting that AZD6244 targets a later stage of OCL differentiation.	AZD 6244	165-172	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	118-123
17876044-4	2007	AZD6244-inhibited tumor growth was associated with increased apoptosis, inactivation of ERK1/2, inhibition of cell proliferation, and down-regulation of cell cycle regulators, including cyclin D1, cdc-2, cyclin-dependent kinases 2 and 4, cyclin B1, and c-Myc.	AZD 6244	0-7	cyclin B1	Mus musculus	238-247
17510321-3	2007	AZD6244 blocks constitutive and cytokine-stimulated ERK1/2 phosphorylation and inhibits proliferation and survival of human MM cell lines and patient MM cells, regardless of sensitivity to conventional chemotherapy.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	52-58
17510321-4	2007	Importantly, AZD6244 (200 nM) induces apoptosis in patient MM cells, even in the presence of exogenous interleukin-6 or BMSCs associated with triggering of caspase 3 activity.	AZD 6244	13-20	caspase 3	Homo sapiens	156-165
17510321-6	2007	AZD6244 down-regulates the expression/secretion of osteoclast (OC)-activating factors from MM cells and inhibits in vitro differentiation of MM patient PBMCs to OCs induced by ligand for receptor activator of NF-kappaB (RANKL) and macrophage-colony stimulating factor (M-CSF).	AZD 6244	0-7	TNF superfamily member 11	Homo sapiens	220-225
17510321-6	2007	AZD6244 down-regulates the expression/secretion of osteoclast (OC)-activating factors from MM cells and inhibits in vitro differentiation of MM patient PBMCs to OCs induced by ligand for receptor activator of NF-kappaB (RANKL) and macrophage-colony stimulating factor (M-CSF).	AZD 6244	0-7	colony stimulating factor 1	Homo sapiens	231-267
17510321-6	2007	AZD6244 down-regulates the expression/secretion of osteoclast (OC)-activating factors from MM cells and inhibits in vitro differentiation of MM patient PBMCs to OCs induced by ligand for receptor activator of NF-kappaB (RANKL) and macrophage-colony stimulating factor (M-CSF).	AZD 6244	0-7	colony stimulating factor 1	Homo sapiens	269-274
17876044-5	2007	The AZD6244-doxorubicin combined protocol not only promoted apoptosis but also induced a synergistic effect not seen in single-agent-treated tumors, including increased expression of the p130 RB tumor suppressor gene.	AZD 6244	4-11	nucleolar and coiled-body phosphoprotein 1	Mus musculus	187-191
17876044-6	2007	Our study provides a strong rationale for clinical investigation of combination therapy with the mitogen-activated protein/ERK kinase 1/2 inhibitor AZD6244 and doxorubicin in patients with HCC.	AZD 6244	148-155	mitogen-activated protein kinase 1	Mus musculus	123-126
17876044-4	2007	AZD6244-inhibited tumor growth was associated with increased apoptosis, inactivation of ERK1/2, inhibition of cell proliferation, and down-regulation of cell cycle regulators, including cyclin D1, cdc-2, cyclin-dependent kinases 2 and 4, cyclin B1, and c-Myc.	AZD 6244	0-7	cyclin D1	Mus musculus	186-195
17876044-4	2007	AZD6244-inhibited tumor growth was associated with increased apoptosis, inactivation of ERK1/2, inhibition of cell proliferation, and down-regulation of cell cycle regulators, including cyclin D1, cdc-2, cyclin-dependent kinases 2 and 4, cyclin B1, and c-Myc.	AZD 6244	0-7	cyclin-dependent kinase 1	Mus musculus	197-202
17876044-4	2007	AZD6244-inhibited tumor growth was associated with increased apoptosis, inactivation of ERK1/2, inhibition of cell proliferation, and down-regulation of cell cycle regulators, including cyclin D1, cdc-2, cyclin-dependent kinases 2 and 4, cyclin B1, and c-Myc.	AZD 6244	0-7	cyclin-dependent kinase 2	Mus musculus	204-236
34644519-5	2022	Inhibition of ERK/MAPK signaling pathway with selumetinib abolished IL-6-stimulated increase in IDE protein level and deceased in ANP secretion in H9C2 cells.	AZD 6244	46-57	Eph receptor B1	Rattus norvegicus	14-17
17361222-0	2007	ZD6474 induces growth arrest and apoptosis of human leukemia cells, which is enhanced by concomitant use of a novel MEK inhibitor, AZD6244.	AZD 6244	131-138	mitogen-activated protein kinase kinase 7	Homo sapiens	116-119
17392524-6	2007	In keeping with the observation that 20S reduction has little effect on mitogen-activated protein kinase kinase 1/2 (MEK1/2) signaling in either ER-positive or ERBB2-positive models, only the MEK-1/2 inhibitor AZD6244 consistently improved the antitumor activity of bortezomib.	AZD 6244	210-217	mitogen-activated protein kinase kinase 1	Homo sapiens	192-199
17237274-0	2007	Targeted inhibition of the extracellular signal-regulated kinase kinase pathway with AZD6244 (ARRY-142886) in the treatment of hepatocellular carcinoma.	AZD 6244	85-92	mitogen-activated protein kinase 1	Mus musculus	27-64
17237274-3	2007	In the present study, we determined the efficacy of a specific MEK1/2 inhibitor AZD6244 (ARRAY-142886) in treatment of HCC.	AZD 6244	80-87	mitogen-activated protein kinase kinase 1	Mus musculus	63-69
17237274-4	2007	Treatment of primary HCC cells with AZD6244 led to growth inhibition, elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase, but inhibition of ERK1/2 and p90RSK phosphorylation.	AZD 6244	36-43	caspase 3	Mus musculus	99-108
17237274-4	2007	Treatment of primary HCC cells with AZD6244 led to growth inhibition, elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase, but inhibition of ERK1/2 and p90RSK phosphorylation.	AZD 6244	36-43	caspase 7	Mus musculus	113-122
17237274-4	2007	Treatment of primary HCC cells with AZD6244 led to growth inhibition, elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase, but inhibition of ERK1/2 and p90RSK phosphorylation.	AZD 6244	36-43	poly (ADP-ribose) polymerase family, member 1	Mus musculus	136-162
17237274-4	2007	Treatment of primary HCC cells with AZD6244 led to growth inhibition, elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase, but inhibition of ERK1/2 and p90RSK phosphorylation.	AZD 6244	36-43	mitogen-activated protein kinase 3	Mus musculus	182-188
17237274-4	2007	Treatment of primary HCC cells with AZD6244 led to growth inhibition, elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase, but inhibition of ERK1/2 and p90RSK phosphorylation.	AZD 6244	36-43	ribosomal protein S6 kinase, polypeptide 2	Mus musculus	193-199
17237274-8	2007	AZD6244-induced growth suppression was associated with inactivation of ERK1/2 and p90RSK, and up-regulation of activated caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase.	AZD 6244	0-7	mitogen-activated protein kinase 3	Mus musculus	71-77
17237274-8	2007	AZD6244-induced growth suppression was associated with inactivation of ERK1/2 and p90RSK, and up-regulation of activated caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase.	AZD 6244	0-7	ribosomal protein S6 kinase, polypeptide 2	Mus musculus	82-88
17237274-8	2007	AZD6244-induced growth suppression was associated with inactivation of ERK1/2 and p90RSK, and up-regulation of activated caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase.	AZD 6244	0-7	caspase 3	Mus musculus	121-130
17237274-8	2007	AZD6244-induced growth suppression was associated with inactivation of ERK1/2 and p90RSK, and up-regulation of activated caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase.	AZD 6244	0-7	caspase 7	Mus musculus	135-144
17237274-8	2007	AZD6244-induced growth suppression was associated with inactivation of ERK1/2 and p90RSK, and up-regulation of activated caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase.	AZD 6244	0-7	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-184
17237274-10	2007	Targeted inhibition of the MEK-ERK pathway with AZD6244 may represent an alternative approach for the treatment of this disease.	AZD 6244	48-55	midkine	Mus musculus	27-30
17237274-10	2007	Targeted inhibition of the MEK-ERK pathway with AZD6244 may represent an alternative approach for the treatment of this disease.	AZD 6244	48-55	mitogen-activated protein kinase 1	Mus musculus	31-34
33808483-8	2021	Application of the allosterically acting MEK inhibitors (MEKi) trametinib, cobimentinib, refametinib, and selumetinib converted activated MEK1 KinCon reporters back into a more closed inactive conformation.	AZD 6244	106-117	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
33808483-8	2021	Application of the allosterically acting MEK inhibitors (MEKi) trametinib, cobimentinib, refametinib, and selumetinib converted activated MEK1 KinCon reporters back into a more closed inactive conformation.	AZD 6244	106-117	mitogen-activated protein kinase kinase 1	Homo sapiens	138-142
17699718-3	2007	AZD6244 (ARRY-142886) is a potent, selective, and ATP-uncompetitive inhibitor of MAPK/ERK kinase 1/2.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	81-85
17699718-3	2007	AZD6244 (ARRY-142886) is a potent, selective, and ATP-uncompetitive inhibitor of MAPK/ERK kinase 1/2.	AZD 6244	9-20	mitogen-activated protein kinase 3	Homo sapiens	81-85
17699718-4	2007	In vitro cell viability inhibition screening of a tumor cell line panel found that lines harboring BRAF or RAS mutations were more likely to be sensitive to AZD6244.	AZD 6244	157-164	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
17699718-6	2007	Chronic dosing with 25 mg/kg AZD6244 bd resulted in suppression of growth of Colo-205, Calu-6, and SW-620 xenografts, whereas an acute dose resulted in significant inhibition of ERK1/2 phosphorylation.	AZD 6244	29-36	mitogen-activated protein kinase 3	Homo sapiens	178-184
17332304-0	2007	Biological characterization of ARRY-142886 (AZD6244), a potent, highly selective mitogen-activated protein kinase kinase 1/2 inhibitor.	AZD 6244	44-51	mitogen-activated protein kinase kinase 1	Homo sapiens	81-124
34644519-5	2022	Inhibition of ERK/MAPK signaling pathway with selumetinib abolished IL-6-stimulated increase in IDE protein level and deceased in ANP secretion in H9C2 cells.	AZD 6244	46-57	interleukin 6	Rattus norvegicus	68-72
34644519-5	2022	Inhibition of ERK/MAPK signaling pathway with selumetinib abolished IL-6-stimulated increase in IDE protein level and deceased in ANP secretion in H9C2 cells.	AZD 6244	46-57	insulin degrading enzyme	Rattus norvegicus	96-99
34644519-5	2022	Inhibition of ERK/MAPK signaling pathway with selumetinib abolished IL-6-stimulated increase in IDE protein level and deceased in ANP secretion in H9C2 cells.	AZD 6244	46-57	natriuretic peptide A	Rattus norvegicus	130-133
34896211-2	2022	Here, selumetinib-resistant PTC (PTCSR) cell lines, which were characterized by loss of sodium/iodide symporter expression, enhanced insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), and activated V-Erb-B2 avian erythroblastic leukemia viral oncogene homolog 2 (ERBB2) signaling, were initially established using a dose escalation method.	AZD 6244	6-17	insulin like growth factor 2 mRNA binding protein 2	Homo sapiens	133-184
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.	AZD 6244	200-207	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.	AZD 6244	200-207	GLI family zinc finger 1	Homo sapiens	19-23
34515877-0	2022	Phase I study of cediranib, an oral VEGFR inhibitor, in combination with selumetinib, an oral MEK inhibitor, in patients with advanced solid malignancies.	AZD 6244	73-84	mitogen-activated protein kinase kinase 7	Homo sapiens	94-97
34515877-3	2022	Preclinical data with cediranib, an inhibitor of all 3 VEGF receptors, in combination with selumetinib, an inhibitor of MEK 1/2, demonstrated improved tumor control experimentally.	AZD 6244	91-102	mitogen-activated protein kinase kinase 1	Homo sapiens	120-127
34905788-4	2022	Therefore, the recent approval of the MEK inhibitor selumetinib for the treatment of NF1-associated PN provides a long-awaited novel therapeutic option.	AZD 6244	52-63	mitogen-activated protein kinase kinase 7	Homo sapiens	38-41
34896211-2	2022	Here, selumetinib-resistant PTC (PTCSR) cell lines, which were characterized by loss of sodium/iodide symporter expression, enhanced insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), and activated V-Erb-B2 avian erythroblastic leukemia viral oncogene homolog 2 (ERBB2) signaling, were initially established using a dose escalation method.	AZD 6244	6-17	insulin like growth factor 2 mRNA binding protein 2	Homo sapiens	186-193
34896211-2	2022	Here, selumetinib-resistant PTC (PTCSR) cell lines, which were characterized by loss of sodium/iodide symporter expression, enhanced insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), and activated V-Erb-B2 avian erythroblastic leukemia viral oncogene homolog 2 (ERBB2) signaling, were initially established using a dose escalation method.	AZD 6244	6-17	erb-b2 receptor tyrosine kinase 2	Homo sapiens	210-273
34896211-2	2022	Here, selumetinib-resistant PTC (PTCSR) cell lines, which were characterized by loss of sodium/iodide symporter expression, enhanced insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), and activated V-Erb-B2 avian erythroblastic leukemia viral oncogene homolog 2 (ERBB2) signaling, were initially established using a dose escalation method.	AZD 6244	6-17	erb-b2 receptor tyrosine kinase 2	Homo sapiens	275-280
34831012-12	2021	The negative impact on NIS expression induced by the MAPK-activating alterations, NRAS Q61R and BRAF V600E, was partially reversed by the presence of the MEK 1/2 inhibitors AZD6244 and CH5126766.	AZD 6244	173-180	NRAS proto-oncogene, GTPase	Homo sapiens	82-86
34849004-9	2021	In addition, we found that MEK inhibitors, ie, trametinib, selumetinib, PD0325901, and RDEA119, may be feasible targeting agents for KIRP patients.	AZD 6244	59-70	mitogen-activated protein kinase kinase 7	Homo sapiens	27-30
34948154-7	2021	We had three goals: first, to identify the KRAS downstream effectors targeted by mir-16, second, to study the effects of miR-16 restoration on TKI resistance in KRAS-mutated NSCLC both in vitro and in vivo, and finally, to compare miR-16 and the MEK inhibitor selumetinib in reducing KRAS-mutated NSCLC growth in vitro and in vivo.	AZD 6244	260-271	glycerophosphodiester phosphodiesterase 1	Homo sapiens	81-87
34948154-7	2021	We had three goals: first, to identify the KRAS downstream effectors targeted by mir-16, second, to study the effects of miR-16 restoration on TKI resistance in KRAS-mutated NSCLC both in vitro and in vivo, and finally, to compare miR-16 and the MEK inhibitor selumetinib in reducing KRAS-mutated NSCLC growth in vitro and in vivo.	AZD 6244	260-271	mitogen-activated protein kinase kinase 7	Homo sapiens	246-249
34856074-6	2022	We demonstrate that SRC is activated in response to treatment of KRAS-mutant colorectal cell lines with MEK inhibitors (trametinib or AZD6244), and that AZD0424 abrogates this.	AZD 6244	134-141	Rous sarcoma oncogene	Mus musculus	20-23
34856074-6	2022	We demonstrate that SRC is activated in response to treatment of KRAS-mutant colorectal cell lines with MEK inhibitors (trametinib or AZD6244), and that AZD0424 abrogates this.	AZD 6244	134-141	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	65-69
34856074-6	2022	We demonstrate that SRC is activated in response to treatment of KRAS-mutant colorectal cell lines with MEK inhibitors (trametinib or AZD6244), and that AZD0424 abrogates this.	AZD 6244	134-141	midkine	Mus musculus	104-107
34856074-7	2022	Cell lines treated with trametinib or AZD6244 in combination with AZD0424 had reduced EGFR, FAK and SRC compensatory activation, and, cell viability was synergistically inhibited.	AZD 6244	38-45	epidermal growth factor receptor	Mus musculus	86-90
34856074-7	2022	Cell lines treated with trametinib or AZD6244 in combination with AZD0424 had reduced EGFR, FAK and SRC compensatory activation, and, cell viability was synergistically inhibited.	AZD 6244	38-45	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
34856074-7	2022	Cell lines treated with trametinib or AZD6244 in combination with AZD0424 had reduced EGFR, FAK and SRC compensatory activation, and, cell viability was synergistically inhibited.	AZD 6244	38-45	Rous sarcoma oncogene	Mus musculus	100-103
34831012-12	2021	The negative impact on NIS expression induced by the MAPK-activating alterations, NRAS Q61R and BRAF V600E, was partially reversed by the presence of the MEK 1/2 inhibitors AZD6244 and CH5126766.	AZD 6244	173-180	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
34831012-12	2021	The negative impact on NIS expression induced by the MAPK-activating alterations, NRAS Q61R and BRAF V600E, was partially reversed by the presence of the MEK 1/2 inhibitors AZD6244 and CH5126766.	AZD 6244	173-180	mitogen-activated protein kinase kinase 1	Homo sapiens	154-161
34196005-1	2021	Selumetinib (ARRY-142886), an oral, potent and highly selective allosteric MEK1/2 inhibitor, is approved by the US FDA for the treatment of pediatric patients aged 2 years and older with neurofibromatosis type 1 with symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	75-81
34216687-6	2021	A confined kinase inhibitor screen revealed that PPP2R4-depletion induced resistance against selumetinib (MEK inhibitor), but unexpectedly sensitized cells for temsirolimus (mTOR inhibitor), in vitro and in vivo.	AZD 6244	93-104	protein phosphatase 2 protein activator	Mus musculus	49-55
34216687-6	2021	A confined kinase inhibitor screen revealed that PPP2R4-depletion induced resistance against selumetinib (MEK inhibitor), but unexpectedly sensitized cells for temsirolimus (mTOR inhibitor), in vitro and in vivo.	AZD 6244	93-104	mitogen-activated protein kinase kinase 7	Homo sapiens	106-109
34196005-1	2021	Selumetinib (ARRY-142886), an oral, potent and highly selective allosteric MEK1/2 inhibitor, is approved by the US FDA for the treatment of pediatric patients aged 2 years and older with neurofibromatosis type 1 with symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	187-211
34196005-1	2021	Selumetinib (ARRY-142886), an oral, potent and highly selective allosteric MEK1/2 inhibitor, is approved by the US FDA for the treatment of pediatric patients aged 2 years and older with neurofibromatosis type 1 with symptomatic, inoperable plexiform neurofibromas.	AZD 6244	13-24	mitogen-activated protein kinase kinase 1	Homo sapiens	75-81
34196005-1	2021	Selumetinib (ARRY-142886), an oral, potent and highly selective allosteric MEK1/2 inhibitor, is approved by the US FDA for the treatment of pediatric patients aged 2 years and older with neurofibromatosis type 1 with symptomatic, inoperable plexiform neurofibromas.	AZD 6244	13-24	neurofibromin 1	Homo sapiens	187-211
34251024-0	2021	Selumetinib for optic pathway glioma: Seeing through the fog, (not yet) the end of the tunnel?	AZD 6244	0-11	zinc finger protein, FOG family member 1	Homo sapiens	57-60
34680330-6	2021	An in-silico drug screen predicted two MEK inhibitors (Trametinib and Selumetinib) as effective compounds for high-risk SCC based on the Cancer Cell Line Encyclopedia, which is supported by a higher p-MEK1/2 immunohistochemical staining of high-risk HNSCC.	AZD 6244	70-81	mitogen-activated protein kinase kinase 7	Homo sapiens	39-42
34680330-6	2021	An in-silico drug screen predicted two MEK inhibitors (Trametinib and Selumetinib) as effective compounds for high-risk SCC based on the Cancer Cell Line Encyclopedia, which is supported by a higher p-MEK1/2 immunohistochemical staining of high-risk HNSCC.	AZD 6244	70-81	mitogen-activated protein kinase kinase 1	Homo sapiens	201-207
34735879-7	2021	As a result, AZD-6244 enhanced the conversion of iPS cells into CSCs and upregulated AKT phosphorylation as same as GDC-0879 and PD0325901.	AZD 6244	13-21	thymoma viral proto-oncogene 1	Mus musculus	85-88
34247190-6	2021	Targeting MEK1 by RNAi or clinically applicable MEK1 inhibitors AZD6244 and GSK1120212 reduces MACC1 tyrosine phosphorylation and restricts MACC1-induced metastasis formation in mice.	AZD 6244	64-71	mitogen-activated protein kinase kinase 1	Mus musculus	10-14
34541874-1	2022	OBJECTIVE: To evaluate the safety and efficacy of selumetinib, a novel MEK inhibitor, for the treatment of plexiform neurofibromas (PN) in patients with neurofibromatosis type 1 (NF1).	AZD 6244	50-61	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
34541874-1	2022	OBJECTIVE: To evaluate the safety and efficacy of selumetinib, a novel MEK inhibitor, for the treatment of plexiform neurofibromas (PN) in patients with neurofibromatosis type 1 (NF1).	AZD 6244	50-61	neurofibromin 1	Homo sapiens	153-177
34541874-1	2022	OBJECTIVE: To evaluate the safety and efficacy of selumetinib, a novel MEK inhibitor, for the treatment of plexiform neurofibromas (PN) in patients with neurofibromatosis type 1 (NF1).	AZD 6244	50-61	neurofibromin 1	Homo sapiens	179-182
34388689-6	2021	Selumetinib has shown an overall response rate of 68% in children with NF1 and symptomatic inoperable PNs, and was associated with pain improvement and a manageable adverse events profile.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	71-74
34604034-5	2021	One major advance is the FDA approval of the MEK inhibitor selumetinib for the treatment of NF1-associated plexiform neurofibroma.	AZD 6244	59-70	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
34604034-5	2021	One major advance is the FDA approval of the MEK inhibitor selumetinib for the treatment of NF1-associated plexiform neurofibroma.	AZD 6244	59-70	neurofibromin 1	Homo sapiens	92-95
34247190-6	2021	Targeting MEK1 by RNAi or clinically applicable MEK1 inhibitors AZD6244 and GSK1120212 reduces MACC1 tyrosine phosphorylation and restricts MACC1-induced metastasis formation in mice.	AZD 6244	64-71	mitogen-activated protein kinase kinase 1	Mus musculus	48-52
34247190-6	2021	Targeting MEK1 by RNAi or clinically applicable MEK1 inhibitors AZD6244 and GSK1120212 reduces MACC1 tyrosine phosphorylation and restricts MACC1-induced metastasis formation in mice.	AZD 6244	64-71	metastasis associated in colon cancer 1	Mus musculus	95-100
34247190-6	2021	Targeting MEK1 by RNAi or clinically applicable MEK1 inhibitors AZD6244 and GSK1120212 reduces MACC1 tyrosine phosphorylation and restricts MACC1-induced metastasis formation in mice.	AZD 6244	64-71	metastasis associated in colon cancer 1	Mus musculus	140-145
34127699-2	2021	In the present study, the neuroprotective effect of selumetinib (a MEK-ERK inhibitor) on acrolein-induced neurotoxicity was investigated in vitro using primary cultured cortical neurons.	AZD 6244	52-63	mitogen-activated protein kinase kinase 7	Homo sapiens	67-70
34127699-7	2021	Moreover, selumetinib prevented acrolein-induced programmed cell death via decreasing active caspase 3 (a hallmark of apoptosis) as well as RIP (receptor-interacting protein) 1 and RIP3 (biomarkers for necroptosis).	AZD 6244	10-21	caspase 3	Homo sapiens	93-102
34127699-2	2021	In the present study, the neuroprotective effect of selumetinib (a MEK-ERK inhibitor) on acrolein-induced neurotoxicity was investigated in vitro using primary cultured cortical neurons.	AZD 6244	52-63	mitogen-activated protein kinase 1	Homo sapiens	71-74
34127699-7	2021	Moreover, selumetinib prevented acrolein-induced programmed cell death via decreasing active caspase 3 (a hallmark of apoptosis) as well as RIP (receptor-interacting protein) 1 and RIP3 (biomarkers for necroptosis).	AZD 6244	10-21	receptor interacting serine/threonine kinase 1	Homo sapiens	140-143
34127699-7	2021	Moreover, selumetinib prevented acrolein-induced programmed cell death via decreasing active caspase 3 (a hallmark of apoptosis) as well as RIP (receptor-interacting protein) 1 and RIP3 (biomarkers for necroptosis).	AZD 6244	10-21	receptor interacting serine/threonine kinase 1	Homo sapiens	145-176
34127699-4	2021	Co-treatment of selumetinib blocked acrolein-induced ERK phosphorylation.	AZD 6244	16-27	mitogen-activated protein kinase 1	Homo sapiens	53-56
34127699-7	2021	Moreover, selumetinib prevented acrolein-induced programmed cell death via decreasing active caspase 3 (a hallmark of apoptosis) as well as RIP (receptor-interacting protein) 1 and RIP3 (biomarkers for necroptosis).	AZD 6244	10-21	receptor interacting serine/threonine kinase 3	Homo sapiens	181-185
34127699-5	2021	Furthermore, selumetinib reduced acrolein-induced increases in heme oxygenase-1 (a redox-regulated chaperone protein) and its transcriptional factor, Nrf-2 as well as FDP-lysine (acrolein-lysine adducts) and alpha-synuclein aggregation (a pathological biomarker of neurodegeneration).	AZD 6244	13-24	heme oxygenase 1	Homo sapiens	63-79
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	37-48	NFE2 like bZIP transcription factor 2	Homo sapiens	78-83
34127699-5	2021	Furthermore, selumetinib reduced acrolein-induced increases in heme oxygenase-1 (a redox-regulated chaperone protein) and its transcriptional factor, Nrf-2 as well as FDP-lysine (acrolein-lysine adducts) and alpha-synuclein aggregation (a pathological biomarker of neurodegeneration).	AZD 6244	13-24	NFE2 like bZIP transcription factor 2	Homo sapiens	150-155
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	37-48	heme oxygenase 1	Homo sapiens	84-88
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	37-48	mitogen-activated protein kinase kinase 7	Homo sapiens	237-240
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	37-48	mitogen-activated protein kinase 1	Homo sapiens	241-244
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	222-233	mitogen-activated protein kinase kinase 7	Homo sapiens	237-240
34127699-8	2021	In conclusion, our study showed that selumetinib inhibited acrolein-activated Nrf-2-HO-1 pathway, acrolein-induced protein conjugation and aggregation as well as damage in neurite outgrowth and cell death, suggesting that selumetinib, a MEK-ERK inhibitor, may be a potential neuroprotective agent against acrolein-induced neurotoxicity in the CNS neurodegenerative diseases.	AZD 6244	222-233	mitogen-activated protein kinase 1	Homo sapiens	241-244
34127699-5	2021	Furthermore, selumetinib reduced acrolein-induced increases in heme oxygenase-1 (a redox-regulated chaperone protein) and its transcriptional factor, Nrf-2 as well as FDP-lysine (acrolein-lysine adducts) and alpha-synuclein aggregation (a pathological biomarker of neurodegeneration).	AZD 6244	13-24	synuclein alpha	Homo sapiens	208-223
35178860-6	2022	Fifty-four percent of patients were managed conservatively, 28% surgically, and 19% are either taking or due to start a mitogen-activated protein kinase kinase (MEK) inhibitor (selumetinib or trametinib), either through a clinical trial or compassionate usage scheme.	AZD 6244	177-188	mitogen-activated protein kinase kinase 7	Homo sapiens	120-159
34066061-5	2021	The only approved drug, the MEK inhibitor Selumetinib, displays a variable and partial therapeutic response.	AZD 6244	42-53	mitogen-activated protein kinase kinase 7	Homo sapiens	28-31
34066061-10	2021	However, combinatorial treatment with both the FAK inhibitor Defactinib (VS-6063) and Selumetinib (AZD6244) fully suppressed colony growth.	AZD 6244	86-97	protein tyrosine kinase 2	Homo sapiens	47-50
34666331-0	2021	The Synergistic Inhibitory Effect of Combining MK-2206 and AZD 6244 in MARIMO Cells Harboring a Calreticulin Gene Mutation.	AZD 6244	59-67	calreticulin	Homo sapiens	96-108
34150845-9	2021	The anticancer drug sensitivity analysis indicated that ZC3H13 expression had a positive relationship with anticancer drugs such as selumetinib, dabrafenib, cobimetinib, trametinib, and hypothemycin (p < 0.001).	AZD 6244	132-143	zinc finger CCCH-type containing 13	Homo sapiens	56-62
34666331-3	2021	Hence, we aimed to initially explore the mechanism of AKT activation and observe the synergistic inhibitory effect of combining AKT (MK-2206) and MAPK kinase (AZD 6244) inhibitors in MARIMO cells.	AZD 6244	159-167	AKT serine/threonine kinase 1	Homo sapiens	54-57
35588700-7	2022	Selumetinib and trametinib, two oral MEK-inhibitors, have been approved for recurrent or refractory OPGs in association with the angiogenetic inhibitor bevacizumab.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	37-40
35568702-17	2022	High expression of HIST1H1E was resistant to trametinib, selumetinib, RDEA119, docetaxel and 17-AAG, High expression of UBE2C was resistant to masitinib, and Low expression of ERO1B made the EC more sensitive to FK866.	AZD 6244	57-68	H1.4 linker histone, cluster member	Homo sapiens	19-27
35617514-0	2022	Osimertinib plus selumetinib in EGFR-mutated, non-small cell lung cancer after progression on EGFR-TKIs: A Phase 1b, open-label, multicenter trial (TATTON Part B).	AZD 6244	17-28	epidermal growth factor receptor	Homo sapiens	32-36
35523987-0	2022	Discovery of novel targets and mechanisms of MEK inhibitor Selumetinib for LGG treatment based on molecular docking and molecular dynamics simulation.	AZD 6244	59-70	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
35523987-1	2022	Based on molecular docking and molecular dynamics simulation, to find a new target and mechanism of MEK inhibitor Selumetinib in the treatment of low-grade glioma (LGG), and to provide theoretical guidance for its clinical medication.	AZD 6244	114-125	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
35489723-5	2022	RESULTS: Lenvatinib and a MEK inhibitor, selumetinib, suppressed SREBP1 expression in BHT-101 but not FTC-133 cells.	AZD 6244	41-52	mitogen-activated protein kinase kinase 7	Homo sapiens	26-29
35523987-6	2022	Through protein interaction (PPI), gene enrichment analysis, and gene difference analysis, one effective target of Selumetinib was finally screened, CDK2 mainly existing in the cytoplasm, endoplasmic reticulum, and plasma membrane; the target plays a role in the treatment of LGG by inhibiting the signal pathways of PI3K Akt and participating in biological processes such as peptide amino acid modification, regulation of intracellular signal transduction, and positive regulation of cell metabolism.	AZD 6244	115-126	cyclin dependent kinase 2	Homo sapiens	149-153
35523987-6	2022	Through protein interaction (PPI), gene enrichment analysis, and gene difference analysis, one effective target of Selumetinib was finally screened, CDK2 mainly existing in the cytoplasm, endoplasmic reticulum, and plasma membrane; the target plays a role in the treatment of LGG by inhibiting the signal pathways of PI3K Akt and participating in biological processes such as peptide amino acid modification, regulation of intracellular signal transduction, and positive regulation of cell metabolism.	AZD 6244	115-126	AKT serine/threonine kinase 1	Homo sapiens	322-325
35523987-7	2022	CDK2 may be a new direction of Selumetinib in the clinical treatment of LGG.	AZD 6244	31-42	cyclin dependent kinase 2	Homo sapiens	0-4
35489723-5	2022	RESULTS: Lenvatinib and a MEK inhibitor, selumetinib, suppressed SREBP1 expression in BHT-101 but not FTC-133 cells.	AZD 6244	41-52	sterol regulatory element binding transcription factor 1	Homo sapiens	65-71
35489723-9	2022	Lenvatinib and selumetinib decreases SREBP1 expression in the BRAF-mutant cell line BHT-101.	AZD 6244	15-26	sterol regulatory element binding transcription factor 1	Homo sapiens	37-43
35489723-9	2022	Lenvatinib and selumetinib decreases SREBP1 expression in the BRAF-mutant cell line BHT-101.	AZD 6244	15-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
35363510-2	2022	Patients with tumors harboring mutations or fusions driving activation of the mitogen-activated protein kinase (MAPK) pathway were treated with the MEK inhibitor selumetinib.	AZD 6244	162-173	mitogen-activated protein kinase kinase 7	Homo sapiens	148-151
35467749-0	2022	Selumetinib in Children with Neurofibromatosis Type 1 and Asymptomatic Inoperable Plexiform Neurofibroma At Risk for Developing Tumor-Related Morbidity.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	29-53
35467749-1	2022	BACKGROUND: Selumetinib was recently approved for treatment of inoperable symptomatic plexiform neurofibromas (PNs) in children with neurofibromatosis type 1 (NF1).	AZD 6244	12-23	neurofibromin 1	Homo sapiens	133-157
35467749-1	2022	BACKGROUND: Selumetinib was recently approved for treatment of inoperable symptomatic plexiform neurofibromas (PNs) in children with neurofibromatosis type 1 (NF1).	AZD 6244	12-23	neurofibromin 1	Homo sapiens	159-162
35410754-1	2022	PURPOSE: Selumetinib (ARRY-142886) is an oral, potent, and highly selective allosteric mitogen-activated protein kinase kinase 1/2 inhibitor approved for the treatment of pediatric patients (>=2 years of age) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	9-20	mitogen-activated protein kinase kinase 1	Homo sapiens	87-130
35410754-1	2022	PURPOSE: Selumetinib (ARRY-142886) is an oral, potent, and highly selective allosteric mitogen-activated protein kinase kinase 1/2 inhibitor approved for the treatment of pediatric patients (>=2 years of age) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	9-20	neurofibromin 1	Homo sapiens	214-238
35410754-1	2022	PURPOSE: Selumetinib (ARRY-142886) is an oral, potent, and highly selective allosteric mitogen-activated protein kinase kinase 1/2 inhibitor approved for the treatment of pediatric patients (>=2 years of age) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	87-130
35410754-1	2022	PURPOSE: Selumetinib (ARRY-142886) is an oral, potent, and highly selective allosteric mitogen-activated protein kinase kinase 1/2 inhibitor approved for the treatment of pediatric patients (>=2 years of age) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	22-33	neurofibromin 1	Homo sapiens	214-238
35170228-1	2022	Selumetinib is an oral, potent, and highly selective allosteric MEK1/2 inhibitor approved for the treatment of pediatric patients (aged <=2 years) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	64-70
35170228-1	2022	Selumetinib is an oral, potent, and highly selective allosteric MEK1/2 inhibitor approved for the treatment of pediatric patients (aged <=2 years) with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	152-176
35179724-8	2022	Selumetinib is an oral, small molecule mitogen-activated protein kinase (MEK) agent with antineoplastic activity which is in ongoing trials for treatment of NF1-associated pediatric low-grade gliomas.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	39-71
35179724-8	2022	Selumetinib is an oral, small molecule mitogen-activated protein kinase (MEK) agent with antineoplastic activity which is in ongoing trials for treatment of NF1-associated pediatric low-grade gliomas.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	73-76
35301838-1	2022	INTRODUCTION: Selumetinib is a MEK inhibitor, which is effective with an acceptable safety profile in reducing the volume of symptomatic inoperable plexiform neurofibromas in some clinical trials and also has been recently approved by FDA for use in children aged 2 years or older.	AZD 6244	14-25	mitogen-activated protein kinase kinase 7	Homo sapiens	31-34
35406545-6	2022	In vitro analysis of lentivirally MACC1-manipulated subclones of FLO-1 and OE33 showed enhanced migration induced by MACC1 in both cell line models, which could be inhibited by the MEK1 inhibitor selumetinib.	AZD 6244	196-207	MET transcriptional regulator MACC1	Homo sapiens	34-39
35406545-6	2022	In vitro analysis of lentivirally MACC1-manipulated subclones of FLO-1 and OE33 showed enhanced migration induced by MACC1 in both cell line models, which could be inhibited by the MEK1 inhibitor selumetinib.	AZD 6244	196-207	MET transcriptional regulator MACC1	Homo sapiens	117-122
35406545-6	2022	In vitro analysis of lentivirally MACC1-manipulated subclones of FLO-1 and OE33 showed enhanced migration induced by MACC1 in both cell line models, which could be inhibited by the MEK1 inhibitor selumetinib.	AZD 6244	196-207	mitogen-activated protein kinase kinase 1	Homo sapiens	181-185
35406545-7	2022	In vivo, the efficacy of selumetinib on tumor growths and metastases of MACC1-overexpressing FLO-1 cells xenografted intrasplenically in NOG mice was tested.	AZD 6244	25-36	MET transcriptional regulator MACC1	Homo sapiens	72-77
35406545-9	2022	Treatment with selumetinib led to a significant reduction in metastasis exclusively in the MACC1-positive xenografts.	AZD 6244	15-26	metastasis associated in colon cancer 1	Mus musculus	91-96
35301838-3	2022	EVIDENCE ACQUISITION: Articles describing the use of selumetinib in patients with neurofibromatosis type-1 (NF1) with inoperable plexiform neurofibromas were searched from different electronic databases.	AZD 6244	53-64	neurofibromin 1	Homo sapiens	82-106
35301838-3	2022	EVIDENCE ACQUISITION: Articles describing the use of selumetinib in patients with neurofibromatosis type-1 (NF1) with inoperable plexiform neurofibromas were searched from different electronic databases.	AZD 6244	53-64	neurofibromin 1	Homo sapiens	108-111
35301838-15	2022	CONCLUSIONS: Selumetinib can produce sustained shrinkage in the majority of patients with NF1 and symptomatic plexiform neurofibroma to provide clinically meaningful benefit in functional ability, with more robust evidence in children.	AZD 6244	13-24	neurofibromin 1	Homo sapiens	90-93
35287697-12	2022	The Homer1 protein and selumetinib, a non-ATP competitive MEK1/2 inhibitor, improved the outcome in ICH in Homer1flox/flox/Nestin-Cre+/- mice.	AZD 6244	23-34	mitogen-activated protein kinase kinase 1	Mus musculus	58-64
35289492-0	2022	Selumetinib for symptomatic, inoperable plexiform neurofibromas in children with neurofibromatosis type 1: A national real-world case series.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	81-105
35289492-3	2022	Selumetinib is an oral selective inhibitor of RAS-mitogen-activated protein kinase (MAPK) 1 and 2, which has shown efficacy for tumour shrinkage/stabilisation and symptom improvement.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	46-97
35250023-0	2022	Retracted: The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.	AZD 6244	32-39	mitogen-activated protein kinase kinase 1	Homo sapiens	15-21
35250023-3	2022	The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.	AZD 6244	21-28	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
35250023-3	2022	The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.	AZD 6244	21-28	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	40-44
35246426-3	2022	Induction therapy for ALL involves steroids, with preclinical data suggesting the combination of dexamethasone with the MEK1/2 inhibitor, selumetinib (ARRY-142886) has a synergistic anticancer effect.	AZD 6244	138-149	mitogen-activated protein kinase kinase 1	Homo sapiens	120-126
35246426-3	2022	Induction therapy for ALL involves steroids, with preclinical data suggesting the combination of dexamethasone with the MEK1/2 inhibitor, selumetinib (ARRY-142886) has a synergistic anticancer effect.	AZD 6244	151-162	mitogen-activated protein kinase kinase 1	Homo sapiens	120-126
35171389-0	2022	Selumetinib: a selective MEK1 inhibitor for solid tumor treatment.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	25-29
35017312-0	2022	Efficacy and Safety of Selumetinib in Pediatric Patients With Neurofibromatosis Type 1: A Systematic Review and Meta-analysis.	AZD 6244	23-34	neurofibromin 1	Homo sapiens	62-86
35017312-1	2022	BACKGROUND AND OBJECTIVES: Although the recent approval of selumetinib is expected to transform the management of children with Neurofibromatosis type 1 (NF1), particularly those with symptomatic and inoperable PN, no systematic review has summarized their efficacy and safety based on the latest studies.	AZD 6244	59-70	neurofibromin 1	Homo sapiens	128-152
35017312-1	2022	BACKGROUND AND OBJECTIVES: Although the recent approval of selumetinib is expected to transform the management of children with Neurofibromatosis type 1 (NF1), particularly those with symptomatic and inoperable PN, no systematic review has summarized their efficacy and safety based on the latest studies.	AZD 6244	59-70	neurofibromin 1	Homo sapiens	154-157
35017312-2	2022	This study was conducted to systematically evaluate the efficacy and safety of selumetinib in children with NF1 METHODS: Original articles reporting the efficacy and safety of selumetinib in patients with NF1 were identified in PubMed and EMBASE up to January 28, 2021.	AZD 6244	79-90	neurofibromin 1	Homo sapiens	108-111
35017312-2	2022	This study was conducted to systematically evaluate the efficacy and safety of selumetinib in children with NF1 METHODS: Original articles reporting the efficacy and safety of selumetinib in patients with NF1 were identified in PubMed and EMBASE up to January 28, 2021.	AZD 6244	176-187	neurofibromin 1	Homo sapiens	205-208
35210278-1	2022	BACKGROUND AND PURPOSE: Selumetinib is a promising MAP (mitogen-activated protein) kinase (MEK) 1/2 inhibitor treatment for pediatric low-grade gliomas.	AZD 6244	24-35	mitogen-activated protein kinase kinase 1	Homo sapiens	56-99
35171389-8	2022	Selumetinib (AZD6244) is a second-generation, selective, potent, and non-ATP competitive allosteric MEK1 inhibitor.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	100-104
35171389-8	2022	Selumetinib (AZD6244) is a second-generation, selective, potent, and non-ATP competitive allosteric MEK1 inhibitor.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	100-104
35171389-10	2022	The present paper provides an overview of the MAPK cascade, the role of selumetinib as a MEK1/2 inhibitor, and the related findings of clinical trials for solid tumor treatment.	AZD 6244	72-83	mitogen-activated protein kinase kinase 1	Homo sapiens	89-95
35055192-7	2022	By leveraging recent efforts in the systematic profiling and cataloguing of thousands of small molecule compounds, we identified drugs including selumetinib that specifically target key molecules within the MEK signaling cascade, representing candidates with the potential to be effective in the treatment of these rare and aggressive SCCs.	AZD 6244	145-156	mitogen-activated protein kinase kinase 7	Homo sapiens	207-210
35075200-2	2022	Here, we evaluated combination therapy with MEK inhibitor selumetinib and MDM2 inhibitor KRT-232 in TP53 wild-type and MAPK altered colon and thyroid cancer models.	AZD 6244	58-69	mitogen-activated protein kinase kinase 7	Homo sapiens	44-47
33903938-0	2021	Population pharmacokinetics and exposure-response of selumetinib and its N-desmethyl metabolite in pediatric patients with neurofibromatosis type 1 and inoperable plexiform neurofibromas.	AZD 6244	53-64	neurofibromin 1	Homo sapiens	123-147
33405090-0	2021	Phase II study of selumetinib, an orally active inhibitor of MEK1 and MEK2 kinases, in KRASG12R-mutant pancreatic ductal adenocarcinoma.	AZD 6244	18-29	mitogen-activated protein kinase kinase 1	Homo sapiens	61-65
33405090-0	2021	Phase II study of selumetinib, an orally active inhibitor of MEK1 and MEK2 kinases, in KRASG12R-mutant pancreatic ductal adenocarcinoma.	AZD 6244	18-29	mitogen-activated protein kinase kinase 2	Homo sapiens	70-74
33405090-0	2021	Phase II study of selumetinib, an orally active inhibitor of MEK1 and MEK2 kinases, in KRASG12R-mutant pancreatic ductal adenocarcinoma.	AZD 6244	18-29	KRAS proto-oncogene, GTPase	Homo sapiens	87-91
33405090-2	2021	We conducted a biomarker-driven trial of selumetinib (KOSELUGO ; ARRY-142886), an orally active, allosteric mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor, in pancreas cancer patients with somatic KRASG12R mutations.	AZD 6244	41-52	mitogen-activated protein kinase 1	Homo sapiens	108-148
33405090-2	2021	We conducted a biomarker-driven trial of selumetinib (KOSELUGO ; ARRY-142886), an orally active, allosteric mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor, in pancreas cancer patients with somatic KRASG12R mutations.	AZD 6244	41-52	mitogen-activated protein kinase kinase 1	Homo sapiens	150-156
34007050-5	2021	Importantly, the MEK inhibitor selumetinib synergizes with steroids in both IL7-dependent and IL7-independent steroid resistant pediatric T-ALL PDX samples.	AZD 6244	31-42	mitogen-activated protein kinase kinase 7	Homo sapiens	17-20
34007050-5	2021	Importantly, the MEK inhibitor selumetinib synergizes with steroids in both IL7-dependent and IL7-independent steroid resistant pediatric T-ALL PDX samples.	AZD 6244	31-42	interleukin 7	Homo sapiens	76-79
34007050-5	2021	Importantly, the MEK inhibitor selumetinib synergizes with steroids in both IL7-dependent and IL7-independent steroid resistant pediatric T-ALL PDX samples.	AZD 6244	31-42	interleukin 7	Homo sapiens	94-97
33683166-0	2021	Selumetinib: the first ever approved drug for neurofibromatosis-1 related inoperable plexiform neurofibroma.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	46-65
33683166-6	2021	Recently, the US Food and Drug Administration approved selumetinib for pediatric patients, 2 years of age and older, with neurofibromatosis type 1 who have symptomatic, inoperable tumor.	AZD 6244	55-66	neurofibromin 1	Homo sapiens	122-146
33683166-11	2021	Selumetinib is an inhibitor of MEK1 and MEK2 proteins, which play an important role in the MAPK signaling pathway related to tumor growth.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	31-35
33683166-11	2021	Selumetinib is an inhibitor of MEK1 and MEK2 proteins, which play an important role in the MAPK signaling pathway related to tumor growth.	AZD 6244	0-11	mitogen-activated protein kinase kinase 2	Homo sapiens	40-44
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	9-20	mitogen-activated protein kinase kinase 1	Homo sapiens	59-65
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	9-20	neurofibromin 1	Homo sapiens	143-167
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	9-20	neurofibromin 1	Homo sapiens	169-172
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	59-65
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	22-33	neurofibromin 1	Homo sapiens	143-167
33903938-1	2021	PURPOSE: Selumetinib (ARRY-142886) is a potent, selective, MEK1/2 inhibitor approved in the US for the treatment of children (>= 2 years) with neurofibromatosis type 1 (NF1) and symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	22-33	neurofibromin 1	Homo sapiens	169-172
33296125-0	2021	Phase I Study of Afatinib and Selumetinib in Patients with KRAS-Mutated Colorectal, Non-Small Cell Lung, and Pancreatic Cancer.	AZD 6244	30-41	KRAS proto-oncogene, GTPase	Homo sapiens	59-63
32414848-8	2021	As hypothesized, superior inhibition of ALL proliferation was observed in KMT2A-AFF1 PDX models treated with entospletinib and the MEK inhibitor selumetinib versus vehicle or inhibitor monotherapies (p<0.05).	AZD 6244	145-156	lysine methyltransferase 2A	Homo sapiens	74-79
32414848-8	2021	As hypothesized, superior inhibition of ALL proliferation was observed in KMT2A-AFF1 PDX models treated with entospletinib and the MEK inhibitor selumetinib versus vehicle or inhibitor monotherapies (p<0.05).	AZD 6244	145-156	AF4/FMR2 family member 1	Homo sapiens	80-84
32414848-8	2021	As hypothesized, superior inhibition of ALL proliferation was observed in KMT2A-AFF1 PDX models treated with entospletinib and the MEK inhibitor selumetinib versus vehicle or inhibitor monotherapies (p<0.05).	AZD 6244	145-156	mitogen-activated protein kinase kinase 7	Homo sapiens	131-134
32414848-10	2021	Combination therapy with vincristine or selumetinib further enhanced treatment effects of SYK inhibition.	AZD 6244	40-51	spleen associated tyrosine kinase	Homo sapiens	90-93
33536190-8	2021	The AKT inhibitor MK-2206 reduced AKT1/2/3 phosphorylation in SW620 xenograft tumors 2 to 4 hours post-dose, and the MEK inhibitor selumetinib reduced MEK1/2 and ERK1/2 phosphorylation by up to 50% and >90%, respectively.	AZD 6244	131-142	mitogen-activated protein kinase kinase 7	Homo sapiens	117-120
33536190-8	2021	The AKT inhibitor MK-2206 reduced AKT1/2/3 phosphorylation in SW620 xenograft tumors 2 to 4 hours post-dose, and the MEK inhibitor selumetinib reduced MEK1/2 and ERK1/2 phosphorylation by up to 50% and >90%, respectively.	AZD 6244	131-142	mitogen-activated protein kinase kinase 1	Homo sapiens	151-157
33536190-8	2021	The AKT inhibitor MK-2206 reduced AKT1/2/3 phosphorylation in SW620 xenograft tumors 2 to 4 hours post-dose, and the MEK inhibitor selumetinib reduced MEK1/2 and ERK1/2 phosphorylation by up to 50% and >90%, respectively.	AZD 6244	131-142	mitogen-activated protein kinase 3	Homo sapiens	162-168
33296125-5	2021	Therefore, this phase I trial was initiated with the pan-HER inhibitor afatinib plus the MEK inhibitor selumetinib in patients with KRASmt, PIK3CA wild type tumors.	AZD 6244	103-114	mitogen-activated protein kinase kinase 7	Homo sapiens	89-92
33354735-1	2021	Selumetinib, a highly specific mitogen-activated protein kinase 1/2 inhibitor, is approved for children older than 2 years of age with neurofibromatosis 1 who have inoperable plexiform neurofibromas.	AZD 6244	0-11	mitogen-activated protein kinase 12	Homo sapiens	31-67
33296125-5	2021	Therefore, this phase I trial was initiated with the pan-HER inhibitor afatinib plus the MEK inhibitor selumetinib in patients with KRASmt, PIK3CA wild type tumors.	AZD 6244	103-114	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	140-146
33850471-9	2021	Compared with control Schwann cells, the YAP inhibitor CA3 might have a more sensitive effect (IC50: NC=0.96+-0.04, shNF1=0.71+-0.02, P<0.05) on the shNF1 Schwann cell model than the classic MEK1/2 inhibitor selumetinib (IC50: NC=14.36+-0.95, shNF1=24.83+-0.98, P>0.05).	AZD 6244	208-219	Yes1 associated transcriptional regulator	Rattus norvegicus	41-44
33850471-9	2021	Compared with control Schwann cells, the YAP inhibitor CA3 might have a more sensitive effect (IC50: NC=0.96+-0.04, shNF1=0.71+-0.02, P<0.05) on the shNF1 Schwann cell model than the classic MEK1/2 inhibitor selumetinib (IC50: NC=14.36+-0.95, shNF1=24.83+-0.98, P>0.05).	AZD 6244	208-219	carbonic anhydrase 3	Homo sapiens	55-58
33721151-6	2021	Selumetinib has become the first FDA-approved targeted therapy for NF1 following its demonstrated efficacy for inoperable plexiform neurofibroma.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	67-70
33712511-1	2021	On April 10, 2020, the U.S. Food and Drug Administration (FDA) approved selumetinib (KOSELUGO, AstraZeneca) for the treatment of pediatric patients 2 years of age and older with neurofibromatosis type 1 (NF1) who have symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	72-83	neurofibromin 1	Homo sapiens	178-202
33712511-1	2021	On April 10, 2020, the U.S. Food and Drug Administration (FDA) approved selumetinib (KOSELUGO, AstraZeneca) for the treatment of pediatric patients 2 years of age and older with neurofibromatosis type 1 (NF1) who have symptomatic, inoperable plexiform neurofibromas (PN).	AZD 6244	72-83	neurofibromin 1	Homo sapiens	204-207
33712511-6	2021	Risks of selumetinib are consistent with mitogen-activated protein kinase (MEK) inhibitor class effects including ocular, cardiac, musculoskeletal, gastrointestinal and dermatologic toxicities.	AZD 6244	9-20	mitogen-activated protein kinase kinase 7	Homo sapiens	41-73
33712511-6	2021	Risks of selumetinib are consistent with mitogen-activated protein kinase (MEK) inhibitor class effects including ocular, cardiac, musculoskeletal, gastrointestinal and dermatologic toxicities.	AZD 6244	9-20	mitogen-activated protein kinase kinase 7	Homo sapiens	75-78
33354735-1	2021	Selumetinib, a highly specific mitogen-activated protein kinase 1/2 inhibitor, is approved for children older than 2 years of age with neurofibromatosis 1 who have inoperable plexiform neurofibromas.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	135-154
33354735-2	2021	By selectively binding to mitogen-activated protein kinase 1/2 proteins, selumetinib can arrest the mitogen-activated protein kinase/extracellular signal-regulated kinase signaling pathway that regulates critical cellular responses.	AZD 6244	73-84	mitogen-activated protein kinase 12	Homo sapiens	26-62
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	82-89	mitogen-activated protein kinase kinase 1	Homo sapiens	201-207
33631016-5	2021	METHODS: We present results from children with recurrent/progressive OPHGs treated on a PBTC phase 2 trial evaluating efficacy of selumetinib, (AZD6244, ARRY-142886) a MEK-1/2 inhibitor.	AZD 6244	153-164	mitogen-activated protein kinase kinase 1	Homo sapiens	168-175
33627767-7	2021	Our candidate drug findings are discordant with (i.e., reverse) SARS-CoV-2 transcriptome signatures generated in vitro, and a subset are also identified in transcriptome signatures generated from COVID-19 patient samples, like the MEK inhibitor selumetinib.	AZD 6244	245-256	mitogen-activated protein kinase kinase 7	Homo sapiens	231-234
33978635-0	2021	Selumetinib normalizes Ras/MAPK signaling in clinically relevant neurofibromatosis type 1 minipig tissues in vivo.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	65-89
33978635-1	2021	Background: The MEK1/2 inhibitor selumetinib was recently approved for neurofibromatosis type 1 (NF1)-associated plexiform neurofibromas, but outcomes could be improved and its pharmacodynamic evaluation in other relevant tissues is limited.	AZD 6244	33-44	mitogen-activated protein kinase kinase 1	Homo sapiens	16-22
33978635-1	2021	Background: The MEK1/2 inhibitor selumetinib was recently approved for neurofibromatosis type 1 (NF1)-associated plexiform neurofibromas, but outcomes could be improved and its pharmacodynamic evaluation in other relevant tissues is limited.	AZD 6244	33-44	neurofibromin 1	Homo sapiens	71-95
33978635-1	2021	Background: The MEK1/2 inhibitor selumetinib was recently approved for neurofibromatosis type 1 (NF1)-associated plexiform neurofibromas, but outcomes could be improved and its pharmacodynamic evaluation in other relevant tissues is limited.	AZD 6244	33-44	neurofibromin 1	Homo sapiens	97-100
33978635-2	2021	The aim of this study was to assess selumetinib tissue pharmacokinetics (PK) and pharmacodynamics (PD) using a minipig model of NF1.	AZD 6244	36-47	neurofibromin 1	Homo sapiens	128-131
33978635-6	2021	Selumetinib concentrations were higher in CNS tissues from NF1 compared to WT animals.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	59-62
33978635-8	2021	Basal p-ERK levels were significantly higher in NF1 minipig optic nerve compared to WT and were reduced to WT levels (60%) with selumetinib.	AZD 6244	128-139	mitogen-activated protein kinase 1	Homo sapiens	8-11
33978635-8	2021	Basal p-ERK levels were significantly higher in NF1 minipig optic nerve compared to WT and were reduced to WT levels (60%) with selumetinib.	AZD 6244	128-139	neurofibromin 1	Homo sapiens	48-51
33978635-10	2021	Conclusions: Selumetinib reduces MAPK signaling in tissues clinically relevant to NF1, effectively normalizing p-ERK to WT levels in optic nerve but resulting in abnormally low levels of p-ERK in the skin.	AZD 6244	13-24	neurofibromin 1	Homo sapiens	82-85
33549085-4	2021	Selumetinib, an inhibitor of mitogen-activated protein kinase (MEK) 1 and 2, has been the first molecule to demonstrate the ability of tackling the growth of PNs.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	29-75
33549085-7	2021	The first case of peripheral edema occurred in a 7-year-old boy affected by a severe form of NF1, after two years of treatment with selumetinib at the standard dose (25 mg/m2twice a day).	AZD 6244	132-143	neurofibromin 1	Homo sapiens	93-96
32876513-7	2021	The IGF2BP1-SRC/ERK2 axis is targetable by the SRC-inhibitor saracatinib and MEK-inhibitor selumetinib.	AZD 6244	91-102	insulin-like growth factor 2 mRNA binding protein 1	Mus musculus	4-11
32876513-7	2021	The IGF2BP1-SRC/ERK2 axis is targetable by the SRC-inhibitor saracatinib and MEK-inhibitor selumetinib.	AZD 6244	91-102	Rous sarcoma oncogene	Mus musculus	12-15
32876513-7	2021	The IGF2BP1-SRC/ERK2 axis is targetable by the SRC-inhibitor saracatinib and MEK-inhibitor selumetinib.	AZD 6244	91-102	mitogen-activated protein kinase 1	Mus musculus	16-20
32876513-7	2021	The IGF2BP1-SRC/ERK2 axis is targetable by the SRC-inhibitor saracatinib and MEK-inhibitor selumetinib.	AZD 6244	91-102	midkine	Mus musculus	77-80
33748440-0	2021	Phase I trial of the MEK inhibitor selumetinib in combination with thoracic radiotherapy in non-small cell lung cancer.	AZD 6244	35-46	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
33748440-2	2021	Selumetinib inhibits MEK and enhances effects of radiotherapy in preclinical studies.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
33622407-13	2021	Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model.	AZD 6244	87-98	midkine	Mus musculus	38-41
33622407-13	2021	Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model.	AZD 6244	87-98	amphiregulin	Mus musculus	78-82
33978635-10	2021	Conclusions: Selumetinib reduces MAPK signaling in tissues clinically relevant to NF1, effectively normalizing p-ERK to WT levels in optic nerve but resulting in abnormally low levels of p-ERK in the skin.	AZD 6244	13-24	mitogen-activated protein kinase 1	Homo sapiens	113-116
33978635-10	2021	Conclusions: Selumetinib reduces MAPK signaling in tissues clinically relevant to NF1, effectively normalizing p-ERK to WT levels in optic nerve but resulting in abnormally low levels of p-ERK in the skin.	AZD 6244	13-24	mitogen-activated protein kinase 1	Homo sapiens	189-192
33978635-11	2021	These results suggest that selumetinib exerts activity in NF1-associated CNS tumors by normalizing Ras/MAPK signaling and may explain common MEK inhibitor-associated dermatologic toxicities.	AZD 6244	27-38	neurofibromin 1	Homo sapiens	58-61
33978635-11	2021	These results suggest that selumetinib exerts activity in NF1-associated CNS tumors by normalizing Ras/MAPK signaling and may explain common MEK inhibitor-associated dermatologic toxicities.	AZD 6244	27-38	mitogen-activated protein kinase kinase 7	Homo sapiens	141-144
33273059-0	2021	AZD0364 is a potent and selective ERK1/2 inhibitor which enhances anti-tumour activity in KRAS mutant tumour models when combined with the MEK inhibitor selumetinib.	AZD 6244	153-164	mitogen-activated protein kinase kinase 7	Homo sapiens	139-142
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	69-80	mitogen-activated protein kinase kinase 1	Homo sapiens	52-58
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	69-80	KRAS proto-oncogene, GTPase	Homo sapiens	124-128
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	69-80	mitogen-activated protein kinase kinase 1	Homo sapiens	201-207
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	82-89	KRAS proto-oncogene, GTPase	Homo sapiens	124-128
33273059-7	2021	We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor selumetinib (AZD6244, ARRY142886) enhances efficacy in KRAS mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition.	AZD 6244	91-101	KRAS proto-oncogene, GTPase	Homo sapiens	124-128
33273059-9	2021	The AZD0364 and selumetinib combination also results in significant tumour regressions in multiple KRAS mutant xenograft models.	AZD 6244	16-27	KRAS proto-oncogene, GTPase	Homo sapiens	99-103
33416182-3	2021	The aim of the present study was to elucidate the anticancer effects of the MEK inhibitor Selumetinib on two low-grade glioma cell lines and the possible underlying effects on intracellular signal transduction.	AZD 6244	90-101	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
33416182-4	2021	The two cancer cell lines displayed different levels of sensitivity to Selumetinib, as Res186 cells were resistant (IC50>1 microM), whereas Res259 cells were sensitive (IC50<=1 microM) to MEK inhibition.	AZD 6244	71-82	mitogen-activated protein kinase kinase 7	Homo sapiens	188-191
33416182-5	2021	Despite the different levels of sensitivity, Selumetinib mediated the phosphorylation of AKT and MEK in both cell lines and suppressed the phosphorylated MAPK cascades.	AZD 6244	45-56	AKT serine/threonine kinase 1	Homo sapiens	89-92
33416182-5	2021	Despite the different levels of sensitivity, Selumetinib mediated the phosphorylation of AKT and MEK in both cell lines and suppressed the phosphorylated MAPK cascades.	AZD 6244	45-56	mitogen-activated protein kinase kinase 7	Homo sapiens	97-100
33416182-6	2021	In addition, Selumetinib induced cell cycle arrest at the G0/G1 phase by downregulating the expression levels of cyclin D1 and p21 and upregulating those of p27 compared with those in the control cells.	AZD 6244	13-24	cyclin D1	Homo sapiens	113-122
33416182-6	2021	In addition, Selumetinib induced cell cycle arrest at the G0/G1 phase by downregulating the expression levels of cyclin D1 and p21 and upregulating those of p27 compared with those in the control cells.	AZD 6244	13-24	cyclin dependent kinase inhibitor 1A	Homo sapiens	127-130
33416182-6	2021	In addition, Selumetinib induced cell cycle arrest at the G0/G1 phase by downregulating the expression levels of cyclin D1 and p21 and upregulating those of p27 compared with those in the control cells.	AZD 6244	13-24	dynactin subunit 6	Homo sapiens	157-160
33416182-8	2021	In conclusion, the results of the present study provided three low-grade glioma cell line models characterized by sensitivity, intrinsic and acquired resistance to Selumetinib, which may be usuful tools to study new mechanisms of chemoresistance to MEK inhibitors and to explore alternative therapeutic strategies in low-grade gliomas for personalization of treatment.	AZD 6244	164-175	mitogen-activated protein kinase kinase 7	Homo sapiens	249-252
33137541-0	2021	Targeted inhibition of glutamine metabolism enhances the antitumor effect of selumetinib in KRAS-mutant NSCLC.	AZD 6244	77-88	KRAS proto-oncogene, GTPase	Homo sapiens	92-96
33137541-5	2021	CB839, an efficient glutaminase inhibitor, synergized with the MEK inhibitor selumetinib to enhance antitumor activity in KRAS-mutant NSCLC cells and xenografts, and the therapeutic response could be well identified by 18F-FDG PET imaging.	AZD 6244	77-88	mitogen-activated protein kinase kinase 7	Homo sapiens	63-66
33137541-5	2021	CB839, an efficient glutaminase inhibitor, synergized with the MEK inhibitor selumetinib to enhance antitumor activity in KRAS-mutant NSCLC cells and xenografts, and the therapeutic response could be well identified by 18F-FDG PET imaging.	AZD 6244	77-88	KRAS proto-oncogene, GTPase	Homo sapiens	122-126
32888253-3	2020	The present study aimed to use proteomic methods to probe into the role of the EGF-EGFR-angiogenesis axis in the tumorigenesis of glioma and access the therapeutic efficacy of selumetinib on glioma.	AZD 6244	176-187	epidermal growth factor	Mus musculus	79-82
33052075-1	2020	We analyzed responsiveness of KRAS-mutated CRC cell lines with distinctive MSI status against mitogen-activated protein kinase (MEK) inhibitor (selumetinib; AZD) and/or B-raf proto-oncogene (BRAF) kinase inhibitor (vemurafenib; PLX).	AZD 6244	144-155	KRAS proto-oncogene, GTPase	Homo sapiens	30-34
32880495-5	2020	EXPERT OPINION: Selumetinib is an oral selective allosteric inhibitor of MEK1 and MEK2 kinases.	AZD 6244	16-27	mitogen-activated protein kinase kinase 1	Homo sapiens	73-77
32880495-5	2020	EXPERT OPINION: Selumetinib is an oral selective allosteric inhibitor of MEK1 and MEK2 kinases.	AZD 6244	16-27	mitogen-activated protein kinase kinase 2	Homo sapiens	82-86
32880495-10	2020	A phase II trial showed that the addition of selumetinib to docetaxel improved response rates and progression-free survival (PFS) in chemotherapy-pretreated KRAS-mutated NSCLC patients; however, a subsequent phase III study did not confirm these findings.	AZD 6244	45-56	KRAS proto-oncogene, GTPase	Homo sapiens	157-161
32880495-11	2020	There are several highly successful non-NSCLC selumetinib trials involving, e.g., patients with neurofibromatosis type 1 related tumors and children with low-grade BRAF-driven gliomas.	AZD 6244	46-57	neurofibromin 1	Homo sapiens	96-120
32880495-11	2020	There are several highly successful non-NSCLC selumetinib trials involving, e.g., patients with neurofibromatosis type 1 related tumors and children with low-grade BRAF-driven gliomas.	AZD 6244	46-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-168
33081092-4	2020	In our study, we investigated the MEK inhibitor selumetinib and PI3K/mTOR dual inhibitor BEZ235 alone and in combination in BRAF-only mutant and BRAF + PI3K/PTEN double mutant cancer cells using short- and long-term 2D viability assays, spheroid assays, and immunoblots.	AZD 6244	48-59	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
33081092-4	2020	In our study, we investigated the MEK inhibitor selumetinib and PI3K/mTOR dual inhibitor BEZ235 alone and in combination in BRAF-only mutant and BRAF + PI3K/PTEN double mutant cancer cells using short- and long-term 2D viability assays, spheroid assays, and immunoblots.	AZD 6244	48-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	145-149
33081092-5	2020	In the 2D assays, selumetinib was more effective on BRAF-only mutant lines when compared to BRAF + PI3K/PTEN double mutants.	AZD 6244	18-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
32607696-6	2020	Based on this finding and subsequent demonstration of clinical benefit, the MEK inhibitor selumetinib recently received approval by the United States Food and Drug Administration (FDA) for children with symptomatic pNF.	AZD 6244	90-101	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
32358092-5	2020	Mice were treated with interferon gamma (IFNgamma) intraperitoneally for 3 days or with the mitogen-activated protein kinase kinase (MEK1/2) inhibitor selumetinib by oral gavage for 24 hours.	AZD 6244	151-162	mitogen-activated protein kinase kinase 1	Mus musculus	133-139
32358092-12	2020	In vitro, selumetinib downregulated cellular and membrane levels of PD-L1 of tumor cells by 50% as measured by Western blotting and flow cytometry.	AZD 6244	10-21	CD274 antigen	Mus musculus	68-73
32590414-2	2020	MEK inhibition using selumetinib has led to promising results with improved progression-free survival.	AZD 6244	21-32	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
32975370-7	2020	In contrast, selumetinib prolonged survival of animals bearing MPNST xenografts, and this correlated with decreased pERK and Ki67 staining.	AZD 6244	13-24	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	116-120
32975370-9	2020	Thymidine uptake, assessed by 18 F-FLT PET/CT, positively correlated with Ki67 expression in different xenograft models and in response to selumetinib.	AZD 6244	139-150	fms related receptor tyrosine kinase 1	Homo sapiens	35-38
33245731-4	2020	We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells.	AZD 6244	54-65	mitogen-activated protein kinase kinase 7	Homo sapiens	8-11
33245731-4	2020	We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells.	AZD 6244	54-65	angiotensin converting enzyme 2	Homo sapiens	73-77
32601387-6	2020	We used dual-energy X-ray absorptiometry (DXA) to assess tumor-associated changes in bone mineral density (BMD) in an individual with NF1 following treatment with the MEK inhibitor selumetinib.	AZD 6244	181-192	neurofibromin 1	Homo sapiens	134-137
32601387-6	2020	We used dual-energy X-ray absorptiometry (DXA) to assess tumor-associated changes in bone mineral density (BMD) in an individual with NF1 following treatment with the MEK inhibitor selumetinib.	AZD 6244	181-192	mitogen-activated protein kinase kinase 7	Homo sapiens	167-170
32888253-3	2020	The present study aimed to use proteomic methods to probe into the role of the EGF-EGFR-angiogenesis axis in the tumorigenesis of glioma and access the therapeutic efficacy of selumetinib on glioma.	AZD 6244	176-187	epidermal growth factor receptor	Mus musculus	83-87
32888253-12	2020	Selumetinib treatment showed tumor reduction effect in EGFR-positive glioblastoma xenograft mouse model.	AZD 6244	0-11	epidermal growth factor receptor	Mus musculus	55-59
32888253-14	2020	Selumetinib could target the EGFR pathway and possibly improve the prognosis of EGFR-positive glioma.	AZD 6244	0-11	epidermal growth factor receptor	Mus musculus	29-33
32888253-14	2020	Selumetinib could target the EGFR pathway and possibly improve the prognosis of EGFR-positive glioma.	AZD 6244	0-11	epidermal growth factor receptor	Mus musculus	80-84
32644232-1	2020	A 12-year-old girl with neurofibromatosis type 1 and a large facial plexiform neurofibroma had been participating in a selumetinib clinical trial for the past 5 years.	AZD 6244	119-130	neurofibromin 1	Homo sapiens	24-48
32272491-8	2020	The use of MEK inhibitors is likely to increase substantially with the expected upcoming approval of selumetinib for a specific indication for treatment of plexiform neurofibromas in NF1.	AZD 6244	101-112	mitogen-activated protein kinase kinase 7	Homo sapiens	11-14
32336014-4	2020	Here, we report that the RAF dimer inhibitors, lifirafenib (BGB-283) and Compound C, show a strong synergistic effect with MEK inhibitors (MEKi), including mirdametinib (PD-0325901) and selumetinib, in suppressing the proliferation of K-RAS-mutated non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) cell lines.	AZD 6244	186-197	zinc fingers and homeoboxes 2	Homo sapiens	25-28
32336014-4	2020	Here, we report that the RAF dimer inhibitors, lifirafenib (BGB-283) and Compound C, show a strong synergistic effect with MEK inhibitors (MEKi), including mirdametinib (PD-0325901) and selumetinib, in suppressing the proliferation of K-RAS-mutated non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) cell lines.	AZD 6244	186-197	mitogen-activated protein kinase kinase 7	Homo sapiens	123-126
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	epidermal growth factor receptor	Homo sapiens	34-38
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	mitogen-activated protein kinase kinase 1	Homo sapiens	62-73
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	CD274 molecule	Homo sapiens	128-133
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	CD274 molecule	Homo sapiens	143-148
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	epidermal growth factor	Homo sapiens	34-37
33099927-6	2020	Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-gamma.	AZD 6244	85-96	interferon gamma	Homo sapiens	191-200
32540097-7	2020	We demonstrate that the expression of point mutation of lamin A in muscle cells increases cellular stiffness compared with cells expressing wild type lamin A and that the chemical agent selumetinib, an inhibitor of the ERK1/2 signaling, reversed the mechanical alterations in mutated cells.	AZD 6244	186-197	lamin A/C	Homo sapiens	56-63
32540097-7	2020	We demonstrate that the expression of point mutation of lamin A in muscle cells increases cellular stiffness compared with cells expressing wild type lamin A and that the chemical agent selumetinib, an inhibitor of the ERK1/2 signaling, reversed the mechanical alterations in mutated cells.	AZD 6244	186-197	lamin A/C	Homo sapiens	150-157
32540097-7	2020	We demonstrate that the expression of point mutation of lamin A in muscle cells increases cellular stiffness compared with cells expressing wild type lamin A and that the chemical agent selumetinib, an inhibitor of the ERK1/2 signaling, reversed the mechanical alterations in mutated cells.	AZD 6244	186-197	mitogen-activated protein kinase 3	Homo sapiens	219-225
32939452-0	2020	The MEK inhibitor selumetinib reduces spinal neurofibroma burden in patients with NF1 and plexiform neurofibromas.	AZD 6244	18-29	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
32939452-0	2020	The MEK inhibitor selumetinib reduces spinal neurofibroma burden in patients with NF1 and plexiform neurofibromas.	AZD 6244	18-29	neurofibromin 1	Homo sapiens	82-85
32939452-2	2020	The MEK inhibitor selumetinib shrinks the majority of plexiform neurofibromas (PNs) in patients with NF1.	AZD 6244	18-29	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
32939452-2	2020	The MEK inhibitor selumetinib shrinks the majority of plexiform neurofibromas (PNs) in patients with NF1.	AZD 6244	18-29	neurofibromin 1	Homo sapiens	101-104
32793908-4	2020	We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells.	AZD 6244	54-65	mitogen-activated protein kinase kinase 7	Homo sapiens	8-11
32793908-4	2020	We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells.	AZD 6244	54-65	angiotensin converting enzyme 2	Homo sapiens	73-77
32533336-3	2020	Selumetinib, an inhibitor of mitogen-activated protein kinase (MEK) 1 and 2, was reported to induce a clinical response in pediatric subjects with inoperable PN.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	29-75
32585592-3	2020	Here, we develop a new MEK inhibitor designated as KZ-02 that exhibits unexpectedly higher cytotoxicity than its starting compound AZD6244, a well-known MEK inhibitor, in colorectal cancer (CRC).	AZD 6244	131-138	mitogen-activated protein kinase kinase 7	Homo sapiens	23-26
32585592-3	2020	Here, we develop a new MEK inhibitor designated as KZ-02 that exhibits unexpectedly higher cytotoxicity than its starting compound AZD6244, a well-known MEK inhibitor, in colorectal cancer (CRC).	AZD 6244	131-138	mitogen-activated protein kinase kinase 7	Homo sapiens	153-156
32585592-6	2020	Mechanistic study revealed that MEK inhibition by AZD6244 leads to increased Pim-1 expression, which could be a general mechanism behind the compromised cell-killing activity of MEK inhibitors.	AZD 6244	50-57	mitogen-activated protein kinase kinase 7	Homo sapiens	32-35
32585592-6	2020	Mechanistic study revealed that MEK inhibition by AZD6244 leads to increased Pim-1 expression, which could be a general mechanism behind the compromised cell-killing activity of MEK inhibitors.	AZD 6244	50-57	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	77-82
32585592-6	2020	Mechanistic study revealed that MEK inhibition by AZD6244 leads to increased Pim-1 expression, which could be a general mechanism behind the compromised cell-killing activity of MEK inhibitors.	AZD 6244	50-57	mitogen-activated protein kinase kinase 7	Homo sapiens	178-181
32754596-3	2020	Based on the notion that HDAC inhibitors may reactivate the expression of genes favoring cell response to drugs, the aim of this study was to investigate the interaction between the HDAC6-specific inhibitor ricolinostat (ACY1215) and the MEK-inhibitor selumetinib (AZD6244) to identify effective combinations in prostate cancer models.	AZD 6244	252-263	histone deacetylase 6	Homo sapiens	182-187
32754596-3	2020	Based on the notion that HDAC inhibitors may reactivate the expression of genes favoring cell response to drugs, the aim of this study was to investigate the interaction between the HDAC6-specific inhibitor ricolinostat (ACY1215) and the MEK-inhibitor selumetinib (AZD6244) to identify effective combinations in prostate cancer models.	AZD 6244	252-263	mitogen-activated protein kinase kinase 7	Homo sapiens	238-241
32754596-3	2020	Based on the notion that HDAC inhibitors may reactivate the expression of genes favoring cell response to drugs, the aim of this study was to investigate the interaction between the HDAC6-specific inhibitor ricolinostat (ACY1215) and the MEK-inhibitor selumetinib (AZD6244) to identify effective combinations in prostate cancer models.	AZD 6244	265-272	histone deacetylase 6	Homo sapiens	182-187
32754596-3	2020	Based on the notion that HDAC inhibitors may reactivate the expression of genes favoring cell response to drugs, the aim of this study was to investigate the interaction between the HDAC6-specific inhibitor ricolinostat (ACY1215) and the MEK-inhibitor selumetinib (AZD6244) to identify effective combinations in prostate cancer models.	AZD 6244	265-272	mitogen-activated protein kinase kinase 7	Homo sapiens	238-241
32754596-6	2020	RNAi-mediated knockdown of HDAC6 in selumetinib-treated 22Rv1 cells resulted in increased apoptosis.	AZD 6244	36-47	histone deacetylase 6	Homo sapiens	27-32
32284325-2	2020	We have previously demonstrated that combination of the ALK inhibitor crizotinib with the MEK inhibitor selumetinib was highly effective at reducing cell viability of ALK-positive non-small-cell lung cancer (H3122) cells.	AZD 6244	104-115	mitogen-activated protein kinase kinase 7	Homo sapiens	90-93
32284325-2	2020	We have previously demonstrated that combination of the ALK inhibitor crizotinib with the MEK inhibitor selumetinib was highly effective at reducing cell viability of ALK-positive non-small-cell lung cancer (H3122) cells.	AZD 6244	104-115	ALK receptor tyrosine kinase	Homo sapiens	167-170
32629964-6	2020	We then used primary cells to assess the therapeutic potential of MLN3651, a neddylation inhibitor which impacts the activity of the CRL family of E3 ubiquitin ligases and the MAPK/ERK kinase (MEK1/2) inhibitor selumetinib.	AZD 6244	211-222	mitogen-activated protein kinase kinase 1	Homo sapiens	193-199
32629964-8	2020	The combination of MLN3651 and the MEK1/2 inhibitor selumetinib prevented the increase in Raf/MEK/ERK activity, and had an additive effect compared with either treatment alone.	AZD 6244	52-63	mitogen-activated protein kinase kinase 1	Homo sapiens	35-41
32629964-8	2020	The combination of MLN3651 and the MEK1/2 inhibitor selumetinib prevented the increase in Raf/MEK/ERK activity, and had an additive effect compared with either treatment alone.	AZD 6244	52-63	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
32629964-8	2020	The combination of MLN3651 and the MEK1/2 inhibitor selumetinib prevented the increase in Raf/MEK/ERK activity, and had an additive effect compared with either treatment alone.	AZD 6244	52-63	mitogen-activated protein kinase 1	Homo sapiens	98-101
32272491-8	2020	The use of MEK inhibitors is likely to increase substantially with the expected upcoming approval of selumetinib for a specific indication for treatment of plexiform neurofibromas in NF1.	AZD 6244	101-112	neurofibromin 1	Homo sapiens	183-186
32187457-13	2020	CONCLUSIONS: In this phase 2 trial, most children with neurofibromatosis type 1 and inoperable plexiform neurofibromas had durable tumor shrinkage and clinical benefit from selumetinib.	AZD 6244	173-184	neurofibromin 1	Homo sapiens	55-79
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	34-45	mitogen-activated protein kinase kinase 1	Homo sapiens	94-100
32504375-2	2020	Selumetinib has been granted orphan drug status as adjuvant treatment for thyroid cancer (in the USA) and as treatment for neurofibromatosis type 1 (in the USA and the EU) and, based on the results of the phase II SPRINT trial, was recently approved in the USA in paediatric patients with neurofibromatosis type 1 and symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	123-147
32504375-2	2020	Selumetinib has been granted orphan drug status as adjuvant treatment for thyroid cancer (in the USA) and as treatment for neurofibromatosis type 1 (in the USA and the EU) and, based on the results of the phase II SPRINT trial, was recently approved in the USA in paediatric patients with neurofibromatosis type 1 and symptomatic, inoperable plexiform neurofibromas.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	289-313
32504375-3	2020	This article summarizes the milestones in the development of selumetinib leading to this first approval for the treatment of paediatric patients aged >= 2 years with neurofibromatosis type 1 who have symptomatic, inoperable plexiform neurofibromas.	AZD 6244	61-72	neurofibromin 1	Homo sapiens	166-190
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	52-92
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	94-100
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	25-32	mitogen-activated protein kinase 1	Homo sapiens	52-92
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	25-32	mitogen-activated protein kinase kinase 1	Homo sapiens	94-100
32504375-1	2020	Selumetinib (KOSELUGOTM; AZD6244, ARRY-142886) is a mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor being developed by AstraZeneca for the treatment of tumours associated with neurofibromatosis and various cancers.	AZD 6244	34-45	mitogen-activated protein kinase 1	Homo sapiens	52-92
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	54-65	midkine	Mus musculus	26-29
31913576-5	2020	Through the conduct of a longitudinal cohort study and early phase clinical trials, the MEK inhibitor selumetinib was identified as the first active therapy for the NF1-related peripheral nerve sheath tumors called plexiform neurofibromas (PNs).	AZD 6244	102-113	mitogen-activated protein kinase kinase 7	Homo sapiens	88-91
31913576-5	2020	Through the conduct of a longitudinal cohort study and early phase clinical trials, the MEK inhibitor selumetinib was identified as the first active therapy for the NF1-related peripheral nerve sheath tumors called plexiform neurofibromas (PNs).	AZD 6244	102-113	neurofibromin 1	Homo sapiens	165-168
32108293-0	2020	Selumetinib for plexiform neurofibromas in neurofibromatosis type 1: a single-institution experience.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	43-67
32108293-4	2020	Selumetinib (AZD6244/ARRY-142886) is a mitogen-activated protein kinase enzyme (MEK1/2) inhibitor and works by targeting the MAPK pathway.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	80-86
32108293-4	2020	Selumetinib (AZD6244/ARRY-142886) is a mitogen-activated protein kinase enzyme (MEK1/2) inhibitor and works by targeting the MAPK pathway.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	80-86
32108293-4	2020	Selumetinib (AZD6244/ARRY-142886) is a mitogen-activated protein kinase enzyme (MEK1/2) inhibitor and works by targeting the MAPK pathway.	AZD 6244	21-32	mitogen-activated protein kinase kinase 1	Homo sapiens	80-86
32108293-6	2020	Herein, we describe a single institutional experience with selumetinib for inoperable PN in NF-1.	AZD 6244	59-70	neurofibromin 1	Homo sapiens	92-96
32108293-7	2020	METHODS: Case series study of demographics, clinical, baseline characteristics, treatment effect, and follow-up of consecutive genetically confirmed NF1 patients with inoperable PN associated with significant or potential significant morbidity treated with selumetinib (April 2018 to April 2019).	AZD 6244	257-268	neurofibromin 1	Homo sapiens	149-152
31942645-6	2020	In this study, we demonstrate that the MEK/ERK inhibitor AZD6244 has potent antiviral efficacy in vitro against DENV-2, DENV-3, and Saint Louis encephalitis virus (SLEV).	AZD 6244	57-64	mitogen-activated protein kinase kinase 7	Homo sapiens	39-42
31942645-6	2020	In this study, we demonstrate that the MEK/ERK inhibitor AZD6244 has potent antiviral efficacy in vitro against DENV-2, DENV-3, and Saint Louis encephalitis virus (SLEV).	AZD 6244	57-64	mitogen-activated protein kinase 1	Homo sapiens	43-46
31942645-13	2020	There was also an increase in IL-1beta and TNF-alpha levels in mice that were infected with D2S20 and treated with AZD6244 in comparison to infected mice that were treated with the vehicle only.	AZD 6244	115-122	interleukin 1 alpha	Mus musculus	30-38
31942645-13	2020	There was also an increase in IL-1beta and TNF-alpha levels in mice that were infected with D2S20 and treated with AZD6244 in comparison to infected mice that were treated with the vehicle only.	AZD 6244	115-122	tumor necrosis factor	Mus musculus	43-52
32181767-9	2020	Finally, in non-V600 BRAF mutant cell lines combined inhibition of pan-RAF and MEK with sorafenib/AZ628 and selumetinib showed significantly stronger cell growth, cell migration and Erk activation inhibition and also increased apoptosis induction compared to single treatments.	AZD 6244	108-119	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
32181767-9	2020	Finally, in non-V600 BRAF mutant cell lines combined inhibition of pan-RAF and MEK with sorafenib/AZ628 and selumetinib showed significantly stronger cell growth, cell migration and Erk activation inhibition and also increased apoptosis induction compared to single treatments.	AZD 6244	108-119	zinc fingers and homeoboxes 2	Homo sapiens	22-25
32181767-9	2020	Finally, in non-V600 BRAF mutant cell lines combined inhibition of pan-RAF and MEK with sorafenib/AZ628 and selumetinib showed significantly stronger cell growth, cell migration and Erk activation inhibition and also increased apoptosis induction compared to single treatments.	AZD 6244	108-119	mitogen-activated protein kinase kinase 7	Homo sapiens	79-82
32181767-9	2020	Finally, in non-V600 BRAF mutant cell lines combined inhibition of pan-RAF and MEK with sorafenib/AZ628 and selumetinib showed significantly stronger cell growth, cell migration and Erk activation inhibition and also increased apoptosis induction compared to single treatments.	AZD 6244	108-119	mitogen-activated protein kinase 1	Homo sapiens	182-185
32102484-6	2020	Additional targeting of the RAS/RAF/MEK/MAPK pathway with the allosteric MEK1/2 inhibitor AZD6244 showed synergistic effects on the viability of MPNST cell lines in vitro in comparison to the dual AKT/mTOR inhibition.	AZD 6244	90-97	zinc fingers and homeoboxes 2	Mus musculus	32-35
32102484-6	2020	Additional targeting of the RAS/RAF/MEK/MAPK pathway with the allosteric MEK1/2 inhibitor AZD6244 showed synergistic effects on the viability of MPNST cell lines in vitro in comparison to the dual AKT/mTOR inhibition.	AZD 6244	90-97	midkine	Mus musculus	36-39
32102484-6	2020	Additional targeting of the RAS/RAF/MEK/MAPK pathway with the allosteric MEK1/2 inhibitor AZD6244 showed synergistic effects on the viability of MPNST cell lines in vitro in comparison to the dual AKT/mTOR inhibition.	AZD 6244	90-97	mitogen-activated protein kinase kinase 1	Mus musculus	73-79
32102484-6	2020	Additional targeting of the RAS/RAF/MEK/MAPK pathway with the allosteric MEK1/2 inhibitor AZD6244 showed synergistic effects on the viability of MPNST cell lines in vitro in comparison to the dual AKT/mTOR inhibition.	AZD 6244	90-97	mechanistic target of rapamycin kinase	Mus musculus	201-205
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	54-65	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	34-42
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	54-65	phosphatase and tensin homolog	Mus musculus	177-181
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	54-65	transformation related protein 53	Mus musculus	182-187
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	67-74	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	34-42
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	67-74	phosphatase and tensin homolog	Mus musculus	177-181
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	67-74	transformation related protein 53	Mus musculus	182-187
31911549-7	2020	Therapeutic inhibition of MEK and p110beta/PI3K using Selumetinib (AZD6244, ARRY-142886) and AZD8186, two drugs that are currently in clinical trials, increased the survival of Pten;Trp53-null mice without major toxicity.	AZD 6244	76-87	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	34-42
31839677-6	2020	RESULTS: In melanomas of patients on the selumetinib but not the placebo arm, two gene signature components, dual-specificity protein phosphatase 4 (DUSP4) and ETS translocation variant 4 (ETV4), were expressed more highly in responders than non-responders.	AZD 6244	41-52	dual specificity phosphatase 4	Homo sapiens	109-147
31785810-4	2020	In this study, we found that phosphorylation of DNA-PKcs, which is the key factor of non-homologous end joining (NHEJ) pathway, was remarkably overexpressed in ionizing radiation (IR)- and Selumetinib resistant UM cells.	AZD 6244	189-200	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	48-56
31785810-6	2020	Inhibition of DNA-PKcs by NU7441 significantly impaired DNA repair and re-sensitized resistant UM cells to radiation and Selumetinib both in vitro and in vivo.	AZD 6244	121-132	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	14-22
31839677-6	2020	RESULTS: In melanomas of patients on the selumetinib but not the placebo arm, two gene signature components, dual-specificity protein phosphatase 4 (DUSP4) and ETS translocation variant 4 (ETV4), were expressed more highly in responders than non-responders.	AZD 6244	41-52	dual specificity phosphatase 4	Homo sapiens	149-154
31839677-6	2020	RESULTS: In melanomas of patients on the selumetinib but not the placebo arm, two gene signature components, dual-specificity protein phosphatase 4 (DUSP4) and ETS translocation variant 4 (ETV4), were expressed more highly in responders than non-responders.	AZD 6244	41-52	ETS variant transcription factor 4	Homo sapiens	189-193
31839677-8	2020	In contrast, DUSP4-depleted cells showed enhanced cell survival and increased resistance to both selumetinib and trametinib.	AZD 6244	97-108	dual specificity phosphatase 4	Homo sapiens	13-18
31839677-9	2020	CONCLUSIONS: ETV4 and DUSP4 associated with clinical response to docetaxel plus selumetinib.	AZD 6244	80-91	ETS variant transcription factor 4	Homo sapiens	13-17
31839677-9	2020	CONCLUSIONS: ETV4 and DUSP4 associated with clinical response to docetaxel plus selumetinib.	AZD 6244	80-91	dual specificity phosphatase 4	Homo sapiens	22-27
31786775-3	2020	In the present study, the effect of AZD6244 (an ATP non-competitive MEK1/2 inhibitor) on acrolein-induced neuroinflammation was investigated using BV-2 cells and primary cultured microglia.	AZD 6244	36-43	mitogen-activated protein kinase kinase 1	Mus musculus	68-74
31786775-6	2020	Furthermore, Western blot assay showed increases in phosphorylated ERK in BV-2 cells subjected to LPS (1 mug/mL) or acrolein (30 muM); these increases were blocked by AZD6244 (10 muM).	AZD 6244	167-174	mitogen-activated protein kinase 1	Mus musculus	67-70
31786775-7	2020	At the same time, AZD6244 attenuated LPS-induced TNF-alpha (a pro-inflammatory cytokine) and cyclooxygenase-II (COX II, a pro-inflammatory enzyme).	AZD 6244	18-25	tumor necrosis factor	Mus musculus	49-58
31786775-9	2020	In addition, AZD6244 inhibited acrolein-induced increases in activated caspase 1 (a biomarker of inflammasome activation) and heme oxygenase-1 (a redox-regulated chaperone protein) in BV-2 cells.	AZD 6244	13-20	caspase 1	Mus musculus	71-80
31786775-9	2020	In addition, AZD6244 inhibited acrolein-induced increases in activated caspase 1 (a biomarker of inflammasome activation) and heme oxygenase-1 (a redox-regulated chaperone protein) in BV-2 cells.	AZD 6244	13-20	heme oxygenase 1	Mus musculus	126-142
31285371-6	2019	Moreover, a novel TGFbeta1/ERK/PHD2-mediated pathway regulating HIF1alpha stability in PROC was discovered.Results: YC-1 and selumetinib resensitized PROC cells to cisplatin.	AZD 6244	125-136	latent transforming growth factor beta binding protein 1	Homo sapiens	18-26
31452046-8	2019	The combination of simvastatin and MEK inhibitor AZD6244 synergistically reduced THP1 cell proliferation compared to simvastatin alone and AZD6244 alone (IC50 values: 0.88 uM in simvastatin, 0.32 uM in AZD6244, and 0.23 uM in combination of simvastatin and AZD6244).	AZD 6244	49-56	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
31452046-8	2019	The combination of simvastatin and MEK inhibitor AZD6244 synergistically reduced THP1 cell proliferation compared to simvastatin alone and AZD6244 alone (IC50 values: 0.88 uM in simvastatin, 0.32 uM in AZD6244, and 0.23 uM in combination of simvastatin and AZD6244).	AZD 6244	49-56	GLI family zinc finger 2	Homo sapiens	81-85
31452046-8	2019	The combination of simvastatin and MEK inhibitor AZD6244 synergistically reduced THP1 cell proliferation compared to simvastatin alone and AZD6244 alone (IC50 values: 0.88 uM in simvastatin, 0.32 uM in AZD6244, and 0.23 uM in combination of simvastatin and AZD6244).	AZD 6244	139-146	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
31452046-8	2019	The combination of simvastatin and MEK inhibitor AZD6244 synergistically reduced THP1 cell proliferation compared to simvastatin alone and AZD6244 alone (IC50 values: 0.88 uM in simvastatin, 0.32 uM in AZD6244, and 0.23 uM in combination of simvastatin and AZD6244).	AZD 6244	139-146	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
31452046-8	2019	The combination of simvastatin and MEK inhibitor AZD6244 synergistically reduced THP1 cell proliferation compared to simvastatin alone and AZD6244 alone (IC50 values: 0.88 uM in simvastatin, 0.32 uM in AZD6244, and 0.23 uM in combination of simvastatin and AZD6244).	AZD 6244	139-146	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
31602313-5	2019	A systematic analysis of preclinical data for a failed phase III trial of selumetinib combined with docetaxel in lung cancer suggests potential indications in pancreatic and colorectal cancers with KRAS mutation.	AZD 6244	74-85	KRAS proto-oncogene, GTPase	Homo sapiens	198-202
31827192-4	2019	In this study the combined effect of crizotinib and the MEK inhibitor selumetinib was investigated in both crizotinib naive (H3122) and crizotinib resistant (CR-H3122) ALK-positive lung cancer cells.	AZD 6244	70-81	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
31827192-4	2019	In this study the combined effect of crizotinib and the MEK inhibitor selumetinib was investigated in both crizotinib naive (H3122) and crizotinib resistant (CR-H3122) ALK-positive lung cancer cells.	AZD 6244	70-81	ALK receptor tyrosine kinase	Homo sapiens	168-171
31804471-4	2019	We also examined functional roles for Kras activation in dysplasia progression using Selumetinib, a MEK inhibitor, which is a downstream mediator of Kras signaling.	AZD 6244	85-96	midkine	Mus musculus	100-103
31804471-4	2019	We also examined functional roles for Kras activation in dysplasia progression using Selumetinib, a MEK inhibitor, which is a downstream mediator of Kras signaling.	AZD 6244	85-96	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	149-153
31645898-3	2019	To identify possible causes of resistance to MEK inhibition, we generated a model of resistance by long-term treatment of AML cells with AZD6244 (selumetinib).	AZD 6244	137-144	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
31649535-3	2019	MK2206 or AZD6244, representative Akt and Erk1/2 inhibitors, respectively, profoundly sensitized bladder cancer cells to THP treatment.	AZD 6244	10-17	mitogen-activated protein kinase 3	Homo sapiens	42-48
31285371-6	2019	Moreover, a novel TGFbeta1/ERK/PHD2-mediated pathway regulating HIF1alpha stability in PROC was discovered.Results: YC-1 and selumetinib resensitized PROC cells to cisplatin.	AZD 6244	125-136	mitogen-activated protein kinase 1	Homo sapiens	27-30
31285371-6	2019	Moreover, a novel TGFbeta1/ERK/PHD2-mediated pathway regulating HIF1alpha stability in PROC was discovered.Results: YC-1 and selumetinib resensitized PROC cells to cisplatin.	AZD 6244	125-136	egl-9 family hypoxia inducible factor 1	Homo sapiens	31-35
31285371-6	2019	Moreover, a novel TGFbeta1/ERK/PHD2-mediated pathway regulating HIF1alpha stability in PROC was discovered.Results: YC-1 and selumetinib resensitized PROC cells to cisplatin.	AZD 6244	125-136	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-73
31285371-10	2019	Inhibition of TGFbeta1 by SB431542, ERK by selumetinib, or HIF1alpha by YC-1 efficiently overcame platinum resistance both in vitro and in vivo The results from clinical samples confirm activation of the ERK/PHD2/HIF1alpha axis in patients with PROC, correlating highly with poor prognoses for patients.Conclusions: HIF1alpha stabilization is regulated by TGFbeta1/ERK/PHD2 axis in PROC.	AZD 6244	43-54	latent transforming growth factor beta binding protein 1	Homo sapiens	14-22
31285371-10	2019	Inhibition of TGFbeta1 by SB431542, ERK by selumetinib, or HIF1alpha by YC-1 efficiently overcame platinum resistance both in vitro and in vivo The results from clinical samples confirm activation of the ERK/PHD2/HIF1alpha axis in patients with PROC, correlating highly with poor prognoses for patients.Conclusions: HIF1alpha stabilization is regulated by TGFbeta1/ERK/PHD2 axis in PROC.	AZD 6244	43-54	mitogen-activated protein kinase 1	Homo sapiens	36-39
30846494-5	2019	Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines.	AZD 6244	28-35	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
30846494-5	2019	Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines.	AZD 6244	28-35	zinc fingers and homeoboxes 2	Homo sapiens	137-140
30846494-5	2019	Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines.	AZD 6244	37-48	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
30846494-5	2019	Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines.	AZD 6244	37-48	zinc fingers and homeoboxes 2	Homo sapiens	137-140
30846494-9	2019	The AZD6244/LBH589 combination was specifically active in cell lines with more BIM:MCL-1 complexes at baseline; resistant cell lines had more BIM:BCL-2 complexes.	AZD 6244	4-11	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	83-88
30846494-9	2019	The AZD6244/LBH589 combination was specifically active in cell lines with more BIM:MCL-1 complexes at baseline; resistant cell lines had more BIM:BCL-2 complexes.	AZD 6244	4-11	BCL2 apoptosis regulator	Homo sapiens	146-151
31201369-10	2019	Based on the HPC3 cell model, we found that the DSTYK mutation promoted cell migration and invasion of HPC3 cells via activation of ERK1/2 signaling, which was inhibited by the MEK/ERK inhibitor AZD6244.	AZD 6244	195-202	dual serine/threonine and tyrosine protein kinase	Homo sapiens	48-53
31201369-10	2019	Based on the HPC3 cell model, we found that the DSTYK mutation promoted cell migration and invasion of HPC3 cells via activation of ERK1/2 signaling, which was inhibited by the MEK/ERK inhibitor AZD6244.	AZD 6244	195-202	mitogen-activated protein kinase 3	Homo sapiens	132-138
31201369-10	2019	Based on the HPC3 cell model, we found that the DSTYK mutation promoted cell migration and invasion of HPC3 cells via activation of ERK1/2 signaling, which was inhibited by the MEK/ERK inhibitor AZD6244.	AZD 6244	195-202	mitogen-activated protein kinase kinase 7	Homo sapiens	177-180
31201369-10	2019	Based on the HPC3 cell model, we found that the DSTYK mutation promoted cell migration and invasion of HPC3 cells via activation of ERK1/2 signaling, which was inhibited by the MEK/ERK inhibitor AZD6244.	AZD 6244	195-202	mitogen-activated protein kinase 1	Homo sapiens	132-135
31201369-11	2019	The DSTYK mutation was also shown to upregulate the expression of two metastasis-related molecules: MMP2 and MMP9 in HPC3 cells; however, this effect was attenuated by AZD6244 treatment.	AZD 6244	168-175	dual serine/threonine and tyrosine protein kinase	Homo sapiens	4-9
31201369-11	2019	The DSTYK mutation was also shown to upregulate the expression of two metastasis-related molecules: MMP2 and MMP9 in HPC3 cells; however, this effect was attenuated by AZD6244 treatment.	AZD 6244	168-175	matrix metallopeptidase 2	Homo sapiens	100-104
31201369-11	2019	The DSTYK mutation was also shown to upregulate the expression of two metastasis-related molecules: MMP2 and MMP9 in HPC3 cells; however, this effect was attenuated by AZD6244 treatment.	AZD 6244	168-175	matrix metallopeptidase 9	Homo sapiens	109-113
30655370-0	2019	Glucocorticoids and selumetinib are highly synergistic in RAS pathway-mutated childhood acute lymphoblastic leukemia through upregulation of BIM.	AZD 6244	20-31	BCL2-like 11 (apoptosis facilitator)	Mus musculus	141-144
31141829-4	2019	Recently, a clinical phase I study reported significant shrinkage of plexiform neurofibromas following treatment with the MEK inhibitor selumetinib.	AZD 6244	136-147	mitogen-activated protein kinase kinase 7	Homo sapiens	122-125
31502118-9	2019	Treatment with selumetinib and trametinib, but not dabrafenib, restored the sensitivity to osimertinib and enhanced cell death in the resistant clones with the BRAF G469A mutation.	AZD 6244	15-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	160-164
30655370-1	2019	New drugs are needed for the treatment of relapsed acute lymphoblastic leukemia and preclinical evaluation of the MEK inhibitor, selumetinib, has shown that this drug has excellent activity in those leukemias with RAS pathway mutations.	AZD 6244	129-140	midkine	Mus musculus	114-117
30655370-2	2019	The proapoptotic protein, BIM is pivotal in the induction of cell death by both selumetinib and glucocorticoids, suggesting the potential for synergy.	AZD 6244	80-91	BCL2-like 11 (apoptosis facilitator)	Mus musculus	26-29
31399133-4	2019	Treatment of these cells with the small-molecule MEK inhibitor AZD6244 induces hyperpigmentation, widespread gene expression changes including alteration of genes linked to pigmentation, and extensive epigenomic reprogramming of transcriptionally distinct regulatory regions associated with the active chromatin mark H3K27ac.	AZD 6244	63-70	mitogen-activated protein kinase kinase 7	Homo sapiens	49-52
31461811-11	2019	After treatment with AZD6244 (5, 10 mumol/L), the level of p-ERK1/2 in OVCAR5 and OVCAR8 decreased significantly in dose-dependent manner.	AZD 6244	21-28	mitogen-activated protein kinase 3	Homo sapiens	61-67
31461811-16	2019	AZD6244 could down-regulated the expression of p-ERK1/2 in ovarian cancer cells, accompanied by the decreased proliferation and increased cell apoptosis of ovarian cancer cells.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	49-55
31409052-7	2019	Consistent with this finding, selumetinib, a MEK1/2 inhibitor, suppressed oncogenic activity of CRC cells, and this effect is more profound in combination with cetuximab.	AZD 6244	30-41	mitogen-activated protein kinase kinase 1	Homo sapiens	45-51
30972766-8	2019	Inhibition of the MAPK pathway, using EGFR inhibitors cetuximab and erlotinib or the MEK 1 and 2 inhibitor selumetinib, prevented EGF- and IFNgamma-induced CD274 mRNA and PD-L1 protein and membrane upregulation, but had no effect on IFNgamma-induced MHC-I upregulation.	AZD 6244	107-118	mitogen-activated protein kinase kinase 1	Homo sapiens	85-96
30972766-8	2019	Inhibition of the MAPK pathway, using EGFR inhibitors cetuximab and erlotinib or the MEK 1 and 2 inhibitor selumetinib, prevented EGF- and IFNgamma-induced CD274 mRNA and PD-L1 protein and membrane upregulation, but had no effect on IFNgamma-induced MHC-I upregulation.	AZD 6244	107-118	interferon gamma	Homo sapiens	139-147
30972766-8	2019	Inhibition of the MAPK pathway, using EGFR inhibitors cetuximab and erlotinib or the MEK 1 and 2 inhibitor selumetinib, prevented EGF- and IFNgamma-induced CD274 mRNA and PD-L1 protein and membrane upregulation, but had no effect on IFNgamma-induced MHC-I upregulation.	AZD 6244	107-118	CD274 molecule	Homo sapiens	156-161
31399133-5	2019	Regulatory regions with differentially acetylated H3K27ac regions following AZD6244 treatment are enriched in transcription factor binding motifs of ETV/ETS and ATF family members as well as the lineage-determining factors MITF and SOX10.	AZD 6244	76-83	melanocyte inducing transcription factor	Homo sapiens	223-227
31399133-5	2019	Regulatory regions with differentially acetylated H3K27ac regions following AZD6244 treatment are enriched in transcription factor binding motifs of ETV/ETS and ATF family members as well as the lineage-determining factors MITF and SOX10.	AZD 6244	76-83	SRY-box transcription factor 10	Homo sapiens	232-237
30628057-3	2019	Our efforts were focused on enhancing the activity of the known MEK inhibitor AZD6244 and overcoming the shortcomings existing in current MEK inhibitors.	AZD 6244	78-85	mitogen-activated protein kinase kinase 7	Homo sapiens	64-67
31135266-3	2019	We further demonstrated that the HER2 TKIs in combination with MEK inhibitor, AZD6244, or PI3K inhibitor, GDC0941, yield robust killing in HER2-L755S cancer cells, indicating a novel targeted strategy to overcome HER2-L755S resistance to anti-HER2 treatment.	AZD 6244	78-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	33-37
31135266-3	2019	We further demonstrated that the HER2 TKIs in combination with MEK inhibitor, AZD6244, or PI3K inhibitor, GDC0941, yield robust killing in HER2-L755S cancer cells, indicating a novel targeted strategy to overcome HER2-L755S resistance to anti-HER2 treatment.	AZD 6244	78-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-143
31135266-3	2019	We further demonstrated that the HER2 TKIs in combination with MEK inhibitor, AZD6244, or PI3K inhibitor, GDC0941, yield robust killing in HER2-L755S cancer cells, indicating a novel targeted strategy to overcome HER2-L755S resistance to anti-HER2 treatment.	AZD 6244	78-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-143
31135266-3	2019	We further demonstrated that the HER2 TKIs in combination with MEK inhibitor, AZD6244, or PI3K inhibitor, GDC0941, yield robust killing in HER2-L755S cancer cells, indicating a novel targeted strategy to overcome HER2-L755S resistance to anti-HER2 treatment.	AZD 6244	78-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-143
31151904-0	2019	Selumetinib in paediatric patients with BRAF-aberrant or neurofibromatosis type 1-associated recurrent, refractory, or progressive low-grade glioma: a multicentre, phase 2 trial.	AZD 6244	0-11	neurofibromin 1	Homo sapiens	57-81
31200828-0	2019	Selumetinib in patients receiving standard pemetrexed and platinum-based chemotherapy for advanced or metastatic KRAS wildtype or unknown non-squamous non-small cell lung cancer: A randomized, multicenter, phase II study.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	113-117
31151904-4	2019	We aimed to assess the activity of selumetinib, a MEK1/2 inhibitor, in these patients.	AZD 6244	35-46	mitogen-activated protein kinase kinase 1	Homo sapiens	50-56
31200828-3	2019	Selumetinib (AZD6244, ARRY142886), a MEK1/2 inhibitor combined with chemotherapy in patients with NSCLC was evaluated in two schedules to evaluate efficacy and toxicity.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	37-43
31151904-22	2019	INTERPRETATION: Selumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma.	AZD 6244	16-27	neurofibromin 1	Homo sapiens	140-143
31151904-23	2019	These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children"s Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade glioma both with and without NF1.	AZD 6244	24-35	neurofibromin 1	Homo sapiens	338-341
30987362-7	2019	Integrating all the results, we highlighted 4 miRNAs (mmu-miR-215-5p, mmu-miR-204-5p, mmu-miR-708-3p and mmu-miR-1298-5p) as the key for AZD6244 treatment, mmu-miR-23a-3p as key for XL-147 treatment, and mmu-miR-125a-5p and mmu-miR-16-5p as key for Budesonide treatment.	AZD 6244	137-144	microRNA 7083	Mus musculus	86-100
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	13-24	mitogen-activated protein kinase kinase 1	Homo sapiens	73-79
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	13-24	mitogen-activated protein kinase 1	Homo sapiens	119-123
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	26-33	mitogen-activated protein kinase kinase 1	Homo sapiens	73-79
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	26-33	mitogen-activated protein kinase 1	Homo sapiens	119-123
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	35-46	mitogen-activated protein kinase kinase 1	Homo sapiens	73-79
30317534-1	2019	Introduction Selumetinib (AZD6244, ARRY-142886) is a potent inhibitor of MEK1/2, thereby inhibiting phosphorylation of ERK2.	AZD 6244	35-46	mitogen-activated protein kinase 1	Homo sapiens	119-123
31200667-0	2019	Investigating the potential clinical benefit of Selumetinib in resensitising advanced iodine refractory differentiated thyroid cancer to radioiodine therapy (SEL-I-METRY): protocol for a multicentre UK single arm phase II trial.	AZD 6244	48-59	selenoprotein I	Homo sapiens	158-163
31200667-10	2019	DISCUSSION: The SEL-I-METRY trial will investigate the effect of Selumetinib followed by I-131 therapy on progression-free survival in radioiodine refractory patients with differentiated thyroid cancer showing increased radioiodine uptake following initial treatment with Selumetinib.	AZD 6244	65-76	selenoprotein I	Homo sapiens	16-21
30995478-3	2019	Two MEKis, selumetinib and trametinib, induce T cell activation with increased CTLA-4 expression and, to a lesser extent, PD-1 expression on T cells in vivo after cyclical pulsatile MEKi treatment.	AZD 6244	11-22	cytotoxic T-lymphocyte protein 4	Sus scrofa	79-85
30969964-10	2019	Both were attenuated by the ERK1/2 signaling inhibitors, U0126 and AZD6244.	AZD 6244	67-74	mitogen-activated protein kinase 3	Homo sapiens	28-34
30579838-0	2019	Schedule-dependent synergistic effects of 5-fluorouracil and selumetinib in KRAS or BRAF mutant colon cancer models.	AZD 6244	61-72	KRAS proto-oncogene, GTPase	Homo sapiens	76-80
30706361-9	2019	JAK2/STAT3 inhibitor AG490 synergistically increases effects of AZD6244 on colon cancer in vitro and in vivo.	AZD 6244	64-71	Janus kinase 2	Homo sapiens	0-4
30706361-9	2019	JAK2/STAT3 inhibitor AG490 synergistically increases effects of AZD6244 on colon cancer in vitro and in vivo.	AZD 6244	64-71	signal transducer and activator of transcription 3	Homo sapiens	5-10
30771306-9	2019	Restored inhibition of MAPK signaling by selumetinib led to an increase in autophagic flux in vivo.	AZD 6244	41-52	mitogen-activated protein kinase 1	Homo sapiens	23-27
30706361-1	2019	The study aimed to investigate the reason of HCT116 cell resistance to MEK inhibitor, and the combination treatment effects of MEK inhibitor AZD6244 and JAK2/STAT3 inhibitor AG490 on colon cancer in vitro and in vivo, including cell viability, apoptosis, and explore the partial mechanisms focused on AZD6244 promoted the activation of JAK2-STAT3 pathways.	AZD 6244	141-148	mitogen-activated protein kinase kinase 7	Homo sapiens	127-130
30706361-1	2019	The study aimed to investigate the reason of HCT116 cell resistance to MEK inhibitor, and the combination treatment effects of MEK inhibitor AZD6244 and JAK2/STAT3 inhibitor AG490 on colon cancer in vitro and in vivo, including cell viability, apoptosis, and explore the partial mechanisms focused on AZD6244 promoted the activation of JAK2-STAT3 pathways.	AZD 6244	301-308	Janus kinase 2	Homo sapiens	153-157
30706361-5	2019	HCT116 cell resistance to MEK inhibitor AZD6244, which inhibited the activation of ERK and promoted the activation of JAK2-STAT3 signaling.	AZD 6244	40-47	mitogen-activated protein kinase kinase 7	Homo sapiens	26-29
30706361-5	2019	HCT116 cell resistance to MEK inhibitor AZD6244, which inhibited the activation of ERK and promoted the activation of JAK2-STAT3 signaling.	AZD 6244	40-47	mitogen-activated protein kinase 1	Homo sapiens	83-86
30706361-5	2019	HCT116 cell resistance to MEK inhibitor AZD6244, which inhibited the activation of ERK and promoted the activation of JAK2-STAT3 signaling.	AZD 6244	40-47	Janus kinase 2	Homo sapiens	118-122
30706361-5	2019	HCT116 cell resistance to MEK inhibitor AZD6244, which inhibited the activation of ERK and promoted the activation of JAK2-STAT3 signaling.	AZD 6244	40-47	signal transducer and activator of transcription 3	Homo sapiens	123-128
30706361-6	2019	The combination treatment of AZD6244 and AG490 significantly inhibited cell viability and induced cell apoptosis, and completely inhibited the activation of ERK and JAK2-STAT3 signaling.	AZD 6244	29-36	mitogen-activated protein kinase 1	Homo sapiens	157-160
30706361-6	2019	The combination treatment of AZD6244 and AG490 significantly inhibited cell viability and induced cell apoptosis, and completely inhibited the activation of ERK and JAK2-STAT3 signaling.	AZD 6244	29-36	Janus kinase 2	Homo sapiens	165-169
30706361-6	2019	The combination treatment of AZD6244 and AG490 significantly inhibited cell viability and induced cell apoptosis, and completely inhibited the activation of ERK and JAK2-STAT3 signaling.	AZD 6244	29-36	signal transducer and activator of transcription 3	Homo sapiens	170-175
30706361-8	2019	The treatment of AZD6244 on K-Ras mutations HCT116 cells promoted the activation of JAK2/STAT3 signaling.	AZD 6244	17-24	KRAS proto-oncogene, GTPase	Homo sapiens	28-33
30706361-8	2019	The treatment of AZD6244 on K-Ras mutations HCT116 cells promoted the activation of JAK2/STAT3 signaling.	AZD 6244	17-24	Janus kinase 2	Homo sapiens	84-88
30706361-8	2019	The treatment of AZD6244 on K-Ras mutations HCT116 cells promoted the activation of JAK2/STAT3 signaling.	AZD 6244	17-24	signal transducer and activator of transcription 3	Homo sapiens	89-94
31040916-6	2019	Treatment with a combination of SAB298 and AZD6244 (selumetinib), induced a synergistic growth inhibition, suggesting that the new compound could be used in the clinic as a substitute for, or in combination with MAPK inhibitors.	AZD 6244	43-50	mitogen-activated protein kinase 1	Homo sapiens	212-216
31040916-6	2019	Treatment with a combination of SAB298 and AZD6244 (selumetinib), induced a synergistic growth inhibition, suggesting that the new compound could be used in the clinic as a substitute for, or in combination with MAPK inhibitors.	AZD 6244	52-63	mitogen-activated protein kinase 1	Homo sapiens	212-216
30867799-3	2019	In KRAS-mutated NSCLC cells, the MEK inhibitor, selumetinib, inhibited cell growth in a dose-dependent manner, and its growth-inhibitory effect was enhanced by combined treatment with the p38 inhibitor LY2228820.	AZD 6244	48-59	KRAS proto-oncogene, GTPase	Homo sapiens	3-7
30867799-3	2019	In KRAS-mutated NSCLC cells, the MEK inhibitor, selumetinib, inhibited cell growth in a dose-dependent manner, and its growth-inhibitory effect was enhanced by combined treatment with the p38 inhibitor LY2228820.	AZD 6244	48-59	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
30867799-3	2019	In KRAS-mutated NSCLC cells, the MEK inhibitor, selumetinib, inhibited cell growth in a dose-dependent manner, and its growth-inhibitory effect was enhanced by combined treatment with the p38 inhibitor LY2228820.	AZD 6244	48-59	mitogen-activated protein kinase 14	Homo sapiens	188-191
30847387-5	2019	However, MAPKi (dabrafenib or selumetinib) induced these effects only in BRAF V600E-mutant cells.	AZD 6244	30-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
30847387-6	2019	Combined treatment with panobinostat and MAPKi (dabrafenib or selumetinib) displayed a more robust BRAF V600E-dependent redifferentiation effect than panobinostat alone via further improving the acetylation level of histone at the sodium-iodide symporter (NIS) promoter.	AZD 6244	62-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
30579838-0	2019	Schedule-dependent synergistic effects of 5-fluorouracil and selumetinib in KRAS or BRAF mutant colon cancer models.	AZD 6244	61-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-88
30579838-7	2019	Induction of thymidine kinase 1, a rate-limiting enzyme in salvage pathway, by 5-FU was abrogated by subsequent treatment with selumetinib, and ERK reactivation after selumetinib was prohibited by pretreatment with 5-FU.	AZD 6244	127-138	thymidine kinase 1	Homo sapiens	13-31
30579838-7	2019	Induction of thymidine kinase 1, a rate-limiting enzyme in salvage pathway, by 5-FU was abrogated by subsequent treatment with selumetinib, and ERK reactivation after selumetinib was prohibited by pretreatment with 5-FU.	AZD 6244	167-178	mitogen-activated protein kinase 1	Homo sapiens	144-147
30579838-12	2019	Our results suggest that sequential administration of 5-FU plus selumetinib would be a promising strategy for patients having KRAS or BRAF mutant colon cancers.	AZD 6244	64-75	KRAS proto-oncogene, GTPase	Homo sapiens	126-130
30579838-12	2019	Our results suggest that sequential administration of 5-FU plus selumetinib would be a promising strategy for patients having KRAS or BRAF mutant colon cancers.	AZD 6244	64-75	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
30343534-3	2018	Herein, we aimed to investigate the cause of the limited therapeutic effect of selumetinib, a selective inhibitor of MEK in HNSCC, as MEK/ERK reactivation inevitably occurs.	AZD 6244	79-90	mitogen-activated protein kinase kinase 7	Homo sapiens	117-120
30682205-9	2019	Retinal gliosis was not altered, but selumetinib did block the increase in intraretinal microglia/macrophage Iba-1 fluorescence intensity and acquisition of amoeboid morphology.	AZD 6244	37-48	induction of brown adipocytes 1	Mus musculus	109-114
30682205-10	2019	Conclusions: MAPK/ERK is neuroprotective in some retinal damage models; in RD, selumetinib blocked Muller pERK accumulation and changed the retinal microglia/macrophage phenotype but did not alter photoreceptor survival.	AZD 6244	79-90	mitogen-activated protein kinase 1	Mus musculus	13-17
30682205-10	2019	Conclusions: MAPK/ERK is neuroprotective in some retinal damage models; in RD, selumetinib blocked Muller pERK accumulation and changed the retinal microglia/macrophage phenotype but did not alter photoreceptor survival.	AZD 6244	79-90	mitogen-activated protein kinase 1	Mus musculus	18-21
30257106-12	2018	High Pi-induced downregulation of PDCD4 was abolished by microRNA-21 inhibitors and selective ERK inhibitor (selumetinib) and was reproduced by microRNA-21 mimics.	AZD 6244	109-120	programmed cell death 4	Mus musculus	34-39
30257106-12	2018	High Pi-induced downregulation of PDCD4 was abolished by microRNA-21 inhibitors and selective ERK inhibitor (selumetinib) and was reproduced by microRNA-21 mimics.	AZD 6244	109-120	mitogen-activated protein kinase 1	Mus musculus	94-97
30343534-5	2018	Selumetinib transiently inhibited MAPK signaling and reactivated ERK signaling in HNSCC cells.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	34-38
30343534-5	2018	Selumetinib transiently inhibited MAPK signaling and reactivated ERK signaling in HNSCC cells.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	65-68
30343534-6	2018	Rebound in the ERK and Akt pathways in HNSCC cells was accompanied by increased FGFR3 signaling after selumetinib treatment.	AZD 6244	102-113	mitogen-activated protein kinase 1	Homo sapiens	15-18
30343534-6	2018	Rebound in the ERK and Akt pathways in HNSCC cells was accompanied by increased FGFR3 signaling after selumetinib treatment.	AZD 6244	102-113	AKT serine/threonine kinase 1	Homo sapiens	23-26
30343534-3	2018	Herein, we aimed to investigate the cause of the limited therapeutic effect of selumetinib, a selective inhibitor of MEK in HNSCC, as MEK/ERK reactivation inevitably occurs.	AZD 6244	79-90	mitogen-activated protein kinase kinase 7	Homo sapiens	134-137
30343534-3	2018	Herein, we aimed to investigate the cause of the limited therapeutic effect of selumetinib, a selective inhibitor of MEK in HNSCC, as MEK/ERK reactivation inevitably occurs.	AZD 6244	79-90	mitogen-activated protein kinase 1	Homo sapiens	138-141
30343534-6	2018	Rebound in the ERK and Akt pathways in HNSCC cells was accompanied by increased FGFR3 signaling after selumetinib treatment.	AZD 6244	102-113	fibroblast growth factor receptor 3	Homo sapiens	80-85
30343534-8	2018	The FGFR3 inhibitor PD173074 prevented MAPK rebound and sensitized the response of HNSCC cells to selumetinib.	AZD 6244	98-109	fibroblast growth factor receptor 3	Homo sapiens	4-9
30343534-11	2018	ERK rebound as a result of the upregulation of FGFR3 and the ligand FGF2 diminished the antitumor effects of selumetinib, which was overcome by combination treatment with the FGFR3 inhibitor.	AZD 6244	109-120	mitogen-activated protein kinase 1	Homo sapiens	0-3
30343534-11	2018	ERK rebound as a result of the upregulation of FGFR3 and the ligand FGF2 diminished the antitumor effects of selumetinib, which was overcome by combination treatment with the FGFR3 inhibitor.	AZD 6244	109-120	fibroblast growth factor receptor 3	Homo sapiens	47-52
30343534-11	2018	ERK rebound as a result of the upregulation of FGFR3 and the ligand FGF2 diminished the antitumor effects of selumetinib, which was overcome by combination treatment with the FGFR3 inhibitor.	AZD 6244	109-120	fibroblast growth factor 2	Homo sapiens	68-72
30343534-11	2018	ERK rebound as a result of the upregulation of FGFR3 and the ligand FGF2 diminished the antitumor effects of selumetinib, which was overcome by combination treatment with the FGFR3 inhibitor.	AZD 6244	109-120	fibroblast growth factor receptor 3	Homo sapiens	175-180
30030148-5	2018	Synergistic effects of sorafenib and selumetinib on cell apoptosis and phospho-ERK (p-ERK) were analyzed by caspase-3/7 apoptosis assay and western blot, respectively.	AZD 6244	37-48	caspase 3	Homo sapiens	108-119
30414267-12	2018	Selumetinib treatment had a synergistic effect with erythromycin to reduce the expression of p-MEK1 and p-ERK1, reduce cell proliferation, and increase cell apoptosis.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	95-99
30414267-12	2018	Selumetinib treatment had a synergistic effect with erythromycin to reduce the expression of p-MEK1 and p-ERK1, reduce cell proliferation, and increase cell apoptosis.	AZD 6244	0-11	mitogen-activated protein kinase 3	Homo sapiens	106-110
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	CD274 molecule	Homo sapiens	30-35
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	mitogen-activated protein kinase 1	Homo sapiens	110-114
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	mitogen-activated protein kinase kinase 7	Homo sapiens	115-118
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	CD274 molecule	Homo sapiens	156-161
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	epidermal growth factor receptor	Homo sapiens	182-186
30172884-6	2018	Moreover, the upregulation of PD-L1 by chemotherapy was also attenuated by the treatment with erlotinib and a MAPK/MEK inhibitor (AZD6244), suggesting that PD-L1 is regulated by the EGFR/ERK pathway in ESCC.	AZD 6244	130-137	mitogen-activated protein kinase 1	Homo sapiens	187-190
29945997-7	2018	Interestingly, p53 co-mutation rendered KRASG12C lung tumors less sensitive to combination treatment with selumetinib and chemotherapy.Conclusions: Our data demonstrate that unique KRAS mutations and concurrent mutations in tumor-suppressor genes are important factors for lung tumor responses to MEK inhibitor.	AZD 6244	106-117	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	40-44
30373214-10	2018	By combining Hh signaling inhibitor BMS833923 with RAS downstream MEK signaling inhibitor AZD6244, we observed reduced number of metastatic nodules in several mouse models for pancreatic cancer metastasis.	AZD 6244	90-97	midkine	Mus musculus	66-69
29945997-7	2018	Interestingly, p53 co-mutation rendered KRASG12C lung tumors less sensitive to combination treatment with selumetinib and chemotherapy.Conclusions: Our data demonstrate that unique KRAS mutations and concurrent mutations in tumor-suppressor genes are important factors for lung tumor responses to MEK inhibitor.	AZD 6244	106-117	midkine	Mus musculus	297-300
29945997-7	2018	Interestingly, p53 co-mutation rendered KRASG12C lung tumors less sensitive to combination treatment with selumetinib and chemotherapy.Conclusions: Our data demonstrate that unique KRAS mutations and concurrent mutations in tumor-suppressor genes are important factors for lung tumor responses to MEK inhibitor.	AZD 6244	106-117	transformation related protein 53, pseudogene	Mus musculus	15-18
29959144-6	2018	Treatment of established lines and primary ovarian cancer cultures with Src and MEK inhibitors saracatinib and selumetinib, respectively, showed target kinase inhibition and synergistic induction of apoptosis and cell-cycle arrest in vitro, and tumor inhibition in xenografts.	AZD 6244	111-122	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	72-75
29959144-6	2018	Treatment of established lines and primary ovarian cancer cultures with Src and MEK inhibitors saracatinib and selumetinib, respectively, showed target kinase inhibition and synergistic induction of apoptosis and cell-cycle arrest in vitro, and tumor inhibition in xenografts.	AZD 6244	111-122	mitogen-activated protein kinase kinase 7	Homo sapiens	80-83
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	aldehyde dehydrogenase 1 family member A1	Homo sapiens	75-80
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	epidermal growth factor receptor	Homo sapiens	225-229
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	erb-b2 receptor tyrosine kinase 2	Homo sapiens	230-234
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	erb-b2 receptor tyrosine kinase 2	Homo sapiens	235-240
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	mitogen-activated protein kinase kinase 7	Homo sapiens	271-274
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	411-414
29959144-11	2018	In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting.Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2-mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src-MEK inhibition in clinical trials.	AZD 6244	182-193	mitogen-activated protein kinase kinase 7	Homo sapiens	415-418
29915160-0	2018	The Endosomal Protein CEMIP Links WNT Signaling to MEK1-ERK1/2 Activation in Selumetinib-Resistant Intestinal Organoids.	AZD 6244	77-88	cell migration inducing hyaluronidase 1	Homo sapiens	22-27
30042150-2	2018	Preclinical studies demonstrated Wnt pathway overexpression in KRAS-mutant cell lines resistant to the MEK inhibitor, selumetinib.	AZD 6244	118-129	KRAS proto-oncogene, GTPase	Homo sapiens	63-67
30042150-10	2018	The MTD was selumetinib 75 mg twice daily and cyclosporin A 2 mg/kg twice daily on a 28-day cycle.	AZD 6244	12-23	metallothionein 1E	Homo sapiens	4-7
30116025-4	2018	Basal protein expression was correlated with in vitro response to the MEK inhibitor, selumetinib.	AZD 6244	85-96	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
29915160-0	2018	The Endosomal Protein CEMIP Links WNT Signaling to MEK1-ERK1/2 Activation in Selumetinib-Resistant Intestinal Organoids.	AZD 6244	77-88	mitogen-activated protein kinase kinase 1	Homo sapiens	51-55
29915160-0	2018	The Endosomal Protein CEMIP Links WNT Signaling to MEK1-ERK1/2 Activation in Selumetinib-Resistant Intestinal Organoids.	AZD 6244	77-88	mitogen-activated protein kinase 3	Homo sapiens	56-62
30018229-1	2018	BACKGROUND: The MEK (mitogen-activated protein kinase)-inhibitor selumetinib led to increased radioiodine uptake and retention in a subgroup of patients suffering from radioiodine refractory differentiated thyroid cancer (RR-DTC).	AZD 6244	65-76	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
30018229-1	2018	BACKGROUND: The MEK (mitogen-activated protein kinase)-inhibitor selumetinib led to increased radioiodine uptake and retention in a subgroup of patients suffering from radioiodine refractory differentiated thyroid cancer (RR-DTC).	AZD 6244	65-76	mitogen-activated protein kinase kinase 7	Homo sapiens	21-53
30018229-2	2018	We aimed to analyse the effect of selumetinib on the expression of sodium iodide symporter (NIS; SLC5A5) and associated miRNAs in thyroid cancer cells.	AZD 6244	34-45	solute carrier family 5 member 5	Homo sapiens	97-103
30021885-7	2018	Treatment with an orally bioavailable small-molecule activator of PP2A DT-061, in combination with the MEK inhibitor AZD6244, resulted in suppression of both p-AKT and MYC, as well as tumor regression in two KRAS-driven lung cancer mouse models.	AZD 6244	117-124	midkine	Mus musculus	103-106
30018229-9	2018	Its protein level was found up-regulated in TPC1 and BCPAP cells and down-regulated in C643 and 8505C cells after treatment with selumetinib.	AZD 6244	129-140	two pore segment channel 1	Homo sapiens	44-48
30021885-7	2018	Treatment with an orally bioavailable small-molecule activator of PP2A DT-061, in combination with the MEK inhibitor AZD6244, resulted in suppression of both p-AKT and MYC, as well as tumor regression in two KRAS-driven lung cancer mouse models.	AZD 6244	117-124	AKT serine/threonine kinase 1	Homo sapiens	160-163
30021885-7	2018	Treatment with an orally bioavailable small-molecule activator of PP2A DT-061, in combination with the MEK inhibitor AZD6244, resulted in suppression of both p-AKT and MYC, as well as tumor regression in two KRAS-driven lung cancer mouse models.	AZD 6244	117-124	myelocytomatosis oncogene	Mus musculus	168-171
30018229-10	2018	Treatment with selumetinib caused a down-regulation of hsa-let-7f-5p, hsa-miR-146b-5p and hsa-miR-146b-3p in TPC1 and BCPAP cells.	AZD 6244	15-26	two pore segment channel 1	Homo sapiens	109-113
30021885-7	2018	Treatment with an orally bioavailable small-molecule activator of PP2A DT-061, in combination with the MEK inhibitor AZD6244, resulted in suppression of both p-AKT and MYC, as well as tumor regression in two KRAS-driven lung cancer mouse models.	AZD 6244	117-124	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	208-212
30018229-13	2018	Selumetinib treatment caused an increase of radioiodine uptake, which was significant in TPC1 cells.	AZD 6244	0-11	two pore segment channel 1	Homo sapiens	89-93
29928418-1	2018	The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells.	AZD 6244	223-230	epidermal growth factor receptor	Homo sapiens	102-106
29928418-1	2018	The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells.	AZD 6244	223-230	mitogen-activated protein kinase kinase 7	Homo sapiens	167-206
29928418-1	2018	The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells.	AZD 6244	223-230	epidermal growth factor receptor	Homo sapiens	68-100
29928418-1	2018	The present study investigated the molecular mechanism by which the epidermal growth factor receptor (EGFR) inhibitor cetuximab enhances the antitumor activity of the mitogen-activated protein kinase kinase (MEK) inhibitor AZD6244 in colorectal cancer HT29 cells.	AZD 6244	223-230	mitogen-activated protein kinase kinase 7	Homo sapiens	208-211
29928418-7	2018	Inhibition of EGFR activity using cetuximab partially abrogated the feedback-activation of phosphorylated receptor tyrosine-protein kinase erB-3 (p-HER3) and p-AKT serine/threonine kinase (AKT), as well as prevented reactivation of p-extracellular regulated kinase (ERK) conferred by AZD6244 treatment.	AZD 6244	284-291	epidermal growth factor receptor	Homo sapiens	14-18
29928418-7	2018	Inhibition of EGFR activity using cetuximab partially abrogated the feedback-activation of phosphorylated receptor tyrosine-protein kinase erB-3 (p-HER3) and p-AKT serine/threonine kinase (AKT), as well as prevented reactivation of p-extracellular regulated kinase (ERK) conferred by AZD6244 treatment.	AZD 6244	284-291	AKT serine/threonine kinase 1	Homo sapiens	160-163
29928418-8	2018	Combination of AZD6244 and cetuximab also inhibited HT29 cell xenograft growth in nude mice and suppressed HER3 and p-AKT levels in xenografts.	AZD 6244	15-22	erb-b2 receptor tyrosine kinase 3	Mus musculus	107-111
29928418-8	2018	Combination of AZD6244 and cetuximab also inhibited HT29 cell xenograft growth in nude mice and suppressed HER3 and p-AKT levels in xenografts.	AZD 6244	15-22	AKT serine/threonine kinase 1	Homo sapiens	118-121
29928418-9	2018	The EGFR inhibitor cetuximab enhanced the antitumor activity of the MEK inhibitor AZD6244 in colorectal cells in vitro and in vivo.	AZD 6244	82-89	epidermal growth factor receptor	Homo sapiens	4-8
29928418-9	2018	The EGFR inhibitor cetuximab enhanced the antitumor activity of the MEK inhibitor AZD6244 in colorectal cells in vitro and in vivo.	AZD 6244	82-89	mitogen-activated protein kinase kinase 7	Homo sapiens	68-71
29737325-0	2018	The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.	AZD 6244	21-28	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
29762469-10	2018	Selumetinib caused a significant suppression of HMGA2 in PDTT 1, 2, 4, 5 and HF; whereas sorafenib caused no change of HMGA2 expression.	AZD 6244	0-11	high mobility group AT-hook 2	Homo sapiens	48-53
29526823-2	2018	The aim of this work was to test the efficacy of a complete EGFR-inhibition by osimertinib plus the monoclonal antibody cetuximab or the MEK1/2-inhibitor selumetinib in EGFR-mutated NCLC in vivo models.	AZD 6244	154-165	mitogen-activated protein kinase kinase 1	Homo sapiens	137-143
29526823-2	2018	The aim of this work was to test the efficacy of a complete EGFR-inhibition by osimertinib plus the monoclonal antibody cetuximab or the MEK1/2-inhibitor selumetinib in EGFR-mutated NCLC in vivo models.	AZD 6244	154-165	epidermal growth factor receptor	Homo sapiens	169-173
29526823-6	2018	Moreover, in ex vivo primary cell cultures obtained from osimertinib plus selumetinib-resistant tumors, we found Hedgehog pathway activation and we showed that therapy with an SMO inhibitor plus osimertinib and selumetinib inhibited proliferation and migratory and invasive properties of resistant cells.	AZD 6244	74-85	smoothened, frizzled class receptor	Homo sapiens	176-179
29526823-6	2018	Moreover, in ex vivo primary cell cultures obtained from osimertinib plus selumetinib-resistant tumors, we found Hedgehog pathway activation and we showed that therapy with an SMO inhibitor plus osimertinib and selumetinib inhibited proliferation and migratory and invasive properties of resistant cells.	AZD 6244	211-222	smoothened, frizzled class receptor	Homo sapiens	176-179
29526823-7	2018	CONCLUSIONS: We showed that a dual vertical EGFR blockade with osimertinib plus selumetinib/cetuximab is a novel effective therapeutic option in EGFR-mutated NCLC and that hedgehog pathway activation and its interplay with MAPK is involved in resistance to these combination treatments.	AZD 6244	80-91	epidermal growth factor receptor	Homo sapiens	145-149
29737325-0	2018	The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.	AZD 6244	21-28	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	40-44
29737325-4	2018	The present study evaluated the effect of vemurafenib in combination with the selective MEK1/2 inhibitor AZD6244 on cell survival and explored the mechanism underlying the combined effect of vemurafenib and AZD6244 on thyroid cancer cells harboring BRAFV600E.	AZD 6244	105-112	mitogen-activated protein kinase kinase 1	Homo sapiens	88-94
29737325-13	2018	AZD6244 alone abolished phospho-ERK1/2 (pERK1/2) expression at 48 h, whereas vemurafenib alone downregulated pERK1/2 at 4-6 h, with rapid recovery of expression, reaching the highest level at 24-48 h. Combined treatment for 48 h completely inhibited pERK1/2 expression.	AZD 6244	0-7	mitogen-activated protein kinase 3	Homo sapiens	32-38
29737325-14	2018	Combination treatment with vemurafenib and AZD6244 inhibited cell growth and induced apoptosis by causing cell-cycle arrest, with the corresponding changes in the expression of the cell cycle regulators p27Kip1 and cyclin D1.	AZD 6244	43-50	cyclin dependent kinase inhibitor 1B	Homo sapiens	203-210
29737325-14	2018	Combination treatment with vemurafenib and AZD6244 inhibited cell growth and induced apoptosis by causing cell-cycle arrest, with the corresponding changes in the expression of the cell cycle regulators p27Kip1 and cyclin D1.	AZD 6244	43-50	cyclin D1	Homo sapiens	215-224
29737325-17	2018	Combination treatment with vemurafenib and AZD6244 inhibited ERK signaling and caused cell cycle arrest, resulting in cell growth inhibition.	AZD 6244	43-50	mitogen-activated protein kinase 3	Homo sapiens	61-64
29774094-3	2018	We evaluated the potential of drug combinations to increase the efficacy of the MEK inhibitor selumetinib (AZD6244, ARRY-142886), in UM cell lines and Patient-Derived Xenografts.	AZD 6244	94-105	mitogen-activated protein kinase kinase 7	Homo sapiens	80-83
29719377-8	2018	Activation of ERK was inhibited by the pharmacological inhibitor selumetinib (AZD6244), which effectively promoted RAD001-induced cell death.	AZD 6244	65-76	mitogen-activated protein kinase 1	Homo sapiens	14-17
29528792-2	2018	Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective MEK1/2 inhibitor with a short half-life, which demonstrated single-agent activity in patients with metastatic uveal melanoma in a randomized phase II trial.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	69-75
29528792-2	2018	Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective MEK1/2 inhibitor with a short half-life, which demonstrated single-agent activity in patients with metastatic uveal melanoma in a randomized phase II trial.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	69-75
29528792-2	2018	Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective MEK1/2 inhibitor with a short half-life, which demonstrated single-agent activity in patients with metastatic uveal melanoma in a randomized phase II trial.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	69-75
29719377-8	2018	Activation of ERK was inhibited by the pharmacological inhibitor selumetinib (AZD6244), which effectively promoted RAD001-induced cell death.	AZD 6244	78-85	mitogen-activated protein kinase 1	Homo sapiens	14-17
29348467-5	2018	Treatment with U0126, PD901, and Selumetinib MEK inhibitors triggered growth restraint in all CCA cell lines tested, with the most pronounced growth suppressive effects being observed in K-Ras mutant cells.	AZD 6244	33-44	midkine	Mus musculus	45-48
29446253-9	2018	Mechanistically, a high level of TRIM44 was found to activate MAPK signaling, and a MEK inhibitor, AZD6244, reversed cell EMT and apoptosis endowed by TRIM44 overexpression.	AZD 6244	99-106	tripartite motif containing 44	Homo sapiens	33-39
29446253-9	2018	Mechanistically, a high level of TRIM44 was found to activate MAPK signaling, and a MEK inhibitor, AZD6244, reversed cell EMT and apoptosis endowed by TRIM44 overexpression.	AZD 6244	99-106	mitogen-activated protein kinase kinase 7	Homo sapiens	84-87
29446253-9	2018	Mechanistically, a high level of TRIM44 was found to activate MAPK signaling, and a MEK inhibitor, AZD6244, reversed cell EMT and apoptosis endowed by TRIM44 overexpression.	AZD 6244	99-106	tripartite motif containing 44	Homo sapiens	151-157
28852199-6	2018	Key regulatory proteins within pathways that showed altered phosphorylation following JAK inhibition were targeted using selumetinib and trametinib (MEK), buparlisib (PI3K) and ABT-199 (BCL2), and found to be synergistic in combination with JAK kinase inhibitors in primary T-ALL samples harboring JAK3 mutations.	AZD 6244	121-132	midkine	Mus musculus	149-152
29507618-8	2018	Xenographic tumors induced by miR-630-knockdown PC9 and PC9GR cells in nude mice were nearly suppressed by the combination of gefitinib with the YAP1 inhibitor verteporfin or an MEK/ERK inhibitor AZD6244.	AZD 6244	196-203	microRNA 630	Homo sapiens	30-37
29507618-8	2018	Xenographic tumors induced by miR-630-knockdown PC9 and PC9GR cells in nude mice were nearly suppressed by the combination of gefitinib with the YAP1 inhibitor verteporfin or an MEK/ERK inhibitor AZD6244.	AZD 6244	196-203	proprotein convertase subtilisin/kexin type 9	Homo sapiens	48-51
29507618-8	2018	Xenographic tumors induced by miR-630-knockdown PC9 and PC9GR cells in nude mice were nearly suppressed by the combination of gefitinib with the YAP1 inhibitor verteporfin or an MEK/ERK inhibitor AZD6244.	AZD 6244	196-203	midkine	Mus musculus	178-181
29507618-8	2018	Xenographic tumors induced by miR-630-knockdown PC9 and PC9GR cells in nude mice were nearly suppressed by the combination of gefitinib with the YAP1 inhibitor verteporfin or an MEK/ERK inhibitor AZD6244.	AZD 6244	196-203	Eph receptor B2	Mus musculus	182-185
28070119-11	2018	Using the MEK inhibitor selumetinib, we suppressed TrkB/ERK-MAPK pathway activity in vivo and reduced OCD-like grooming in SPRED2 KO mice.	AZD 6244	24-35	midkine	Mus musculus	10-13
28070119-11	2018	Using the MEK inhibitor selumetinib, we suppressed TrkB/ERK-MAPK pathway activity in vivo and reduced OCD-like grooming in SPRED2 KO mice.	AZD 6244	24-35	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	51-55
28070119-11	2018	Using the MEK inhibitor selumetinib, we suppressed TrkB/ERK-MAPK pathway activity in vivo and reduced OCD-like grooming in SPRED2 KO mice.	AZD 6244	24-35	mitogen-activated protein kinase 1	Mus musculus	56-59
28070119-11	2018	Using the MEK inhibitor selumetinib, we suppressed TrkB/ERK-MAPK pathway activity in vivo and reduced OCD-like grooming in SPRED2 KO mice.	AZD 6244	24-35	sprouty-related EVH1 domain containing 2	Mus musculus	123-129
29670612-11	2018	C37, a small molecule blocking the interaction between FPRs and uPAR, and selumetinib, a clinically approved MAPKK/ERK inhibitor, significantly inhibited FPRs-mediated ROS production in fibroblasts derived from SSc patients.	AZD 6244	74-85	mitogen-activated protein kinase 1	Homo sapiens	115-118
29348467-5	2018	Treatment with U0126, PD901, and Selumetinib MEK inhibitors triggered growth restraint in all CCA cell lines tested, with the most pronounced growth suppressive effects being observed in K-Ras mutant cells.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	187-192
28833380-0	2018	Population pharmacokinetics of the MEK inhibitor selumetinib and its active N-desmethyl metabolite: data from 10 phase I trials.	AZD 6244	49-60	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
28833380-1	2018	AIMS: The aims of the study were to characterize the pharmacokinetics (PK) of selumetinib (AZD6244; ARRY-142886), a mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor in clinical development for various indications, and its N-desmethyl metabolite in healthy volunteers, and evaluate clinically important covariates.	AZD 6244	78-89	mitogen-activated protein kinase kinase 1	Homo sapiens	116-165
29136201-13	2018	Selumetinib 75 mg BID plus docetaxel 60 mg/m2 was not tolerated in this patient population.	AZD 6244	0-11	BH3 interacting domain death agonist	Homo sapiens	18-21
28986121-4	2018	These death responses, however, were reverted to growth arrest responses upon titration of cellular phospho-ERK1/2 levels by the MEK1/2 inhibitor AZD6244.	AZD 6244	146-153	mitogen-activated protein kinase 3	Homo sapiens	108-114
28986121-4	2018	These death responses, however, were reverted to growth arrest responses upon titration of cellular phospho-ERK1/2 levels by the MEK1/2 inhibitor AZD6244.	AZD 6244	146-153	mitogen-activated protein kinase kinase 1	Homo sapiens	129-135
29055717-3	2018	Recent clinical trials have shown promising success for some drugs, notably selumetinib, an inhibitor of MAP kinase kinase (MEK).	AZD 6244	76-87	mitogen-activated protein kinase kinase 7	Homo sapiens	105-122
29055717-3	2018	Recent clinical trials have shown promising success for some drugs, notably selumetinib, an inhibitor of MAP kinase kinase (MEK).	AZD 6244	76-87	mitogen-activated protein kinase kinase 7	Homo sapiens	124-127
29216787-6	2018	Other MEK1/2 inhibitors that are also in advanced stages of clinical development include selumetinib, cobimetinib, and binimetinib.	AZD 6244	89-100	mitogen-activated protein kinase kinase 1	Homo sapiens	6-12
29066719-6	2017	We further analyze two independent breast cancer datasets and find that specific isoforms of IGF2BP2, NECTIN4, ITGB6, and KLHDC9 are significantly associated with AZD6244, lapatinib, erlotinib, and paclitaxel, respectively.	AZD 6244	163-170	insulin like growth factor 2 mRNA binding protein 2	Homo sapiens	93-100
28916199-8	2017	ROCK inhibition specifically ameliorated the phenotype of selumetinib-treated SMA mice demonstrating an efficient ROCK to ERK crosstalk relevant for the SMA pathophysiology.	AZD 6244	58-69	mitogen-activated protein kinase 1	Mus musculus	122-125
28866094-4	2017	In this study, we demonstrated the combination effects of the MEK inhibitor selumetinib and the CDK4/6 inhibitor palbociclib in RAS-driven NSCLC.	AZD 6244	76-87	mitogen-activated protein kinase kinase 7	Homo sapiens	62-65
28866094-6	2017	We used siRNA and pharmacologic inhibition of CDK4 and found that the combination of selumetinib and palbociclib synergistically inhibited RAS-driven NSCLC cases with CDKN2A mutations but not those with wild type CDKN2A.	AZD 6244	85-96	cyclin dependent kinase 4	Homo sapiens	46-50
28866094-6	2017	We used siRNA and pharmacologic inhibition of CDK4 and found that the combination of selumetinib and palbociclib synergistically inhibited RAS-driven NSCLC cases with CDKN2A mutations but not those with wild type CDKN2A.	AZD 6244	85-96	cyclin dependent kinase inhibitor 2A	Homo sapiens	167-173
28866094-6	2017	We used siRNA and pharmacologic inhibition of CDK4 and found that the combination of selumetinib and palbociclib synergistically inhibited RAS-driven NSCLC cases with CDKN2A mutations but not those with wild type CDKN2A.	AZD 6244	85-96	cyclin dependent kinase inhibitor 2A	Homo sapiens	213-219
28866094-8	2017	Selumetinib completely inhibited p-ERK but not p-RB.	AZD 6244	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	33-38
28866094-11	2017	These data suggest that the combination treatment of palbociclib and selumetinib is effective in preclinical models of RAS-driven NSCLC with CDKN2A mutations.	AZD 6244	69-80	cyclin dependent kinase inhibitor 2A	Homo sapiens	141-147
29045535-1	2017	Background: Combination of selumetinib plus docetaxel provided clinical benefit in a previous phase II trial for patients with KRAS-mutant advanced non-small-cell lung cancer (NSCLC).	AZD 6244	27-38	KRAS proto-oncogene, GTPase	Homo sapiens	127-131
28111882-5	2017	PD-L1 and signal transducer and activator of transcription 1 ( STAT1 ) mRNA expression were reduced in the presence of mitogen-activated protein kinase kinase 1.2 (MEK1/2) inhibitors RDEA119 and AZD6244 in CLL 17-71 cells.	AZD 6244	195-202	CD274 molecule	Canis lupus familiaris	0-5
28111882-5	2017	PD-L1 and signal transducer and activator of transcription 1 ( STAT1 ) mRNA expression were reduced in the presence of mitogen-activated protein kinase kinase 1.2 (MEK1/2) inhibitors RDEA119 and AZD6244 in CLL 17-71 cells.	AZD 6244	195-202	signal transducer and activator of transcription 1-alpha/beta	Canis lupus familiaris	10-60
28111882-5	2017	PD-L1 and signal transducer and activator of transcription 1 ( STAT1 ) mRNA expression were reduced in the presence of mitogen-activated protein kinase kinase 1.2 (MEK1/2) inhibitors RDEA119 and AZD6244 in CLL 17-71 cells.	AZD 6244	195-202	signal transducer and activator of transcription 1-alpha/beta	Canis lupus familiaris	63-68
28111882-5	2017	PD-L1 and signal transducer and activator of transcription 1 ( STAT1 ) mRNA expression were reduced in the presence of mitogen-activated protein kinase kinase 1.2 (MEK1/2) inhibitors RDEA119 and AZD6244 in CLL 17-71 cells.	AZD 6244	195-202	dual specificity mitogen-activated protein kinase kinase 2	Canis lupus familiaris	164-170
28791489-7	2017	RESULTS: Inhibition of ERK activation with selumetinib, a MEK1/2 inhibitor, blocked EGF-induced expansion of CD44+/CD24- populations.	AZD 6244	43-54	mitogen-activated protein kinase 1	Homo sapiens	23-26
28791489-7	2017	RESULTS: Inhibition of ERK activation with selumetinib, a MEK1/2 inhibitor, blocked EGF-induced expansion of CD44+/CD24- populations.	AZD 6244	43-54	mitogen-activated protein kinase kinase 1	Homo sapiens	58-64
28791489-7	2017	RESULTS: Inhibition of ERK activation with selumetinib, a MEK1/2 inhibitor, blocked EGF-induced expansion of CD44+/CD24- populations.	AZD 6244	43-54	CD44 molecule (Indian blood group)	Homo sapiens	109-113
28791489-7	2017	RESULTS: Inhibition of ERK activation with selumetinib, a MEK1/2 inhibitor, blocked EGF-induced expansion of CD44+/CD24- populations.	AZD 6244	43-54	CD24 molecule	Homo sapiens	115-119
29066719-6	2017	We further analyze two independent breast cancer datasets and find that specific isoforms of IGF2BP2, NECTIN4, ITGB6, and KLHDC9 are significantly associated with AZD6244, lapatinib, erlotinib, and paclitaxel, respectively.	AZD 6244	163-170	nectin cell adhesion molecule 4	Homo sapiens	102-109
29066719-6	2017	We further analyze two independent breast cancer datasets and find that specific isoforms of IGF2BP2, NECTIN4, ITGB6, and KLHDC9 are significantly associated with AZD6244, lapatinib, erlotinib, and paclitaxel, respectively.	AZD 6244	163-170	integrin subunit beta 6	Homo sapiens	111-116
29066719-6	2017	We further analyze two independent breast cancer datasets and find that specific isoforms of IGF2BP2, NECTIN4, ITGB6, and KLHDC9 are significantly associated with AZD6244, lapatinib, erlotinib, and paclitaxel, respectively.	AZD 6244	163-170	kelch domain containing 9	Homo sapiens	122-128
28599981-4	2017	We sought to evaluate inhibitors of p90RSK family members: BI-D1870 and BRD7389, for their ability to inhibit both proliferation and protein synthesis in patient-derived melanoma cell lines with acquired resistance to combined treatment with the BRAF inhibitor vemurafenib and the mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor selumetinib.	AZD 6244	362-373	ribosomal protein S6 kinase A1	Homo sapiens	36-42
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	100-106
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	0-11	zinc fingers and homeoboxes 2	Homo sapiens	131-134
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	0-11	mitogen-activated protein kinase 1	Homo sapiens	139-142
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	100-106
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	13-20	zinc fingers and homeoboxes 2	Homo sapiens	131-134
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	13-20	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	13-20	mitogen-activated protein kinase 1	Homo sapiens	139-142
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	100-106
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	22-33	zinc fingers and homeoboxes 2	Homo sapiens	131-134
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	22-33	mitogen-activated protein kinase kinase 7	Homo sapiens	100-103
28424891-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric inhibitor of MEK1/2, a component of the RAS/RAF/MEK/ERK pathway which is constitutively activated in many cancers.	AZD 6244	22-33	mitogen-activated protein kinase 1	Homo sapiens	139-142
28424891-14	2017	Overlapping toxicities prevented the escalation of selumetinib to its recommended phase II monotherapy dose of 75 mg BID.	AZD 6244	51-62	BH3 interacting domain death agonist	Homo sapiens	117-120
28931905-0	2017	Ex vivo treatment of patient biopsies as a novel method to assess colorectal tumour response to the MEK1/2 inhibitor, Selumetinib.	AZD 6244	118-129	mitogen-activated protein kinase kinase 1	Homo sapiens	100-106
28849200-6	2017	Based on the sequencing results and associated literatures, AZD6244, a highly selective inhibitor against mitogen-activated protein kinase kinase 1 (MEK1), was chosen as a potential therapy.	AZD 6244	60-67	mitogen-activated protein kinase kinase 1	Homo sapiens	106-147
28849200-6	2017	Based on the sequencing results and associated literatures, AZD6244, a highly selective inhibitor against mitogen-activated protein kinase kinase 1 (MEK1), was chosen as a potential therapy.	AZD 6244	60-67	mitogen-activated protein kinase kinase 1	Homo sapiens	149-153
28849200-7	2017	AZD6244, a highly selective MEK1 inhibitor, was evaluated as effective for the pancreatic cancer PDX model, and thus may provide potential efficacy in the clinical treatment of the patient with pancreatic cancer investigated in the present study.	AZD 6244	0-7	mitogen-activated protein kinase kinase 1	Homo sapiens	28-32
28982310-7	2017	Wortmannin decreased phosphorylated adenosine monophosphate-activated protein kinase protein levels, and AZD6244 increased phosphorylated Akt protein levels.	AZD 6244	105-112	AKT serine/threonine kinase 1	Homo sapiens	138-141
28931905-4	2017	The MEK1/2 inhibitor, Selumetinib (AZD6244, ARRY-142886) was used as a tool compound.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
29113345-6	2017	This in-series Raf-Mek co-targeting synergy was recapitulated in orthotopic mouse xenografts, where SFN and the Mek inhibitor selumitinib (AZD6244) inhibited primary tumor growth and pulmonary metastasis.	AZD 6244	139-146	zinc fingers and homeoboxes 2	Mus musculus	15-18
28620782-7	2017	Furthermore, when treating the triple mutant astrocytes with AZD-6244, an inhibitor of the RAF/MEK/ERK pathway, we found significant reduction in migration through the confined channels when compared to that of controls (83% decrease in 5 x 5 mum2 and 86% in 3 x 5 mum2 channels).	AZD 6244	61-69	zinc fingers and homeoboxes 2	Homo sapiens	91-94
28620782-7	2017	Furthermore, when treating the triple mutant astrocytes with AZD-6244, an inhibitor of the RAF/MEK/ERK pathway, we found significant reduction in migration through the confined channels when compared to that of controls (83% decrease in 5 x 5 mum2 and 86% in 3 x 5 mum2 channels).	AZD 6244	61-69	mitogen-activated protein kinase kinase 7	Homo sapiens	95-98
28620782-7	2017	Furthermore, when treating the triple mutant astrocytes with AZD-6244, an inhibitor of the RAF/MEK/ERK pathway, we found significant reduction in migration through the confined channels when compared to that of controls (83% decrease in 5 x 5 mum2 and 86% in 3 x 5 mum2 channels).	AZD 6244	61-69	mitogen-activated protein kinase 1	Homo sapiens	99-102
28665153-9	2017	Patients treated with MEK inhibitors (Trametinib and Selumetinib) had an increased risk overall of peripheral edema (RR = 3.05, 95% CI = 1.98-4.70; p &lt; .00001), but the MEK inhibitors (Trametinib and Selumetinib) did not increase the risk of high grade edema (RR = 1.88, 95% CI = 0.66-5.35; p = .24).	AZD 6244	53-64	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
28665153-9	2017	Patients treated with MEK inhibitors (Trametinib and Selumetinib) had an increased risk overall of peripheral edema (RR = 3.05, 95% CI = 1.98-4.70; p &lt; .00001), but the MEK inhibitors (Trametinib and Selumetinib) did not increase the risk of high grade edema (RR = 1.88, 95% CI = 0.66-5.35; p = .24).	AZD 6244	53-64	mitogen-activated protein kinase kinase 7	Homo sapiens	172-175
28665153-9	2017	Patients treated with MEK inhibitors (Trametinib and Selumetinib) had an increased risk overall of peripheral edema (RR = 3.05, 95% CI = 1.98-4.70; p &lt; .00001), but the MEK inhibitors (Trametinib and Selumetinib) did not increase the risk of high grade edema (RR = 1.88, 95% CI = 0.66-5.35; p = .24).	AZD 6244	203-214	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
28620782-7	2017	Furthermore, when treating the triple mutant astrocytes with AZD-6244, an inhibitor of the RAF/MEK/ERK pathway, we found significant reduction in migration through the confined channels when compared to that of controls (83% decrease in 5 x 5 mum2 and 86% in 3 x 5 mum2 channels).	AZD 6244	61-69	trafficking protein particle complex subunit 1	Homo sapiens	243-247
28620782-7	2017	Furthermore, when treating the triple mutant astrocytes with AZD-6244, an inhibitor of the RAF/MEK/ERK pathway, we found significant reduction in migration through the confined channels when compared to that of controls (83% decrease in 5 x 5 mum2 and 86% in 3 x 5 mum2 channels).	AZD 6244	61-69	trafficking protein particle complex subunit 1	Homo sapiens	265-269
29113345-6	2017	This in-series Raf-Mek co-targeting synergy was recapitulated in orthotopic mouse xenografts, where SFN and the Mek inhibitor selumitinib (AZD6244) inhibited primary tumor growth and pulmonary metastasis.	AZD 6244	139-146	midkine	Mus musculus	19-22
29113345-6	2017	This in-series Raf-Mek co-targeting synergy was recapitulated in orthotopic mouse xenografts, where SFN and the Mek inhibitor selumitinib (AZD6244) inhibited primary tumor growth and pulmonary metastasis.	AZD 6244	139-146	midkine	Mus musculus	112-115
28807001-0	2017	The MEK inhibitor selumetinib complements CTLA-4 blockade by reprogramming the tumor immune microenvironment.	AZD 6244	18-29	midkine	Mus musculus	4-7
28807001-0	2017	The MEK inhibitor selumetinib complements CTLA-4 blockade by reprogramming the tumor immune microenvironment.	AZD 6244	18-29	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	42-48
28807001-8	2017	RESULTS: Anti-CTLA-4 enhanced the generation of KLH specific immunity following KLH immunization in vivo; selumetinib was found to reduce, but did not prevent, this enhancement of immune response by anti-CTLA-4 in vivo.	AZD 6244	106-117	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	204-210
28807001-10	2017	Combination of anti-CTLA-4 with selumetinib negated this up-regulation of Cox-2 and Arg1, reduced the frequency of CD11+ Ly6G+ myeloid cells, and led to the accumulation of differentiating monocytes at the Ly6C+ MHC+ intermediate state in the tumor.	AZD 6244	32-43	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	74-79
28807001-10	2017	Combination of anti-CTLA-4 with selumetinib negated this up-regulation of Cox-2 and Arg1, reduced the frequency of CD11+ Ly6G+ myeloid cells, and led to the accumulation of differentiating monocytes at the Ly6C+ MHC+ intermediate state in the tumor.	AZD 6244	32-43	arginase 1	Homo sapiens	84-88
28807001-10	2017	Combination of anti-CTLA-4 with selumetinib negated this up-regulation of Cox-2 and Arg1, reduced the frequency of CD11+ Ly6G+ myeloid cells, and led to the accumulation of differentiating monocytes at the Ly6C+ MHC+ intermediate state in the tumor.	AZD 6244	32-43	major histocompatibility complex, class I, C	Homo sapiens	212-215
28807001-12	2017	Finally, we show that pre-treatment, but not concurrent treatment, with selumetinib enhanced the anti-tumor activity of anti-CTLA-4 in the CT26 model.	AZD 6244	72-83	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	125-131
27813079-5	2017	The MEK inhibitor selumetinib-similarly to that of the BRAF-specific inhibitor-also increases PMCA4b levels in both BRAF and NRAS mutant melanoma cells suggesting that the MAPK pathway is involved in the regulation of PMCA4b expression.	AZD 6244	18-29	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
28675058-4	2017	Areas covered: A phase II trial in KRAS-mutant NSCLC had shown significant improvements in PFS and ORR in patients treated with selumetinib plus docetaxel compared to docetaxel alone.	AZD 6244	128-139	KRAS proto-oncogene, GTPase	Homo sapiens	35-39
28675058-5	2017	Disappointing data emerged from the next phase III trial in which the addition of selumetinib to docetaxel in patients with advanced KRAS mutant lung cancer did not improve survival or show clinical benefit.	AZD 6244	82-93	KRAS proto-oncogene, GTPase	Homo sapiens	133-137
28339824-0	2017	A phase I trial of the MEK inhibitor selumetinib (AZD6244) in pediatric patients with recurrent or refractory low-grade glioma: a Pediatric Brain Tumor Consortium (PBTC) study.	AZD 6244	37-48	mitogen-activated protein kinase kinase 7	Homo sapiens	23-26
28339824-0	2017	A phase I trial of the MEK inhibitor selumetinib (AZD6244) in pediatric patients with recurrent or refractory low-grade glioma: a Pediatric Brain Tumor Consortium (PBTC) study.	AZD 6244	50-57	mitogen-activated protein kinase kinase 7	Homo sapiens	23-26
28339824-2	2017	The aim of this study was to determine the recommended phase II dose (RP2D) and the dose-limiting toxicities (DLTs) of the MEK inhibitor selumetinib in children with progressive LGG.	AZD 6244	137-148	mitogen-activated protein kinase kinase 7	Homo sapiens	123-126
28566331-6	2017	We applied our approach to an ongoing phase Ib clinical trial (TATTON) administering AZD9291 and selumetinib to EGFR-mutant lung cancer patients.	AZD 6244	97-108	epidermal growth factor receptor	Homo sapiens	112-116
28938614-0	2017	Phenformin enhances the therapeutic effect of selumetinib in KRAS-mutant non-small cell lung cancer irrespective of LKB1 status.	AZD 6244	46-57	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	61-65
28938614-6	2017	The re-expression of wild type LKB1 increased phospho-ERK level, suggesting that restored dependency on MEK-&gt;ERK-&gt;MAPK signaling might have contributed to the enhanced sensitivity to selumetinib.	AZD 6244	189-200	serine/threonine kinase 11	Mus musculus	31-35
28938614-6	2017	The re-expression of wild type LKB1 increased phospho-ERK level, suggesting that restored dependency on MEK-&gt;ERK-&gt;MAPK signaling might have contributed to the enhanced sensitivity to selumetinib.	AZD 6244	189-200	midkine	Mus musculus	104-107
28938614-10	2017	Finally, in xenograft models bearing isogenic A549 cells, we confirmed that loss of LKB1 confers resistance to selumetinib, and phenformin significantly enhances the therapeutic effect of selumetinib.	AZD 6244	111-122	serine/threonine kinase 11	Mus musculus	84-88
28938614-11	2017	Irrespective of LKB1 status, phenformin may enhance the anti-tumor effect of selumetinib in KRAS-mutant NSCLC.	AZD 6244	77-88	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	92-96
28819429-6	2017	Moreover, the anti-tumor effect of AZD6244 (MEK inhibitor) was evaluated because PDCs harbored a MAP2K1 mutation at the time of resistance to the EGFR plus BRAF inhibitors.	AZD 6244	35-42	mitogen-activated protein kinase kinase 7	Homo sapiens	44-47
28819429-6	2017	Moreover, the anti-tumor effect of AZD6244 (MEK inhibitor) was evaluated because PDCs harbored a MAP2K1 mutation at the time of resistance to the EGFR plus BRAF inhibitors.	AZD 6244	35-42	mitogen-activated protein kinase kinase 1	Homo sapiens	97-103
28819429-10	2017	Investigation of the combined effect of sorafenib and AZD6244 using the calculated combination index (CI) showed synergistic effects of sorafenib and AZD6244 in combination therapy applied to PDCs with the MAP2K1 K57T mutation.	AZD 6244	54-61	mitogen-activated protein kinase kinase 1	Homo sapiens	206-212
28819429-10	2017	Investigation of the combined effect of sorafenib and AZD6244 using the calculated combination index (CI) showed synergistic effects of sorafenib and AZD6244 in combination therapy applied to PDCs with the MAP2K1 K57T mutation.	AZD 6244	150-157	mitogen-activated protein kinase kinase 1	Homo sapiens	206-212
28574827-2	2017	In this study, we analyzed genome-wide gene expression profiling data from 6 sensitive and 6 resistant cell lines to identify candidate genes whose expression changes are associated with responses to a MEK inhibitor, selumetinib (AZD6244).	AZD 6244	217-228	mitogen-activated protein kinase kinase 7	Homo sapiens	202-205
28574827-2	2017	In this study, we analyzed genome-wide gene expression profiling data from 6 sensitive and 6 resistant cell lines to identify candidate genes whose expression changes are associated with responses to a MEK inhibitor, selumetinib (AZD6244).	AZD 6244	230-237	mitogen-activated protein kinase kinase 7	Homo sapiens	202-205
28574827-6	2017	The expression of the ITF-2 was elevated both in primary AZD6244 resistant cell line, LOX-IMVI and acquired resistant cell line, M14/AZD-3.	AZD 6244	57-64	transcription factor 4	Homo sapiens	22-27
28574827-7	2017	Targeted silencing of ITF-2 by siRNA significantly enhanced susceptibility to AZD6244 in resistant cells.	AZD 6244	78-85	transcription factor 4	Homo sapiens	22-27
27813079-5	2017	The MEK inhibitor selumetinib-similarly to that of the BRAF-specific inhibitor-also increases PMCA4b levels in both BRAF and NRAS mutant melanoma cells suggesting that the MAPK pathway is involved in the regulation of PMCA4b expression.	AZD 6244	18-29	ATPase plasma membrane Ca2+ transporting 4	Homo sapiens	94-100
27813079-5	2017	The MEK inhibitor selumetinib-similarly to that of the BRAF-specific inhibitor-also increases PMCA4b levels in both BRAF and NRAS mutant melanoma cells suggesting that the MAPK pathway is involved in the regulation of PMCA4b expression.	AZD 6244	18-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
27813079-5	2017	The MEK inhibitor selumetinib-similarly to that of the BRAF-specific inhibitor-also increases PMCA4b levels in both BRAF and NRAS mutant melanoma cells suggesting that the MAPK pathway is involved in the regulation of PMCA4b expression.	AZD 6244	18-29	NRAS proto-oncogene, GTPase	Homo sapiens	125-129
27813079-5	2017	The MEK inhibitor selumetinib-similarly to that of the BRAF-specific inhibitor-also increases PMCA4b levels in both BRAF and NRAS mutant melanoma cells suggesting that the MAPK pathway is involved in the regulation of PMCA4b expression.	AZD 6244	18-29	ATPase plasma membrane Ca2+ transporting 4	Homo sapiens	218-224
28291381-3	2017	The SELIMETRY trial (EudraCT No 2015-002269-47) aims to investigate the role of the MEK inhibitor Selumetinib in resensitizing advanced iodine refractory differentiated thyroid cancer to radioiodine therapy.	AZD 6244	98-109	mitogen-activated protein kinase kinase 7	Homo sapiens	84-87
28283692-0	2017	Pharmacokinetics and pharmacogenetics of the MEK1/2 inhibitor, selumetinib, in Asian and Western healthy subjects: a pooled analysis.	AZD 6244	63-74	mitogen-activated protein kinase kinase 1	Homo sapiens	45-51
28283692-1	2017	PURPOSE: Emerging data on selumetinib, a MEK1/2 inhibitor in clinical development, suggest a possible difference in pharmacokinetics (PK) between Japanese and Western patients.	AZD 6244	26-37	mitogen-activated protein kinase kinase 1	Homo sapiens	41-47
28385507-3	2017	Importantly, 2 exhibited MEK1 binding affinity with IC5071nM, which is so far the best result for metal complexes and more potent than U0126 (7.02muM) and AZD6244 (2.20muM).	AZD 6244	155-162	mitogen-activated protein kinase kinase 1	Homo sapiens	25-29
28492898-0	2017	Selumetinib Plus Docetaxel Compared With Docetaxel Alone and Progression-Free Survival in Patients With KRAS-Mutant Advanced Non-Small Cell Lung Cancer: The SELECT-1 Randomized Clinical Trial.	AZD 6244	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	104-108
28492898-2	2017	Objective: To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy for advanced KRAS-mutant NSCLC.	AZD 6244	94-105	mitogen-activated protein kinase kinase 7	Homo sapiens	38-77
28492898-2	2017	Objective: To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy for advanced KRAS-mutant NSCLC.	AZD 6244	94-105	mitogen-activated protein kinase kinase 7	Homo sapiens	79-82
28492898-2	2017	Objective: To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy for advanced KRAS-mutant NSCLC.	AZD 6244	94-105	KRAS proto-oncogene, GTPase	Homo sapiens	177-181
28212559-0	2017	The selective MEK1 inhibitor Selumetinib enhances the antitumor activity of everolimus against renal cell carcinoma in vitro and in vivo.	AZD 6244	29-40	mitogen-activated protein kinase kinase 1	Homo sapiens	14-18
27978579-16	2017	Conclusions and Relevance: Dual targeting of the MEK and PI3K/AKT pathways downstream of KRAS by selumetinib plus MK-2206 did not improve overall survival in patients with metastatic pancreatic adenocarcinoma for whom gemcitabine-based chemotherapy had failed.	AZD 6244	97-108	KRAS proto-oncogene, GTPase	Homo sapiens	89-93
28326681-1	2017	Selumetinib (AZD6244, ARRY-142886), a mitogen activated protein kinases (MEK1 and 2) inhibitor, has been granted orphan drug designation for differentiated thyroid cancer.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	73-83
28326681-1	2017	Selumetinib (AZD6244, ARRY-142886), a mitogen activated protein kinases (MEK1 and 2) inhibitor, has been granted orphan drug designation for differentiated thyroid cancer.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	73-83
28019010-0	2017	Pharmacokinetics of a Single Oral Dose of the MEK1/2 Inhibitor Selumetinib in Subjects With End-Stage Renal Disease or Varying Degrees of Hepatic Impairment Compared With Healthy Subjects.	AZD 6244	63-74	mitogen-activated protein kinase kinase 1	Homo sapiens	46-52
29040023-2	2017	We report a patient with disseminated LGG with the BRAFV600E mutation, which was refractory to selumetinib, a MEK inhibitor, but subsequently showed immediate clinical and radiographic response to dabrafenib, a BRAF inhibitor, with sustained effect for 9 months prior to clinical progression.	AZD 6244	95-106	mitogen-activated protein kinase kinase 7	Homo sapiens	110-113
29040023-2	2017	We report a patient with disseminated LGG with the BRAFV600E mutation, which was refractory to selumetinib, a MEK inhibitor, but subsequently showed immediate clinical and radiographic response to dabrafenib, a BRAF inhibitor, with sustained effect for 9 months prior to clinical progression.	AZD 6244	95-106	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
28212559-5	2017	In this study, we evaluated whether the antitumor activity of everolimus against RCC is enhanced by Selumetinib, a selective MEK1 inhibitor.	AZD 6244	100-111	mitogen-activated protein kinase kinase 1	Homo sapiens	125-129
28264648-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric MEK1/2 inhibitor with a short half-life that has shown clinical activity as monotherapy in phase I and II studies of advanced cancer.	AZD 6244	0-11	mitogen-activated protein kinase kinase 1	Homo sapiens	87-93
28276530-6	2017	To overcome treatment evasion and reduce systemic effects, we developed CXCR4-targeted nanoparticles to co-deliver sorafenib with the MEK inhibitor AZD6244 in HCC.	AZD 6244	148-155	C-X-C motif chemokine receptor 4	Homo sapiens	72-77
28276530-6	2017	To overcome treatment evasion and reduce systemic effects, we developed CXCR4-targeted nanoparticles to co-deliver sorafenib with the MEK inhibitor AZD6244 in HCC.	AZD 6244	148-155	mitogen-activated protein kinase kinase 7	Homo sapiens	134-137
28264648-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric MEK1/2 inhibitor with a short half-life that has shown clinical activity as monotherapy in phase I and II studies of advanced cancer.	AZD 6244	13-20	mitogen-activated protein kinase kinase 1	Homo sapiens	87-93
28264648-2	2017	Selumetinib (AZD6244, ARRY-142886) is an oral, potent and highly selective, allosteric MEK1/2 inhibitor with a short half-life that has shown clinical activity as monotherapy in phase I and II studies of advanced cancer.	AZD 6244	22-33	mitogen-activated protein kinase kinase 1	Homo sapiens	87-93
28264648-6	2017	Part A of the study (dose escalation) evaluated safety, tolerability, PK, and maximum tolerated dose (MTD) of selumetinib twice daily (BID) with docetaxel 75 mg/m2 or dacarbazine 1000 mg/m2 administered every 21 days.	AZD 6244	110-121	BH3 interacting domain death agonist	Homo sapiens	135-138
28053239-6	2017	The protective function of MAPK1 on miR-378 was shown in kidney cells treated with the MAPK1 inhibitor, selumetinib, which inhibited mesangial cell hypertrophy in response to TGF-beta1.	AZD 6244	104-115	mitogen activated protein kinase 1	Rattus norvegicus	27-32
28053239-6	2017	The protective function of MAPK1 on miR-378 was shown in kidney cells treated with the MAPK1 inhibitor, selumetinib, which inhibited mesangial cell hypertrophy in response to TGF-beta1.	AZD 6244	104-115	microRNA 378	Rattus norvegicus	36-43
28053239-6	2017	The protective function of MAPK1 on miR-378 was shown in kidney cells treated with the MAPK1 inhibitor, selumetinib, which inhibited mesangial cell hypertrophy in response to TGF-beta1.	AZD 6244	104-115	mitogen activated protein kinase 1	Rattus norvegicus	87-92
28053239-6	2017	The protective function of MAPK1 on miR-378 was shown in kidney cells treated with the MAPK1 inhibitor, selumetinib, which inhibited mesangial cell hypertrophy in response to TGF-beta1.	AZD 6244	104-115	transforming growth factor, beta 1	Rattus norvegicus	175-184
27588400-4	2017	Here we show that the MEK inhibitors Trametinib, Selumetinib and MEK162 severely impair primary RAS-mutant MLL-rearranged infant ALL cells in vitro.	AZD 6244	49-60	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
28094260-0	2017	Targeted therapies: Selumetinib MEKing differences in NF1.	AZD 6244	20-31	neurofibromin 1	Homo sapiens	54-57
27588400-4	2017	Here we show that the MEK inhibitors Trametinib, Selumetinib and MEK162 severely impair primary RAS-mutant MLL-rearranged infant ALL cells in vitro.	AZD 6244	49-60	lysine methyltransferase 2A	Homo sapiens	107-110
28086243-11	2017	Consequently, the MEK-inhibitor selumetinib/AZD6244, in contrast to the PI3K/mTOR-inhibitor dactolisib/NVP-BEZ235, increases growth inhibition when given together with a FASN-blocker.	AZD 6244	32-43	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
28086243-11	2017	Consequently, the MEK-inhibitor selumetinib/AZD6244, in contrast to the PI3K/mTOR-inhibitor dactolisib/NVP-BEZ235, increases growth inhibition when given together with a FASN-blocker.	AZD 6244	32-43	fatty acid synthase	Homo sapiens	170-174
28086243-11	2017	Consequently, the MEK-inhibitor selumetinib/AZD6244, in contrast to the PI3K/mTOR-inhibitor dactolisib/NVP-BEZ235, increases growth inhibition when given together with a FASN-blocker.	AZD 6244	44-51	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
28086243-11	2017	Consequently, the MEK-inhibitor selumetinib/AZD6244, in contrast to the PI3K/mTOR-inhibitor dactolisib/NVP-BEZ235, increases growth inhibition when given together with a FASN-blocker.	AZD 6244	44-51	fatty acid synthase	Homo sapiens	170-174
27599525-0	2017	Selumetinib Attenuates Skeletal Muscle Wasting in Murine Cachexia Model through ERK Inhibition and AKT Activation.	AZD 6244	0-11	mitogen-activated protein kinase 1	Mus musculus	80-83
28179307-0	2017	Selumetinib Inhibits Melanoma Metastasis to Mouse Liver via Suppression of EMT-targeted Genes.	AZD 6244	0-11	IL2 inducible T cell kinase	Mus musculus	75-78
28179307-1	2017	AIM: We investigated the therapeutic effects of a mitogen-activated protein (MEK) inhibitor, selumetinib, in a hepatic melanoma metastasis model and studied its possible mechanism of action.	AZD 6244	93-104	midkine	Mus musculus	77-80
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	integrin alpha 5 (fibronectin receptor alpha)	Mus musculus	144-160
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	integrin alpha 5 (fibronectin receptor alpha)	Mus musculus	162-167
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	jagged 1	Mus musculus	170-178
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	jagged 1	Mus musculus	180-184
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	zinc finger E-box binding homeobox 1	Mus musculus	187-223
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	zinc finger E-box binding homeobox 1	Mus musculus	225-229
28179307-7	2017	Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1).	AZD 6244	30-41	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	279-287
27889832-0	2017	Effects of cytochrome P450 (CYP3A4 and CYP2C19) inhibition and induction on the exposure of selumetinib, a MEK1/2 inhibitor, in healthy subjects: results from two clinical trials.	AZD 6244	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-34
27889832-0	2017	Effects of cytochrome P450 (CYP3A4 and CYP2C19) inhibition and induction on the exposure of selumetinib, a MEK1/2 inhibitor, in healthy subjects: results from two clinical trials.	AZD 6244	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
27889832-0	2017	Effects of cytochrome P450 (CYP3A4 and CYP2C19) inhibition and induction on the exposure of selumetinib, a MEK1/2 inhibitor, in healthy subjects: results from two clinical trials.	AZD 6244	92-103	mitogen-activated protein kinase kinase 1	Homo sapiens	107-113
27889832-8	2017	CONCLUSIONS: Co-administration of CYP3A4/CYP2C19 inhibitors will likely increase exposure to selumetinib, while CYP3A4 inducers will likely reduce its exposure.	AZD 6244	93-104	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-40
27889832-8	2017	CONCLUSIONS: Co-administration of CYP3A4/CYP2C19 inhibitors will likely increase exposure to selumetinib, while CYP3A4 inducers will likely reduce its exposure.	AZD 6244	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
27599525-0	2017	Selumetinib Attenuates Skeletal Muscle Wasting in Murine Cachexia Model through ERK Inhibition and AKT Activation.	AZD 6244	0-11	thymoma viral proto-oncogene 1	Mus musculus	99-102
27599525-2	2017	Previous clinical trials showed that treatment with MEK inhibitor selumetinib resulted in skeletal muscle anabolism.	AZD 6244	66-77	midkine	Mus musculus	52-55
27599525-8	2017	Muscle wasting was attenuated and the expression of E3 ligases, MuRF1 and Fbx32, was inhibited following selumetinib treatment of the gastrocnemius muscle.	AZD 6244	105-116	tripartite motif-containing 63	Mus musculus	64-69
27599525-11	2017	Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group.	AZD 6244	127-138	mechanistic target of rapamycin kinase	Mus musculus	52-56
27599525-11	2017	Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group.	AZD 6244	127-138	thymoma viral proto-oncogene 1	Mus musculus	44-47
28149280-0	2016	The MEK-Inhibitor Selumetinib Attenuates Tumor Growth and Reduces IL-6 Expression but Does Not Protect against Muscle Wasting in Lewis Lung Cancer Cachexia.	AZD 6244	18-29	interleukin 6	Homo sapiens	66-70
27599525-11	2017	Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group.	AZD 6244	127-138	mitogen-activated protein kinase 1	Mus musculus	79-82
27599525-11	2017	Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group.	AZD 6244	127-138	forkhead box O3	Mus musculus	84-90
27599525-11	2017	Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group.	AZD 6244	127-138	glycogen synthase kinase 3 beta	Mus musculus	96-104
27599525-12	2017	These indicated that selumetinib effectively prevented skeletal muscle wasting in cancer cachexia model through ERK inhibition and AKT activation in gastrocnemius muscle via cross-inhibition.	AZD 6244	21-32	mitogen-activated protein kinase 1	Mus musculus	112-115
27599525-12	2017	These indicated that selumetinib effectively prevented skeletal muscle wasting in cancer cachexia model through ERK inhibition and AKT activation in gastrocnemius muscle via cross-inhibition.	AZD 6244	21-32	thymoma viral proto-oncogene 1	Mus musculus	131-134
27599525-13	2017	The study not only elucidated the mechanism of MEK/ERK inhibition in skeletal muscle anabolism, but also validated selumetinib therapy as an effective intervention against cancer cachexia.	AZD 6244	115-126	midkine	Mus musculus	47-50
27599525-13	2017	The study not only elucidated the mechanism of MEK/ERK inhibition in skeletal muscle anabolism, but also validated selumetinib therapy as an effective intervention against cancer cachexia.	AZD 6244	115-126	mitogen-activated protein kinase 1	Mus musculus	51-54
28149280-0	2016	The MEK-Inhibitor Selumetinib Attenuates Tumor Growth and Reduces IL-6 Expression but Does Not Protect against Muscle Wasting in Lewis Lung Cancer Cachexia.	AZD 6244	18-29	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
28149280-5	2016	The mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) inhibitor Selumetinib has been tested in clinical trials for various cancers.	AZD 6244	91-102	mitogen-activated protein kinase kinase 7	Homo sapiens	4-74
28149280-5	2016	The mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) inhibitor Selumetinib has been tested in clinical trials for various cancers.	AZD 6244	91-102	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
28149280-6	2016	Moreover, Selumetinib has also been shown to inhibit the production of IL-6.	AZD 6244	10-21	interleukin 6	Homo sapiens	71-75
28149280-12	2016	Treatment with Selumetinib reduced tumor mass and reduced circulating and tumor IL-6; however MEK inhibition did not preserve muscle mass.	AZD 6244	15-26	interleukin 6	Homo sapiens	80-84
28670440-4	2017	Using this approach, we find that 75% of melanoma cell lines can be treated with either the MEK inhibitor AZD6244 or the HSP90 inhibitor 17AAG.	AZD 6244	106-113	mitogen-activated protein kinase kinase 7	Homo sapiens	92-95